Evomoz notes

Anatomy
Surgery
ENT
Ophthalmology
Orthopaedics
Gen. Radiology
CHAPTER 1

ANATOMY
Cranial Nerve Columns
Motor
"SAVE VA SAVE VASE" Afferent Efferent
Sensory

SSA SVE SVA GSA GVE GVA GSE

Special senses Muscles of Sensory supply to General To glands Autonomic
To muscles
pharyngeal arch tongue Sensory sensations
"Swaad"

1 5 - 5 3 NTS 3,4,6
Trigeminal Nucleus tactus
Smell solitarius Extra-ocular muscles
(Face)
LR⁶SO⁴O³
2 7 7 7 7 7
Vision Ant 2/3 12
8 9 9 9 9 9 Hypoglossal n.
Tongue
Vestibulo- Post 1/3 Jacobson's
cochlear (middle ear)
nerve 10 10 10 10 10 11
Posterior most Arnold's Spinal Acc. nerve
(uvula & soft palate) (External ear) Trapezius

Columns for 3rd CN : GVE and GSE

For 7, 9, 10 CN : All except first and last (SSA and GSE)

Olfactory, Optic, Vestibulo-cochlear

EOM, Hypoglossal
7,9,10 + SAN + trigeminal

GVE/Parasympathetic supply
Cranial nerve Preganglionic Postganglionic
parasympathetic Ganglion parasympatehtic Structures supplied
nucleus

Edinger-Westphal Ciliary ganglion Nasociliary nerve Ciliary muscles

nucleus CN III Short ciliary nerves
Pterygopalatine Lacrimal gland
ganglion Maxillary nerve
Superior salivatory
CN VII Sublingual and
nucleus Submandibular Lingual nerve
ganglion submandibular glands

Inferior salivatory Auriculotemporal Parotid gland

CN IX Otic ganglion
nucleus nerve (Frey's Sx) "Par-Otic gland"
Dorsal motor
CN X Vagal Nerve Heart, lungs upper GI
nucleus
 Ciliary Ganglion
EW nucleus
III nerve
Sphincter pupillae & Ciliaris muscles

Pterygopalatine Ganglion
GPN
Sup. Sal. Nu Lacrimal gland
VII nerve

Chorda tympani nv Submandibular & sublingual gland

Submandibular Ganglion
Inf. Sal. Nu
IX nerve Otic Ganglion
Parotid gland

Dorsal nu of X

X nerve
Smooth muscles & glands of thorax and abdomen

Parasympathetic outflow-craniosacral outflow-III, VII,IX, X, S2, S3, S4

Sympathetic outflow-thoracolumbar outflow-T1 to L2 nerve

Gray and white mater communicantis

Gray is post-ganglonic and unmyelinated Gray Mater White Mater
White is myelinated and preganglionic Contains neuronal Contains myelin
cell bodies sheath (fibres)
Outer part in brain Inner part in brain
Inner part in Spinal Outer part in spinal
cord cord

Trigeminal Nuclei

Centre for jaw reflex

Mesencephalic nu. Proprioception
Only site for pseudo-unipolar neuron in CNS

Principal sensory nu. Touch & pressure

Touch in face is more sensitive

Spinal nu. Pain & temperature

Spines cause pain
 Posterior triangle of neck

Facial branch Mastoid branch

Great auricular nerve

GAN thickened in Leprosy patient
Root value: C2-C3
Runs with EJV
Supplies lobule of ear
Supplies skin at angle of mandible & parotid region
In Frey’s syndrome- ATN communicates to GAN
Injured in parotid Sx - sensory loss in shaving area

Spinal accessory nerve

Runs between investing layer and pre-vertebral layer
Injury in posterior triangle
SCM spared and Trapezius affected
Difficulty in shrugging of shoulder
Difficulty in retraction of scapula
Difficulty in overhead abduction

Cross section at neck

RLN –Tracheo-esophageal groove

X nerve-Inside carotid sheath

Sympathetic chain-between carotid sheath and prevertebral fascia

Phrenic nerve - Ant to scalenus anterior & posterior to PVF

Roots of brachial plexus - between Scalenus anterior and medius

Ansa cervicalis (most commonly damaged in

injury to carotid sheath)

Contents
CCA IJV 1. CCA
2. ICA
X 3. IJV
4. X nerve

Sympathetic chain

Modifications of deep cervical fasica of neck

1. Pre-tracheal fascia : encloses the trachea and thyroid gland
2. Investing layer
3. Pre-vertebral layer : Surrounds the vertebral coloumn and scalene muscles
4. Carotid sheath
Cavernous Sinus

Through the walls Through the sinus

CN 3 (oculomotor) CN 6
CN 4 (trochlear) ICA (hence, Pulsatile
CN 5¹ (Opthalmic div) proptosis seen in
CN 5² (Maxillary ) Carotidocavernous fistula)

Sella turcica
Sellar mass : Pitutary adenoma
Supra-sellar mass : Craniopharyngioma

II

III

IV

VI

XII
IX, X, XI
Sphenoid bone

Lesser wing
Greater Maxillary branch of
wing Sella F. Rotundum
turcica trigeminal nerve nerve (V²)
F.ovale
F. Lacerum
F. Spinosum
MALE through ovale
Middle meningial artery 1. Mandibular branch of
(Injured in EDH) trigeminal nerve (V³)
Nervus spinosum 2. Acc. meningial artery
3. Lesser petrosal nerve
4. Emissary veins

Epidural Hematoma (EDH)

Injury to anterior MMA
Landmark : Pterion
Lemon shaped
Doesn't cross suture lines
Crosses midline

Parietal Frontal

Pterion
Sup. Orbital fissure
Between greater and lesser wing of sphenoid

LFT SoNIA Squamous part of Greater wing of Sphenoid

Outside Inside temporal bone

Lacrimal n Sup. Oculomotor

Frontal n Naso'ciliary Relations of the pterion
Trochlear n Inf. Oculomotor Anterior division of the middle
+ Abducens
meningeal vessels
Opthalmic vein
Middle cerebral vessels
Sylvain fissure
Insula
Optic canal Broca's motor speech area (on the left)
In lesser wing of sphenoid
Optic nerve
Opthalmic artery
Temporal bone

Bill's bar

7 Sup vest
nerve
Falciform
Squamous
part crest
s pa
rt Cochlear Inferior
ou
Pe
tr
nerve vest n

"7 Up Coke down"

External acoustic
meatus
Squamous part of
Tympamic part of temporal bone
temporal bone
Zygomatic process
Mastoid part of
temporal bone
Styloid process
Mastoid process

Occipital bone

Jugular foramen is divided by jugular spine

Pars nervosa : 9th CN + Inf petrosal sinus
Pars vascularis : 10th CN, 11th CN and IJV

Phelp's sign
Destruction of Jugular spine in Glomus Jugulare
Cranial Foramina

Cribriform plate (olfactory n.)

Optic canal
Sup. Orbital fissure
Rotundum
Ovale

Spinosum

F. Lacerum
F.
Magnum
Int. Aud. Meatus

Jugular foramen

Hypoglossal canal.
(12th CN)

FORAMEN LACERUM
At junction of
1. Sphenoid bone
2. Apex of the petrous temporal bone
3. Basilar part of the occipital bone

Traversing structures Fills UP

1. Meningeal branches of 1. ICA
ascending pharyngeal art. 2. Sympathetic plexus
2. Emissary veins 3. DPN
4. GPN

Cranial Nerves
Trochlear nerve
Dorsal origin
Longest intra-dural : Abducents Nerve (dorello's canal)
Internal decussation
Longest intra-osseus : Facial Nerve
Longest intracranial course
Thinnest and smallest

Rule of 17
12 + 5 palsy : Ipsilateral deviation
10 + 7 palsy : Contralateral deviation "Messi and Ronaldo cross contra-lateral"
Pharyngeal clefts and pouches

Clefts

Obliterates

Pouch :
Mesoderm Endoderm Persistence Only 1st cleft forms
1. External auditory canal
Branchial cyst 2. Outer layer of tympanic membrane
Cleft :
Ectoderm

Pouches
Pharyngeal 1st pouch - Middle ear cavity, eustachian tube & mastoid antrum
membrane
2nd pouch - Palatine 2onsil
Site where cleft meets pouch Most common micro-
(1st pharyngeal memb. forms 3rd pouch- Thymus & inferior parathyroid gland deletion syndrome
tymp membrane) DiGeorge syndrome
4th pouch- Superior parathyroid gland
(22q11 deletion syndrome)
Remnant of 5th pouch - Ultimobranchial body
Pharyngeal arches and derivatives

1st arch (M) 2nd arch (S) 3rd arch

Mandibular nerve (V3) Facial nerve (VII) Glossopharyngeal nerve (IX)
Maxillary artery Stapedial artery CCA and ICA

Maxilla and Mandible

Malleus and Incus Stapes (Stapedius muscle) Body and greater horn of hyoid
ZygoMatic bone Styloid process Stylopharyngeus
SphenoMandibular ligament Lesser horn of Hyoid

Muscles of mastication Muscles of facial expression, Buccinator

Mylohyoid Stylohyoid
Anterior belly of digastric Posterior belly of digastric
Tensor veli palatini Platysma, Stapedius

4th arch 6th arch

Vagus and SLN Vagus and RLN
On left : ARCH of Aorta Pulmonary artery
On right : Proximal part of subclavian artery Ductus arteriosus on left side

All soft palate muscles (except TVP) All muscles of Larynx (except Cricothyroid
All muscles of pharynx (except - stylopharyngeus by 4th arch)
by 3rd and cricopharyngues by 6th) Cricopharyngeus
Cricothyroid

3rd arch Stylo-pharyngeus

4th arch
6th arch Crico-pharyngeus 🔁 Crico-thyroid

Dysphagia lusoria Zenker's Diverticulum

Aberrant right subclavian artery
Pulsion pseudo diverticulum in Killian's
Defect in 4th arch
dehiscence
Seen in elderly
Boyce sign
Because thyropharyngeus and
cricopharyngeus have different nerve supply
(different origin)
T/t : Dohlman Procedure

Crico-thyroid
Only Tensor and Adductor of vocal cords
Because 4th arch derivative, supplied by SLN (other muscles by RLN)
In b/l RLN palsy, there is unopposed adduction - Emergency
Tongue

Genioglossus aka Safety muscle of tongue

(doesn't allow tongue to fall back)
Hyoglossus is the only depressor
(towards hyoid)
All muscles supplied by 12th CN except
Palatoglossus (supplied by pharyngeal plexus)

Safety muscles
Tongue - Genioglossus (Genie)
Larynx - Posterior crico arytenoid (ACP)

Development of tongue
MUSCLES - Occipital myotomes (except palatoglossus)
Anterior 2/3 : 1st arch (along with tuberculum impar)
Posterior 1/3 : 3rd arch (hypobranchial eminence)
Genio-hyoid
Posterior most : 4th arch (hypobranchial eminence)
Genio-glossus
Hyo-glossus
Stylo-glossus

Lingual Nerve

Posterior most (4th arch)

Both taste and sensation by
Vagus nerve

Posterior 1/3rd (3rd arch)

Both taste and sensation by
glossopharyngeal nerve

Division of mandibular nerve Anterior 2/3rd (1st arch)

Moves along with chorda tympani (both supply Taste : Chorda tympani
Sensation : Lingual nerve
ant 2/3 tongue)
Most likey to get damaged in sub-mandibular Anterior → Posterior
gland resection
Inserts into hyoglossus muscle 7 → 9 →10
Muscles of mastication

Temporalis
Lateral pterygoid

Masseter Medial pterygoid

All derived from 1st pharyngeal arch

All supplied by Mandibular nerve (except Medial pterygoid - Trigeminal)
All elevators except Lateral pterygoid "LP Lowers"
All protractors except Temporalis which is retractor
Accessory masticator muscle is Buccinator
Structures around 3rd ventricle

Roof of 3rd ventricle

Body of fornix
Corpus
Anterior relations of callosum Choroid plexus
3rd ventricle Body
Septum
pellucidum
Anterior commissure Posterior relations of 3rd ventricle
First commisure to develop
Corpus
Lamina terminalis callosum
Remnant of ant. neuropore spleenium Habenular commissure
III VENTRICLE Pineal gland (aka epithalamus)
Posterior commisure
Floor of 3rd ventricle mid- SC
Aqueduct
brain IC

Optic chiasma
Infundibulum
Mamillary body Pons
IVth
Posterior perforating ventricle
substance

Medulla

Sagittal Section of Brain

Fornix

3rd Ventricle

MB IV nerve

Pitutary VII nerve

Sphenoid Pons
sinus

Medulla
Basilar artery

Fornix connects Hippocampus to Mamillary body

Types of White Mater fibres

Commisural (Connects two hemispheres)

Corpus callosum Parts of corpus callosum
Ant. Commisure
Post. Commisure body
Habenular commisure
Hippocamp. fibres of fornix genu

Assocaition (within same hemisphere) rostrum splenium

Arcuate fasciculus
Sup/inf longitudinal fasciculi
Fornix
Cingulum

Projection (Cortex to deeper structures) R Rostrum

Cortico-spinal tracts G Genu
Cortico-bulbar tract B Body
Optic radiation S Spleenium
Internal capsule
Corona radiata

Limbic System (Papez circuit)

A neural circuit for the control of

emotional expression and memory.
1. Fornix
2. Hippocampus
3. Mamillary body
4. Cingulate gyrus
5. Subiculum
6. Anterior thalamic nuclei

Went to single,
wanted to buy "sab" TERMINATION OF FORNIX
but met aunty. ORIGIN OF FORNIX
Coronal section of brain

Septum pellucidum

Corona radiata Body of Caudate nucleus

Fornix & Choroid plexus

Thalamus

Substantia Nigra

Lentiform nucleus

Forceps minor

Insula

Caudate nucleus
Lentiform nu
Internal capsule
Thalamus

Tapetum

Forceps major

Bulb of post horn of

lateral ventricle
Vascular anatomy of brain

Anterior
Doesn't participate in Middle Cerebral
Circle of Willis Cerebral A2 artery
artery
Enters Lateral sulcus
A1

Direct branch of ICA

Posterior P1 Part of Anterior
Cerebral artery circulation
P2

Superior Cerebellar artery

Anterior Inferior
Cerebellar artery

Runs in internal
acoustic meatus
Posterior Inferior
Cerebellar artery

Circle of Willis aneurysms

ACA and ACOM

Most common location of Berry aneurysm
(aka Saccular aneurysm)
Pressure on optic chiasma can lead to BTHA

PCA and PCOM

Most common aneurysms to "rupture"
Pressure on 3rd CN that runs between PCA and SCA
(Ipsilateral down and out eye)
Blood supply of brain

Blood supply of Cerebral Cortex

ACA
ACA
MCA

PCA
PCA
MCA

Corpus Callosum supplied by

ACA along with ACOM

Blood supply of internal capsule

ACA : Recurrent artery of Heubner (longest)

MCA : Lenticulo striate branch aka Charcot's

ACA and MCA same as anterior limb

Direct branch from internal carotid

MCA : Charcot's artery

Anterior choroidal artery (branch
of Int. Carotid)
Posterolateral branches of PCA

MCA supplies all

Blood supply of dura mater

Anterior cranial fossa : MMA

Middle cranial fossa : MMA
Posterior cranial fossa : Posterior meningial
artery (branch of asce. pharyngeal artery)
Spinal Tracts

Descending tracts Ascending tracts

Pyramidal tract
Cortico - spinal : Voluntary motor control
Cortico- bulbar : Voluntary motor of face, Spino-thalmaic tracts
head, neck.
(Antero-lateral system)
Pain, temperature, crude touch
Extra-pyramidal CS tratcs Crosses over at level of spinal cord
Rubro-spinal : Fine motor
Tecto-spinal : Head-coordination
(tecto : Head in Greek)
Reticulo-spinal : Maintains tone
Vestibulo-spinal : Balance

Brown Sequard Syndrome

Hemi-section of spinal cord
Contra-lateral spino thalamic tract affected
below the level (crosses at level of spinal cord)
Ipsi-lateral dorsal coloumn affected
UMN below the level Dorsal coloumn medial lemniscus pathway
LMN at level of lesion Fine touch, vibration
Conscious proprioception,
Crosses at level of medulla

Spino-cerebellar pathway
Unconscious proprioception
Cerebellum

Cerebellar Cortex Deep Cerebellar

Cerebellar Cortex is the largest collection of inhibitory fibres. Nuclei
Granny (granular cells) is excited to meet mausi (mossy)
D Dentate
Afferents E Emboliform
1. Olivocerebellar & paraolivocerebellar tract are CLIMBING FIBRES G Globose
2. Rest all are MOSSY F Fastigeal
Don't even give fucks

"Mausi will only go to excited olives (like grapes) Efferents most commonly
granny, who stays in ground floor" are climbers
are via Dentate nucleus
Fastigeal is the oldest
Efferents
Purkinje Cells → Deep Cerebellar Nuclei → Efferent from cerebellum deep Cerebellar nuclei

Molecular layer : Basket and stellate cells

Cerebellar Peduncles
Purkinje Layer : Purkinje cells
Superior Cerebellar Peduncle Granular layer : Granule cell and Golgi cells
Dentato-thalamic and Dentato-rubro-thalamic tracts
Ventral spinocerebellar tract

Middle Cerebellar Peduncle

Largest Peduncle
Purely afferent (Cortico-ponto-cerebellar tract)

Inferior Cerebellar Peduncle

Everything else
PURKINJE CELLS

Central part of cerebellum

↓
Vermis
(Maintains truncal balance)

Lateral part of cerebellum

↓
Hemispheres
(Fine movement of limbs)
Basal Ganglia

Cerebral cortex

Caudate nucleus
Striatum
Putamen
Athetosis : Globus Pallidus
Thalamus Chorea : Caudate (Striatum)
Hemiballismus : Sub tHalamic nucleus
Globus pallidus

Subthalamic nucleus

Substantia nigra

Direct pathway
Dopamine acts on D-1 receptor (+)
Striatum inhibits GpI
GpI doesn't inhibit thalamus : Movement
(Double negative is positive)

Indirect pathway GPi (interns inform

Dopamine acts on D-2 receptor (-) the thalamus)
Striatum via a long path excites GpI
GPe (externs
GpI inhibits thalamus : No movement take more time
and do nothing)
No offense, just a
mnemonic!

Parkinsonism
Dopamine : Acetylcholine balance distorted
Direct pathway reduced and indirect pathway increased

Huntington's Chorea
Indirect pathway affected
Tri nucleotide repeat disorder (CAG)
 Thalamic Connections
Inferior col

Mamillary
bodies
Medial nuclei Auditory
MGB
Music cortex

ATN Internal medullary lamina

Papez circuit LGB Visual
Cingulate Ventro- Ventro- Ventro- Light
gyrus anterior posterior cortex
lateral
nucleus nucleus nucleus

Superior col.
Basal Pre Motor Spino- Sensory
Ganglia Cortex thalamic cortex
tract

Superior Motor Posterior : Painful

Cerebellar Cortex
VPM : very painful mouth
peduncle
VPL : very painful limbs
Efferents from cerebellum
Dentato-thalamic
Dentato-rubro-thalamic
From superior Cerebellar peduncle

Hypothalamic Nuclei

Lateral Nucelus Supraoptic nucleus

Hunger and Anger (Ghrelin) ADH release
"Makes you grow laterally" SAD POX

Venteromedial Nucelus Para-ventricular nucleus

Satiety (Leptin) Oxytocin release
Opposite of Lateral nucleus SAD POX
Neurohypophysis
Anterior Nucelus SupraChiasmatic nucleus
Cooling Melatonin release
AC - Anterior cooling Circadian - Chiasmatic
Adenohypophysis

Posterior Nucelus Pre-Optic nucleus

Heat generation GnRH release Anterior pitutary - Surface ectoderm
Opposite of anterior Pre gonadotropin hormone Posterior pitutary - Neuro ectoderm
Brain Stem - Ventral aspect

Crus cerebri
Connects pons to
cerebral hemispheres
Midbrain

III
IV
CN 4 originates from dorsal side
Pons
On midline : 3,4,6,12 (Multiples of 12)
V VI CN 11 : Spinal acc. Nerve (supplies SCM and Trapezius)
VII
VIII
IX
Pyramids
Olives

X
XI

XII

Midbrain stroke syndromes

Multiples of 12
Involves 3rd CN (Ipsilateral down and out pupil)
PCA stroke
eber's

Spino -cerebellar tract

1. Weber's (only 3rd CN involved)

Spino-thalamic tract
3

Sympathetic coloum
3,4 3,4
2. Benedict (3rd CN + Red nucleus) Red hair Benedict Dorsal coloumn
Cortico-spinal

3. Claude (3rd CN + Red + hemi-ataxia) A + B + C

MLF

4. Parinaud (upward gaze palsy) Pari is above 6 5,7,8

5,6,7,8

Pontine stroke Syndromes 12 9,10,11

1. Millard + Gubbler (6th + 7th) Count letters 9,10,11,12
2. Foville (6th +7th + 8th + INO) Fov-ALL
3. Raymond (only 6th) 6th is common like Raymond
M S
MLF (INO) Sensory
Motor : Cort-spinal (Spinothalamic)
Medulla stroke Syndromes (weakness) Spino-cerebellar
Medial lemniscus Sympathetic
Medial medullary syndrome
coloumn (Horner's)
Dejerine Sx
I/L tongue deviation (12th)
Anterior spinal artery > Vertebral artery

Lateral medullary syndrome

WaLLenberg Sx
10th cranial nerve symptoms
Vertebral artery > PICA
Brain Stem - Dorsal aspect (Floor of ventricles)

SC
Quadrigeminal
plate
IC
IV

Abducens nuclei is surrounded by

SCP LMN of 7th nerve
Injury to this area causes LMN palsy
MCP Facial colliculus of facial nerve
Vestibular area
XII Trigone
MCP doesn't ICP
form boundary Xth trigone
6-8-12-10

Cranial Nuclei at the floor of 4th ventricle

VI, VIII, X & XII (not 7th)

Dural venous sinus anatomy

Internal cerebral veins
( Deep veins)
↓
Combine with
Vein of Rosenthal
↓
Vein of Galen
(aka great cerebral vein)
↓
Combines with ISS
↓
IJV Straight sinus
Sinuses meeting at confluence
↓
Vein of Galen malformation T Transverse sinus
Confluence of
O Occipital sinus
sinuses
S Straight sinus
↓
S Sup. sagittal sinus
Transverse sinus
↓
Sigmoid sinus
↓
Combines with superior
and inferior petrosal
sinus to drain into IJV
Cerebral cortex

Primary motor cortex (4) Primary somatosensory

cortex (3,1,2)

Frontal eye field (8)

Broca's
Broca's speech area of Primary Visual Start seeing
left hemisphere (44, 45) cortex (17) people at 17

auditory association cortex (22)

Wernicke's
Primary auditory cortex (41,42)
Heschl's Gyrus

Brodman area 22
Brodman area 44/45 Superior temporal gyrus
Inferior frontal gyrus Inferior branch of MCA
Superior branch of MCA
Wacky speech,
"Broken speech" can't understand,
but can understand hence can't say
Fluency → Frontal lobe
Fertilisation and implantation

Day 1 Zygote

Day 4 Morula (16 celled)

Day 5 Blastocyst (fluid filled)
Day 6 Zona hatching
Day 7 Implantation

Inner cell mass forms epiblast and Endometrium

hypoblast (bilaminar embryonic disc)

Epiblast forms Amniotic cavity

Hypoblast forms primitive Yolk sac

Blastocyst cavity
(forms yolk sac)
GASTRULATION -3rd week
Epiblast replaces hypoblast via primitive Hypoblast
streak to form endoderm and mesoderm Embryonic disc
Epiblast
Epiblast cells then form the ectoderm
Amnion
Amniotic cavity

Trophoblast Cytotrophoblast
Syncytiotrophoblast

Sacro-coccygeal teratoma
Persistence of cells in primitive streak

NEURULATION - 4th week

Cells of primitive streak in mesoderm get
modified to form notochord
(blastospore - n. process - n.canal - n. plate)
Notochord stimulates ectoderm to form
neural tube

Pre-chordal plate Heart starts beating in 4th week of development

Modification of endoderm near the cranial end. Pre-embryonic phase : 1st 2 weeks
Forms buccopharyngeal membrane that forms oral cavity Cap of sperm : Golgi apparatus

Anterior neuropore : Lamina terminalis

Posterior neuropore : Terminal ventricle
Embryology
Remnants of Notochord
NCC Nucleus pulposus
Apical ligament of Dens
Tectorial membrane

Intermediate
mesoderm Para-axial Lateral plate
Notochord
mesoderm mesoderm
Forms
urogenital Axial skeleton SOMATO-PLEURIC
system Skeletal muscles Appendicular skeleton
(except pharyngeal arches) Dermis of front
Dermis of back
SPLANCHNO-PLEURIC
Smooth muscles
Dura mater
Cardiac muscles
RES - Spleen, Microglia

Somites

Adrenal cortex : Mesoderm

Neuro-ectoderm derivatives NCC derivatives Adrenal medulla : NCC
Brain & spinal cord
M Melanocytes Dura : Mesoderm
Oligodendrocytes (myelination in CNS)
O Odontoblasts (tooth) Leptomeninges : NCC
Astrocytes (various functions)
Ependymal cells (production of CSF)
T Tracheal cartilages
E ECL cells (stomach) Anterior pitutary : Surface-ect.
Retina & pigment L Leptomeninges Posterior pitutary : Neuro-ect.
Iris and its muscles
P PNS ganglia (Hirschprung dis.) Enamel/Ameloblast : Surface-ect.
Pineal gland Dentin/Odontoblast : NCC
A Adrenal medulla
Posterior pitutary (SAD POX) S Schwann cells
Sphincter/dilator pupillae : Neuro-ect
S Spiral septum Cilliaris : NCC
E Endo-cardial cushions EOM : Mesoderm
Surface-ectoderm derivatives S Skull cartilages
Lens Everything in brain from
Epithelium of Cornea, Conjunctiva neuroectoderm, except Microglia
Lacrimal, Tarsal glands (macrophages in brain)
Everything in abdomen from
PSM glands (Parotid, Sweat, Mammary)
All three derm layers endoderm, except Spleen
Anterior pitutary Tympanic membrane
Macro-glial cells : Neuro-ectoderm
Vitreous Humor
Micro-glial cells : Lateral plate
Anal canal below pectinate line
mesoderm
Epidermis
Schwann cells : NCC
Olfactory epithelium
Enamel
Urogenital system development

Development of Kidneys
A region of intermediate mesoderm, known as the urogenital
ridge, gives rise to urogenital system.

Pronephros formed initially in cervical region of the embryo

(degenerates eventually)
Mesonephros forms -
(a) Mesonephric duct (Wollfian duct)
(b) Ureteric bud (forms collecting system)
Ureteric bud induces formation of metanephric blastema
(forms the excretory part)

The definitive kidney (metanephros) develops in the pelvic

region before ascending into the abdomen.

Development of Bladder and Urethra

The bladder and urethra are derived from cloaca – a hindgut Allantois
structure (endoderm)
Cloaca Urorectal
The cloaca is divided by uro-rectal septum into urogenital sinus septum
(anterior) and anal canal (posterior) Cloacal
Hindgut
membrane
Uro-genital sinus
Upper part forms the bladder (except trigone, which is formed
by collecting system)
Pelvic part forms entire urethra in female, posterior urethra
in males
Phallic part forms the anterior urethra in males

Allantois
The urinary bladder is initially drained by the allantois.
Obliterated during fetal development and becomes a
fibrous cord – the urachus
Urachus forms : median umbilical ligament

Mullerian : Paramesonephric (females) Genital swelling (sac) Summary

Wolffian : Mesonephric (males) Scrotum Kidney till DCT : Metanephric blastema
Labia majora Collecting system and trigone of
Wolffian Mullerian bladder : Mesonephric duct
Genital ridge (rizz)
Seminal vesicles Fallopian tube Testes Bladder, urethra : Uro-genital sinus
Ejac. duct Uterus Ovaries
Trigone Cervix
Post. urethra Upper 2/3 of vagina Genital fold (2° sac) Umbilical ligaments
Para-oopheron Ventral urethra
Prostatic utricle Labia minora Median : Urachus
Ep-oopheron Appendix of testes MediAL : Umbilical artery
Gartner's cyst (hydatid of Morgagni) Genital tubercle (tube) Lateral : Inf. Epigastric artery
PEG PAt Glans penis
Clitoris
Lig teres hepatis : Left umb. vein
CVS Embryology

Ventricles
Rough part of left : Primitive ventricle
Rough part of right : Bulbus cordis
Smooth part of both : Bulbus cordis

Atria
Rough part of both : Primitive atria
Smooth part of right : Sinus venosus + Right horn
Smooth part of left : Primitive pulmonary veins

Other structures
Left horn : Coronary Sinus
Truncus arteriosus : Roots of great arteries

Inter - atrial septum Inter - ventricular septum

Septum primum formed first
Osteum primum is the opening between septum
primum and endocardial cushions (crucial for right
to left shunt in fetal circulation)

Ventricular septum has "2 components"

Muscular component
Eventually osteum primum is obscured. Cardiac muscles
Osteum secundum formed in upper part of septum
primum as fnestrations Membranous component (NCC derivatives)
Spiral septum : IV septum
Endocardial cushions : AV septum

New septum secundum formed that covers osteum

secundum.
This forms a one way valve known as foramen ovale

Depression : fossa ovalis

Surrounded by : limbus fossa ovalis
When left atrial pressure increases on birth,
foramen ovale is closed.
Fossa ovalis is a depression formed by osteum
secundum (has septum primum as base)
Limbus fossa ovalis formed by septum secundum
(surrounds fossa ovalis)
IVC development

Supracardinal
Infra-renal IVC
Azygous vein
Hemi-azygous vein
Sub cardinal vein
Sub supra anastomosis
Sub cardinal vein Supracardinal
Supra-renal IVC
Gonadal veins
Cardinal veins
Left renal vein

Sub supra anastomosis

Renal IVC

Left Inferior Phrenic vein

Right Inferior Phrenic vein

Hepatic Veins
Right Supra-renal Vein
Left Supra-renal Vein

Right Renal Vein.

Left Renal Vein

Left Gonadal Vein

Right Gonadal Vein-

Right Lumbar Veins Left Lumbar Veins

Median Sacral
Vein
Common Iliac
Veins
GI embryology

Foregut
Till second part of duodenum
Vagus nerve
Stomach rotates by 90°

Midgut
Till 2/3 of transverse colon
At transpyloric plane
Vagus nerve
Rotates 270° anticlockwise (90+180)
Physiological herniation at 6 weeks and
back by 12 weeks

Hindgut
Pelvic plexus
Till Pectinate line of rectum

Superior rectal a.
(branch of IMA) Superior rectal v.
Trans-pyloric plane (L 1) Drain to internal
Visceral innervation
iliac LN
Sub-costal plane (L 3)

Umbilicus (L4- L5)

Inter- tubercular plane
(L 5)

Pectinate
line

Trans-Pyloric plane (L¹)

Origin of (Renal arteries, SMA, Portal vein)
Neck of pancreas Somatic innervation Inferior Inferior Drain to
(Pudendal nerve) rectal a. rectal v. superficial
Hilum of kidney
(branch of inguinal LN
Duodeno-Jejunal flexure pudendal artery)
Termination of spinal cord

Rotation of stomach
The rotation of stomach leads to formation
of greater and lesser sac.
Connection between greater and lesser sac
is known as epiploic foramen

Boundaries of epiploic foramen

(aka Foramen of Winslow)
Superioirly Caudate lobe of liver
Inferioirly 1st part of duodenum
Anteriorly hepato-duodenal ligament
Posteriorly IVC, adrenals
Pringle's manuevere
 Development of Diaphragm

Central Tendon

Crura

Pleuro-
peritoneal
Body wall membrane
mesoderm

Embryologic origin
Muscular part : Body wall mesoderm
I 8 IVC (T8) + Rt phrenic nerve Central tendon : Septum transversum
Central tendon Crura : Dorsal mesentery of esophagus

10 Esophagus (T10) + both Vagus

Persistence of Pleuroperitoneal canal
eggs + Gastric artery (lt)
Muscular part
Bochdalek foramen
AT Aorta, Thoracic duct (T12) +
12 Azygous and hemiazygous vein
Congenital Diaphragmatic Hernia
Crura •Common on left side
•Complication→left lung Hypoplasia

Derivatives of mesogastrium
Derivatives of
ventral mesogastrium Diaphragm Derivatives of
dorsal mesogastrium

1. Triangular ligaments 1. Gastrophrenic ligament

2. Coronary ligaments 2. Gastrosplenic ligament.
3. Falciform ligament
3. Lienorenal ligament
4. Greater omentum
Lesser FaCT Bile duct
4. Lesser omentum Posterior abdominal wall
Phrenico-colic ligament
Prevents the vertical and
Ligamentum teres hepatis downward descent of spleen
(obliterated left umbilical vein)
Cleft lip and palate

Frontonasal prominence
Intermaxillary
Medial nasal process process

Nasal pit

Lateral nasal process

Maxillary prominence
Philtrum
Mandibular prominence

Medial nasal process forms the inter-maxillary process

The intermaxillary process fuses with maxillary process to form Philtrum
Failure of fusion of medial nasal process with maxillary prominence causes cleft lip
Midline cleft lip : failure of fusion of medial nasal processes to form inter-maxillary
process.

Couinaud's Liver Segments

Portal vein divides the liver horizontally

Cantlie's line separates liver into left and right
Imaginary line
aka Cholecysto-vena caval line

7 8 4a 2
Portal vein

6 5 4b 3
Cantlie's line

4b 3 4a 2
5 Portal vein 8 IVC
IVC

6 Kidney 7 Spleen

Portal vein + IVC : Inferior Only IVC : Superior

Shoulder Joint

s
roces
oid p
Greater Corac
tubercle
⬇️
Lesser tubercle

Coracoid process palpated below

⬆️ clavicle (type of atavastic epiphysis)
Base of bicipital
groove

Short head of biceps Pectoralis minor

Coraco-brachialis

SIT muscles
Supra-spinatus
Infra-spinatus
Teres minor

Adduction + Ext. rotation

Except supra-spinatus : Abduction 0-15°

MLM
Sub-capsularis
Pect major aka Forgotten Tendon
Latt. Dorsi
Teres major
Adduction + Int. rotation

Clavipectoral Fascia

Structures Piercing the Clavipectoral Fascia

1. Thoraco-acromial artery. T
2. Lateral pectoral nerve. L
3. Cephalic vein C
Lateral pectoral nerve supplies P. major

Muscles enclosed : P Minor and Subclavius

Subclavian artery

Divided into 3 parts by anterior scalene muscle

1st part
Vertebral artery
Internal-thoracic artery VIT
Thyro-cervical trunk

2nd part
Costo-cervical trunk C
3rd part
Dorso-scapular artery D

Branches of thyro-cervical trunk

Supra-scapular
Transverse cervical STI
Inferior thyroid

Superior thyroid artery is a branch of ECA

Scalenus
Anterior muscle
Blood supply : ⬇️
I
Transverse cervical : Trapezius and SCM T
(innervated by SAN)
Suprascapular : Supra-spinatus and infra-spinatus S
(innervated by supra-scapular nerve)
Phrenic nerve
(anterior to scalene
anterior muscle)

Axillary artery

Divided into 3 parts by Pectoralis minor muscle

1st segment - 1 branch

Superior thoracic 1st rib divides subclavian from axillary artery
3rd segment supplies the surgical neck of humerus
2nd segment - 2 branches
Thoraco-acromial artery
Lateral thoracic artery

3rd segment - 3 branches

Sub-scapular artery
Ant circumflex humoral
Post. circumflex humoral
Brachial artery
Divided into radial and ulnar artery at cubital fossa
Profunda brachii artery : First and largest branch of brachial artery
Ulnar artery forms the common inter-osseus artery which forms the recurrent-inter osseus artery

Cubital Fossa

lateral
MP Medial
Medial Pronator

MBBR
Medial - Lateral
(nerve artery muscle nerve)

Median cubital vein (aka anti cubital vein)

is preferred for blood draw.

Anatomical snuff box

Medial boundary : Ex P L
Lateral boundary : Ab P L, Ex P B
Ab pee le
ex bhi pee

Only content: Radial artery

Roof : Cephalic vein, Superficial br of radial n.
Also the area supplied by radial nerve
Brachial Plexus

C5 Re
tro Musculocutaneous nv.
-cl
C6 av Supplies
icu
lar Biceps
Brachialis
C7 Coracobrachialis

C8 Continues as lateral
cutaneous nerve of forearm
T1

Musculocutaneous nv.
Axillary nerve
Radial nv.
Median nerve
Ulnar nv.

Erb's Palsy

Upper trunk

C⁵ - C⁶

Axillary nerve Musculocutaneous nerve

Biceps brachi Flexion,

Deltoid BBC muscles Brachialis Supination
Abduction 15-90° Coracobrachialis
Klumpke’s palsy
Adducted Extended elbow
Lower trunk shoulder Pronated forearm

C8, T1
Medial and ulnar nerve Policeman’s tip hand
Intrinsic muscles of hand

Hyperextension at MCP
joints Flexion at IP joints
(Reverse of Lumbricals action)
CLAW HAND

T/t : Knuckle bender splint

 Ulnar Nerve

Motor Sensory
All interossei Medial 1.5 fingers (both
3rd and 4th lumbricals dorsal and palmar)
Hypothenars
Adductor policis
cUbital tunnel (GraveyADD)

Ulnar Paradox
FDP (Medial half) More prominent claw hand when injury at lower levels
than at upper level.
At upper levels (more proximal injury) FDP is paralysed -
lesser flexion and hence lesser prominent claw hand

gUyon's canal

Book test (Froment Sign)

Thumb can't adduct but
flex (Add policis affected)

Median Nerve

Motor Sensory
All flexors of forearm Lateral 3.5 fingers
AIN - deeper muscles, pure (palmar side)
motor Tips of fingers of lateral
1st and 2nd lumbricals 3.5 on dorsal side
Thenars (except Adductor
pollicis)

FDP (Lateral half) Anterior inter-

osseus nerve
FPL
"weak OK sign"
Weak OK sign Hand of Benediction Ape thumb
FDS Thumb can adduct but Can't flex lateral finger
Palmar won't flex (FPL affected) (FDP/Lumbricals affected)
Flexor retinaculum
cutaneous
branch
 Radial Nerve (C5-T1) entire brachial plexus

Motor Sensory
All extensors of arm Lateral 3.5 fingers
PIN- deeper muscles (dorsal side)
(purely motor)

TRICEPS
Extension of
elbow
M
ECRL
Wrist extensor
supplied from
above the elbow

M U
U R
PIN

SUPERFICIAL BRANCH
Cutaneous branch,
supplies the skin
(Lateral 3.5 of hand)

Nerve injuries in humeral fractures

Axillary nerve injury

Surgical neck Regimental badge sensory loss
Loss of abduction (15-90°) → supplies deltoid

Radial nerve injury

Spiral groove
Innervates all Extensor muscles of arm & forearm
Causes wrist drop
Treatment : Cock up splint

Median nerve (AIN injury)

Not directly related to Most of the Flexor muscles of forearm
humerus
Intrinsic muscles in hand
labourer's nerve

Medial epicondyle

Ulnar nerve injury

FCU (ulnar deviation ) & part of FDP (forearm)
Intrinsic muscles in hand
Lateral epicondyle Musician's nerve
Tardy Ulnar nerve injury
(LCH) Cubitus valgus deformity
 ULNAR NERVE MEDIAN NERVE
Supplies hand muscles mostly Supplies forearm flexors mostly
(musician's nerve) (Labourer's nerve)

Adductor Pollicis
Book test
Flexor digiti minimi Flexor pollicis brevis Weak OK sign
(Froment Sign)
Can't add. thumb Abductor digiti minimi Can't flex thumb
Abductor pollicis brevis
FPL intact FPL affected
Add. policis affected Opponens digiti minimi Opponens pollicis Add. policis intact
(present deeper)
Palmaris brevis
(subcutaneous)

Lumbricals and Inter-ossei

Numbering from lateral to medial
Lumbricals originate from FDP (flexor digitorum profundus) ALL INTEROSSEI-ULNAR NERVE
Inter-ossei as the name says are from bone to bone vowels stick

Lumbricals Inter-ossei

Bi-pinnate Uni-pinnate
ULNAR NERVE MEDIAN NERVE

3rd Lumbrical 2nd Lumbrical

4th Lumbrical 1st Lumbrical Palmar Dorsal

interossei interossei
muscles muscles

PAD DAB
Unipennate Bipennate
Absent on middle finger Middle finger has 2
Test - CARD test Test - EGAWA test

Knuckle bender splint

 Wrist Joint
Radio-Carpal joint
E Elbow
Distal end of ulna doesn't participate S Shoulder
in formation of wrist Joint 16 yrs H Hip
Involves 1. Radius A Ankle
2. Art. Disc
17-19 yrs Ki Knee
3. SLT carpals
19 yrs Wrist Wrist
Fuses at last 19 years

Carpal bones
Scaphoid - Lunate
Triquetrum - Pisiform
Hamate - Capitate
Trapezoid - Trapezium

The
Here Comes Appearance of ossification centres
Thumb
Pinky Capitate : 1 month (earliest)
To Long
Hamate : 2 months
So
Tri-quetrum : 3 years
Lunate : 4 years
Scaphoid : 5 years

Trapezium, Trapezoid : 6 years

Pisiform : 12 years (most late)

Elbow Joint

Medial epicondyle
Lateral epicondyle

Capitulum of humerus
Trochlea of humerus Lateral Medial Olecranon process
Olecranon process epicondyle epicondyle
Trochlear notch
Coronoid process
Radial head Appearance of oss. centres Fusion
Radial notch
2 yrs C Capitellum 14 yrs L Lateral epic.
Neck
4 yrs R Radial head 15 yrs M Medial epic.
Tuberosity of ulna 6 yrs I Internal epic. (medial) 16 yrs O Olecranon
Radial tuberosity 8 yrs T Trochlear
10 yrs O Olecranon
12 yrs E External epic. (lateral)
 Appendicular muscles of back

Dorsal
"scapular"
nerve
Arm abduction
Levator
scapulae
Trapezius
Rhomboid
Trapezius and
minor serr. anterior
SAN
SAN
LTN
Rhomboid
major

Deltoid
Latissimus Thoraco Axillary n.
dorsi "dorsal"
nerve
Supra-spinatus
Supra-scapular nerve

Winging of scapula
Inferior border of scapula moves medially or laterally.

Medial winging
Serratus anterior muscle weakness.
Long thoracic nerve dysfunction
Lateral winging
Trapezius muscle weakness.
Spinal accessory nerve dysfunction
Iliacus and psoas major

Psoas Major
Iliacus

Ilio-psoas tendon
(inserts at lesser trochanter) Psoas abscess
(Seen in TB)

Lumbar plexus

Sub-costal nerve
Vulnerable to injury
behind kidney
Ilio-inguinal and ilio-hypogastric nerve

Genito-femoral nerve (on psoas)

Vulnerable to injury
Lateral cutaneous nerve of thigh (on iliacus)
behind caecum
Femoral nerve (lateral to psoas)
Obturator nerve (medial to psoas)

Genitofemoral nerve
LCNT in Laproscopic hernia repair
Genital branch Gen-fem nerve (L1-L2)
Efferent for cremasteric reflex Ilio-inguinal in open repair
Sensory over anterior scrotum Genital branch Ilio-hypogastric in mesH hernioplasty
Femoral branch
Femoral branch
Afferent for cremasteric reflex
Sensory over medial thigh
Femoral and Obturator nerve
(over femoral triangle)
L2-L4
Obturator (medial to psoas)
Lateral cut. nerve of thigh supplies medial compartment
Can get compressed deep to LCNT (L2-L3) of thigh.
inguinal ligament Femoral (lateral to psoas)
Leads to meralgia parasthetica supplies anterior compartment
Burning sensation in lateral thigh of thigh.
 Hip Joint

ANTERIOR
ASIS

AIIS

Greater
trochanter POSTERIOR
PIN
Gluteus minimum structures
Gluteus medius
Pudendal nerve
Int. Pudendal vessels
AbIR at hip
Nerve to Obturator int
(Weakness causes
Trendelenberg gait) Ischial spine

Superior gluteal nerve

Gluteal tuberosity
Lesser trochanter
Gluteus maximus
Ilio-psoas
Extension and ER of hip
Inferior gluteal nerve

SGN and
vessels
IGN and Piriformis
vessels
Sciatic
nerve
Gluteus medius

Piriformis

Gemellus superior
Obturator internus
Gemellus inferior
Greater sciatic foramen
Quadratus femoris

Above piriformis
Superior gluteal nerve and vessels
Below piriformis
Inferior gluteal nerve and vessels
Sciatic nerve
Nerve to quad. Femoris SGN supplies
Femoral cutaneous nerve Glut medius and minimus
PIN structures TFL (tensor fascia lata)

IGN supplies
Lesser sciatic foramen Gluteus maximus
PIN structures
Sciatic Nerve
Tendon to Obturator internus
Largest nerve of sacral plexus
Posterior comp. of thigh
Anterior compartment of thigh
1. Tensor fascia lata
2. Sartorius
3. Quadriceps femoris
TFL
→ Vastus lateralis
Gluteus maximus
→ Vastus medialis
→ Vastus intermedia (deep) Inserts on ITB

→ Rectus femoris

Main action : Flexion at hip joint Iliotibial band Contracture in Polio

Modification of
Fascia Lata of thigh
Rectus femoris has additional
action of extension at knee joint. Hip joint- FABER Knee joint -FER

Nerve : Femoral nerve

Femoral triangle
AS
IS CUS
ILIA
Pectineus AS M
AJO
R
PSO
EUS
TIN
ING
. LIG PEC
.
PUBIC
Sartorius TUBERCLE
Flexion at hip

Sar
Flexion at knee
tor
ius

MEDIAL
Vastus OR
-ADDUCT
lateralis Rectus femoris
LATERAL

S
LONGU
Flexion at hip
Vastus Extension at knee
medialis

Extension at knee

IS
AS
FEMORAL NERVE

Femoral nerve FEMORAL ARTERY

FEMORAL VEIN
LYMPH NODES
L2 L3 L4

Iliacus
Pectineus
MEDIAL

Inguinal lig
LATERAL

PD AD
Hip joint Sartorius
Quadriceps Medial cut. nerve of thigh
femoris Intermediate cut. nerve
of thigh
Sartorius forms Lateral boundary
Great saphenous vein

(isn't a part of femoral triangle)

Saphenous nerve Adductor longus forms medial boundary
Skin of medial side of leg & foot (is a part of base)
Femoral sheath has femoral artery and vein
Medial to lateral (VAN)
surAL - LAteral Cloquet lymph nodes present (most medial)
Posterior compartment of thigh

}
Biceps femoris
Semi-membranosus Hamstring muscles
Semi-tendinosus

Popliteal fossa
Membranous-
Medial
Boundaries
Supero -Medial : Semi-membranosus
Supero - Lateral : Tendon of biceps femoris
Inferiorly : medial and lateral head of gastrocnemius

Contents
Tibial nerve (sciatic divides into tibial and CPN)
Common peroneal nerve
(hooks around fibula → foot drop → steppage gait)
Popliteal vein and artery

Sciatic nerve
L4, L5, S1, S2, S3

Largest branch of sacral plexus Deep to Piriformis

Hamstrings
n
mo e
a com nerv
k
a ular
fib TIBIAL NERVE
Neck of
fibula

Superficial Deep Tibia is medial, hence

peroneal Tibialis causes inversion
peroneal nerve nerve
Pernoeus longus Dorsi-flexors Plantar-flexors
(evertors) (invertors) Tibial nerve injury
Pernoeus brevis Plantar flexors and inverters
Tibialis Tibialis affected
anterior posterior Dorsi-flexed and everted foot

Common peroneal nerve injury

Dorsi flexors and evertors
Skin over affected
MPN LPN Foot drop and inverted foot
dorsum
High steppage gait
Skin over 1st web space
Compartments of leg

Deep peroneal n
Ant tibial artery

No neurovascular bundle

Ischiorectal fossa

Obturator
internus
Obturator fascia
Ext anal sphincter

Pudendal canal

• Pudendal nerve
• Internal pudendal vessels

Contents of IRF
1. Fat
2. Pudendal canal and its contents
3. Inferioir rectal veins and nerves
↓
Can be injured in drainage
of IRF infections
Lungs
Lobes of lungs
Left lung has 2 lobes and a cardiac notch
Right lung has 3 lobes (additional middle lobe)
Left lung can have a small lobe below cardiac notch
known as lingula
Hila of lungs
Right lung has 2 bronchi (ep-arterial and hypo-
arterial) above and below pulmonary artery
Left lung has only one bronchi
Anterior ro Posterior : VAB
Phrenic nerve passes anterior to the hila of lungs to
supply the diaphragm

Eparterial
bronchus
Right pulmonary Left pulmonary
Bronchial
artery artery
arteries
Superior pulmonary vein Hyparterial Superior pulmonary vein
bronchus
Inferior pulmonary vein Left principal Inferior pulmonary vein
bronchus

Pulmonary
ligament

Heart
Transverse pericardial sinus
Separates the arterial end of the heart tube from
the venous end.
Aorta and pulmonary trunk lie anterior to the sinus
and the superior vena cava lies posterior to it.
Therefore, during surgery, a clamp passed through
the transverse sinus stops the blood flow from the
aorta and pulmonary trunk.

Area posterior to sternum

Right ventricle
Right atria forms the right lateral
margin along with SVC
Conduction system of heart

SA Node
Located at the upper part of the crista terminalis, at the
junction of the superior vena cava opening to the right
atrium.
This is also the junction between the parts of the right
atrium derived from sinus venosus and primitive atria.

AV Node
Located at interatrial septum near the opening of the
coronary sinus.
It is located in the center of the Koch triangle.

Coronary Circulation

Anterior Posterior
aortic sinus aortic sinus

RCA LCA
Conus
AV groove Anterior MI : LAD
branch
Lateral MI : LCX

PDA LAD Inferior MI : RCA

Posterior Left Anterior Posterior MI : PDA
descending artery descending
(Decides dominance) (widow's artery)
Supplies Posterior LV wall Supplies Anterior LV wall
Posterior 1/3 of septum Anterior 2/3 of septum

Right Marginal artery

Left Circumflex (LCX)
(Acute)
↓
Venous Drainage Left Marginal artery
Everything drains into Coronary Sinus (obtuse)
except Anterior Cardiac vein (ACV)
Intercostal Arteries and Veins

Upper 9 ICS Anterior intercostal arteries

2 anterior intercostal arteries 1 - 6 ICS, internal thoracic artery branches
1 posterior intercostal artery 7 - 9 ICS, musculophrenic artery branches
10 - 11 ICS, no anterior intercostal artery
10th and 11th ICS
No anterior intercostal arteries Posterior intercostal arteries
1 posterior intercostal artery There are 11 pairs of posterior intercostal arteries.
The first 2 pairs are branches of the superior
intercostal artery, a branch of the costocervical trunk.
The lower 9 pairs are branches of the descending
Subclavian artery thoracic aorta.
The right posterior intercostal arteries are longer than
Internal thoracic those on the left (because aorta is on left)
artery
Posterior intercostal arteries are responsible for
Anterior intercostal rib nothing in coarctation of aorta.
arteries

Right and Left

brachiocephalic

Musculophrenic
artery
Left superior
Superior epigastric intercostal
Right superior
artery
intercostal

Azygos Accessory
vein hemiazygos

Hemiazygos

Intercostal Nerves

Derived from the thoracic vertebrae - T1 to T11.

They lie between the internal intercostal and
innermost intercostal muscles. VAN
T3-T6 are known as typical intercostal nerves
(supply only thoracic wall) while atypicals supply
other structures as well
T1 and T2 supply upper limb
T7-T11 supply the abdominal wall
Major arterial branches

Abdominal aorta
Celiac trunk Left gastric art.
Right gastric art.

↓
Common Splenic art.
Gastro-

↓
Rt. gastro- hepatic art. Branches to the spleen and pancreas
duodenal
↓ Left gastro-epiploic artery
epiploic artery artery
Proper hepatic
Superior
artery
pancreaticoduo
denal artery Right and left hepatic art.
Cystic artery (from rt. Hepatic)
Right gastric art.

Common hepatic art.

Abdominal aorta

Celiac axis
Splenic
Left gastro-epiploic artery
arterty
Left gastric art.

Proper help. artery

Gastroduodenal artery
Right gastric art.
Superior pancreaticoduodenal artery
Duodenal branches
Right gastro- epiploic artery

Pancreatic branches
Inferior panreatico-
duodenal artery
(branch of SMA)
Lesser curve Greater curve
(small name) (Large name)
Lt. Gastric Lt. Gastro-epiploic
Rt. Gastric Rt. Gastro-epiploic

Internal iliac artery

Anterior branch Posterior branch
(everything else) SIL
Sup. Gluteal art
Iliolumbar artery
Lateral sacral artery
 Abdominal Wall

Flat muscles (lateral) Vertical muscles

Ext oblique Int oblique Trans. Abdominis Rectus abdominis Pyramidalis

Largest and most Fibres Deepest Long paired muscle Small triangular
superficial flat perpendicular Deeper to this Split by linea alba muscle
muscle. to ext. oblique muscle is (formed by tendons of
forms inguinal transversalis fascia lateral muscles)
ligament

Lower fibres of int. oblique and trans abdominis form conjoint tendon

Rectus sheath Anterior wall of rectus sheath (thick)

Rectus Abd
The rectus sheath is formed by the aponeuroses of the EO
IO
three flat muscles and encloses the vertical muscles. TA Posterior wall of rectus
sheath (deficient)

Arcuate line
Approximately midway between the umbilicus and the
pubic symphysis, all the aponeuroses move to the
anterior wall of the rectus sheath.
At this point, there is no posterior wall to the sheath
and rectus abdominis is in direct contact with the
transversalis fascia.

Anterior wall fascia Ext. oblique modifications

P
Inguinal ligament
No deep fascia (hence can distend) Pectineal ligament
At umbilicus splits into : superficial •Ligament of Poupart
•Modification of External oblique aponeurosis Linea alba
Camper and deep fibrous Scarpa.
Scarpa continue to cover scrotum and
I Inguinal ligament

labia majora.
L Lacunar ligament

ASIS Ligament of Cooper

Pectineal ligament

Inguinal ligament
Reflected part of
inguinal ligament

Pubic tubercle
Lacunar ligament
• Gimbernat’s Ligament
• Medial to femoral ring
Inguinal canal
Passasge for Spermatic cord in males and Round ligament of uterus in females.
Ilioinguinal nerve enters the canal through the side and not through the deep ring.
Hernia via inguinal canal : Indirect hernia

2 Muscles (int. oblique, trans. abdominis) Superior wall

2 Aponeurosis (int. and external oblique) Anterior wall
2 Ligaments (Inguinal, lacunar) Lower wall
2 Ts (Transversalis fascia, Conjoint tendon) PosTerior wall
↓
Lower fibres of int. oblique and
trans abdominis fused

External spermatic fascia

aster mus
em c Internal spermatic fascia
Cr

le

Vas. Def and its artery. Spermatic cord enters

Cremasteric
artery Deep inguinal ring
A defect in fascia
transversalis
3 arteries: testicular, ductus deferens, Poster
Anterio ior wa
cremasteric r wall ll
3 nerves: genital branch of genitofemoral,
cremasteric, autonomics
Superficial inguinal ring
3 other things: vas deferens, pampiniform
Floor
plexus, lymphatics
Spermatic cord exits

Inguinal lymph nodes

Superficial inguinal lymph nodes Deep inquinal lymph nodes

Horizontal group along the lower Along the femoral vein
border of inguinal ligament
Vertical group along Great
saphenous vein
 Pelvis
Modifications of Pubococcygeus
Levator ani

Pelvic diaphragm
1. Pubo-urethralis
Pubo-coccygeus Bladder
Obturator internus
2. Pubo-vaginalis
Ilio-coccygeus
Pelvic diaphragm
3. Pubo-rectalis Ischio-coccygeus Deep
Urogenital diaphragm
space

Ischiocavernosus
Muscle of continence Bulbospongiosus Superficial
over crus
over bulb Superficial perineal space
fascia
(Colle's Fascia)

Perineal membrane Bulb/ bulbospongiosus

Inferior layer of UGD
Crus/ Ischiocavernosus

Bladder
Obturator internus
Superficial transverse
perineal muscle
Perineal body Pelvic diaphragm
External anal sphincter
(10 muscles) Deep Urogenital
space diaphragm
Ischiocavernosus
Bulbospongiosus over crus
Superficial
Paired muscles (4) over bulb Superficial perineal space
1. Superficial transverse fascia
(Colle's Fascia)
perineal muscle
2. Deep transverse Unpaired muscles (2)
perineal muscle 1. External anal sphincter
3. Bulbospongiosus 2. Longitudinal muscles of
4. Levator ani anal canal

Pelvic diaphragm
Scarpa's fascia is a continuation of the anterior Superior layer of UGD
Scarpa’s fascia
abdominal fascia and forms Dartos muscle. DPP
Perineal membrane
Dartos continues as Colle's fascia which along with
perineal membrane forms Superficial peroneal pouch. SPP
Deep perineal pouch between perineal membrane and
superior layer of UGD.
Colle’s fascia

Dartos muscle

EXTRAVASATION OF URINE
In anterior trauma, urine can move into Bladder
Detrusor muscle
Space around penis
Internal sphincter
Scrotum Bulbar urethra
Ant. Abdominal wall Prostatic urethra Anterior
Thigh Posterior
Penile urethra
In posterior trauma, urine collects Membranous urethra
in deep perineal pouch External
sphincter
 Joints
1. Fibrous joints Syn-arthrosis : Fibrous joints (can't move)
2. Cartilaginous joints (primary and secondary) Amphi-arthrosis : Cartilaginous joints (some movement)
3. Synovial joints Diarthrosis : Synovial joints (freely movable)

Fibrous Joints SSG

Sutures Syndesmosis Gomphosis

Plain suture,
e.g. frontonasal suture am
ou
s
S q u u tu re
s
De
n
s u tic u
tu la
re te

Serrate suture Squamous suture,

between parietal temporal bone - parietal bone

Ala of Rostrum of
vomer sphenoid
Denticulate suture Schindylesis
Lambdoid suture of Sphenoid and ala of vomer
occipital bone

Cartilaginous Joints
Primary cartilaginous Secondary cartilaginous
(Syn-chondrosis) (Symphysis)
Bones are joined by hyaline cartilage (less rigid, Bones are joined by fibro cartilage (more rigid,
more flexible) less flexible)
Epiphyseal growth plates Pubic symphysis / IV discs / Sterno-manubrial
Costo-chondral joints (rib-cartilage) and 1st
costo-sternal joint (1st rib - sternum).
Synovial Joints
Ball and socket Condylar
Hip TM joint
Shoulder Knee joint
Incudo-stapedial (IS is BS)
Talo-Calacaneo-Navicular

Saddle Hinge
Incus- malleus Elbow
Calcaneo-cuboid Knee
1st carpo-metacarpal Inter-phalangeal
Sterno - clavicular

Ellipsoid Plane synovial

Atlanto-occipital (C0-C1) Acromio-clavicular
yELL YES first
Costo-vertebral
Costo-transverse
Costo-sternal

Inter-carpal
Pivot Inter-tarsal
Atlanto-axial (C1-c2)
Say NO second

Plane Saddle

Saddle
Icudo-malleolar joint

True ribs first 7

Ball and Socket
Incudo-stapedial joint Typical ribs 3-9
Floating ribs 11 and 12

Symphisis are manubrio-sternal and xiphi-sternal

Synchondrosis : 1st costo-sternal and all costo-chondral

Synovial : "TVS" Costo transverse, costo vertebral,

consto sternal (except 1st costo sternal)
Dermatomes

T-2 : Axilla

T-4 : Nipples

C6 : Thumb
T-6 : siXphoid

T-10 : Umbilicus

T-12 : Inguinal Ligament

C5 - C6 - C7 - C8 - T1

C7 : Middle finger

L-2 : Mid Anterior thigh

L-3 : Knee

L-4 : Medial Calf

L-5 : Lateral Calf +
Dorsum of foot
Histology

GI Histology
Mouth and esophagus : Non keratinised stratified
squamous
Stomach : Simple squamous (with mucus cells)
Duodenum : Broad villi + Brunner's glands
Duodenum Jejenum
Jejunum : Tongue shaped villi (Broad villi) (Tongue shaped villi)
Ileum : Flat villi + Peyer patches Brunner's glands

Large intestine : Goblet cells

Anal canal (Above PL) : Simple coloumnar
Anal canal (Below PL) : Non keratinised stratified
squamous

Ileum Large intestine

(Flat villi) Goblet cells
Peyer's Patches

Paneth cells
(Produces substances
that kill bacteria) Mouth/Esophagus
Lamina propria
Connective tissue found below
basement membrane in mucous
lined tissues.

Tongue Histology

Circumvallate papillae Fungiform papillae Filliform papillae

Largest in size Has taste buds and Smallest and most
Placed near sulcus sensory cells numerous
terminalis Keratinised
No taste buds
Respiratory Histology
PNS, Tracheal, Bronchus, Proximal bronchiole : Cilliated pseudo stratified coloumnar
Terminal bronchiole : Cilliated coloumnar
Respiratory bronchiole : Simple coloumnar
Alveolus : Simple squamous

Respiratory bronchiole Alveolar duct and sac Alveoli

Uro-genital tract
PCT, DCT : Simple Cuboidal
Ovary : Simple cuboidal
Collecting part : Transitional epithelium
Male structures : Pseudo strat coloumnar with
stereo cilia
Fallopian tube : Cilliated coloumnar
Uterus + Endocervix : Simple Coloumnar Transitional epithelium Pseudo-strat columnar
Ectocervix + Vagina : Stratified Squamous Urinary bladder with stereo-cilia
Ureter Testes
Calyces Vas-deferens
Posterior urethra Epididymis
Prostate gland

Cilliated coloumnar Simple cuboidal Squamo-coloumnar junction of cervix

Fallopian tube PCT, DCT Ectocervix + Vagina : Str squamous
Ovaries Endocervix + Uterus : Simple coloumnar
Cartilages

Elastic Hyaline Fibro-cartilage

Chondrocytes Chondrocytes Chondrocytes

individually in lacunae forming cell nests present in rows
No calcifications Calcification with old age Calcification with bone
Type 2 collagen Major articular cartilage repair
Type 2 collagen Type 1 collagen
Perichondrium present No perichondrium
(but absent in epiphyses All symphyses
and articulations)

Muscles

Skeletal muscle Cardiac muscle Smooth muscle

Striations Inter-calated discs
Lymphoid tissue
In Lymph nodes, lymphatic nodule in outer cortex
Spleen has a splenic arteriole inside lymphatic nodule
Tonsils have surface epithelium and a tonsilar crypt.
No nodule in thymus

Lymph node Spleen

le
Capsu
White pulp

Cortex Red Pulp

Trabeculae
Lymphatic nodule
(B Lymphocytes)
Medulla
Paracortex GC Lymphatic
(T Lymphocytes) nodule

Splenic arteriole
inside nodule

Palatine Tonsil
Hassal's Corpuscle
Thymus
Tonsilar
crypt

Cortex

Medulla

⬆️ Incomplete
Lymphatic septation
nodule

Pancreas and Thyroid

Pancreas Thyroid Follicles
Follicular Cells

Colloid
The clear space around the
colloid is a shrinkage
artifact.

Islets of Langerhans
Lightly stained clusters of
endocrine cells
Sebaceous glands
Apocrine
Mammary glands
Ceruminous glands (ear)
Moll's gland in eyelids (blockage causes stye)
Sweat glands in axilla and groin
Ecrine/merocrine
Sweat glands in rest of body
Tear glands
Salivary glands
Goblet cells
Holocrine
Sebaceous glands
Seba Meibo
Meibomian glands
Pear-shaped glands
Pale staining cells that produce sebum
Holocrine secretion

Paneth Cells (Zymogen cells)

Found in deeper part of intestinal crypts
Rich in Zinc
Lysosomal action to destroy bacteria
 Cardiac muscle Skeletal muscle Muscular artery

Foliate Papilla Hyaline Cartilage Fibrous cartilage

Lymph node
Pancreas Striated Duct

Sebaceous gland Spleen Cerebellum

Thymus Elastic Cartilage

Circumvallate Papilla
CHAPTER 2

SURGERY
Sutures

Sub-cuticular suture
Simple interrupted suture Horizontal matress suture Intra-dermal stitch, beneath
the epidermis
Better cosmetic results
Monocryl 3.0 commonly used
for this

Simple continuous suture

Single knot known as Vertical matress suture
Aberdeen knot

JENKIN'S RULE
1cm
Length of suture should be 4 times
the length of wound Purse-string suture
Sutures should be placed at 1 cm Used in :
1cm
intervals and more than 1 cm from 1. Cervical cerclage
the wound edge 2. Rectal prolapse
3. Thiersch wiring
(for non-absorbable sutures)

Type of sutures

Absorbable Non absorbable

Natural Synthetic Natural Synthetic

1. Catgut 1. Monocryl 1. Silk (black) 1. Nylon
Made from sheep ileum submucosa 2. Vicryl Used for skin sutures 2. Prolene
Preservative : Isopropyl alcohol 3. PDS and to secure drains 3. Polyester
Used for Tubectomy 4. Dexon Nylon used for tendons and
nerves
Monocryl used for sub-cutaneous
Prolene has maximum tensile
sutures (better cosmesis)
strength (used as mesh
Vicryl is violet
material and to suture rectus
PDS used for Whipple's
sheath)
Dexon has maximum risk of infection
 Important Knots

Similar Crossings are

Square knot Granny's knot
crossings "upar-niche"
Surgeon's knot
aka Reef knot aka Pseudo-square knot
More secure Not secure
Surgeons are twisted
"Square is a symmetrical shape" "Granny is upar-niche"

Important Bags

Closed drains

Romovac
Mastectomy
Thyroidectomy

Abdominal drain bag Chest tube bag

No water level line Water level line at bottom
Jackson Pratt
Abdominal drain

Mechanism of Chest tube drainage bag

Open to air
From patient To patient

When the patient inhales,

Water level provides a seal the water seal prevents
(usually 2cm) entrainment of room air

Jackson Pratt abdominal drain

On exhalation : On inhalation :
Bubbling Water rises
Retractors

Z
Czerny

Deaver's

D
Balfour
Self retaining abdominal retractor
"All four"
L
Langenbach

Perkins
Self retaining

M
Retracts small incisions
"Small perks" Morris
D

Doyen's

Joll's
Self retaining
Thyroid retractor

Blades

Bard Parker Handle

10 11 12 15
Skin and I&D Suture Minor
muscle removal OT
Miscellaneous Instruments

Malecot Catheter
Supra-pubic cystotomy
Thick abscess drain

Pigtail Catheter
Draining abscess DJ stent
Ureteral stenting

Monopolar cautery Bipolar cautery

Requires a cautery pad Doesn't need a cautery pad
Electrolyte free fluids such as Normal saline can be used
glycine or mannitol are used.
Has 2 switches :
1. Blue : AC, coagulate "Blue - Glue"
2. Yellow : DC, cuts

Cautery Pad
Needed with monopolar cautery
 Post-Op Fever

POD : 1-3 "wind"

Lung atelectasis
M/c on day - 1
Prevention : Incentive spirometry, antibiotics

Wind - Water - Land

POD : 3-4 "water"
Urinary tract infection
Most common cause of post-op fever overall
Prevention : Short term foley use

POD : 4-5 "land"

Deep vein thrombosis
Prevention : Early mobilisation, compression socks, heparin

Incentive Compression
POD : 7+ (but less than a month) spirometry socks
Surgical site infection
Prevention : Pre-operative antibiotics

Surgical Site Infections

Definition : Infection of surgical site within 30 days of surgery (or 1 year if a prosthesis was implanted)

Grading of SSI Risk of SSI

1. Southampton Grading 1. Clean : 2 % risk

0 - Normal healing Planned procedure
1 - Bruising/Hematoma Not entering GI/GU/Respi
2 - Erythema eg. Mastoidectomy, Hernia repair
3 - Serous discharge
4 - Pus 2. Clean-contaminated : 2-10 % risk
5 - Tissue breakdown Planned procedure
Entering GI/GU/Respi
2. ASEPSIS Score eg. LSCS. TURP, lobectomy

A - Additional treatment needed 3. Contaminated : 10-20 % risk

S¹ - Serous discharge
Emergency procedure < 4 hours
E - Erythema
Breach in sterile technique
P - Pus
eg. Cholecystectomy with acute inflammation
S² - Separation of deeper tissue
I - Isolation of bacteria in culture
4. Dirty : >20 % risk
S³ - Stay in hospital > 14 days
Emergency procedure > 4 hours
Score of < 10 : Satisfactory healing
Purulent wounds
Score of > 40 : Severe SSI
eg. Abscess
Intra-Abdominal Abscess
Most common site
Supine : Hepato-renal pouch (aka Morrison's pouch)
Ambulatory : Pelvis
Most common overall : Pelvis

TOC Hepato-renal pouch Recto-uterine pouch

Pigtail catheter drainage (Morrison's) (Pouch of Douglas)

Burst Abdomen
Pathognomic sign : Salmon color sero-sanguinous discharge
Management : Bogota bag/Uro bag laparostomy

Salmons compiled
1. Tympanic membrane : Otosclerosis
2. h/p : Amyloidosis (Congo red)
3. Abscess : Burst abdomen

Nerve Injuries
Breast surgery / axilla clearance : Inter costo brachial trunk
Thyroid surgery : SLN (ELN) > RLN
Parotid surgery
a) Deviation of angle of mouth : Marginal mandibular n.
b) Anaesthasia at angle of mouth : Greater auricular n.
c) Frey's syndrome : Auriculo-temporal n.

Submandibular surgery : Lingual n. (related to Wharton's duct)

Hernia surgery
a) Lap hernia surgery : Lat. Cutaneous n. of thigh (also involved in Meralgia Parasthetica)
b) Open hernia surgery : Ilio inguinal n. (loss of sensation at root of penis)
c) Mesh entrapment : Ilio hypogastric n.
Thymectomy : Phrenic n.
 TRAUMA - Basics
Trauma Algorithm
1. Primary survery : Identify emergencies Primary Survery
2. Resuscitation : Treat emergency A : Airway + C-Spine stabilisation
3. Secondary survery : Identify other injuries B : Breathing + Ventilation
4. Definitive care : Make a management plan C : Circulation
D : Disability (GCS)
E : Exposure & environment control
Damage Control Surgery
It's a staged approach in trauma surgery that focuses
In field setting
on saving the life over anatomical reconstruction.
C-ABCDE is done
Stage 1 : Primary life saving surgery C = Control bleeding
Hemostasis (control active hemorrhage)
Drainage of septic contamination
Temporary abdominal closure

Stage 2 : Damage control resuscitation (in ICU)

ICU management aimed to tackle the trauma triad of
death (Hypothermia, Met acidosis, Coagulopathy)
Coagulopathy

Philadelphia Collar
Severe
(used for C-Spine stabilisation)
blood
loss

Radiological adjuncts to Primary Survery

Hypothermia Acidosis
1. eFAST
2. CXR
Judicious use of IV fluids (< 1L, permissive hypotension)
Early use of blood products (1:1:1 ratio)
3. Pelvic X-Ray
Prevent or reverse coagulopathy (use of TEG) CT scan or MRI are never part of primary survery

Stage 3 : Definitive surgery

Back Examination
Full GI repair
Temporary or permanent abdominal closure Done only in secondary survey
Log roll maneuver (5 people needed)
Stage 4 : Abdominal closure PR examination is done in back
In patients on whom abdominal closure was not performed examination

CRASH-2 Trial
Clinical Randomisation of an Antifibrinolytic in
Significant Haemorrhage

1gm Tranexamic acid over 10 minutes

Give within 3 hours of injury
Significantly reduces mortality in trauma Log roll maneuver
 TRAUMA - Shock
SIRS (Systemic Inflammatory Response Syndrome) : SIRS criteria ≥ 2 SIRS criteria
Sepsis : SIRS + Identified focus of infection
1. Core temperature : > 38°C or < 36°C
Severe Sepsis : Sepsis + End organ damage
2. Respiratory rate : > 20/min (or pCO² > 32 mm Hg)
Septic Shock : Severe sepsis + Hypotension refractory to resuscitation
3. Heart rate : > 90/min
with ≥ 3L fluids
4. White blood cell count : > 12,000/μL or < 4000/μL
MODS (Multiple Organ Dysfunction Syndrome) : Septic shock + Multiple
5. Band form neutrophils : > 10 %
end organ damage
≥ 2 criteria required to categorise as SIRS

Prognostic Scores for patients in Shock

A. qSOFA score (done for patients not in ICU) "SIR doesn't measure BP"
1. GCS < 15 "GaRBa"
2. Resp. rate > 22/min
3. BP (systolic) < 100 mm/hg

B. SOFA score (done in ICU)

1. qSOFA (PiO² instead of RR)
2. Billirubin (for hepatic function) Types of shock
3. Creatinine (for renal function)
Cardiogenic (heart failure)

C. Revised Trauma Score Hypovolemic (trauma)

Similar to qSOFA (GCS, RR, SBP)
Obstructive (cardiac tamponade / pneumothorax)
D. Trauma and Injury Severity Score (TRISS) Distributive (sepsis /anaphylaxis)
1. Revised trauma score
2. Injury severity Neurogenic (spinal cord injury / anaesthasia)
3. Age

Classification of Shock

Cardiac output : low Cardiac output : low Cardiac output : High

SVR : high (compensation) SVR : low (no compensation) SVR : Very low (peripheral pooling)

Check CVP Neurogenic shock Distributive shock

(Central venous pressure) Bacterial toxin mediated vasodilation of
peripheral vessels in sepsis

High Low
(Heart can't push) (not enough blood)

Cardiogenic or Hypovolemic shock

Obstructive shock
TRAUMA - Hypovolemic Shock
Grading of hypovolemic Shock
Class 1 : <15% blood loss (< 1L)
No changes otherwise Heart rate
No treatment needed
Shock Index =
SBP
eg. Blood donation
Normal : 0.5 - 0.7
Class 2 : 15-30% blood loss (1 - 1.5 L)
High : > 0.9 (requires resuscitation)
HR increases
Pulse pressure decreases
Fluid resuscitation
Class 3 : 31-40% blood loss (1.5 - 2L) Modified Shock Index = Heart rate
Urine output decreases 15 | 30 | 45 MAP
GCS lowers
Requires blood products
Class 4 : >40% blood loss (> 2 L)
Urine output further decreases
Requires massive blood transfusion

Fluid resuscitation in hypovolemic shock

Fluid type : Isotonic crystalloids (warmed)
Amount : < 1L (damage control resuscitation)
Indicator of adequate resuscitation : Urine output (1ml/kg/hr)

Indicator to estimate fluid required : Central venous pressure

Lab parameter to check tissue perfusion : Lactate (base deficit)

TRAUMA - Triage

Description Colour

Immediate Red Active hemorrhage, Pneumothorax, Cardiac arrest, Severe shock

Urgent Yellow Opthalmic/CNS issue, Fractures

Delayed Green Walking-wounded

Dead White/Black
 TRAUMA - Pneumothorax
Presence of air in the pleural space (which can result in partial or complete collapse of the lung)
1. Tension Pneumothorax : If pneumothorax causes obstructive shock
2. Spontaneous Pneumothorax : Seen in tall-thin-male-smoker with family history (managed conservatively)

A very close d/d of Tension Pneumothorax is Cardiac tamponade

Both present with Obstructive shock and Distended JVP

Characteristic of Tension Pneumothorax : Tracheal shift (to opposite side),

reduced breath sounds, hyper resonant chest
Characteristic of Cardiac Tamponade : Muffled heart sounds

Management of Tension Pneumothorax : Needle Thoraco-stomy/ICD

Management of Cardiac Tamponade : Emergency Thoraco-tomy Right sided Pneumothorax

Management of Pneumothorax

Patient stable Patient unstable

Intercostal drain Emergency Needle Throaco-stomy

placement (Needle decompression)

Intercostal drain placement when

Triangle of Safety patient is stable

Needle thoraco-stomy

ADULT CHILD

5th ICS MAL 2nd ICS MCL

"Adult has 5 letters"

Anatomical space in axilla through which M-Mode Ultrasound

intercostal drain can be placed safely
The boundaries include :
1. Line through apex of axilla
2. Ant. Border of lat dorsi
3. Lat. Border of Pect. major
4. Line through Nipple / 5th ICS

Seashore sign Barcode/Stratosphere sign

Normal lung Pneumothorax
Thoraco-stomy : Hole in thorax
Sea-shore is chill Barcode or stratosphere -
Thoraco-tomy : Opening up thorax and normal stressfull things
TRAUMA - Hemothorax and other chest trauma

Empyema Thoracis

Collection of pus in pleural space

Left sided Hemothorax Right sided
Management algorithm :
(Can't be differentiated from "Massive" Hemothorax
Pleural effusion on CXR) ICD insertion
↓
VATS
Management of hemothorax (Video-assisted
ICD insertion in triangle of safety thoracoscopic surgery)
Thoraco-tomy (opening up the thorax) indicated when ↓
1. More than 1.5L blood drained in 1st hour Decortication
2. More than 200cc of blood per hour for 2-4 hours

Flail chest

Fracture of Ribs
The flail part contracts while inspiring
and expands while expiration
(paradoxical respiration)
Treatment : Oxygen + Opioids
In case of respiratory failure : PPV

Paradoxical respiration in flail chest

 TRAUMA - Abdominal trauma

Abdominal Trauma

Blunt Trauma Penetrating trauma

(Most common organ injured : Spleen) (Most common organ injured : Liver > Stomach)

Stable Unstable Stable Unstable

eFAST Start IV fluids Start IV fluids

CECT scan

eFAST Shift to OT/ Laprotomy

Shift to OT/ Laprotomy

eFAST(-) eFAST(+) eFAST done here to
fluid absent fluid present localise the site of Pneumo-peritoneum
bleed if possible, Presence of free air in peritoneal cavity
before shifting to CXR finding : Air under diaphragm
Observation CECT scan OT Occurs secondary to intestinal perforation
(IOC)
Management : Immediate OT / Laprotomy
AAST grading

eFAST
extended Focussed assessment sonography in trauma

Initial investigation in all cases of blunt trauma of

abdomen (not IOC)
Helps to detect any intra-abdominal bleed
Sensitivity : 100ml of fluid
Can't be used for :
1. Retroperitoneal injuries
2. Subcutaneous emphysema Air under diaphragm

Inter Costal Spaces for pneumothorax

(done only in eFAST)

Abdominal Compartment
Syndrome
Abdominal pain + Distention + Hypotension
Sub xiphod for following abdominal Trauma
pericardial effusion Management : Immediate OT / Laprotomy

Spleeno-renal
Hepato-renal pouch Signs in Spleenic injuries
pouch 1. Ballance's sign : Dullness on percussion in LUQ
(Morrison's) 2. Kehr's sign : Referred pain in shoulder

Pelvic pouch
(Pouch of Douglas)
 AAST Grading
American Association for the Surgery of Trauma
Done for abdominal organs like Liver,
Spleen and Kidney in trauma
Needs a CECT scan
Grading :

For Liver/Spleen For Kidney

Grade 1 : Laceration < 1 cm Grade 1 : No Laceration
Grade 2 : Laceration 1-3 cm Grade 2 : Laceration < 1 cm
Grade 3 : Laceration > 3 cm Grade 3 : Laceration > 1 cm
Grade 4 : Peri-hilar injury
Grade 5 : Entire hilum injured /
Shattered kidney
Liver Spleen
Grade 4 : One lobe < 75% injured Grade 4 : Peri-hilar injury
Grade 5 : One lobe > 75% injured Grade 5 : Entire hilum injured /
Shattered spleen

TRAUMA - Retroperitoneal trauma

Maneuvers to explore
Zone 1 : Aorta and IVC abdomen for Aorta & IVC
Zone 2 : Kidneys and adrenals
Zone 3 : Pelvic vasculature For Aorta
Mattox maneuver
Zone wise management Left medial visceral rotation
Zone 1 : Exploration
Zone 2 : Observation For IVC
Zone 3 : External pelvic compression Kocher's/Cattle Brasch maneuver
Right medial visceral rotation

TRAUMA - Diaphragmatic and Aortic Injury

Diaphragmatic Injury Aortic Injury

M/c mode : Penetrating injury M/c site : Isthumus
M/c organs to herniate : Stomach IOC : CT-Angio,
(left sided herniation is more Trans-esophageal echo
common) Initial management : Beta
IOC : CECT (for stable) blockers (medical management)
Wide mediastinum
Management : Repair via Definitive Management : EVAR
abdominal approach (Endovascular Aortic Aneurysm
ICD is contraindicated Repair)
 TRAUMA - Bladder trauma
Suspected case of bladder trauma
Gross hematuria
Inability to void
Low abdominal pain CT-Cysto-Urethro-graphy
CT scan of the bladder and urethra
Put a Foley's Catheter after filling the bladder with dye
(the dye is put via the foley's catheter)
Hematuria

CT-Cysto-Urethro-graphy

Extra-peritoneal Intra-peritoneal
bladder rupture bladder rupture
(more common) (Surgical emergency)

Leave the Foley's catheter in Immediate OT / Laprotomy

place for 10 days

TRAUMA - Urethral trauma

Suspected case of Urethral trauma Retrograde Urethro-graphy

Blood at tip of meatus Dye is injected into the urethra (retrograde) and an X-ray
Inability to void image is taken.
(Foley's Catheter is contraindicated)

Retrograde urethro-graphy (IOC) Prostatic

urethra
Pen Membranous
Confirmed urethral trauma ile u
reth urethra
ra

Supra-pubic cysto-stomy
Have to palpate the bladder for this procedure, Bulbar
urethra
hence wait for bladder to fill if it's not distended. peno-bulbar junction

Anterior urethra Posterior urethra

Wait for 4-6 weeks Penile and Bulbar urethra Membranous and Prostatic
Injured in Straddle injury urethra
Injured in Pelvic fracture
Delayed urethroplasty "Membrane around prostate"
TRAUMA - Head trauma

Epidural/Extradural Sub Dural

Sub Arachnoid Hemorrhage
Hemorrhage (EDH) Hemorrhage (SDH)
Patient presents with worst headache of
Arterial hemorrhage Venous bleed life aka "Thunderclap headache"
(Middle meningial art.) (bridging veins) Traumatic > Berry aneurysm rupture
Trauma at "Pterion" Trivial injury in elderly Initial investigation : NCCT
Doesn't cross sutures (but Can present few days IOC : CT Angio
can cross midline) after the traumatic event. Gold standard inv : Digital subtraction
Lucid interval more Can cross sutures (but angiography (DSA)
prominent here. can't cross midline) Associated with ADPKD (berry aneurysms)
IOC : NCCT IOC : NCCT Management : Angiography + stenting
Indications for surgical Treatment : Burr hole
treatment (Decompressive decompression
craniotomy)
1. Raised ICP causing
Micro bleeds
midline shift > 0.5cm
2. Thickness > 1cm
3. GCS drop by 2

Drugs contraindicated in head injury

1. Steroids : Have been found to increase mortality
2. Morphine (Opioids) : Can cause respiratory
depression

Diffuse Axonal Injury

Patient presents with very low GCS (comatose) but
normal NCCT with h/o head trauma
IOC : MRI (SWI)
Caused due to white mater shearing
Most sensitive marker : β amyloid precursor protein
H/p : Shows significant findings after 12 hours
 Burns
1st degree 2nd degree 3rd degree 4th degree
(only epidermis) (Dermis also inv.) (Full thickness) (Muscle or bone inv.)

Painful Painful or Painless Painless & dry Extensive loss of

Doesn't blister or scar Wet Contractures present tissue
T/t : Keep it open Blisters and scars High risk of infection
Risk of infection T/t : Skin grafting
Use running water but never use ice T/t : Might require
(Ice causes vasoconstriction) surgery

Cause of death in Burns Wallace's rule of 9

Immediate : Asphyxia > Neurogenic Shock To calculate body surface area
Early : Hypovolemia (For both front and back)
Late : Sepsis (m/c organism is Pseudomonas) Each upper limb and head : 9
Overall most common cause : Sepsis Each lower limb, thorax, abdomen : 9×2

Fluid management in Burns

Fluid of choice : Ringer's Lactate (lactate
helps to counter the acidosis)
Fluid of choice in children : RL + DNS
Duration : 1st ½ in 8 hrs, 2nd ½ in 16 hrs
Amount of fluid is determined by latest ATLS
guidelines :
1. Adults : 2 mg/kg/bsa
2. < 14yr : 3 mg/kg/bsa
3. Electrical injury : 4 mg/kg/bsa (due to
risk of rhabdomyolysis)

Buzzwords in Burns
On h/p : Burr cells
Gastric ulcers : Curling's ulcer
Slow growing sq. cell ca. : Marjolin's
ulcer (radioresistant tumor)

Silver sulfadiazine and Silver nitrate Cerium Nitrate

ointment (active against pseudomonas) Increases cell mediated immunity
(Best treatment for Burns)
 Important Scores

Glasgow Coma Scale (GCS)

Eye opening (E⁴)

4 : Spontaneously
3 : To speech
2 : To pain
1 : Doesn't open

Verbal response (V⁵)

5 : Oriented
4 : Confused
3 : Only words Formula : E⁴V⁵M⁶
2 : Only sounds
Maximum GCS : 15
1 : No response
Minimum GCS : 3
Motor response (M⁶) Minimum GCS-P : 1
6 : Obeys commands
5 : Localise pain
4 : Flexion (withdrawal) GCS 13-15 : Mild Injury
3 : Decerebrate (abnormal flexion) GCS 9-12 : Moderate injury
2 : Decorticate (abnormal extension) GCS ≤8 : Severe injury
1 : No response

Pupil (subtract from GCS to get GCS-P)

0 : If both pupils reacti
1 : If only one pupil reactive
2 : If no pupil reactive

Mangled Extremity Severity Score

Helps determine whether a mangled limb should be amputated or not
Parameters included are
S : Shock
I : Ischemia
V : Velocity (of impact)
A : Age
 Thyroid

Thyroid examination

To check for nodules To check for invasion

Pizzillo's method Crile's Method Lahey's Method Pemberton's method Berry's method
Can detect small nodules Thumb used Palms used SVC invasion ICA invasion
CT : Crile's - Thumb ✋🏻 Hey 👋🏻

Thyroid carcinoma

Papillary carcinoma Medullary carcinoma Follicular carcinoma

Most common thyroid cancer Originates from C-cells (para- Second most common thyroid
Excellent prognosis follicular cells) cancer
Classic microscopic findings: Very agressive tumor Arises from follicular cells
Orphan Annie nuclei, Marker: Calcitonin Diagnosis requires capsular or
psammoma bodies Associated with MEN 2 syndromes vascular invasion (not seen in
Spreads via lymphatics (cervical (RET mutations) FNAC)
nodes commonly involved) Mainstay of treatment: Surgery Spread is primarily
Mainstay of treatment : Surgery (Total thyroidectomy + lymph node hematogenous (lungs, bone,
(total thyroidectomy) ± RAI dissection) liver)
No role of RAI Treatment: Surgery (Total
thyroidectomy) + RAI (for high-
risk cases)

Anaplastic carcinoma of thyroid

Worst prognosis

Thyroid lobectomy Sub-total Total

(In hemithyroidectomy, thyroidectomy thyroidectomy
isthumus is also removed)
 Thyroglossal Cyst Retrosternal Goitre
A congenital anomaly resulting from incomplete Thyroid gland extending into the mediastinum,
obliteration of the thyroglossal duct below the thoracic inlet.
During
embryogenesis,
the thyroid gland
develops from the
foramen cecum
at the base of the
tongue and
migrates
downward to the
neck through the
thyroglossal
duct, which
normally Can be primary or secondary
obliterates
Primary Retrosternal Goitre : ectopic thyroid tissue
in the mediastinum (rare)
Characteristic movement: Moves upward with Secondary Retrosternal Goitre : downward extension
swallowing or tongue protrusion. of a cervical goitre (>90% of cases)
Most common location: Near the hyoid bone
Treatment of choice: Sistrunk procedure Presenting features
Compression signs (dyspnoea, dysphagia, SVC
Most common complication : Infection of the cyst
syndrome)
Rare complication: Malignant transformation
Pemberton’s sign: Classic clinical feature.
(papillary carcinoma of thyroid).
Treatment
Surgical removal (via a cervical approach)

Swelling moves with swallowing and

protrusion of tongue.

Parathyroid Adenoma
Most common cause of primary hyperparathyroidism
Causes hypercalcemia "Bones, Stones, Groans, and Psychiatric Moans"
Associated with MEN-1 syndrome Miami Criteria
IOC: Tc ⁹⁹ Sestamibi scan To ensure PTH adenoma
is removed completely
Treatment of choice: Parathyroidectomy (Miami criteria)
> 50% decline in serum
Complications : Postoperative hypocalcemia (hungry bone syndrome)
PTH in 10 minutes

Parathyroid autotransplantation
To ensure some parathyroid function is left after complete parathyroidectomy.
Commonly transplanted in the forearm (brachioradialis muscle) or in the
sternocleidomastoid muscle.
Complications of thyroid surgery
Complications of thyroid surgery

Intra-operative Post-operative

1. Hemorrhage 1. Hemorrhage
Post operative hemorrhage can be life threatening due
2. Injury to Recurrent Laryngeal Nerve (RLN)
to airway compression (urgent surgical evacuation)
(m/c nerve to be injured in thyroid surgeries)
2. Hypocalcemia
Unilateral injury : Hoarseness or weak voice
Bilateral injury : Airway obstruction and stridor Most common cause is compromised blood supply to
parathyroids from Inferior thyroid artery
3. Injury to Superior Laryngeal Nerve - external branch Presents after 2-3 days
Low pitched voice Clinical signs : Chvostek's sign and Trousseau's sign

Baehr's triangle
Landmark for safe thyroid surgery to prevent RLN injury.

Thyroid cartilage

Boundaries
CCA
Chovstek sign
ITA Facial muscles spasm Trousseu sign
RLN on percussion Carpo-pedal spasm on
Beahr's inflating BP cuff
triangle

3. Thyrotoxic Crisis (Thyroid Storm)

Thyrocervical
trunk
Rare complication, seen in patients with untreated
Inferior thyroid artery hyperthyroidism.
Recurrent laryngeal nerve To prevent : Pre-op Beta blockers & antithyroid drugs

MEN Syndromes
MEN 1 (aka Wermer Sx) : 3 P’s – Parathyroid (Adenoma), Pancreas (Gastrinoma), Pituitary (Prolactinoma)
MEN 2A (aka Sipple Sx): Medullary ca. of thyroid, Pheochromocytoma, Parathyroid adenoma
MEN 2B (aka MEN 3) : Medullary ca. of thyroid, Pheochromocytoma, Mucosal neuromas, Marfanoid habitus.

Genetic Mutation
MEN 1: MEN1 gene on chromosome 11
MEN 2A & 2B: RET proto-oncogene on chromosome 10

Prophylactic Thyroidectomy
Done for Medullary ca of thyroid (agressive tumor)
MEN 2A: 5 yrs
MEN 2B : 1 yr
 Breast Carcinoma
Breast carcinoma is the most common malignancy in women worldwide. Mammography
Screening for breast carcinoma :
Annual mammogram : All women after 40 yrs of age
Annual MRI : For high risk patients after 30 yrs of age
On suspicion of breat carcinoma in screening, triple assessment is done :
i. Clinical features
ii. Histopathology (core needle biopsy)
iii. Radiological assessment
The modality of radiological assessment could be
USG : in young (< 40 yrs) & lactating females (r/o abscess)
MRI : high risk patients & patients with breast implants
Mammography : for everyone else

Why mammogram not done High risk patients :

in young patients? a. Family h/o breast carcinoma
Breast tissue in younger women b. BRCA +
is denser, which makes c. Recurrence
mammograms less effective d. Patient on radiotherapy Micro-calcifications
Mammogram is most sensitive for
microcalcifications (highly suggestive of malignancy)

Based on the radiological assessment, a BIRADS score is assigned.

Breast Imaging Reporting and Data System
Core biopsy needle
BI-RADS 0 : Additional imaging needed
BI-RADS 1 : Normal (continue screening)
BI-RADS 2 : Benign breast mass
BI-RADS 3: < 2% risk of malignancy (requires 6-month follow-up)
BI-RADS 4 & 5 : 2-95% risk of malignancy (Biopsy recommended)
BI-RADS 6 : Biopsy-proven malignancy

Management of breast cancer :

Treatment of breast cancer is multidisciplinary, involving surgery,
radiation, systemic therapies (hormonal, chemotherapy, and targeted
therapy), and palliative care for advanced disease.
a. BCS (breast conservation sx) + Radiotherapy : early-stage disease
b. Mastectomy : for large tumors, multicentric disease BRCA 1 (chr 17) BRCA 2 (chr 13)
c. Hormonal Therapy : ER/PR-positive tumors. "17 year olds" "13 yeard olds"
d. HER2-positive tumors: Treated with Trastuzumab Triple negative Luminal A type
e. Triple-negative breast cancer (TNBC): Chemotherapy ± type breast cancer Breast cancer
immunotherapy. Bad prognosis Risk of male breast
f. Neoadjuvant therapy: Shrinks tumors pre-surgery in locally Indication for cancer
advanced cases. prophylactic Assocaited with
g. Adjuvant therapy: Post-surgery treatment to reduce recurrence. mastectomy Fanconi's anaemia
h. Metastatic disease: Focus on palliation and systemic therapy.
 Breast carcinoma one liners Breast conservation therapy
1. Breast conservation surgery : Resection of
Most common location : Upper outer quadrant (more tissue present)
tumor with 1 cm margins (breast is
Sporadic breast cancer is more common than familial
preserved)
M/c gene involved :
2. Sentinel lymph node biopsy (a secondary
a. Sporadic breast cancer : P53 gene
incision made at axilla)
b. Familial breast cancer : BRCA 1 gene
3. Mandatory radiotherapy
Most important prognostic marker : Axillary lymph node involvement
Most common complication after mastectomy : Seroma (collection of Survival rates are similar to mastectomy when
fluids in a surgically created cavity) combined with radiotherapy

Structures removed in radical mastectomy Axillary lymph nodes

1. Radical mastectomy Level 1 Level 3
a. Breast + NAC (nipple areolar complex)
1. Anterior group Level 2
b. Pectoralis muscles (major + minor) 2. Posterior group
c. Level 1,2,3 axillary lymph nodes (aka subscapular) Level 1
3. Lateral group
2. Modified radical mastectomy Level 2
"Pectoralis major spared in all"
(behind p.monor)
a. Patey's MRM : Pectoralis minor also spared (P - P.minor)
1. Central group
b. Scanlon MRM : Pectoralis minor incised (S-Scalpel) 2. Inter-pectoral group
c. Auchincloss MRM : Pectoralis minor retracted (Claw retracts)
Level 3
Contraindication to radical mastectomy : Distant mets 1. Apical group
 Breast Carcinoma classification
Breast carcinoma can be classified based on either histological or molecular features

A. Histological classification Van Nuys Prognostic index

Used for DCIS management.
1. Invasive carcinomas
Based on "GAMS"
a. Invasive Ductal Carcinoma (most common type)
G : Grade
b. Invasive Lobular Carcinoma
A : Age
2. Non invasive carcinoma M : Margin
a. Ductal carcinoma in situ (DCIS) S : Size
b. Lobular carcinoma in situ (LCIS) Interpretation
Low scores : BCT (BCS + RT)
High scores : mastectomy
B. Molecular classification No role of chemo in DCIS

Based on receptor status and gene expression profiling

ER/PR (+) ER/PR (-)

Check Ki-67 Check Her-2 (on

immunohistochemistry)

Ki-67 (-) Ki-67 (+)

Low proliferation High proliferation

Luminal A type Luminal B type

Most common type More agressive than
Best prognosis luminal A
Treated with hormonal therapy Treated with hormonal
Examples of breast carcinoma of therapy + Chemotherapy
this type are : If Her2(+) on IHC, its
a. Papillary known as triple positive
b. Tubular breast cancer
c. Mucinous
d. Lobular
Her-2 (+) Her-2 (-)

Her2 enriched Triple Negative

Treated with Her2-targeted Poor prognosis
therapy : Trastuzumab Cytokeratins (+)
(aka Herceptin) aka Basal type
S/e of therapy : Cardiotoxic Treated with chemotherapy
If resistant to Trastuzumab, (good response to t/t)
drug used : Lapatinib Examples include :
a. BRCA - 1 (+) tumors
b. Secretory type
c. Medullary type
"Secretary Medussa is bad"
 Immunohistochemistry scores Paget's disease of breast
(for Her-2 status) Rare form of breast cancer that involves the epidermis
IHC scores range from 0 to 3 of the nipple and areola (d/d : Eczema)
Negative for Her2 : Score of 0 and 1 Associated with an underlying DCIS or invasive breast ca.
Equivocal (FISH needed to confirm) : Score 2 Diagnosis : Skin punch biopsy showing Paget cells
Positive for Her2 : Score 3 Treatment : Central cone excision + Radiotherapy
FISH is the gold standard when IHC is equivocal.

Paget's is unilateral
with no itching while
eczema is bilateral
with itching
Score 0 Score 1 Score 2 Score 3

Stain used : Di-amino-benzidine

Breast Carcinoma - TNM Staging

T staging N staging
T⁰ : Non invasive tumor (DCIS/LCIS) N⁰ : No lymph nodes involved
T¹ : < 2 cm N¹ : Axillary LN (mobile)
T² : 2-5 cm "T : 2 & 5" N² : Divided into 2 stages
T³ : > 5 cm (spread to other organs) N² a : Axillary LN (matted)
T⁴ : Further divided into 4 stages N² b : Internal mammary LN
T⁴ a : Serratus Anterior involved N³ : Divided into 3 stages
T⁴ b : Peau de orange / Ulceratons / Satelite lesions "PUS" N³ a : Infra-clavicular LN
T⁴ c : Cutaneous involvement N³ b : Int.mammary + Axilalry LN
T⁴ d : Inflammatory breast cancer (poor prognosis) N³ c : Supra clavicular LN

Treatment based on T stage

T (0,1,2) : Breast conservation therapy M staging
T 3 : Neo-adjuvant chemo + Mastectomy + RT Based on metastasis (present or not)
T 4 : Only palliative treatment

Prefixes
eg. cTNM, pTNM
C : Clinical
P : Pathological
Y : Neo-adjuvant Multifocal Multicentric
M : Multifocal in same in different quadrants
quadrant of same breast Peau de orange appearance
Due to blockage of superficial lymphatics
(Stage : T4b)
 Benign breast tumors (BIRADS -2)

Fibroadenoma of breast Phyllode's tumor

Most common benign breast tumor Differentiated from fibroadenomas by their rapid
Typically occurs in young women (15–35 years) growth and histological features.
Mobile, well-circumscribed, painless lump Classic histological feature : Leaf like growth pattern
"breast mouse" Seen in females >40 yrs
No malignant potential in simple Mainstay of treatment : wide local excision with
fibroadenomas. ≥1 cm margins (to avoid recurence)
Has malignant potential

Popcorn calcification Leaf-like growth pattern

Approach to Nipple Discharge

Nipple discharge

Green Bloody

Duct Ectasia Single duct Multiple ducts

Dilatation of lactiferous ducts
Fluid accumulates in the dilated ducts leading to Rule out breast
infection and inflammation. carcinoma
Seen in peri-menopausal females
Smoking is a known risk factor.
Characteristic broken needle clacifications on X-ray Intra-ductal Papilloma
Total duct excision - Hadfield's Surgery
Small, wart-like tumor within a lactiferous duct
Solitary intra-ductal papilloma has no malignant
potential.
Treatment : Microdochectomy (micro-doch-ectomy)

Broken needle
clacifications
Breast - Miscellaneous

Mastitis Gynaecomastia
Mastitis can be either lactational or non-lactational. > 2 cm sub-areolar breast tissue in males
1. Lactational mastitis
Occurs due to milk stasis and bacterial infection, most Physiological gynaecomastia seen with
a. Neonates (due to maternal estrogen)
commonly by Staphylococcus aureus.
b. Adolescence (excess estradiol)
Treatment : Antibiotics (Dicloxacillin)
c. Senescence (testosterone drops)
Breastfeeding has to be continued
2. Non-lactational mastitis "Pseudo-gynaecomastia seen in fat people"
Associated with duct ectasia and smoking.
Inflammatory breast carcinoma (T4d) has to be ruled
out in non lactational mastitis.

Male breast cancer

Prognosis and management same as
Mastitis
female breast cancer
Associated with BRCA-2 mutation
Seen in old age (60-70 yrs)
Breast Abscess Most common type : DCIS
Complication of untreated mastitis
Characterised by pus formation
IOC : USG
Treatment Breast conditions associated
i. Aspiration of pus (if failed then do a 2nd attempt)
ii. If aspiration fails twice : Incision and Drainage with smoking
1. Paget's disease
2. Duct ectasia
3. Mondor's disease
Sclerosing thrombophlebitis of
Breast reconstruction flaps
the subcutaneous veins of the
anterior chest wall
TRAM flap DIEP flap
4. Zuska's disease
(Transverse rect. abd. (Deep inferior epigastric
Sub-areolar asbcess
pedicel flap) perforator)

"Looks like T" Flap is transplanted

Only skin and fat moved
Attached flap
Preserves abdominal strength
Abdomen becomes weak
Quicker, less intense recovery
Uses superior epigastric artery
(preferred flap)
Inflammation of vein in Mondor's disease
Arterial Occlusion
Arterial occlusion

Acute occlusion Chronic occlusion

Surgical emergency Characterised by intermittent claudication (pain due to
Presents with sudden bilateral lower anaerobic metabolism)
limb ischemia and absent pulses. M/c cause is atherosclerosis
M/c cause is cardioembolic events M/c muscles affected : Calf muscles (femoral artery occlusion)
(atrial fibrillation) Initial investigation : USG doppler
IOC : CT angiography IOC : CT angiography
Management : Gold standard : DSA + Baloon angioplasty
Immediate anticoagulation with Treatment : Baloon angioplasty +/- stenting
heparin
Urgent surgical intervention Ankle-Brachial index : tells about the degree of occlusion
(catheter based treatment) Normal : > 0.9
Complications : Intermittent claudication : 0.5 - 0.9
Reperfusion injury : toxic Critical limb ischemia : 0.3 - 0.5
metabolites leads to acidosis, Gangrene : < 0.3 "Three - Gangree"
hyperkalemia and myoglobinuria
Boyd's classification for intermittent claudication :
Grade 1 : Pain relieved on walking
Grade 2 : Pain on walking
Ankle brachial index (ABI) Grade 3 : More pain on walking (compelled to take rest)
Grade 4 : Pain even at rest

Sites of chronic arterial occlusion

Claudication (pain) is at one level below the artery occluded

Aorta (buttock claudication)

Leriche Syndrome
Buttock claudicaltion + Impotence Iliac (thigh claudication)
Due to aorto-iliac occlusion (Impotence due
to compromised supply of internal Iliac artey)
Treatment : Aorto-femoral bypass
Femoral (calf claudication)

Baloon angioplasty
Done for chronic arterial occlusion

Popliteal (foot claudication)

Stent is closed
Atherosclerotic plaque

-Balloon inflated
Stent is expanded

Expanded stent
is left in place
 Aneurysms
Abnormal dilation or bulging of a blood vessel, caused by a weakness in the vessel wall
Most commons :
Vessel overall : Circle of Willis - Berry aneurysm (Junction of ant.cerebral and ACOM)
Extra-cranial vessel : Abdominal aorta (infra-renal)
In Ehlers Danlos Syndrome/ Marfan Syndrome/ Bicuspid aortic valve : Thoracic aorta
Peripheral vessel : Popliteal
Pseudo-aneurysm : Does not involve all layers (outer layer - tunica adventitia, is intact)
Yin yang sign
Initial investigation : USG Doppler
(on Doppler USG)
IOC : CT angiography
Bi-directional flow of blood
IOC in unstable : TEE
in an aneurysm
(Trans-esophageal echocardiogram)
Management : EVAR
(endovascular aneurysm repair)
Indication to surgically manage :
a. Any symptompatic aneurysm
b. Large size
> 5.5 cm in males
Crisoid aneurysm
> 5 cm in females Draped Aorta sign
Type of arterio-venous
c. Rapid increase in size (on CT)
hemangioma
0.6 cm in 6 months
1 cm in 1 year

Aortic Dissection
An aortic dissection is an emergency
Tear develops in the intima (inner layer) of the aorta, leading to blood
flowing between the layers of the vessel wall, creating a false lumen
Most common cause : Hypertension
Other risk factors : Ehlers Danlos Syndrome/ Marfan Syndrome/ Bicuspid
aortic valve
Characteristic presentation : Sudden, severe tearing or ripping chest
pain radiating to the back or abdomen
Asymmetrical blood pressure (between arms)
Aorta shows a true
IOC : CT angiography lumen and a false lumen
IOC in unstable : TEE (Trans-esophageal echocardiogram)

Classification of aortic dissection

1. Stanford classification
Stanford A : Ascending aorta involved (needs immediate surgical mx)
Stanford B : Only descending aorta involved (medical mx with IV esmolol)
2. De-Bakey classification
Stanford A is De-Bakey 1 and 2 based on descending aorta involvement
Stanford B is De-Bakey 3

Double Barreled Aorta

Less severe form of aortic dissection (doesn't progress) A (Ascending aorta ± B (Only descending
descending aorta) aorta involved)
2 intimal tears (forms a false channel)
 Varicose Veins
Dilated & tortuous superficial veins
Commonly seen in lower limbs
Cause : valvular incompetence and venous reflux Mickey mouse sign
Concept : on USG
Valves normally only allow movement from down to up and (indicates SFJ incompetence)
from superficial to deep veins (not the other way)
Valve insufficiency leads to venous reflex and consequent
varicose veins
Dilated SFJ indicates SFJ insufficiency (Mikey mouse sign) Saphenofemoral Junction
Tests for SFJ incompetence :
i. Brodie-Trendelenburg test
Great Saphenous vein
ii. Morrissey's test (Superficial System)
iii. Schwartz test
Femoral Vein
Common sites of varicose veins: (Deep System)

a. Great saphenous vein (most common) - Saphenous nerve injury

b. Small saphenous vein - Sural nerve injury
Small Saphenous vein
Gold standard investigation: Duplex ultrasonography
(Superficial System)
First-line : Conservative management (compression stockings)
TOC for large varicose veins: Endovenous ablation (EVLA) or Perforating Veins

Radiofrequency ablation (RFA)

Complication : Venous ulcers (commonly located near the medial
malleolus, known as Gaiter's area)

Klippel-Trenaunay syndrome Perforating veins reflux

Varicose veins IOC : Fegan's test
Port-wine stain TOC : Sclerotherapy
Limb hypertrophy

CEAP Classification
For categorizing venous disorders and determining treatment strategies
CEAP stands for : Clinical - Etiological - Anatomical - Pathophysiological
Duplex ultrasonography is essential for anatomical and pathophysiological
classification

Clinical classification
C1 : Telangiectasia or reticular veins Reticular veins
C2 : Varicose veins "Varicose veins in 2 legs"
C3 : Edema "3 is E"
C4 : Skin-subcutaneous tissue changes
C4-a : Pigmentation or eczema
C4-b : Lipodermatosclerosis or atrophie blanche
C4-c : Corona phlebectatica
C5 : Healed
C6 : Active ulcer "Active sex" Atrophie Blanche Lipodermatosclerosis

Gaiter's zone
At medial mallelolus
Venous (stasis) ulcers

Corona Phlebectatica
 Deep venous thrombosis (DVT)
Formation of a blood clot (thrombus) in the deep veins of leg
Most common site of DVT : Calf veins (e.g., posterior tibial and peroneal veins)
Most common cause : Post op patients (lack of movement) - Prophylaxis is essential

First-line imaging: Duplex USG

Most sensitive test: D-dimer (used to rule out DVT in low-risk patients) Calf swelling,
Other tests for DVT : erythema and
a. Modified Perthe's test warmth with pain
b. Pratt test (mostly unilateral )
Clinical signs in DVT :
i. Homan's sign (pain on foot dorsifelxion) "Homan - heels"
ii. Moses sign (pain on squeezing calf muscles)
Gold standard investigation: Venography (invasive procedure, hence not commonly done)

Initial anticoagulant of choice: LMWH for 3 motnths

Complications : Pulmonary embolism (PE) and post-thrombotic syndrome

Right (normal) Left (with DVT) Triphasic

Normal arteries
artery artery

Biphasic
Arterial stenosis (mild)
vein does not
Vein completely compress in DVT
compressed
Monophasic
Arterial stenosis (severe)
With compression Normal veins

Duplex Ultrasonography

Lymphedema
Accumulation of lymphatic fluid in the tissue Brunner's staging
Occurs due to impaired lymphatic drainage
Stage 0 : Sub-clinical
Chronic swelling, most commonly in the limbs
Stage 1 : Pitting edema
Treatment : Debulking procedures (e.g., Charles procedure)
(subsides with elevation)
Classification : Stage 2 : Non pitting edema
(not relieved with elevation)
Stage 3 : Fibrosis
Primary lymphedema Secondary lymphedema

1. Congenital lymphedema (Milroy disease) More common cause of

Present at birth or within the first year of life lymphedema
Mostly bilateral presentation MCC : Filariasis
Management : VLNT (Vascular lymph node transfer) Other causes
2. Lymphedema praecox (Meige disease) a. Post op. patients
Onset during puberty or early adulthood b. Varicose veins
More commonly in females "Meige is a female" c. Trauma
Mostly unilateral presentation
Stewart Treves Syndrome
Angiosarcoma in patients with long
Both conditions show AD transmission
standing lymphedema
Occurs 10-20 years after a surgery
Ulcers

Arterial ulcers Neuropathic ulcers

Shiny and thin ulcers Aka Diabetic ulcer or
Tip of toe/ anterior shin Trophic ulcer
Lateral malleolus Associated with loss of
Dry ulcer with necrotic sensation
eschar Present on plantar aspect
of foot
Punched out ulcer

Venous ulcers Pressure ulcers

Gaiter's area (medial Pressure > 30 mm Hg
malleolus) Ischium/Gluteal tuberosity
Ulcers with sloping (other pressure sites)
edge aka Decubitus ulcer or
Wet & exudative ulcer Bed sores
Management : Negative
pressure at -125 mm Hg

Grading of pressure ulcers

Grade 1 : Non blanchable erythema

Grade 2 : Partial thickness skin loss Negative pressure wound therapy

(epidermis and dermis) -125 mm Hg

Grade 3 : Full thickness skin loss

(Involves subcutaneous tissue)

Grade 4 : Involves muscle or bone Hyperbaric oxygen therapy

(tissue necrosis) Causes neovascularisation and reduces oxidative stress
Lesser occurence of ischemic reperfusion injury
Side effect : Middle ear barotrauma
 Urolithiasis
Formation of calculi (stones) in the urinary tract (including the kidneys, ureters, bladder, and urethra)
If the stone is impacted in ureters it can cause renal colic (sudden severe flank pain)

Types of urinary stones

a. Calcium Oxalate stone
Most common urinary stones
Ca-oxalate mono-hydrate stones : Dumbell shaped "Mona is dumb"
Ca-oxalate di-hydrate stones : Envelope shaped
Risk factors : Hyper-calciuria, hyper-oxaluria, hypo-citraturia (citrate binds to calcium)
b. Struvite stone
Ca-Ox stone Ca-Ox stone
aka Triple phosphate stone (Calcium, magnesium, and ammonium phosphate) (Monohydrate) (Dihydrate)
aka Staghorn stone because of the gross shape of renal calculi
Microscopic appearance : Coffin lid shaped "Dead stag"
Seen in alkaline urine (all other stones seen in acidic urine)
Associated with UTI - urea splitting organisms (eg Proteus)
(makes the urine alkaline by producing ammonia)
c. Uric acid stone
Risk factors: Hyperuricemia, gout
Struvite stone Uric acid stone
Microscopic appearance : Rhomboid
d. Cystine stone
Seen to cystinuria (defect in PCT, COLA amino acids lost in urine)
Microscopic appearance : Hexagonal crystals "6tine stones"
Hard stones
e. Ammonium urate stone
Cystine stone Ammonium urate
Associated with Laxative use
stone
Microscopic appearance : Apple thorn shaped

Initial investigation : USG (some stones are radiolucent, hence X-ray not done)
IOC : NCCT

Management
a. Conservative management - stones < 0.5 cm
High fluid intake
Urine alkalisation with Pottasium citrate (for acidic stones)
Extracorporeal shock wave lithotripsy
Allopurinol for uric acid stones
Thiazides are used for hyper-calciuria
Alpha blockers (tamsulosin) for distal ureteric stones
b. Extracorporeal shock wave lithotripsy (ESWL) - stones < 2 cm
Done only for soft stones (can't be done for Cystine stones)
Not done if there is associated - infection/obstruction/bleeding diathesis
Also avoided in pregnancy/adults/children
Percutaneous nephrolithotomy
c. Percutaneous nephrolithotomy (PCNL) - stones > 2 cm
Done for larger stones (eg. Staghorn calculi)
Done for cases where ESWL is not possible
d. Retrograde intra renal surgery (RIRS)
Minimally invasive procedure, performed using a ureteroscope
Done for complex cases or residual stones after ESWL or PCNL.
Contraindication : Active UTI & larger stones (PCNL is preferred) Retrograde intra renal surgery
 IV Pyelogram - Special signs

Intravenous Pyelogram (IVP)

Hand-shaking calyces / flower vase app

Horse-shoe kidney
Congenital anomaly where the kidneys are fused at lower poles
Fused part is known as isthumus
Due to the fusion, ascent is prevented by IMA 1. Fish hook : Retrocaval ureter
Increased risk of RCC 2. Maiden waist : Retroperitoneal fibrosis
Most common complication : Hydronephrosis 3. Drooping lily : Duplex kidney
Associated genetic disorder : Turner syndrome 4. Hand shaking calyces / Flower vase : Horse shoe kidney
Conservative management 5. Cobra head : Ureterocele

Site affected
in RP fibrosis

Fish hook sign Maiden waist app.

Retrocaval ureter Retroperitoneal fibrosis
Right ureter posterior to inf. vena cava aka Ormond’s disease
Complications : Hydronephrosis and recurrent UTIs Fibrous tissue in the retroperitoneum - leads to
ureteral obstruction
Associated with IgG4 related disease

Drooping lily sign

Duplex Kidney
One of the kidneys have an extra collecting system Cobra/Adder head app.
(which may or may not drain into an ectopic ureter)
Urterocele
Most common congenital renal anomaly
Weigert-Meyer rule: Cystic dilatation of the terminal portion of
Upper pole ureter is prone to obstruction "vowels stick" the ureter
Lower pole ureter is prone to reflux Associated with duplex kidney

Complication of ectopic ureter in females: Continuous dribbling of urine.

PUJ obstruction
Functional or anatomical blockage at the junction of the renal
pelvis and proximal ureter
MCC is congenital anomalies in development
Obstruction leads to hydronephrosis (dilatation of renal pelvis
and calyces), if untreated, results in progressive renal damage.
Investigations :
Initial investigation : USG
IV Pyelogram shows "Ballooned renal pelvis" with delayed
excretion of contrast
Gold standard : Radiotracer scans with MAG-3 or DTPA
Indications for surgery (pyeloplasty) :
Recurrent UTIs
Bilateral obstruction
Right PUJ obstruction on IVP
Poor renal function (<40%) in the affected kidney

Renal Tuberculosis
Renal TB is a form of genitourinary tuberculosis
(GU TB is most common form of extrapulmonary TB)
Sterile pyuria is a hallmark finding
Other classic fidndings
a. on IV Pyelogram
Moth eaten calyx
Thimble bladder (extremely contracted and fibrosed bladder)
Kerr kink (sharp kink at the pelvi-ureteric junction)
b. on X-ray
Putty kidney (renal calcification)
c. on Cystoscopy
Golf hole app. of ureter opening U/L calcified kidney B/L calcified kidney
Pallor of mucosa around ureteric orifice (earliest finding) on X ray on X ray
Autonephrectomy is seen in later stages of renal TB (Putty kidney) (Medullary nephro
Surgical intervention is required for strictures, non-functioning calcinosis)
kidneys, or severe bladder involvement.

Vesico Ureteral Reflux (VUR)

Retrograde flow of urine from the bladder into the ureters
Causes recurrent UTIs and renal scarring Voiding cystourethrogram
MCC is congenital defect - primary VUR
Secondary VUR is caused due to increased pressure in bladder
a. Bladder outlet obstruction (e.g., posterior urethral valves)
b. Chronic cystitis
c. Ureteral anomalies (e.g., duplex system, ureterocele)
IOC : Voiding cystourethrogram
Grading system :
Grade I: Reflux into the ureter only (without dilatation)
Grade II: Reflux into the renal pelvis (without dilatation)
Grade III: Mild dilatation of ureter or renal pelvis 1. Bladder is filled with dye using a catheter
Grade IV: Moderate dilatation with tortuous ureter and blunting of calyces 2. Patient is asked to void (urinate)
Grade V: Severe dilatation 3. Series of X-rays taken while the patient urinates
Renal Cell Carcinoma
Historical names of renal cell carcinoma Paraneoplastic syndromes:
Hypernephroma a. Hypercalcemia (PTHrP production)
Grawitz tumor b. Stauffer syndrome : Non-metastatic hepatic dysfunction

Etiology Investigations:
Environmental factors Initial investigations : USG
IOC : Contrast enhanced CT (large heterogeneous mass)
Cigarette smoking (strongest risk factor)
Obesity and hypertension. Large homogeneous black lesion in kidneys on CT would be an
Chronic renal failure and dialysis angio-myo-lipoma (associated with Tuberous Sclerosis)
Genetic factors
Von Hippel-Lindau (VHL) disease (chromosome 3p)
MET proto-oncogene mutation
Birt-Hogg-Dubé syndrome

Histological subtypes
a. Clear Cell RCC
Most common type Large heterogeneous mass - Black homogeneous lesion -
Associated with VHL mutation RCC Angiomyolipoma
b. Papillary RCC
2nd most common Management:
Associated with MET gene mutation Surgery is mainstay (chemo and radio resistant)
Psammoma bodies can be seen on h/p
a. Radical nephrectomy
c. Chromophobe RCC Standard treatment
Best prognosis Large or centrally located tumors
d. Collecting Duct (Bellini duct) RCC b. Partial nephrectomy
Rare but aggressive tumor Tumor size < 4 cm
Worst prognosis Bilateral tumors
e. Medullary RCC
Associated with sickle cell trait

Poly-cystic kidney disease

ADPKD (Autosomal dominant PKD) ARPKD (Autosomal recessive PKD)
More common Less common
Age on onset > 30 yrs More severe
M/c presentation : Hypertension Presents at infancy and childhood
50% patients get ESRD by age of 60 yrs 50% of newborns born with ARPKD die
Genes affected (infant renal failure)
PKD-1 gene (chr 16) Genes affected
PKD-2 gene (chr 4) PKHD-1 gene (chr 6)
Diagnosis : USG (Ravine's criteria used)
Age < 40 yrs : ≥ 3 cysts (U/L or B/L)
Age 40 - 60 yrs : ≥ 2 cysts (in each kidney)
Age > 60 yrs : ≥ 4 cysts (in each kidney)
Treatment : Vasopressin antagonists

Smaller cysts
(Smooth outer contour )

Large cysts
(Rough outer contour )
 Carcinoma of Prostate and BPH
Carcinoma of Prostate
Most common cancer in men > 65 years
Most common histological type : Adenocarcinoma
Presentation : Lower urinary tract symptoms (LUTS)
Prostate Central Zone
(Frequency, urgency, nocturia, weak stream)
Urethra Transitional Zone
Rule out : Benign prostatic hyperplasia (BPH)
Investigations : Peripheral Zone

a. Screening
i. Prostate-specific antigen (PSA):
Normal range: < 4 ng/mL (for age > 60 yrs)
PSA > 10 ng/mL : Malignancy
BPH originates from transitional zone
PSA 4-10 : Rule out BPH / Prostatitis / UTI
(presents early)
ii. Digital rectal examination (DRE): Adenocarcinoma originates from peripheral zone
Hard, irregular prostate with nodules : Malignancy (presents late)
Smooth and firm prostate enlargement : BPH
b. Confirmatory
i. TRUS (transrectal USG) guided biopsy Benign Prostatic Hyperplasia
Gleason score based on architectural pattern of Non-cancerous enlargement of the prostate gland
tumor glands (Scores range from 2 to 10) Cause : Increased activity of dihydrotestosterone (DHT)
ii. MRI Compressed prostatic urethra : bladder outlet obstruction
iii. PMSA PET : For mets On DRE : Enlarged, smooth, firm prostate
Elevated PSA ( > 4 ng/ml)
Management :
a. Medical management :
i. α1-blockers:
Relieve obstruction by relaxing prostatic smooth muscle
Inhibits the dynamic component of BPH
Drugs: Tamsulosin, Alfuzosin, Doxazosin
ii. 5α-reductase inhibitors:
Reduce prostate size by inhibiting DHT synthesis
Inhibits the static component of BPH
Drugs: Finasteride, Dutasteride
b. Surgical management :
Metastasis
Indicated in case of any complication like AUR,
Hematogenous spread
Predominantly to bones (osteoblastic mets) recurrent UTIs, bladder stones or failure of medical
Spread to lumbar vertebrae - via Batson venous plexus therapy.
Isolated liver mets is rare Gold standard surgery : Transurethral Resection of
Retroperitoneal and pelvic lymph nodes are commonly Prostate (TURP)
involved (prostate is retroperitoneal organ)

Management
a. Localised disease
Active surveillance:
For low-risk, well-differentiated tumors
(Gleason ≤ 6, PSA < 10 ng/mL)
If life expectancy < 10 years
Radical prostatectomy
Healthy patients with life expectancy > 10 years
Complications : Hydronephrosis, > 200 ml residual
Distal limit of resection : Verumontanum
urine, raised BUN, erectile dysfunction.
M/c complication : Retrograde ejaculation (injury at
b. Advanced disease with organ invasion internal urethral sphincter)
Androgen deprivation therapy (ADT) + Radiotherapy TURP Syndrome
GnRH agonists (Leuprolide, Goserelin) or GnRH
Absorption of large volumes of hypo-osmolar irrigation fluid
antagonists (Degarelix)
during TURP (distilled water used with monopolar cautery)
Flutamide (androgen antagonist)
Hyponatremia + Altered mental status
Orchidectomy (rarely done now)
Prevention : Use of isotonic fluids with bipolar cautery
 Testicular Tumors
Most common solid tumors in males aged 15–35 years
Presents as painless testicular mass
Cryptorchidism (undescended testis) is the most
significant risk factor
Associated with Klinefelter syndrome
Classification :
a. Germ Cell Tumors (GCTs) – 95% of cases
i. Seminomas – Most common germ cell tumor Schiller Duval bodies
ii. Non-seminomatous germ cell tumors Seen with Yolk sac tumor
Yolk sac tumor (endodermal sinus tumor)
Choriocarcinoma
Investigations :
Embryonal carcinoma
Teratoma Initial investigation : USG scrotum + Tumor markers
Mixed germ cell tumors AFP : Yolk sac tumor "Yolk has protein"
b. Sex Cord-Stromal Tumors – 5% of cases HCG : Choriocarcinoma "Chorionic"
i. Leydig cell tumor (Reinke Crystalloids) LDH : Seminoma
ii. Sertoli cell tumor Biopsy/FNAC : Never done (can cause local seeding)
Iii. Granulosa cell tumor IOC for Tumor staging : High inguinal radical orchidectomy
Open biopsy : frozen section using Chevassu Maneuver
Staging and Management :
For metastasis : CECT
Scrotal mass + Positive tumor markers Prostate is a retroperitoneal organ
Commonly involves para-aortic lymph nodes
Check for lymph node involvement

No Lymph node involvement Lymph nodes involved

Stage 1 Stage 2 (local mets), Stage 3 (distant mets)

Chemo-therapy (one cycle) Adjuvant chemotherapy
For seminoma (highly radiosensitive) Chemotherapy regimen : BEP (Bleomycin, Etoposide, Cisplatin)
add radiotherapy with chemotherapy f/b Retro-peritoneal lymph node dissection

Undescended Testes (Cryptorchidism)

Failure of one or both testes to descend into scrotum
Most common congenital anomaly of the male genitalia
Higher incidence in preterm infants
Spontaneous descent occurs in most cases by 6 months of age
Normal Testicular Descent occurs in two phases:
Transabdominal phase (up to 10 weeks gestation)
Inguinoscrotal phase (from 26–35 weeks gestation)
Most common location: Inguinal canal
(presents with empty scrotum and inguinal mass)
Management :
a. Observation
In neonates, spontaneous descent may occur by 6 months of age.
If descent does not occur by 6 months, intervention is required.
b. Surgical Treatment - Orchidopexy
Indicated if the testis does not descend by 6–12 months.
Procedure involves mobilizing the testis and fixing it in the scrotum.
Early surgery (before 1 year) improves fertility potential and reduces cancer risk
c. Orchidectomy
Done in postpubertal males with undescended testes due to high cancer risk
M/c associated cancer : Seminoma
Other testicular conditions

Testicular torsion Varicocele

Twisting of spermatic cord Abnormal dilatation and tortuosity of the
Compromised blood supply - Ischemia pampiniform venous plexus in the spermatic cord due
(surgical emergency) to venous reflux.
Presenting features : Left side is more common (Left testicular vein drains
Pain into the left renal vein at a right angle, increasing
Absent cremasteric reflex venous pressure)
Assymetric scrotum Classic clinical finding : "Bag of worms" appearance
Management : Most common cause of correctable male infertility
Immediate exploration of both testes IOC : USG with Doppler
(within 6 hours)
Treatment: Varicocelectomy (for symptomatic cases
Differential diagnosis : Epididymitis
or infertility)
(Phren's sign - pain relieved on lifting the testes)

Normal Twisting of
spermatic cord Normal Varicocele

Testicle

Cystic swllings of Testes Hydrocele


Both are painless, cystic swellings that Most common cause of painless scrotal swelling
transilluminate Accumulation of fluid within the tunica vaginalis leading to
USG done to differentiate scrotal swelling.
a. Spermatocele Can be congenital or acquired
Contains milky fluid with sperm Congenital hydrocele is due to patent processus vaginalis
"Barley water fluid" Acquired hydrocele is m/c and is mostly idiopathic.
b. Epididymal Cyst IOC : USG
Clear, serous fluid without sperm Transillumination test : Positive in uncomplicated
"Chinese lantern illumination" hydrocele
Surgical procedures for hydrocele
a. Lord’s (plication)
b. Jaboulay’s (eversion) hydrocelectomy
Spermatocele or
Epididymal cyst
Carcinoma of bladder
Most common histological type : Transitional cell carcinoma (~90%)
Presents as painless hematuria
Gold standard investigation : Cystoscopy with biopsy
Risk factors:
a. Smoking (most significant risk factor)
b. Schistosomiasis (squamous cell carcinoma)
c. Occupational exposure to aromatic amines (adenocarcinoma)
Management :
If very small : Intravesical BCG and cystoscopic removal
If moderate size : Trans urethral resection of bladder tumor (TURBt)
If invades muscle : Radical cystectomy TURBt
BCG contraindications: Gross hematuria, immunosuppression..

Penile conditions
Congenital conditions of the penis

1. Hypospadias
Most common congenital anomaly of urethra
Urethral opening on the ventral side (under-surface) of the penis.
Associated with chordee (ventral curvature)

2. Epispadias
Urethral opening on the dorsal surface (upper surface) of the penis. Hypo-spadias Epi-spadias
Often associated with bladder exstrophy
- Both don't cause obstruction or UTI For penis, dorsal is upper and
- Management for both : Surgical correction ventral is under surface
- Circumcision is contraindicated (foreskin needed for repair)

Inflammatory conditions of the penis

1. Balanitis
Inflammation of the glans penis
Common causes : Poor hygiene, infections (Candida, bacterial)
Higher risk in uncircumcised males
If prepuce also inflammed along with glans : Balanoposthitis
Treatment: Antifungal/antibacterial therapy and proper hygiene

2. Peyronie’s Disease
Fibrosis of tunica albuginea
Penile curvature during erection
Associated with pain and erectile dysfunction

Pre-malignant lesions of the penis Malignant lesions of the penis

1. Carcinoma in situ Squamous cell carcinoma
Penile shaft : Bowen's disease Most common malignant lesion of the penis
Glans penis : Erythroplasia of Queyrat "Glans is red" Painless ulcer of penis : Always r/o SCC
Risk factors:
2. Condyloma acuminatum
a. Uncircumcised status
Caused by HPV 6 and 11 (low malignant potential)
b. HPV infection - 16,18
3. Leukoplakia c. Chronic irritation
White plaques due to chronic irritatoion Management : Surgery (Penectomy)
 Hernia

Indirect inguinal hernia Direct inguinal hernia

More common type of inguinal hernia Herniation through Hesselbach’s triangle Inferior epigastric
vessels
Herniation through the deep inguinal ring Medial to the inferior epigastric vessels Indirect
inguinal
Lateral to the inferior epigastric vessels Caused by weakness of the posterior wall of hernia Direct inguinal
Caused by patent processus vaginalis the inguinal canal. hernia
More common in children and young adults More common in elderly men due to Femoral
vessels
Can extend into the scrotum abdominal wall weakness.
Femoral
"Old man Hesselbach speaks direclty" hernia

Femoral hernia Obturator hernia

More common in females, especially Most common in elderly, multiparous,
multiparous women (however m/c hernia in emaciated women.
females in indirect inguinal hernia) Howship-Romberg sign: Medial thigh pain
Located below the inguinal ligament (inguinal exacerbated by hip movements.
hernia located above it) High risk of strangulation
Strangulation is the most common Surgical management
complication due to the narrow femoral ring.

Important named Hernias Boundaries of Hesselbach Triangle

1. Amyand’s Hernia Medial: Lateral border of rectus abdominis.
Inguinal hernia containing the appendix, may present with appendicitis Lateral: Inferior epigastric vessels
2. Littre’s Hernia Inferior: Inguinal ligament
Hernia sac contains Meckel’s diverticulum "Meckel's Diverticulum is litter"
Inferior epigastric vessels
3. Gibson’s Hernia
Hernia with hydrocele "Gibbons have large testicles"
4. Pantaloon Hernia
Both direct and indirect inguinal hernias on the same side.
Resembles a pair of pantaloons
5. Sliding Hernia
Inguinal
Retroperitoneal organ forms part of the sac "Slides into retroperitoneum" Rectus abdominis
ligament
Sigmoid colon or bladder muscle
6. Richter’s Hernia Hesselbach (medial border)
triangle
Involves the antimesenteric border of the bowel.
May cause diarrhea "Rich with diseases"
7. Laugier's Hernia
Herniation through weakness of lacunar ligament
8. Ogilvie’s Hernia Zieman's 3 finger technique
Congenital direct hernia "Ugly baby - Ogilvie" Index finger: Indirect hernia
9. Maydl’s Hernia Middle finger: Direct hernia
Two loops of bowel form a “W” configuration inside the hernial sac, with the Ring finger : Femoral hernia
apex being necrosed due to strangulation.
Also known as hernia en W
Bowel "may die - Maydl's"

Umbilical hernia : Seen in neonates

Para-umbilical hernia : Seen in obese adults
Infra-umbilical hernia : Spigelian hernia
Hernia mimicking peptic ulcer : Epigastric hernia
Hernia repair
Types of Hernia repair 1. Emergency surgery : Done in cases of
i. Strangulation
1. Open Hernia Repair ii. Bowel obstruction
a. Bassini’s repair iii. Bowel infarction
b. Shouldice repair (Multilayered tissue repair)
c. Lichtenstein tension-free mesh repair : Most 2. Reduction and elective surgery later
commonly performed open repair i. For young patients
ii. All femoral hernias (chance of strangulation)
2. Laparoscopic Hernia Repair iii. Hernia with increasing size
Preferred especially for bilateral or iv.
recurrent hernias. 3. Only observation
Done in elderly, if the hernia is not causing any
For large hernia defects, mesh fixation is severe symptom
essential to prevent recurrence

Nerves injured in inguinal hernia repair

Important triangles in hernia surgery
1. Open : Ilio-inguinal nerve "Vowels stick"
1. Triangle of Doom Loss of sensation at root of penis
Contains external iliac artery and vein (risk 2. Laparoscopic : Lateral cut. nerve of thigh
of vascular injury)
Tingling/numbness/burning pain in outer thigh -
Mesh fixation is avoided in this area to
merlagia parasthetica
prevent vascular injury
Boundaries :
3. Mesh repair : Ilio-hypogastric nerve
Medial: Vas deferens 4. Numbness over anterior thigh : Genitofemoral n.
Lateral: Gonadal vessels
Base: Peritoneal reflection

2. Triangle of Pain
Contains important nerves (femoral branch
of Genitofemoral nerve and LCNT)
Injury to nerves in this area can lead to
chronic pain or numbness Corona Mortis
Boundaries :
Medial: Gonadal vessels Aberrant obturator
Lateral: Iliopubic tract artery anastomosis
Base: Peritoneal reflection with pelvic vessels.
Present in 1/3
population
ct

Life threatening
Va
tra

sd

bleeding if it's injured

Gonadal
ic

Vessels

ef
ub

er

during hernia repair.

-P

en
io

s
Ill

PAIN DOOM

Peritoneal reflection
Peritoneal reflection and gonadal vessels are common
Salivary Gland
Sialolithiasis
Formation of salivary stones (sialoliths) within the salivary glands
Leads to obstruction of saliva
Pain and swelling during meals are hallmark symptoms Sialolith under
Submandibular gland is most commonly involved (>90%) NCCT (IOC)
Management :
Sialoendoscopy is a minimally invasive technique for stone removal
Surgery (gland excision) is indicated in recurrent or complicated cases

Benign Salivary Gland Tumors Malignant Salivary Gland Tumors

1. Pleomorphic Adenoma 1. Mucoepidermoid Carcinoma
Most common salivary gland tumor (60–70%) Most common malignant salivary gland tumor
Site : Parotid gland (superficial lobe) Site: Parotid gland > minor salivary glands
Clinical features: Painless swelling that lifts the ear lobe Management : Surgical excision
IOC : FNAC 2. Adenoid Cystic Carcinoma
Surgery : Superficial parotidectomy
Site : Submandibular gland and minor salivary glands
2. Warthin’s Tumor Tendency for perineural invasion (causes pain or facial
Second most common benign tumor nerve palsy)
aka Papillary Cysto lymphoma Management : Surgery + radiotherapy (high recurrence and
Exclusively in the parotid gland, often bilateral distant metastasis common)
Associated with smoking (seen in elderly)
Shows hot spot in Tc⁹⁹ scan

Cystic lesions of head and neck

Dermoid Cyst Sebaceous Cyst Cystic Hygroma Branchial Cyst

Congenital cystic lesion Obstruction of a sebaceous Congenital lymphatic Incomplete obliteration of
Trapped ectodermal tissue gland duct malformation . the 2nd branchial cleft
during embryogenesis Has a punctum (a dark dot Transilluminates Lateral side of the neck,
T/t : Excision in the middle) T/t : Sclerotherapy anterior to the
T/t : Excision (surgical excision if large) sternocleidomastoid
T/t : Excision

Ranula Plunging ranula

Ranula means body of frog A ranula that extends
Mucous retention cyst arising beyond the mylohyoid
from obstruction of a sublingual muscle into the neck
gland duct Swelling in the floor of the
T/t : Marsupialization (unroofing mouth along with a
the cyst) cervical swelling
High recurrence (removal of Treatment : removal of
sublingual gland done) sublingual gland
Carotid body tumor
Rare, highly vascular tumor arising from the carotid body (chemoreceptor)
It's a paraganglioma (associated with SDH gene mutation)
Slow-growing, pulsatile mass
Shows side-to-side mobility but not vertical mobility (Fontaine’s sign)
Salt and pepper appearance on MRI
Lyre's sign on angiography

Pulsatile neck mass

Lyre's sign Salt and pepper app.

(angiography) (MRI)

Carcinoma of lip
Squamous cell carcinoma is the most common type of lip cancer
Lower lip is more commonly involved than the upper lip
If upper lip involved : Basal cell carcinoma (BCC)
Major risk factors include
Chronic sun exposure
Tobacco use
Actinic cheilitis
Management :
a. If no lymph nodes involved : Excision with wide margins
b. If lymph nodes involved : Neck dissection + Radiotherapy
(Flaps needed if >1/3 of lip removed)

Abbe-Estlander flap
Esophagus

Achalasia Cardia Other motility disorders of esophagus

Failure of LES to relax
Diffuse esophageal spasm (DES)
Raised LES pressure + loss of esophageal peristalsis
Dysphagia (initially more to liquids), regurgitation and wt. loss Uncoordinated,
Barium Swallow : Bird-beak appearance (smooth tapering) non-propulsive
Gold standard investigation : Manometry esophageal contractions
Chicago classification based on Manometric findings Presents with
Type 1 : Only LES pressure increased (classic) intermittent dysphagia
Type 2 : Pan-esophageal increased pressure and chest pain
Type 3 : Spastic contraction Manometry shows
Treatment :
simultaneous,
Endoscopic: Pneumatic dilation, botulinum toxin injection
high-amplitude
Surgical: Heller’s myotomy, POEM (peroral endoscopic myotomy)
contractions (>120 mmHg)
Infections associated with Achalasia Cardia
Barium swallow : Corkscrew app. of
HSV - 1 esophagitis
Chaga's disease esophagus
Management :
a. CCB and nitrates
b. Esophageal myotomy in refractory cases

Nutcracker esophagus
(aka Jackhammer esophagus)
Most common esophageal motility disorder
Excessively strong peristaltic contractions
(>220 mmHg)
Bird beak app. Rat tail app. Management : CCB and nitrates
(smooth tapering) (rough tapering) (botulinum toxin in severe cases)
Achalasia Cardia Esophageal Carcinoma

Esophageal Carcinoma Sievert's Classification

IOC : Endoscopy + Biopsy for esophageal carcinoma
Types of esophageal carcinoma

Squamous cell ca. Adenocarcinoma Type 1

M/c cancer of esophagus Affects lower sections of

Affects upper and middle esophagus
sections of esophagus Associated with Type 2
Associated with GERD
Smoking, alcohol Barret's esophagus Type 3
Achalasia Cardia
Plummer Vinson Syndrome
Corrosive esophagitis
(alkali/acid ingestion)

Leiomyoma is the m/c benign esophageal tumor Type 1 and 2 : Esophageal ca.
(arises from the smooth muscle layer) Type 3 : Treated as gastric ca
 Gastro-Esophageal Reflux Disease Barret's esophagus
(GERD) Intestinal metaplasia of esophagus in chronic GERD
Reflux of acidic gastric contents due to LES dysfunction Risk factors :Male, obesity, GERD, smoking
Damage to the esophageal mucosa causes inflammation IOC : Endoscopic biopsy
(esophagitis) and may progress to complications Goblet cells are characteristic of the condition
Heartburn and regurgitation are hallmark features Alician blue is used for staining (stains goblet cells)
Symptoms worse after meals or lying down 1% risk of adenocarcinoma
Investigations : Seattle protocol for biopsy
(a biopsy procedure used to detect dysplasia and early
24 hour pH monitoring is gold standard
cancers in Barrett's esophagus)
Endoscopy for complications
Complication : Barrett’s esophagus (risk for esophageal
adenocarcinoma)
Management :
PPIs are first line for therapy
Nissen fundoplication for refractory cases

Nissen fundoplication
Most common complication : Gas bloat syndrome
360° plication
Other plications
a. Dor : 180° (anterior)
b. Toupet : 180°-270° (posterior)

Esophageal Rupture Booerhaave's Syndrome

Most common cause : Iatrogenic Sudden increase in intra-esophageal
MCC of spontaneous rupture : Boerhaave’s Syndrome pressure, often due to violent vomiting or
Can complicate as mediastinitis (Fever, tachycardia, retching
tachypnea) Seen commonly in alcoholics
IOC : CECT with Oral Contrast (Barium is C/I) Clinical signs : Mackler's triad "CVS"
Widened mediastinum on imaging and Hamman sign on Chest pain
auscultaion (crunching sound with heart beat) Vomiting/Retching
Subcutaneous emphysema
Early surgery (< 24 hours) is lifesaving
Iatrogenic small tears are managed conservatively
Differential diagnosis : Mallory Weiss tear
M - Mucosal tear (not a full thickness tear)
Also seen in alcoholics
Conservative management

Widened mediastinum
 Esophageal Webs and Rings

Web Rings

Single ring Multiple rings

Schatzki Ring Feline Esophagus

Benign condition Seen in Eosinophilic
Causes intermittent dysphagia esophagitis
Ring can be at Idiopathic condition
GE junction : "A" ring Diagnostic hallmark : Multiple
Squamo-coloumnar jn : "B" ring mucosal rings on barium
"B" ring is more common swallow
Associated with Plummer Vinson Syndrome
Associated with GERD and Associated with atopy
(aka Petterson Kelly Syndrome)
Hiatal hernia (eg. asthma)
R/f : Post menopausal females
Triad of
a. Esophageal webs (post-cricoid region)
b. Dysphagia
c. Iron deficiency anemia
Can cause Squamous cell carcinoma of
esophagus

Oesophageal constrictions Oesophageal ulcers

Punched out sulcers : HSV esophagitis
Serpingenous ulcers : CMV esophagitis
Plaques and peudomembrane : Candida esophagitis
Gastric cancers
Most common gastric cancers is adenocarcinoma (>90% of cases) Lauren (Histological) classification of
Other types include gastric adenocarcinoma
a. Lymphomas
b. Gastrointestinal stromal tumors (GISTs)
c. Neuroendocrine tumors Intestinal type Diffuse type
More common in males Associated with H. pylori Poorly differentiated
Risk factors include : Forms gland-like structures Can cause linitis plastica
i. H.pylori infection (most significant r/f) More common in older (stomach walls become thick)
ii. Alcohol and smoking patients Associated with CDH1
iii. Low fiber diet mutation (hereditary)
Younger patients
Sites of metastases: Has worse prognosis
Virchow's Node: Left supraclavicular Other classification systems
Irish node : Left axillary "vowels stick"
Japanese : Early gastric ca.
Sister Mary Joseph Nodule: Umbilical metastasis
Bormann : Late gastric ca.
Krukenberg Tumor: Ovarian metastasis
Dawson : For GI lymphoma
Blumer’s Shelf: Rectal mass felt on DRE "blum - bum"

Diagnostic Gold Standard: Endoscopy with biopsy

Surgical Gold Standard: Gastrectomy with D2 lymphadenectomy
Linitis Plastica
Prognosis: Early detection improves survival significantly

Gastrointestinal Stromal Tumor (GIST) Gastric Lymphoma

Origin: Interstitial cells of Cajal (pacemaker cells of GIT) Malignancy of lymphoid tissue in
Most common mesenchymal tumor of the GI tract the stomach
Most Common Site: Stomach Includes :
Markers: Positive for KIT (CD117) and DOG1 (most specific) MALT lymphoma (more common)
Treatment: DLBCL
Surgery for localized disease MALT lymphoma strongly linked to
Imatinib for advanced/metastatic disease H. pylori infection (H. pylori
Syndromic Associations: Carney's traid eradication is the first-line
a. Gastric GIST treatment for MALT lymphoma)
b. Paraganglioma 117 DLBCL is treated with
c. Pulmonary chondroma chemotherapy (R-CHOP)
KIT and DOG1

Neuroendocrine Tumors (NETs) of the Stomach

aka gastric carcinoids

Origin : Enterochromaffin-like (ECL) cells in the gastric mucosa
Positive for neuroendocrine markers :
Chromogranin A
Synaptophysin
Classification :
Type 1 : asso. with Chronic atrophic gastritis (e.g. pernicious anemia)
Type 2 : asso. with Zollinger-Ellison syndrome and MEN1
Type 3 : sporadic (most aggressive)
Other Gastric Conditions

Cerebriform stomach Watermelon stomach Arterial Spurt

Menetrier's disease GAVE Dieulafoy's lesion
(Gastric antral vascular ectasia)
Hyperplastic gastropathy Non-ulcerated lesion causing massive
Reason : Overexpression of TGF-α Dilated blood vessels in gastric antrum upper GI bleeding
Giant gastric folds and reduced acid Causes occult blood loss and Iron Reason : tortuous submucosal artery
secretion due to excessive deficiency anemia that erodes through the mucosa without
proliferation of the gastric mucosa Management : CO² laser an associated ulcer
Protein-losing gastropathy Endoscopy is the gold standard
Increased risk of gastric (diagnostic + therapeutic)
adenocarcinoma

Colorectal cancer
(Gene mutations are covered under Integrated GIT)

Most Common Type: Adenocarcinoma

Screening
Begin at 50 years (or earlier in high-risk populations)
Tests include:
i. FOBT (fecal occult blood test) annually - if
positive then colonoscopy
ii. or Colonoscopy every 10 years (gold standard)
iii. or Flexible sigmoidoscopy every 5 years Sigmoidoscopy Colonoscopy
Right vs. Left Colon Symptoms: 25 cm >150 cm
Right: Occult bleeding "right is red"
Left: Obstruction, altered bowel habits
Surgical Treatment: Colectomy
(followed by a colectomy or ileostomy)
Markers: CEA for monitoring recurrence
Metastatic Sites: Liver > lungs > peritoneum

Chemo regime for various GI tumors

1. Esophageal and gastric : ECF (epirubicin + cisplatin+ FU)
2. Small intestine : 5-FU Ileostomy Colostomy
3. Colorectal: FOLFOX
More chance of More chance of a
4. Anal canal : Negro regimen (chemo-radiation)
electrolyte loss para-stomal hernia
(Hyponatremia) and
skin excoriation
 Intestinal obstruction
Patient presents with the following symptoms : Complications :
Abdominal pain: Colicky pain Strangulation: Ischemia of bowel due to
Vomiting: Early in SBO, late in LBO compromised blood supply
Distension: More in LBO Perforation: Leads to peritonitis
Obstipation: Inability to pass stool or flatus Sepsis: Due to bacterial translocation
Electrolyte imbalances: Hypokalemia,
Initial management : metabolic alkalosis (due to vomiting)
Nil Per Oral (NPO): No oral intake
IV Fluids: Correct dehydration and electrolyte imbalance
Nasogastric Tube: Decompress bowel Paralytic ileus
Functional obstruction of the intestines
Investigations : Absent bowel sounds : Diagnostic hallmark
Initial investigation : Abdominal X-ray + CXR (erect) M/c cause : Postoperative
Management: Mainly supportive, treat underlying cause
CXR (erect) done to rule out perforation
Differentiate from mechanical obstruction using CT scan
IOC : CECT

Approach to intestinal obstruction

Large bowel obstruction Small bowel obstruction

More peripheral More central
Presence of haustrations (incomplete Lesser diameter of dilated bowel
mucosal folds) M/c cause : Adhesions (post-op)
M/c cause : Malignancy Management : Conservative
Greater diameter of dilated bowel > 6cm
Management: Surgery
(exploratory lapratomy)
Ileal obstruction Jejunal obstruction
Featureless Valvulae conniventes
(dilated jejunal loops)

"Large haustra small conni"

 Acute appendicitis
Inflammation of the appendix
Commonly caused by luminal obstruction (fecolith)
and subsequent infection.
It is a common surgical emergency 3
2/ 2/
3

Signs and symptoms :

Localized tenderness at McBurney's point associated
McBurney's point
with low grade fever, anorexia, N&V
2/3 the distance from navel to RSIS
(high grade fever indicates complications)
Rebound tenderness suggests peritoneal irritation
Special signs:
a. Rovsing’s sign: RLQ pain on palpation of LLQ
b. Psoas sign: Pain on hip extension (retrocecal
appendicitis)
Rebound tenderness Rovsing's sign
c. Obturator sign: Pain on internal rotation of the
flexed hip (pelvic appendicitis)

Diagnosis :
Clinically Murphy's triad is indicative of acute appendicitis Psoas sign Obturator sign
a. Pain in RIF
b. Nausea or vomiting
c. Fever
NOTE : Murphy's sign seen in acute cholecystitis
Another clinical scoring system used is Alvarado score
(score > 7 is highly suggestive and requires surgery)

M Migration of pain to RLQ ------- 1

A Anorexia ---------------------------- 1
N Nausea and vomiting ------------ 1
T Tenderness in RLQ --------------- 2
R Rebound pain --------------------- 1
E Elevated temperature ---------- 1
L Leukocytosis ---------------------- 2
S Shift of WBCs count to left ---- 1

Investigations :
Initial investigation : USG
Incisions at McBurney's point
IOC in pediatric age group : USG 1. Lanz : Skin crease incision
IOC in adults : CECT 2. Grid-iron : Muscle splitting "iron splits"
IOC in pregnancy : MRI 3. Rutherford Morrison : Muscle cutting

Appendiceal lump
Forms when the inflamed appendix becomes
surrounded by omentum and bowel loops,
Most common
localizing the infection.
It is a sequela of delayed presentation in acute
appendicitis.
Ochsner-Sherren regimen (conservative
management) is the first-line treatment.
 GI bleed

Upper GI bleed Lower GI bleed

Bleeding proximal to the ligament of Treitz Bleeding distal to the ligament of Treitz
MCC : Peptic Ulcer Disease > Variceal bleeding MCC : Diverticulosis > Angiodysplasia
Hemetemesis and malena (dark tarry stools) (m/c site for diverticulosis : Sigmoid colon)
seen in UGI bleed (m/c site for angiodysplasia : Caecum)
Other causes : Colon cancer, IBD hemorrhoids
Approach to UGI bleed Hematochezia (fresh, bright red blood in stools)
seen in LGI bleed.
Management : Colonoscopy
Resuscitation
Polyp

Upper GI endoscopy
(done within 24 hours,
diagnostic + therapeutic)
Normal colon Polyp

Polyp Snare Colonoscope

No re-bleed Re-bleeding

Prophylaxis : UGI endoscopy Colonoscope

β blockers
2nd attempt

Re-bleeding

TIPS
Transjugular Intrahepatic
Portosystemic Shunt

Forrest Classification
For UGI bleed in peptic ulcer disease
Suggests risk of re-bleed based on endoscopic app.
TIPS
r/o re-bleed maximum for 1 and minimum for 3
Side effect : Hepatic encephalopathy
1 : Spurting/oozing blood Early complication : Capsular rupture
2 : Non bleeding vessel/adherent clot Late complication : Stent thrombosis
3 : Clean based ucler

Baloon Tamponade devices (for UGIB)

Done in hemodynamically unstable patients that can't undergo endoscopy

Tc⁹⁹ scan
Most sensitive investigation
Sengstaken-blakemore Minnesota Linton for GI bleed (done for LGIB)
(2 baloons) (2 baloons, many ports) (single gastric baloon) Can find obscure bleeds in
small intestine
 Diverticulosis
Diverticuli are outpouchings of the colonic mucosa and Diverticulosis Diverticulitis
submucosa through weak areas of the muscle layer Mere presence Inflammation
of Diverticula
Commonly asymptomatic but can cause complications like of Diverticula
a. Bleeding (m/c cause of LGIB)
b. Diverticulitis (inflammation of the diverticuli)
Most common site : Sigmoid Colon
Risk factor : Chronic constipation in old age, low fiber diet
Hallmark of diverticular bleeding : Painless hematochezia
Bleeding
IOC : CT Scan (barium enema or colonoscopy are contraindicated
for diagnosis - can complicate into diverticulitis)
Management of bleeding :
a. Mild bleeding : High fiber diet (prevents progression & recurrence) Saw tooth sign
b. Heavy bleeding : Endoscopic intervention (clipping, cauterization) Seen on barium
enema if done in
Diverticulosis
Hinchey Classification (for Diverticulitis) Enema howsoever is
1 : Peri-colonic abscess contraindicated for
2 : Pelvic abscess diagnosis of
3 : Purulent peritonitis diverticulosis
4 : Feculent peritonitis

Peptic Ulcer Disease

Imbalance between aggressive factors (acid, pepsin) and
defensive factors (mucus, bicarbonate) Modified Johnson Classification
(for gastric ucler)
1. H.pylori (most common cause) : disrupts mucosal defense
and increases acid secretion
2. NSAIDs: Inhibit prostaglandin synthesis, reducing mucosal 1 is less (lesser cirvature)
defense (prostaglandins protect the mucosa) 2 is both (stom. & duod.)
3 is pre
3. Zollinger-Ellison syndrome : Gastrinoma causing 4 is door (GE junction)
hyperacidity 5 is NSAIDS (5 letters)
4. Other factors : Stress, alcohol consumption, smoking.
Type 1 : Lesser curve
Duodenal ulcers Gastric ulcers
Younger patients Older patients Associated with acid hypersecretion
Due to increased acid Due to impaired mucosal
secretion defense (normal-low acid
H pylori is strongly secretion)
associated NSAIDs are common cause
Relieved by food Worsens with food (due to
High risk of bleeding and acid secretion)
perforation (very close to Lower risk of bleeding or
gastro-duodenal artery) perforation Type 2 : Stomach + Type 3 : Pre-pyloric
Lower risk of malignancy Malignancy must be rule out Duodenal

Endoscopy: Gold standard

Can diagnose and classify peptic ulcers (Forrest classification)
Actively bleeding ulcers can be managed
Biopsy gastric ulcers to rule out malignancy.

Management:
Medical : PPIs, triple therapy for H.pylori eradication "CAP"
(Clarithromycin + Amoxicillin + PPI for 14 days)
Type 4 : Near G-E Type 5 : NSAID
Surgical : Vagotomy junction induced
(selective vagotomy has high recurrence)
 Anal fistula (Fistula-in-Ano)
Abnormal communication between anal canal & perianal skin
MCC : Infection of anal glands (aka Cryptoglandular abscess)
Classified based on Parks’ Classification:
Intersphincteric (Most Common): Between both sphincters
Levator ani
Transsphincteric: Passes through both sphincters muscle
Suprasphincteric: Above the sphincter complex
Extrasphincteric: Does not involve sphincter muscles Puborectalis muscle

Goodsall's rule Internal anal sphincter

Anterior fistulas : Straight track
Posterior fistulas : Curved track to midline External anal sphincter
(Excception : Anterior fistula >3cm, also have curved track)

Intersphincteric
fistula
Extrasphincteric Superficial
fistula fistula
Suprasphincteric
fistula
Transsphincteric fistula

IOC : Pelvic MRI

Management :
Low fistulas : Fistulotomy
High fistulas : Seton placement

Hemorrhoids (Piles)
Hemorrhoids are swollen and inflamed vascular structures
Internal hemorrhoids External hemorrhoids
in the anal canal (normal part of anatomy)
Increased intra-abdominal pressure causes distension and Arise above the Arise below the
dentate line dentate line
prolapse of the hemorrhoidal vascular plexus (chronic
Covered by mucosa Covered by skin and
constipation, pregnancy, obesity, low fiber diet) and not painful painful
Associated with Associated with
Internal hemorrhoids graded based on degree of prolapse mucus discharge pruritis
Grade I: only bleeding Can prolapse
Grade II: Prolapse that reduces spontaneously
Grade III: Prolapse requiring manual reduction
Grade IV: Irreducible prolapse

Management :
Grade I-II: Conservative or rubber band ligation
Grade III-IV: Surgery (Hemorrhoidectomy)

Pilonidal Cyst
Cyst or abscess near the natal cleft of the buttocks, often
containing hair, debris, and granulation tissue.
Risk factors :
Prolonged sitting
Obesity
Excessive body hair
Deep natal cleft
Treatment : Incision and drainage
 Rectal Prolapse
Protrusion of the rectal wall through the anus
Abdominal approach Perineal approach
May involve only the mucosa (partial prolapse) or the full
thickness of the rectal wall (complete prolapse, seen in elderly) Preferred for fit adults Done for elderly or unfit
Procedures include Procedures include
a. Ripstein (ant.rectopexy) a. Delorme's
Conservative management : For mild prolapse or early stages
b. Well's (post. rectopexy) b. Altemeier's
a. High-fiber diet
c. Moskowitz c. Thiersch circlage
b. Kegel exercises : Strengthen pelvic muscles
Difficult to perform but Easier to perform but has
lower recurrence higher recurrence
Surgical management : Persistent or severe prolapse
Can be done via abdominal or perineal approach "Rip abdomen well"

Mesenteric Cysts
Rare intra-abdominal cystic lesions that develop in the mesentery
Most common cause : Congenital malformations of lymphatic
vessels
Clinical presentation : Palpable, mobile, and non-tender abdominal
mass
Tillaux's sign is a hallmark diagnostic sign : cyst moves only
perpendicular to axis of mesentery
Investigations
Initial : USG
Definitive : CT/MRI
Tillaux Sign Mesenteric cyst
Management : Complete surgical excision

Syndromes related to GI surgery

Short bowel Syndrome
Dumping Syndrome
Malabsorption resulting from extensive resection of
Ingested food moves too quickly from the stomach the small intestine
into the small intestine, often following gastric surgery Presents with :
Can be classified into : Diarrhea and steatorrhea
Nutritional deficiencies
Electrolyte imbalances
Early dumping Late dumping Management :
Occurs 15-30 mins after Occurs 1-3 hrs after TPN in acute phase
taking food taking food Medical mx : Teduglutide (GLP ² analogue)
Rapid gastric emptying Rapid glucose Surgical mx : Lengthening procedures
causes hyperosmolar absorption causes (Bianchi, Step, Kimura)
jejunal chyme (water reactive hypoglycemia
moves into intestines) (increased insulin
Presents with : release) Refeeding Syndrome
Hypotension Presents with :
Rapid reintroduction of nutrition after prolonged
Tachycardia Hypoglycemia
Diarrhea starvation or malnutrition
Sudden carbohydrate intake triggers insulin secretion
Management : Small frequent meals Intracellular shifts of phosphate, potassium, and
magnesium, leading to deficiencies "KMPan = Seizures"
Presents with seizures and confusion (can cause
arrythmias and heart failure if uncorrected)
Gall stones
Stones formed in the gallbladder or biliary tract due to change in concentration of bile
Causes of gall stone formation :

Increased cholesterol Bile pigment excess Decreased bile salts

Obesity (Pigment stones) No enterohepatic circulation
Dyslipidemia M/c stones in Asia (occurs at Ileum)
Radio-opaque stones Short bowel syndrome
Cholesterol Stones UDCA tablets are not effective Ileal loop resection
M/c in western world Can be further classified Bariatric surgeries
Radiolucent stone CRASH diet
(can't be seen on x-ray)
UDCA tablets are effective Brown Black Mixed stones
pigment stones pigment stones Combination of cholesterol
Biliary infections Formed due to and pigment stones
(eg. Ascaris) excessive bilirubin
Causes primary Associated with
CBD stones hemolytic disorders

Conditions associated with gall stone

Obstruction of the cystic duct by a gallstone : Biliary colic
Intense, episodic, RUQ pain, often after fatty meals

Prolonged obstruction causes gallbladder wall inflammation : Acute cholecystitis

Persistent RUQ pain associated with N&V
Murphy’s sign positive (pain on deep inhalation while deep palpation of RUQ)
Classic patient : Fat fertile female of 40 Posterior acoustic shadowing
IOC : USG (requirements for diagnosis include) by gall stone
i. Posterior acoustic shadowing seen with gall stones
ii. Gallbladder wall thickening (> 4 mm) with pericholecystic fluid

Obstruction of the CBD by a gallstone : Choledocholithiasis

RUQ pain + Obstructive Jaundice
Elevated ALP, GGT, and bilirubin levels
Initial investigation : USG
IOC : MRCP (can detect stones better than USG) non invasive
Gold standard : ERCP (diagnostic + therapeutic) but invasive

Infection of the biliary tree due to bile stasis from a stone in the CBD : Cholangitis
MRCP ERCP
Charcot’s Triad: Fever, RUQ pain, jaundice
Reynolds’ Pentad: Triad + hypotension + altered mental status

Obstruction of the pancreatic duct by a gallstone : Gallstone pancreatitis Pneumobilia

Most common cause of acute pancreatitis
Severe epigastric pain radiating to the back
Elevated serum amylase/lipase

Gallstone erodes through GB wall into the small intestine : Gallstone ileus
Mechanical small bowel obstruction (m/c site is ileum)
Air in the biliary tree (pneumobilia) - hallmark finding on X-ray
Rigler's triad : Pneumobilia + Small bowel obstruction + Gall stone Distended small bowel loops

Gallstone in the cystic duct compresses the common hepatic duct : Mirizzi Syndrome CT findings in gallstone ileus
"Painless" obstructive jaundice
Choledochal Cyst
Congenital cystic dilation of the bile ducts
Increased risk of cholangiocarcinoma
Classification : Todani Classification
Type I: Fusiform dilation of the extrahepatic bile duct (most common)
Type II: Saccular diverticulum of the extrahepatic bile duct
Type III (Choledochocele): Cystic dilation of the intraduodenal portion of extrahepatic bile duct
Type IV: Multiple cysts
IVa: Both intrahepatic and extrahepatic bile ducts "A - All"
IVb: Only in extrahepatic ducts "B - Baahar"
Type V (Caroli’s Disease): Cystic dilation of intrahepatic bile ducts

Fusiform Saccular Intraduodenal A - All B - Baahar Only intra-hepatic

m/c type diverticulum portion dilatation Multiple cysts bile ducts affected

Management :
Roux-en-Y hepatico jejunostomy for all (except Todani iii and v)
Todani iii (Choledochocele) : ERCP
Todani v (Caroli's disease) : No treatment (Liver transplant is needed)

Cholangiocarcinoma
Malignant tumor arising from the bile duct epithelium Intrahepatic

Risk factors are :

a. Chronic Biliary Inflammation
i. Primary sclerosing cholangitis (PSC) not PBC Perihilar
ii. Choledochal cysts Near junction of left and
b. Liver flukes (Opisthorchis, Clonorchis) right hepatic ducts
c. Liver Diseases
i. Chronic viral hepatitis (HBV, HCV) Distal
ii. Nonalcoholic fatty liver disease
d. Thorotrast (historical use as a radiographic contrast agent)
Stomach

Management based on location :

Intrahepatic: Liver resection Liver
Perihilar (aka Klatskin tumor) - m/c location
Liver resection with bile duct excision
Biliary reconstruction Galbladder
Distal: Pancreaticoduodenectomy (Whipple procedure)
(Pylorus + Duodenum) + (GB + Cystic duct + CBD) Head of Pancreas
+ (Head of pancreas) removed
All cut ends anastomosed with jejenum - Pancreaticojejunostomy, Duodenum
Gastrojejunostomy and Choledochojejunostomy Parts of the body removed

Whipple procedure
 Bile duct injuries
Trauma to the biliary tree, commonly occurring as a complication of
hepatobiliary surgeries, particularly laparoscopic cholecystectomy
Presentation : Increased post op drain or post op jaundice
Initial investigation : USG
Most sensitive investigation : HIDA scan
Management : Pigtail catheter drainage
If no resolution with pigtail catheter : ERCP

Strasberg Classification for bile duct injuries

Cystic duct leak Aberrant duct injured CBD injured CBD transected
(m/c type) (Right post. sectoral duct) (partial cut) (End to end cut)
B - Ligated "Baandhna" Further classified from E1-E5
C - Cut

Liver disease severity scores

(Helps prioritise patients for transplantation)

MELD PELD Child Turcotte Pugh Score

Model for end stage Pediatric end stage assess the severity of chronic liver disease
liver disease liver disease A Albumin (reduced)
Creatinine Albumin (low) B Bilirubin (raised)
Billirubin Billirubin C Coagulopathy (PT, INR)
INR INR D Distention - Ascites
(Revised MELD has Encephalopathy (measured using
Age < 1 year E
included Na+ levels)
Growth failure West Haven criteria)

ABI instead of CBI

CBI +
2 age related criterias
Na+

King's college criteria for severity

in paracetamol induced liver failure
Barcelona Clinic Staging System
Arterial pH < 7.30 staging hepatocellular carcinoma (HCC)
Or Performance status (evaluates physical capability)
H Hepatic Encephalopathy (grade 3 or 4) Child Pugh score (for liver function)
C Coagulopathy (PT or INR raised) Tumor burden
C Creatinine raised a. Number of nodules
"King has HCC" HCC b. Presence of metastasis
Treatment options
Multinodular : TACE (Trans Arterial Chemo Embolisation)
Portal invasion : Sorafenib
Pancreas
Accessory pancreatic duct
Sphincter of Oddi dysfunction (duct of Santorini)
"Santorini - Secondary"
aka Biliary dyskinesia
Stenosis of sphincter of the sphincter Gallbladder

IOC : ERCP Common bile duct

Gold standard : Manometry Minor papilla

"Milwaukee" classification system used Major papilla

Type 3 : Only biliary pain (no evidence of dilated Sphincter of Oddi
duct) - Managed medically with PPI Ampulla of Vater
Type 2 : Biliary pain with some objective evidence Main pancreatic duct
(dilated duct or raised LFT) - Manometry needed (duct of Wirsung)
for confirmation
Type 1 : Recurrent biliary pain with objective
evidence of obstruction - Sphinctorotomy
Complications : Pancreatitis and recurrent Pancreatic divisum : Congenital anomaly of pancreas
where the two ducts don't fuse (asymptomatic)
biliary obstruction

Acute Pancreatitis
Caused due to premature activation of pancreatic Atalanta classification for acute pancreatitis
enzymes (e.g. trypsin) inside the pancreas
Characterised by either :
Fluid collection around pancreas
< 1 month < 1 month
Pancreatic necrosis
M/c cause : Gallstones (2nd mcc is alcohol)
(alcohol is mcc of chronic pancreatitis )
M/c cause in children : Trauma
Iatrogenic risk factor : ERCP > 1 month > 1 month

Clinical features :
Severe epigastric pain radiating to the back,
associated with N&V
Worsens with fatty meals
Investigations :
Elevated serum Amylase (raised earlier) and
serum Lipase (more specific)
LFT (raised alk. phos suggests gallstones)
USG - first line to detect gallstones
CECT (gold standard) Sentinel loop sign
No parenchymal enhancememnt by IV contrast
on CT in pancreatitis
Score assigned based on CECT : Balthazar score
Abdominal X-ray : Sentinel loop, colon cut off sign Colon cut off sign

Abdominal signs in severe pancreatitis :

a. Cullen’s Sign: Periumbilical bluish discoloration
b. Grey Turner’s Sign: Flank ecchymosis
c. Fox's sign : Discolouration in inguinal region
d. Bryant's sign : Bluish discoloration of the scrotum
Severity score in acute pancreatitis - BISAP score
(BUN, Impaired mental status, SIRS, Age, Pleural effusion)
Management :
IV fluids + Antibiotics
Surgical debridement is not done (associated
with high mortality)
 Chronic Pancreatitis Pancreatic Pseudocyst
Chronic injury leads to recurrent inflammation of Non-epithelialized - cystic fluid collection following
pancreatic tissue pancreatitis or trauma
Fibrosis and calcification result in: MCC : Alcoholic chronic pancreatitis
Loss of exocrine function (malabsorption) Management : EUS guided drainage
Loss of endocrine function (diabetes) Complications associated with pseudocyst
M/c cause : Alcohol Splenic vein thrombosis
Genetic cause : Mutations in PRSS1, CFTR, or Duodenal obstruction
SPINK1 (tropical pancreatitis) genes Perforation of cyst
Portal vein thrombosis (if near head of pancreas)
Investigations : Bile duct stenosis (if near head of pancreas)
Pancreatic calcifications on imaging (pathognomic)
Secretin stimulation test (gold standard trest for
exocrine insufficiency)
Fetal elastase reduced in exocrine insufficiency Splenic vein
Surgical management :
a. Puestow Procedure (aka Lateral
pancreaticojejunostomy) tail removed in chronic
dilatation of pancreatic ducts
b. Frey’s Procedure in which pancreatic head Duodenum
is cored out "Frey's syndrome seen in head" Portal vein
c. Duval's procedure : Distal part of pancreas removed
+ Roux en y pancreatico-jejunostomy
d. Beger's procedure : Duodenum preserving
pancreatic head surgery "Beggar's duodenum" Pain management in chronic pancreatitis : Celiac plexus block

Pancreatic Neoplasms Pancreatic Neuro Endocrine tumors

Features of pancreatic neoplasms : Most commons :
a. Desmoplastic reaction (growth of dense connective M/c NET : Non functional tumors
tissue around the tumor - makes it resistant to M/c functional NET : Insulinoma
chemo and radio therapy) M/c NET in MEN-1 syndrome : Gastrinoma
b. Perineural invasion cancer cells invade nerves and
IOC for NETs : DOTANOC - PET
spread through them
Insulinoma : Presents with Whipple's triad
Exocrine neoplasms are more common than
Symptoms of hypoglycemia (sweating, seizures)
endocrine neoplasms
after fasting
a. Pancreatic (ductal) Adenocarcinoma: m/c Blood sugar levels < 55 mg/dl
pancreatic neoplasm overall Symptoms improve on taking glucose
b. IPMN : High-risk features, require resection
c. Mucinous cystadenoma : Middle-aged women Gastrinoma
Can cause parietal cell hypertrophy known as
Risk factors :
Zollinger Ellison syndrome
a. Smoking M/c location : Passaro's triangle
b. Chronic pancreatitis
c. Genetic :
i. K-ras mutation Passaro's triangle
ii. Peutz-Jeghers syndrome
Serum marker : CA 19-9 (> 80% patients)
Symptoms for tumor at head of pancreas : Glucagonoma
Present's early with obst. jaundice (waxing and Can cause - Necrotic migratory erythema along
weaning type of jaundice) with hyperglycemia
Courvoisier's law : palpable, non-tender gallbladder
in jaundiced patients is due to a tumor
(Exception : Mirizzi's syndrome) Necrotic migratory
erythema
Symptoms for tumor at body or tail :
Present's late
Miscellaneous

Skin grafting Fournier's Gangrene

Split-Thickness Skin Graft Full-Thickness Skin Graft

aka Thiersch graft aka Wolfe graft
Epidermis + Partial dermis Epidermis + Dermis
M/c donor site : Thigh Donor site : Post-auricular,
Undergo secondary Supra-clavicular
contractures (hence poor Undergo primary
cosmetic results) contractures (hence better
cosmetic results)

Gangrene of the scrotum (testes

are usually spared)
Surgical emergency (associated
with high mortality, > 50%)
Humby skin Mixed aerobic + anaerobic
grafting knife infection

Abnormal wound healing Anatomical landmarks

characterized by excessive collagen deposition in hepatobiliary surgeries

Keloid Hypertrophic scar

Fibrous tissue growth extending Fibrous tissue growth confined to the
beyond the wound margin wound margin
Hepatocystic triangle
Develops weeks to months after injury Develops shortly after injury
A/w pruritus, pain, or tenderness No associated symptoms
M/c location : Sternum Location : Skin with high tesion
On h/p : Disorganized collagen fibers On h/p : Organised collagen fibers Calot triangle
High recurrence rate, often difficult to No recurrence, and mostly resolves
manage spontaneously
Hepatocystic triangle
Boundaries:
Inferior surface of the liver
Common hepatic duct
Cystic duct
Contents:
Right hepatic artery
First line management : Triamcinolone
Cystic artery (within the
If refractory ( > 12 months) : Excision + Radiation
triangle)
Lymph nodes

Calot triangle
Terms in surgical checklist
Boundaries: "3 C"
Sign in : Before induction of anesthasia Common hepatic duct
Time out : Before skin incision "skin time" Cystic duct.
Sign out : Before patient leaves OT Cystic artery
Contents:
Cystic lymph node (of
Lund)
CHAPTER 3

ENT
Paranasal Sinuses

1. Frontal sinus
2. Ethmoidal sinus (anterior
group and posterior group)
3. Maxillary sinus (first sinus to
develop)
4. Sphenoid sinus

(at birth only maxillary and ethmoid

sinus are present)

Sinusitis
Inflammation of the paranasal sinuses

Investigations
IOC : HRCT Temporal bone
Gold standard : FESS

Potts puffy tumor

Ethmoidal Sinusitis
Complication of frontal sinusitis
Most common sinusitis in children Sub periosteal abscess in frontal bone
Periorbital swelling Ring enhancement + central necrosis
Retro-orbital pain

Maxillary sinusitis
Most common sinusitis in adults
Cheek pain / tooth-ache

Frontal sinusitis
Frontal headache
Worsens on leaning forward
Complicates as cranial osteomyelitis Subperiosteal abscess of orbit
(pott's puffy tumor) Most commonly associated with
ethmoidal sinusitis
Sphenoid sinusitis Reason : venous supply of ethmoid and
Pain radiating to occiput orbit are same
Diplopia
Cavernous sinus thrombosis could be a
complication
 X ray views for para-nasal sinuses

Modified Waters view Caldwell view

Water's view : best for Maxillary sinus Best for Frontal sinus
Modified water's view (aka Pierre's view): Maxillary sinus Stenver's view
open mouth, can view Sphenoid sinus obscured by temporal Visualisation of Cochlear implants
aka occipito - mental view bone (petrous part)
Posterior ethmoidal sinus can't be seen aka occipito frontal
(all other sinuses can be visualised) view

W for M
(Water's for Maxillary)

Cold Front
(Caldwell for frontal)

Down town via foramen

magnum Cochlear implants enter via
Towne's view round window
(Towne's for formaen
Shows foramen magnum
magnum and sella turcica)
and sella turcica
Used to diagnose apex
petrositis

Law's/ Schullers view Sino dural angle

Mastoid air cells seen Determines pneumatisation of
Sino dural angle (Citelli's angle) mastoid air cells
*Citelli's abscess : in digastric muscle, complication of CSOM Decreases in sclerosis
*Bezold abscess : in SCM muscle
 Nasal Turbinates

Superior turbinate
Superior meatus Nasal turbinates are present on the
Ethmoidal air cells lateral walls of nose
Ethmoidal air cells
These turbinates form passages for
Middle turbinate air which are known as meatus.
Middle meatus
Middle and superior turbinates are
Maxillary sinus parts of the ethmoidal bone
Inferior turbinate is a separate bone
Inferioir meatus
Inferior turbinate

Nasal septum

Drainage Drainage from sphenoid sinus into

1. Inferior meatus : NLD from eye the spheno ethmoidal recess
2. Middle meatus : Frontal,
Ant. ethmoidal, Maxillary Naso-frontal duct draining frontal sinus
3. Superior meatus : Post. ethmoidal and anterior ethmoid sinus
4. Spheno-ethmoidal recess : Sphenoid
Drainage from maxillary sinus

Drainage from nasolacrimal duct

Ethmoidal air cells

Anterioir most : Agger Nasi (aage)

Largest : Bulla Ethmoidalis (bulla : bada)
Infraorbital : Haller cell (hall below orbit)
Optic nerve compression : ONodi cell
Pneumatised middle turbinate : Concha Bullosa (like a bulla : Bullosa)

Concha bullosa Haller cell Pneumatised

Pneumatised middle turbinate Ethmoid air cells at the floor superior turbinate
of orbit
Related to the roof of
maxillary sinus
Osteomeatal Complex
1. Opening of maxillary sinus (ostium)
2. Uncinate process
3. Bulla ethmoidalis
Bulla Ethmoidalis
4. Infundibulum
5. Hiatus semilunaris

Infundibulum

Ostium

Double density sign

Allergic fungal sinusitis
Non invasive
Peanut butter nasal discharge
Bent and Kuhn's critera used for dx
(fungal culture is a minor criteria)

Inverted Papilloma (Ringertz tumor)

Old age, M>F

Arises from Schnederian membrane
Hyperintense tumor on MRI
Cerebriform appearance on endoscopy
Management : Surgical (Moure incision)
No bony erosions seen here (d/d is maxillary
cancer which shows bone erosion)
Inverted papilloma Cerebriform app on
on MRI endoscopy

Other "cerebriform" appearances

1. Mycoises fungoides (shape of nucleus) 2. Menetrier's disease (gross appearance of stomach)
Pautriers microabscess TGF alpha overexpression
Protein losing enteropathy
Carcinoma of maxillary sinus
Risk factors Types of incisions for maxillary sinus
1. Nickel : Squamous cell carcinoma (m/c type)
2. Wood : Adenocarcinoma wood ad

Ohngren's line
Cancers below the line have good prog
Cancers above the line have bad prog

Moure Weber ferguson

Lateral rhinotomy/ Total maxillectomy
medial maxillectomy in carcinoma of
Used in surgery of Maxillary sinus
inverted papilloma
(Ringertz tumor)
Moure is less

Coldwell luc approach

Gluck Sorensen incision Maxillary sinus surgeries
(used for total laryngectomy) Infra-orbital nerve most commonly damaged

Nasopharyngeal Carcinoma
Presents as cervical lymphadenopathy
Originates from fossa of Rosenmuller
Can lead to serous otitis media (in adults)
Associated with EBV (Ebstein Bar Virus)

Trotter's triad
1. Trigeminal neuralgia (5th CN)
2. Palatal palsy (10th CN) "5, 10, CHL"
3. Cond. hearing loss (glue ear)
(all ipsilateral)

Sampter's triad seen with intrinsic asthma

Sam has asthma
Juvenile nasopharyngeal angiofibroma
Male adolescent with epistaxis Radkowski staging
Highly vascular tumor that originates from the
sphenopalatine foramen
Limited to nose and nasopharynx
Internal maxillary artery is the major feeding vessel
IOC is CE-CT (biopsy is contraindicated because of high Extension into para nasal sinuses
vascularity) Extension into the pterygopalatine
Management : Embolisation f/b surgical removal fossa
Radiotherapy for Intra-cranial spread Occupies the entire pterygopalatine
Radkowski staging is used to stage the tumor fossa (Homan Miller sign)

Involvement of the infratemporal

fossa

Erosion of the skull base, minimal

intra-cranial extension

Erosion of the skull base, extensive

intra-cranial extension

Male adolescent with Homan Miller sign

Stage 2 b
epistaxis
Anterior bowing of the
posterior wall of maxillary sinus

Nasal Polyps
Nasal Polyps Principle of Nasal polyps
According to Bernoulli's principle, when air flows
Ethmoidal polyp Antro-choanal polyp through a fixed space, the pressure in that space
aka Middle meatal polyps Usually unilateral decreases.
Usually bilateral (from maxillary sinus) In the nasal cavity, a constricted meatus can have a
Multiple Solitary negative pressure due to Bernoulli's principle. This
Seen in adults Seen in children negative pressure can suck the sinuses' mucosa
Allergic cause Infectious cause mostly into the nasal cavity : forming polyps
Medical management is Surgical management is
preferred preferred
Surgical mx : FESS Surgical mx : FESS
Sampter's triad
A - one, unilateral, young 1. Ethmoidal polyps
2. Asthma
3. Aspirin hypersensitivity

Young's Syndrome
1. Recurrent rhinits
2. Nasal polyps
3. Infertility

1. Allergic rhinits : Pale and edematous mucosa

2. Inflammatory rhinits : Red and swollen mucosa
Diseases of nose

Rhinoscleroma Rhinosporidiosis
Caused by Klebsiella Rhinoscleromatis Caused by Rhinosporidium Seeberi
Woody nose known as Tapir/Hebra nose h/o swimming in ponds
Russel bodies / Mikulicz cells are characteristic More prevalent in South India
findings on histopathology Seen in immunocompetent individuals
DOC : Streptomycin + Tetracycline Sporangium with endospores are seen
on histopathology
DOC : Excision + Dapsone

Sporangium with endospores

Woody nose Foamy histocytes

(Hebra nose/Tapir) (Mikulicz cells)
Red fleshy mass in nose/tongue

Atrophic rhinitis Rhinophyoma

aka Empty nose syndrome
Roomy nasal cavity
Merciful anosmia (patient is unaware
of foul discharge coming from nose)
Etiology can be either

Primary atrophic rhinitis Secondary atrophic

(Ozaena) rhinitis aka Potato nose
Rare degenrative 1. TB of nose Sebaceous gland hypertrophy
condition of the nose 2. Syphilis Associated with acne rosacea
Cause by Klebsiella 3. Rhinoscleroma,
Ozaenae 4. Wegner's Granulomatosis
5. DNS (presents with Deviated Nasal Septum
unilateral atrophic rhinitis)
Presents with congestion on
Immediate mx : Nasal douching one side and roomy cavity
Definitive mx : Modified Young's procedure on the other side (risk of
atrophic rhinitis)
Cottle's test for diagnosis
Preferred treatment
nowdays is septoplasty
(conservative, uses Freer's
incision)

SMR (sub mucosal resection) is

not preferred (non conservative,
uses Killian's incision)
Trauma

CSF Rhinorrhea HRCT of nose and PNS

M/c site : Cribriform plate of ethmoidal bone in trauma
M/c site for traumatic CSF leak : Fovea ethmoidalis defect
Handkerchief test : CSF will be non sticky while mucus is sticky
IOC : β² transferrin
(β² glycoprotein in APLA, β² microglobulin in Multiple myeloma)

Tear drop sign

Orbital blowout fracture (base of orbit)
aka Trapdoor fracture (Inferior rectus is
trapped)
Halo test
CSF when mixed with blood
will form a halo/target sign

Le-fort fracture
Fractures of mid face
Pterygoid plate involvement is common to all
It's of 3 types

Frontal mucocele
h/o trauma

Fractures of septal cartilage

Floating palate Pyramidal Complete cranio
aka Guerin # injury facial dysfunction
No CSF rhinorrhea
Guerin sign seen
(Greater palatine
artery hematoma)
Jarjaway Chevallet
Goes straight up like
a Chevrolet car
Ulrich classification
(for temporal bone #) Battle sign
Bruising behind
Longitudinal Transverse
the ear
Middle ear injury Internal ear injury
Indicative of base
TM rupture SNHL
of skull #
CHL 7th CN involved
Appears after
a-long the bone several days of
trauma
Epistaxis

Anterior epistaxis Posterior epistaxis

Seen in children Seen in elderly
MCC is trauma Hypertensive : Sphenopalatine artery
Little's area (Kisselbach's Woodruf's area (5-10% bleeds) : posterior
plexus) part of middle turbinate
Relatively asier to manage Difficult to manage

Management
Internal carotid artery
algorithm for
Ophthalmic artery epistaxis
Anterior Posterior ethmoidal artery
ethmoidal artery Trotter's maneuver
(Doesn't participate in
Kisselbach's plexus)
(aka Hippocratic method)

Kisselbach's plexus

Nasal packing

Branches of
sphenopalatine TELSPA
Branches of artery (Total endoscopic ligation of
facial artery Sphenopalatine artery)
Sphenopalatine artery
aka artery of epistaxis
Greater Lesser palatine
palatine artery
artery Branches of ECA ligation
Facial artery Maxillary artery (Maxillary & Facial artery)
External carotid
artery
ECA ligation

Branches of ICA ligation

(Ethmoidal arteries)

(ICA never ligated)

Nasal packing tampon

Trotter's maneuver
(aka Hippocratic method)

Nasal packing with gauge roll

External ear

Helix
Superior
crus

Inferior crus

Concha
Antihelix Tragus
Antitragus
Incisura terminalis
No cartilage present
Eustachian tube Lobule here
EAC
Lampert's end-aural
incision through this
in pediatric patients,
EAC vs Eustachian tube to reach mastoid.

EAC is 24 mm (use AC at 24°)

Eustachian tube is 36 mm
Both tubes are bony near middle ear
EAC is more bony,
cartilage : bone = 1:2 (8mm, 16mm)
Eustachian tube is more cartilaginous,
bone : cartilage = 1:2 (12mm, 24mm)

EAC cartilaginous part has Foramen of Santorini

Absence of anti-helix Darwin's
(saints are soft)
EAC bony part has Foramen of Huschke known as bat ear Tubercle

Development of external ear

Development of pinna Development of EAC and TM

1st and 2nd pharyngeal arches form 6 hillocks 1st pharyngeal cleft forms the EAC
1st hillock forms Tragus Tympaic membrane formed by fusion of fusion of
Other hillocks form the rest of pinna 1st cleft with 1st pouch (has all 3 germ layers)

If 1st cleft and 2nd cleft don't fuse properly, it forms

pre-auricular sinus Pre-auricular sinus

aka Sharpnell's membrane

Always anterio- inferior Boxer's/Pugilistic/Cauliflower ear

Determines left/right H/o trauma
tymp. membrane (this is right TM) immediate I and D
mc site of rupture / myringotomy /
gromett insertion
 Nerves supplying the external ear and TM

Anterior aspect of EAC

Branch of mandibular div of
trigeminal nerve
Referred pain from : dental
conditions, parotid, TM joint,
anterior 2/3rd of tongue
An
te
rio
r

Posterior superior
part of EAC (face is
superior)
Hitzelberger sign in
Acoustic neuroma Glossopharyngeal nerve (CN 9)
Supplies medial side of tympanic
membrane (Jacobson's nerve)
Referred pain from
1. Acute tonsillitis
Postero inferior aspect 2. Peritonsillar abscess
Referred pain from Cervical Spondylitis 3. Carcinoma of base of tongue
of EAC
Can cause syncope if
syringing done in
postero inferior
direction.
Referred pain from :
"Hence syringing always done in postero superior direction"
Carcinoma of larynx,
pharynx

Auriculotemporal nerve

Lesser occipital nerve

Greater auricular
nerve

Facial and-
Vagus nerve
Greater auricular nerve
Facial and-
Vagus nerve Supplies a greater section of
ear auricle

Lateral Surface Medial Surface

Diseases involving external ear

Sessile exostosis
(osteochodroma of ear)
aka Surfer's ear
Multiple bony swellings

Generalized otitis externa Keratosis Obturans

aka Swimmer's ear Presence of desquamated
Caused by Pseudomonas aeruginosa cells in EAC
T/t : Topical fluoroquinolones
General swimmers flow (fluroq.)

Malignant otitis externa

H/o diabetes mellitus
Whitish discharge from ear
Pseudomonas aeruginosa
t/t : 3rd gen cephalosporins
Tc⁹⁹ scan to confirm Bullous myringitis
malignant but safe (ceph) Intensely painful condition
Caused by HSV or Mycoplasma
 Middle ear

Anterior wall
T Tensor tympani muscle (Supplied by mandibular nerve) Tensor tympani
Tegmen tympani muscle
E Eustachian tube opening roof of mid. ear
A Artery : Internal Carotid artery

Aditus
Posterior wall Opening to
mastoid antrum
Oval window
1. Mastoid antrum
Pyramidal
2. 7th CN (vertical part) eminence Eustachian
Promontory
3. Pyaramidal eminence (stapedial muscle tube
Chorda
originates from here) tympani
nerve entry

Facial nerve.
Medial to pyramids Lateral to pyramids (VII) Round Chorda tympani
window nerve exit
Sinus tympani (m/c site of Facial recess area (used to Internal
residual cholesteatoma) approach middle ear via mastoid) carotid artery
Internal jugular vein

Facial recess area

Medial wall
1. Promontory (with Jacobson's nerve)
2. Processus cochleariformis (tensor tympani
Facial n.
hooks around it)
Pyramidal 3. Oval and round windows
eminence
4. LSC impression
Footplate is 5. Facial canal prominence
Sinus tympani
medial

Scutum/Attic
Malleus
Incus

Stapes
17 : 1 X 1.3 : 1 = 22 : 1
Areal ratio Lever ratio Transformer ratio
Tympanic
membrane
Oval
window Area of TM Due to ear Overall effect
compared to oval ossicles
window
All joints of ear ossicles are synovial joints
Malleus-incus : Saddle
Incus-stapes : Ball and socket
I-S is B-S
Otosclerosis
Sclerosed ear ossicles (conductive hearing loss)
B/L but affects one ear first followed by other
AD transmission, affects 20-40 year olds
Hearing better in noisy surroundings (paracusis)
Gelle's test : Negative
Schwartz sign (salmon pink TM) in active otosclerosis (t/t : NaF)
TOC : Stapedotomy > Stapedectomy
Associated with Van Der Hooeve's syndrome
1. Otosclerosis Schwartz sign
2. Blue sclera (salmon pink TM)
3. Osteogenesis imperfecta

Siegel's speculum
used for Gelle's test On applying pressure,
causes ossicular chain
fixation
In normal patients leads to
reduced hearing (positive
Gelle's)
Carhart notch is a depression
Negative Gelle's seen with
in the bone-conduction at
otosclerosis (ossicular chain
2000 Hz.
already fixed)
This is a characteristic finding
seen with autosclerosis

Glomus Tumor
Most common benign neoplasm of middle ear
The tumour consists of paraganglionic cells derived from the neural crest cells
Clinical presentation: Pulsatile tinnitus
Can be of 2 types : Glomous Jugulare, Glomus Tympanicum
In Glomus Jugulare : 9th to 12th cranial nerve can be involved
Biopsy is contraindicated (vascular tumor, can bleed)
On MRI : Salt and pepper appearance

Brown's sign : Blanching on pressure

(vascular tumor)

Phelp's sign : Erosion of carotico jugular spine

(on CT)

Rising sun sign

Seen with Glomus
Tympanicum
 Development of Inner ear

Maculae
Utricle Hair cells present in utricle
Pars Superior Endolymphatic sac and saccule
Vestibular part
SCC Responcible for linear
accelerations.
Saccule
Pars Inferior Cristae
Cochlear duct
Hair cells present in ampulla
of the SCC.
Endolymphatic duct Responcible for rotational
Form's endolymphatic sac accelerations.
Otic vesicle Cochlear part Surgical landmark : Donaldson's line

Perilymph

Endolymph
Cristae of SCC
Endolymphatic sac
(rotational)

Utricle -Utriculosaccular duct Cochlea

(Horizontal) Endolymph
Saccule (Vertical) 2.75 turns
Rich in K+ (like ICF)
Ductus reuniens High frequency at base
Production is from stria
Low frequency at apex
vascularis (in cochlea)
Very low frequency of people Absorption is through
Duct of cochlea
get to apex endolymphatic sac (not
functional in Menieres'
disease)

Scala Vestibuli Helicotrema

(Opens at oVal window)
Scala media
Scala
Oval vestibuli Organ of
window Corti
Stria Vascularis Scala
ne Produces endolymph tympani
embra Scala Media
r m
sne
Reis Organ of Corti
Round window
Tectorial membrane
Basilar membrane + Hair cells

Outer hair cells

Inner hair cells Outer hair cells
Inner hair cells
Less in number More in number
Single row 3-4 rows
Flask shaped Cylindrical
Afferent supply Efferent supply
Scala Tympani Transmit auditory Modulate function
(Opens at round window) stimuli of inner hair cells
Resistant to Vulnerable to
damage damage

Blood supply of inner ear : Labyrinthine artery (branch of AICA)

Outer hair cells responcible for Oto acoustic emmisions

Ménière's disease
aka Endolymphatic hydrops
Endolymphatic sac unable to drain endolymph efficiently
Affects inner ear, hence both hearing and balance affected
U/L episodic tinnitus, vertigo and SNHL
Low frequency hearing loss in audiogram (apex of cochea affected)
Tulio's phenomenon : Vertigo on loud sound
Tumarkin phenomenon : Drop attacks on loud sound
IOC : Electro-cochleo-graphy

Management
Initial management for all
Low salt diet
Avoid cafeine, chocolate, alcohol and tobacco

3-6 months trial of diuretics (if lifestyle modification not

useful)
Meniette's device Silverstein's microwick
For acute attacks : Oral, IM, or intratympanic steroids Pulses of micropressure Deliver otic medication to
inner ear via round window
Treatment failure
Meniett device
⬇️
Endolymphatic sac enhancement surgery
⬇️
Gentamicin perfusion (ototoxic drug)
⬇️
Labyrinthectomy

* Vestibular neurectomy is not done (not useful)

Donaldson's line
Landmark for
endolymphatic sac surgery

BPPV
Benign Paroxysmal Positional Vertigo
Calcium crystals dislodged from utricle and enter semi-circular canals
Vertigo has a horizontal as well as vertical component
Sudden vertigo on moving head to a certain position

Dix Hallpike maneuver Epley's maneuver

For diagnosis Treatment
Vestibular Schwannoma
aka Acoustic neuroma
Most common tumor of the cerebello-pontine angle
Arises from inferior vestibular branch of the vestibulocochlear nerve
Hitzelberger sign : Involvement of 7th CN early in the course of disease
(hypoasthesia of posterio-superior EAC)
Bilateral seen in Neurofubromatosis type 2
Mx : Gamma knife surgery

H/p of the tumor shows two distinct tissue types

Ice cream cone shaped

tumor at CP angle

Antoni A Antoni B
Cellular zones Acellular zone
Verrucay bodies

Auditory Pathway

Cochlear hair cells (inner hair cells)

Spiral ganglion
ECOLIMA

E Eighth nerve
C Cochlear nuclei
O Olivary complex (superior)
L Lateral lemniscus
I Inferior colliculus
M Medial geniculate body
A Auditory cortex
 Subjective hearing tests

Normal hearing SNHL

Pure tone audiometry

1. Air bone gap : CHL (gap in conduction)
2. No gap, decreased gap : SNHL
3. Downslope (high frequency affected) : Presbyacusis,
ototoxicity, NIHL
4. Upslope (low frequency affected) : Meniere's disease
5. Acoustic dip at 4000 Hz : Early NIHL
6. Cahart's notch at 2000 Hz : Otosclerosis CHL (air bone gap)
Cant differentiate Cochlear from Retrochochlear

Meniere's Presbyacusis/totoxicity/NIHL Otosclerosis - Cahart's notch Early NIHL

(upsloping) (downsloping) (BC dip at 2000 Hz) (BC and AC dip at 4000 Hz)

Tuning fork tests

1. Rinne's Test
Can repeat
words at
is it still ringing test
higher
intensity Plateau

Positive Negative
Roll over AC > BC BC > AC
phenomenon

Normal SNHL CHL U/L severe SNHL

Sound transmits to the
opp. ear via bones

2. Weber's Test
Wee bit lateralised
Speech audiogram Not lateralised : Normal
Lateralised to one side
Speech reception threshold : Lowest intensity of sound at
which the patient can repeat 50% of words.
This is plotted for various sound intensities (amplifications) Ipsilateral to Contralateral to
Plateau : Cochlear hearing defect hearing defect
Roll over : Retro cochlear (Rock and roll is retro music) CHL SNHL

"IC or CS" one set can only have one C

ABC test, Schwabach test : SNHL
Gelle's test is also subjective
 Objective hearing tests

Tympanometry
aka impedance audiometry
Middle ear pathology tested
Reflection of sound by tympano
ossicular system OAE BERA
(oto acoustic emmisions ) (Brainstem evoked responce audiometry)
1. As : Autoscelrosis
Outer hair cells Pathologies of auditory pathway
2. Ad : Discontinuity of ossicular chain
Screening test only (Retrochochlear)
3. C : Retracted tympanic membrane
Best test to determine Cochlear vs
4. B : Rupture/Fluid in middle ear
Retrochochlear

Wave 5 is most important

Corresponds to lateral lemniscus:
diagnosis of acoustic neuroma

Cochlear vs Retro-cochlear hearing loss

Cochlear Retrochochlear
Hair cells are damaged Lesion in 8th nerve
Recruitment is present (higher intensity Tone decay and stapedial reflex decay
sounds percieved louder than normal) are significant (due to nerve fatigue)
SISI is positive Roll over phenomenon is present.

S.I.S.I.
Short increment sensitivity index
This test is based on recruitment
Positive in cochlear pathologies
Sis recruits for coachella (cochlea)
Acute Otitis Media
Eustachian tube blocked
⬇️
Air present in middle ear cavity Middle ear
absorbed
⬇️
Retracted Negative
pressure Eustachian tube
Negative pressure created TM
⬇️
Tympanic membrane retracted
⬇️
Pain

Causes

Infection No infection

ASOM OME
(Acute suppurative (Otitis media with effusion)
otitis media) aka Serous otitis media / Glue ear
mcc : Strep pneumonia mcc in adults : Nasopharyngeal carcinoma
mcc in children : Adenoid hypertrophy

Cartwheel appearance
Congested TM in ASOM Glue ear (OME)

Lighthouse sign
Pulsatile otorrhea in ASOM

Treatment for both conditions

Myringotomy + Gromett insertion

Incision in ASOM : Curvilinear Gromett insertion/ incision is always

Incision in OME : Radial done in AIQ (antero-inf. quadrant)
Curved bacteriae
Chronic Suppurative Otitis Media (CSOM)
Chronic / permanent perforation of tympanic
membrane
Cholesteatoma
Can be due to chronic infection or cholesteatoma
CSOM can be classified as Sq. epithelium of ext ear
Ext. ear
CSOM
Fibrous layer of TM
Middle ear
Tubo-tympanic Attico-antral Mucosa of middle ear
aka safe type CSOM aka unsafe type CSOM
Mastoid not affected Mastoid affected Cholesteatoma in
T/t : Myringoplasty T/t : Mastoidectomy middle ear
(temporalis fascia used)

Types
Canal wall Canal wall
1. Congenital : Epidermal cells in middle ear
up down
Posterior wall not Posterior wall
(Levenson criteria)
removed removed 2. Primary acquired : No h/o ear infection or perforation
Recurrence Makes middle ear 3. Secondary acquired : Outer squamous epithelium
Requires second look cavity very large (can migrates to inner ear via perforation
surgery after 6 months get infected easily)
No 2nd look needed

Complications of CSOM
1. Mastoiditis : Most common complication, can form abscesses 1. Citelli's abscess : Occipital abscess
2. Facial nerve palsy 2. Bezold abscess : Sternocleidomastoid muscle
3. Labyrinthitis : Fistula sign (vertigo on pressing tragus) 3. Post auricular abscess : Pushes earlobe
False negative fistula sign : When labyrinth is dead 4. Zygomatic abscess
4. Petrositis : Gardenigo's triad
5. Greissenger sign : Mastoid edema due to thrombosis of Gardenigo's Triad
emissary veins Seen with Apical petrositis
6. Meningitis 1. Retro orbital pain (5th CN)
2. 6th CN palsy
3. Ear pain

Perforated TM in CSOM Greisenger sign

GreiseL syndrome is for non-

traumatic atlanto-axial subluxation
 Laryngeal framework
Rule of 3 for laryngeal framework Hyaline cartilages
3 unpaired (Thyroid, Cricoid, Epiglottis) Get calcified with age
Cartilaginous skeleton
Thyroid, cricoid and arytenoids
C³ - C⁶ 3 paired (Arytenoid, Corniculate, Cuneiform)
All others are elastic cartilages

Epiglottis
Hyoid Bone
(Not a part of laryngeal framework)
Sup. laryngeal
Artery, Vein, Nerve Thyro-hyoid membrane
Extrinsic cartilage of larynx
Superior laryngeal vessels and nerve pass
Thyroid cartilage
through this
Laryngocele protrudes via this structure

Cricothyroid membrane
Cricoid cartilage Intrinsic cartilage of larynx
(Ring shaped cartilage) Cricothyrotomy for emergency intubation

Tracheal Cartilages

Epiglottis

Corniculate and cuneiform Thyroid cartilage

Arytenoid

Cricoid cartilage

Epiglottis Ary-epiglottic fold

(Quadrangular membrane)
Cuneiform cartilage
Epiglottis
Vocal cords

Arytenoids and Cuneiform

 Endoscopic view of larynx

Vestibular folds False vocal cords

True vocal cords

False vocal cords

Vestibular folds present above the true vocal cords
Function is to protect and lubricate the true vocal cords
If false vocal cords produce sounds, its known as "Dysphonia Epiglottis
Plica Ventricularis"
Area between true and false vocal cords is known as vestibule

Vestibule Saccule
The area between true and false vocal cords
Has a pocket of space known as saccule Sub-glottic
space
Saccule
Saccule is known as oil can of larynx because it's rich in
mucus glands.
Cystic dilatation of saccule seen in Laryngocele

Laryngocele
Cystic dilatation of saccule
Seen commonly in trumpet players
Herniation of larynx through thyrohyoid membrane
Swelling moves with deglutition
Bryce sign : Hissing sound on pressing the bulge
Treatment : Marsupialisation

Boyce sign seen in Zenker's diverticulum

Pediatric vs Adult larynx

Adult Larynx Pediatric Larynx Subglottic stenosis

Cylindrical Conical Congenital or acquired
C³ - C⁶ level Higher : C¹-C² level narrowing of the
Leaf shaped epiglottis Omega shaped epiglottis subglottic airway
Narrowest portion is glottis Narrowest portion is subglottis Cotton Myer staging
Treatment : Mitomycin C
Because of these variations, infants can breath while suckling milk

Laryngeal disorders on endoscopy

Laryngeal papillomatosis Vocal nodules

H/o viral warts in mother Stress to vocal cords
HPV 6,11 Bilateral
If u/l : Vocal polyp

TB larynx Reinke's edema

Turban shaped epiglottis Submucosal edema
Rat bitten appearance Associated with GERD, smoking
Rx : micro laryngeal stripping

Laryngomalacia
Omega sign
Inspiratory stridor
Increase in stridor : Crying
Decrease in stridor : Prone position
Resolve spontaneously in 2 yrs

Carcinoma of Larynx
Most common : Glottic (early presentation, best prognosis)
T staging
1. One subsite involved (normal vocal cords mobility)
2. 2 subsites (vocal cords mobility decreased)
3. Pre/para glottic or post cricoid (vocal cords fixed)
4. Everything else
Treatment
T1-T2 : Radiotherapy > Partial laryngectomy
T3-T4 : Total laryngectomy
Laryngeal disorders on X ray

Thumb Sign (Acute epiglottitis)

Fever, toxic looking child
Hot potato voice
Child spontaneously takes Tripod position (easier to breathe)
Strep pneum > Hem. Infl B (due to vaccination against H.influenza)
Mx: Intubate, IV antibiotics (3rd gen cephalosprins)

Steeple Sign (Acute laryngo tracheo bronchitis)

aka Croup
Narrowed subglottis
Barking cough
MCC : Parainfluenza virus
Mx: Racemic epinephrine for mild to moderate cases
(no role of antibiotics)
Dexamethasone for severe disease

Multiple linear opacities at hilum

(Viral bronchiolitis)
aka Bronchial flu
MCC : RSV (respiratory syncytial virus)
Common in cold seasons
Prophylaxis : Palivizumab
Rx : Ribavirin

Isolated hperlucency of hemithorax

(Foreign body aspiration)
Most common foreign body aspirated are peanuts 🥜
Mx : Bronchoscopy and removal

Rigid brochoscopy : Therapeutic

Flexible bronchoscopy : Diagnostic
Nerve supply of Larynx

Vagus nerve

Superior laryngeal Recurrent laryngeal

nerve nerve
Internal branch of SLN provides Motor supply to larynx
Sensory supply to larynx (cough (except cricothyroid)
reflex, prevents aspiration)
External branch of SLN supplies
Cricothyroid muscle (only tensor and
adductor)
Sensory : SLN

ILN paralysis : No sensory supply, hence no cough : Aspiration

ELN paralysis : No supply to cricothyroid, hence no tension : Low pitch
SLN paralysis : Aspiration + Low pitch

RLN paralysis : Only cricothyroid functional (adducted vocal cords) : Can't breathe
Emergency tracheostomy needed. (Def mx : Type 2 thyroplasty)

Complete paralysis : Cadaveric position of vocal cords, aspiration + aphonia

Thyroplasty
Type 1 : Medialisation (1 head, medial)
Type 2 : Lateralisation (2 hands, lateral)
Type 3 : Shortening / relaxation : Done for puberophonia (3 : pubis, short)
Type 4 : Lengthening / tightening : Done for androphonia (4 : legs, long)

1 Gutzmann test for puberophonia

2 2

4
Pharynx
Common passage for air and food
C¹ - C⁶ Nasopharynx
Tonsils are arranged in Waldeyer's ring C¹ Skull base to soft palate
Pharyngeal muscles
C² Oropharynx
C³ Hyoid to cricoid

Inner longitudinal Outer circular C⁴

Laryngopharynx
1. Stylo-pharyngeus C⁵ Along with larynx
2. Salpingo-pharyngeus Constrictors C⁶
3. Palato-pharyngeus (superior, middle
Lined by bucco-pharyngeal fascia and inferior)

Gaps between constrictor muscles

Base of skull
1. Eustachian tube
Sinus of Morgagni 2. TVP, LVP
3. Ascending palatine artery
Superior constrictor

1. Glosso-pharyng nerve
2. Stylo-pharyngeus muscle
Zenker's diverticulum
Between thyro-pharyngeus and
crico-pharyngeus : Area of
Middle constrictor
weakness known as Killian's
triangle
Sup. Laryngeal nerve and Seen at old age (non coordination
vessels (via thyrohyoid memb.) of muscles during swallowing)
It's a false diverticulum (only
Inferior constrictor mucose and sub-mucosa involved)
Boyce sign (gurgling sound on
palpation)
T/t : Dohlman procedure
(endoscopic diverticulotomy)
Tonsils

Mcc of tonsilitis : Beta hemolytic strep

Referred otalgia in tonsilitis : Due to glossopharyngeal nerve
present in tonsillar bed (referred pain via Jacobson's nerve)
Blood supply of tonsils : Branches of ECA (major supply is via
tonsillar branch of facial artery)
Intra-op haemorrhage in tonsillectomy : From tonsillar vein
Reactionary haemorrhage : Within 24 hours (due to improper
clipping action by superior constrictor)

Adenoid hypertrophy
Nasal obstruction with recurrent otitis media in a child
Characteristic adenoid facies can be seen (flat nose,
high arched palate, long face and dental crowding)
Dx : Lateral X ray of head and neck, endoscopy
Mx : Intranasal steroids and antibiotics
Adenoidectomy done only for significant symptoms
which includes : Sleep apnea and Otitis media

Peritonsillar abscess (quinsy)

Uvula pushed to opposite side
No neck mass (if present it's
parapharyngeal abscess)
Management : Incision and drainage
Tonsillectomy done later.

Parapharyngeal abscess Retropharyngeal abscess

Neck swelling Neck swelling
Uvula pushed Uvula not pushed
aka prevertebral abscess

Site for I and D

Ludwig's vs Vincent's angina

Ludwig's angina Vincent's angina

Old male aka acute necrotising ulcerative gingivitis
Floor of mouth cellulitis Mixed bacteria-spirochetal infection
Fever + tooth ache + dysphagia Predisposing factors : Poor oral hygiene and
Polymicrobial infection Immunosuppression
t/t : I & D + Antibiotics Shows membrane over tonsil

Ludwig is a clean
white owl

Tracheostomy vs Laryngectomy

Tracheostomy Laryngectomy
Most common position is 2-3rd Larynx removed and an opening is
tracheal ring (mid tracheostomy) made to allow air into trachea
High tracheostomy : Causes cricoid
inflammation and subglottic stenosis
(only done in case of Ca. Larynx)
Low tracheostomy : Lower risk of
infection (can complicate due to
presence of important structures
around)

To facilitate speaking, voice

prosthesis are used.
Tracheo-esophageal prosthesis are
the preferred voice prosthesis.
Laryngoscopy vs Rhinoscopy mirror

Indirect laryngoscopy mirror Posterior rhinoscopy mirror

(St. Clair Thompson mirror)

VESPA

Radical neck dissection

Structures always removed
1. Lymph nodes
1a - Submental LN
1b - Submandibular LN
2,3,4 - Along jugular vein
5 - Posterior triangle nodes
(Level 6 LN removed in central
neck dissection not in radical)
2. Sub-mandibular glands
3. Parotid tail

Structures spared
Type 1 : SAN
Type 2 : SAN + IJV Lymph node levels of neck
Type 3 : SAN + IJV + SCM muscle
CHAPTER 4
OPHTHALMOLOGY
 Corneal Epithelium

Non keratinised
Stratified squamous epithelium
Corneal epithelium
With cilia
Bowman's membrane
Not a true basement membrane (PAS negative)
Can't regenerate, hence forms scar tissue
Ca²+ deposition in band shaped keratopathy →

Stroma of cornea
Thickest layer Rx : EDTA
Has keratocytes
Glycosaminoglycans (Keratan sulphate)
Type 1 collagen evenly organised

Dua's Layer Strongest layer Secreted continuously by endothelium

Descemet's membrane Termination is known as Schwalbe's line
Corneal endothelium KF ring in Wilson's
Metabolically active ↓
Maintains dehydration
<500 : hazy cornea
Keratic precipitates present in
ant. uveitis in this layer

Rx : Triamterene + Zinc

Corneal Tests and Instruments

Corneal topography

Endothelial cell count Pachymeter Keratometry Pentacam

Normal : 2400 - 3000 Measures corneal Measures corneal curvature Based on Scheimpflug
< 500 : Hazy cornea thickness using USG imaging
Ker-Curvature
PT
Placido disc
 Corneal Infections
Bacterial ulcer Fungal ulcer
Pneumococcus is MCC h/o trauma with vegetative matter
h/o contact lens use : Pseudomonas Hypopyon : Non sterile and immobile
Hypopyon : Sterile and mobile (fungal hyphae makes the pus immobile)
(occurs due to bacterial toxins) Signs >>> pain
Satelite lesions
Hypopyon MCC of corneal ulcer in contact lens
"mis-use" is Acanthamoeba ulcer
Immune ring (Wesley's)
Collection of pus in anterior chamber
Seen in bacterial and fungal corneal ulcers

Acanthamoeba ulcer
h/o contact lens mis-use
Pain >>> signs
Ring abscess
DOC : PHMA (Poly Hexa Methylene Biguanide)

Fungal ulcer Acanthamoeba ulcer

Satelite lesions Ring abscess
Immune ring (Wesley's)

Viral ulcer
Fluroscein stain Rose Bengal stain
Most common cause is HSV
Cobalt blue light
Corneal sensation is lost
(loss of corneal reflex)
SPK - Dendritic - Geographical
T/t : Acyclovir 3% ointment
Steroids are contraindicated
Superficial punctate keratitis Dendritic ulcer Geographical ulcer (cause thinning of cornea)

Dyes used for corneal ulcer

Tear film producion
Fluroscein dye
Base of ulcer
Cobalt blue light is used
Ulcer appears green
Bengal is a
peripheral
Rose bengal stain
state
Margins of corneal ulcer Lipid Layer
Used in Schimmer tear test (Sjogren syndrome) (Meibomian glands)
Irritant (used at the end)
Aqueous Layer
(Lacrimal glands)
Mucin Layer
Non infective keratitis
(Epithelial cells)
Neuroparalytic keratitis
Due to 7th CN palsy
Unable to close eyes →Exposure keratitis Tear breakup time < 10s : Mucin deficiency
Mucin deficiency is associated with Vit A deficiency
Interstitial keratitis (xeropthalmia)
inflammation of stroma
seen in congenital syphilis
Keratoconus

Munson's sign : Lower eyelid

protrudes on down gaze
Vogt's striae
(Haab's striae seen in Bupthalmos) Munson's sign Vogt's striae Fleischer ring
Fleischer ring : Iron deposition
(KF ring in copper deposition)
Rizutti sign on oblique light
Oil droplet reflex on Opthalmoscopy
ScissoRing on Retinoscopy
Corneal Rizutti sign ScissoRing reflex Oil-droplet reflex
topgraphy

Management
INTACS
Keratoplasty
C³R : Collagen
cross linking with
riboflavin
INTACS rings

Munson's sign Vogt's striae

Corneal opacity

Nebular grade corneal opacity

Opacity of <1/3 of corneal thickness
Details of iris can be made out

Macular grade corneal opacity

Opacity of > 1/3 and < 1/2 of corneal thickness
Details of iris are blurred Arcus senilis
aka Gerontoxon
Leukomatous grade corneal opacity Seen in elderly
Opacity of > 1/2 of corneal thickness Lipid deposition : Lucid interval of Vogt
Details of iris are can not be seen Pseudogerontoxon : VKC (Spring Catarrh)

Adherent Leukoma
Iris involved

L-M-N
(in reverse)
Scleromalacia perforans
Complication of RA
 Visual field defects

Nasal fibres
Defect in visual field of
cross over
L eye R eye

1 Optic Nerve lesion : I/L anopia

7 Macula Optic nerve
1 2 Optic chiasma : Bitemporal hemianopia
3 Optic tract
Optic chiasm ➡️
2- 4 Meyer loop 3 Wernickie's
(temporal lobe) Optic tract : C/L Homonymous hemianopia hemianopic pupil

Superior quadrantanopia (Meyers loop)

Dorsal optic 5
4
STeMI
radiation Sup → Temp → Myers
(parietal lobe) 5 Inferior quadrantanopia (Baum's loop)
3
(6 if PCA infarct) 6 PCA (macular sparing)

7 Macular lesion

Junctional scotoma
Causes of BTHA (Seen in meningioma)
aka heteronymous hemianopia

3rd ventricular glioma

Pituitary adenoma (mc) Pitutary adenoma
Craniopharyngioma- occur in
Rathke's pouch
ACA aneurysm
Cavernous sinus thrombosis

Craniopharyngioma
 Light reflex

Afferent Efferent
Optic nerve Oculomotor nerve
Optic tract Cilliary ganglion
Skips LGB Short ciliary nerve
Pre-tectal nucleus
(relays to opp side)
EW nucleus

Causes of light near dissociation

ARP (tertiary syphillis)
Adie's tonic pupil (idiopathic)

AFFERENT PATHWAY DEFECT EFFERENT PATHWAY DEFECT

ISOCORIA AN-ISOCORIA

Optic nerve damaged Argyl Robertson Pupil

Total/ absolute afferent pupillary defect (TAPD/AAPD) Light near dissociation
aka Amaurotic pupil Accomodation reflex present, light reflex absent
When light on normal eye, both constrict and in Seen in tertiary syphillis
abnormal eye none.
Adie's Tonic Pupil
Optic neuritis Light near dissociation
Relative afferent pupillary defect (RAPD) Parasympatehtic post-ganglionic
aka Marcus Gunn pupil light fibres are damaged
When light on normal eye, both constrict Idiopathic and resolves
and in abnormal eye both dilate spontaneously
(paradoxical dilation) RAPD
More common in females
Seen in Multiple Sclerosis Swinging flashlight test Associated with absent knee
reflex
Constricts on 0.125% pilocarpine
Wernicke's Pupil
Localises to optic tract in a patient with hemi-anopia Pharmacological Mydriasis
Light on the blind half produces no light reflex Here even accomodation reflex is absent
Doesn't constrict with 0.125% pilocarpine
 Opthalmoscopy
Direct opthalmoscopy Indirect opthalmoscopy
More magnification (14 times) Less magnification (3 times)
Only 2 DD can be seen (periphery 9 DD can be seen (periphery can
can't be seen) be seen)
Direct image seen Inverted image seen
No stereopsis Stereopsis possible
Examination not possible through Examination through hazy media
hazy media possible

Lord Jagannath with big eyes

2 disc
(fovea centralis) is present in
diameters
temple (temporal side)

Optic Atrophy
Primary Optic atrophy Secondary Optic atrophy
Optic nerve etiology Secondary to papilledema
Chalky white disc (chalks used in primary classes) Grey disc
Distinct margins Blurred margins (Blurred and grey)
Causes Gliosis (fibrosis) of optic nerve head
1. Compression of ON Central scotoma (expansion of blind spot)
2. Hereditary optic neuropathy Other causes :
3. Nutritional optic atrophy 1. AION (Anterioir ischemic optic neuropathy)
2. Papillitis

Diseases affecting optic nerve

Multiple Sclerosis Neuromyelitis Optica
Retrobulbar neuritis is m/c presentation aka Devic's disease
in adults (the optic disc appears normal) Auto-immune demyelinating disease
Both doc and patient can't see anything Antibodies against aquaporin 4
Painful u/l loss of vision U/l or b/l optic neuritis (papillitis) within a
No VFD few weeks of transverse myelitis
IOC : CE MRI (demyelination of spinal cord)

Neuro-retinitis
Optic neuritis (Papillitis) + Macular star
 Layers of Retina
Retina is "outer"
Dark stained are nuclear layers Outer 4 layers supplied by Short posterioir cilliary artery
Plexiform between nuclear layers Inner 6 supplied by central retinal artery
Rods and cones hyperpolarise

Inner nuclear layer

Internal limiting membrane Amacrine cells
Muller cells
Nerve fiber layer Horizontal cells

CRA
Ganglion cell layer Ganglion cells (3° neurons)
Inner plexiform layer
Inner nuclear layer Bipolar cells (2° neurons)
Outer plexiform layer CME, hard exudates
Short Outer nuclear layer
Post. External limiting membrane
cilliary Photoreceptor layer Rods and cones (1° neurons)
art.
RPE Retinal detachment occurs at RPE

Choroid Blood retinal barrier

Outer : RPE (causes CSR)
Inner : Capillary permeability of CRA,
at OPL (causes CME)

Macular disorders
FFA OCT FFA OCT

Ink blot/
Flower petal Petalloid
mushroom RPE detached

Central Serous retinopathy Cystoid MACULAR edema

Outer blood retinal barrier breached Inner blood retinal barrier breached Amsler's Grid
RPE Outer plexiform layer Detects metamorphopsia
Steroids and Type A personality are Irvin Gass / PG analogues / Niacin and macular problems
risk factors toxicity Grid has straight lines
Laser photo-coagulation if >4 months Rx : Steroids
Steroids are contraindicated Photostress test
To determine if disease is at
optic nerve or macula
ERG : Retinitis pigmentosa
EOG : Best's disease (Arden's
ratio decreased)
Diabetic retinopathy

Non Proliferative DR Proliferative DR

Pan retinal photocoagulation

nd Yag, double frequency laser
(532nm)

Cotton wool spots Hard exudates Neovascularisation

Microaneurysms (Present in OPL) Sub hyaloid hemorrhages
Flame shaped hemorrhages Boat shaped hemorrhages
ETDRS : Early treatment DR study
Severe NPDR : VEG-F inhibitors T/t : PRP
4mm above the limbus

VEG-F inhibitors
Intravitreal injection
Micro-aneurysms (earliest sign) : INL
Screening "bro Rani bewava, afli peg"
Dot and blot haemorrhages : OPL
Type 1 : Within 5 years of diagnosis
Hard exudates (due to leaked lipids) : OPL Brolucizumab
Type 2 : At the time of diagnosis
Flame shaped haemorrhages : NFL Ranibizumab
Cotton wool spots (soft exudates) : Axonal Bevacizumab
infarcts in NFL Aflibercept
Pegaptanib

"MINL HOPL"

Hypertensive retinopathy

Salu's sign : S shaped deflection of veins

AV nicking
Gunn sign : Tapering of veins at either ends
Bonnet : Dilatation of veins at junction
Arteriolar
attenuation
Normal artery : vein diameter → 2:3
In hypertensive retinopathy (further attenuation) → 1:3
Copper wiring
 Fundus Spotters

Cherry red spot Splashed Ketchup Roth Spots

Neiman picks CRVO Infective endocarditis
Tay Sachs also seen in
100 day glaucoma
CRAO Acute leukemia
(Ocular Emergency) Rubeosis iridis Diabetes
New vessels in iris Sickle cell anemia
Berlin's edema
(Traumatic) 2° open angle g. HIV
Trabecular meshwork blocked due SLE
to fibrovascular membrane

2° angle closure g.
Contracture of fibrovascular
membrane pulls the iris forming
peripheral anterior synechiae

T/t VEGF

Salt and pepper retinopathy Pizza pie appearance Headlight in fog Macular scar
Congenital Syphilis CMV retinitis Toxoplasmosis Punched out lesions in retina
Congenital Rubella (In HIV CD⁴ < 50) Untreated Toxoplasmosis
Refsum's disease T/t: Ganciclovir
HSV retinitis

Eale's disease
Idiopathic inflammatory venous
occlusion (phlebitis)
Primarily affects the peripheral retina
that is periphlebitis
Characterized by recurrent bilateral
vitreous hemorrhage

Candle wax drippings

Seen in Sarcoidosis
 Age related Macular disorders

ARMD can be of dry type or wet type

Wet type is when it's associated with neo-vascularisation

AREDS -2
(Age related eye disease studies 2)
Vit C, E (Vit A not included)
Cu, Zn
Lutein, Zeaxanthin
Drusens Lipofuscin deposition
Between RPE and seen on fundal imaging
Bruch's membrane

Retinal detachment
Types of retinal detachment
Scleral buckling
Rhegmatogenous : (Rhegma = Broken)
Horse shoe shaped tear
Seen with Trauma/ Myopia/ Surgery
"Curtain falling in front of eye"

Exudative : Fluid filled

Dome shaped detachment Horse shoe shaped tear
Rhegmatogenous
Shifting fluid sign
retinal detachment

Tractional
Tent shaped detachment

Treatment
Scleral buckling
Retinopexy (inject sulfur-hexachloride or silicone or air) Retinopexy
B scan showing exudative
retinal detachment

Retinoblastoma

Sporadic 60%, Hereditary 40%

M/c inheritance is AD
Leukocorea
Most common presentation of Rb Rb gene on chromosome 13q14
Other causes of Leukocorea Trilateral Rb : b/l Rb + Pinealoblastoma Calcium deposition
1. Persistent hyperplastic as seen on CT
primary vitreous (PPHV) Most common route of spread : Direct
2. Endopthalmitis invasion (with optic nerve)
3. Congenital cataract
Treatment for unilateral Rb : Enucleation
Treatment for bilateral Rb : VEC regime
Clinical presentation of Rb : (Vincristine, Etoposide, Carboplatin)
Leukocorea > Esotropia > Glaucoma

Associated with Osteosarcoma

 Arterial
attenuation

On
fundus
examination

Waxy Pale Bony

optic disc Spicules

Egg yolk appearance Silent choroid on FFA

Retinitis Pigmentosa
Best macular dystrophy Stargardt disease
Autosomal recessive disease (Chr 3q) Autosomal Dominant Most common macular
Rod - cone dystrophy (rods more affected) transmission dystrophy
Night blindness and ring scotoma (tunnelling Lipofuscin deposition Cone dystrophy
of vision) (egg yolk app) Fish flecks (bronze beaten
IOC : ERG IOC : EOG (Arden's ratio appearance due to
No treatment available (only counsel about decreased) lipofuscin deposition)
the vision loss) Bull's eye can also be seen
Poor prognosis if : XLR
Associated with : Lawrence Moon Biedl sx

Bull's eye maculopathy

1. Chloroquine toxicity (>5 yrs)
2. Stargardt disease
 Conjunctiva

Pterygium Pingeculla
Only Conjunctival disease Localised conjuctival
which affects vision overgrowth
Abnormal proliferation of
limbal stem cells
Limbal stem cells marker :
ABCG 2
Pre-auricular lymph node
t/t : Excision + autograft
Sub-mandibular lymph node

Grey and
pale

Red and
glistening

Follicles Papules
Hypertrophied vascular core
Lymphoid aggregates
A and B : Allergic and Bacterial
Viruses and Toxins
VKC : Spring Catarrh
Chlamydia (Trachoma) Giant Papillary Conjunctivitis
Giant papillary conjunctivitis
seen with contact lens use

VKC (Spring Catarrh)

Pre-adolescent boy (5-14 years)
Ropy discharge
Cobblestone papilla
Horner Tranta dots
Horner tranta dots
Pseudogerontoxon
Pseudogerontoxon Gerontoxon limbal dots consisting of
DOC : Olapatadine + Steroids
Deposition of eosinophils (Arcus Senilis) degenerated epithelial
in cornea cells and eosinophils

MCC of bacterial conjunctivitis : Staph Aureus

Hyperacute blenorrhea : Gonorrhea Neonatal conjunctivitis
Angular conjunctivitis : Moraxella
Conjunctivitis < 30 days of birth

Chlamydia A-C : Trachoma (ABC of Trachoma)

If within 24 hrs : Chemical con. Due to AgNO3
Chlamydia D-K : Inclusion conjunctivitis (neonates and adults)
2 - 5 days : Gonococal (t/t is ceftriaxone)
5 - 14 days : Chlamydial (t/t is erythromycin)
Acute hemorrhagic conjunctivitis
aka Apollo Conjunctivitis MCC in developed countries is chlamydial
Adenovirus 2, Cox A24, Enterovirus 70
(ACE 2 24 70)
Self resolving in 2-3 days
 Trachoma
Chlamydia SAFE strategy by WHO
Serovars A, B, Ba, C

WHO (FISTO)
Follicles (Sago grains)
Inflammation For trichiasis Single dose
Scarring (Arlt's line) Azithromycin
Water washed disease
Trichiasis p/o
Opacity of cornea

Limbal conditions
Herbert's Pits Trachoma
Horner tranta dots VKC Arlt's line Herbert's Pits Pannus
Cicatrical scar in Limbal pits (left after Superficial vascularisation
conjunctiva healing of follicles) of cornea
 Glaucoma Visual field changes + Optic disc changes + ↑IOP

Trabecular meshwork IOP

blocked > 21mm Hg or
Iris touches lens > 5mm Hg difference in
both eyes

Open angle glaucoma Closed angle glaucoma

Seen in elderly Acute painful red eye
Gradual and painless LOV Shallow anterior chamber is a
Trabecular meshwork risk factors Mid dilated and fixed
blocked Iris touches cornea, closes pupil in glaucoma
Rx : Trabeculectomy/ angle and aqueous drainage is
trabeculoplasty impaired.
Rx : Laser Iridotomy

Pupillary block

Vogt's Triad (ACG) Management of ACG

Iris atrophy A : Acetazolamide (reduces production)
Glaucomflecken (anterior M : Mannitol
sub-capsular opacity) P : Pilocarpine (Cholinergic, causes miosis and Iris bombe

Pigment dispersion in prevents synechae)

corneal endothelium
Anterior lens and posterioir DOC for acute PACG : Pilocarpine
cornea deposits of iris debris Definitive treatment : Laser Iridotomy (Nd Yag) PAS - peripheral anterior
synechiae

Visual field changes Optic Disc changes

Earliest change : Isoptre contraction

Paracentral
Scotoma

Siedel's
scotoma
Nasal field lost

Enlarged optic cup (vertically enlarges)

Arcuate Cup : Disc ratio > 0.3
scotoma Loss of neuroretinal rim ( inferior first)
Peripapillary atrophy
Bayonetting sign (double angulation of vessels)
Ring
scotoma
KRUKENBERG SPINDLES (Open angle)
Present on back of cornea
Total field loss Pigmentory glaucoma : constant rubbing and friction
between pigment iris epithelium and lens
Temporal field
These pigment particles block the trabecular
lost at late stages
meshwork → POAG
Glaucoma Instruments

Inner margins
Schiotz indentation should touch
Goniometry
tonometer
Angle of anterior chamber
Uses total internal reflection

Structures seen
Goldman's aplanation tonometer Can Cilliary body band
Gold standard See Scleral spur
Imbert fick law : P= F/A This Trabecular meshwork
Stuff Schwalbe's line

Self/digital/rebound Raised Low Normal

tonometer IOP IOP

Pseudo exfoliation syndrome Bupthalmos

Seen in elderly (Congenital Glaucoma)
Risk of POAG Blepharospasm
Humphreys static VFA Photophobia
Lacrimation

Anti-Glaucoma drugs
Drugs that decrease aqueous production Increased Trabecular outflow
1. Carbonic anhydrase inhibitors 1. Pilocarpine
1. Acetazolamide DOC for acute angle closure glaucoma
2. Brinzolamide S/e of NLD stenosis
3. Dorzolamide
2. Netarsudil
Rho-kinase inhibitor
2. Alpha agonists
S/e of Vortex keratopathy
1. Apraclonidine (s/e : Lid lag)
Alpha 2 agonists
2. Brimonidine (s/e : Apnea)
3. Dipivefrine (s/e : Black conjunctiva)
Non-selective alpha agonist Increased Uveo-scleral outflow
3. Beta blockers PGF-2 alpha analogues
(s/e : reduced corneal sensation) Latanoprost and Bimatoprost
1. Timolol S/e of heterochromia iridis,
2. Betaxolol (preferred) hypertrichosis, CME and uveitis
 Lens
Capsule is thinnest at posterior pole
Thickest at pre-equatorial region

Lenticonus Ectopia lentis

Anterior Posterior Marfan syndrome

Supero temporal (fan out)
Alport Sx Lowe Syndrome
(oculo-cerebro-renal
syndrome) Homocystinuria
B 6/9/12 deficiency
Inferonasal (in)
Marfanoid habitus and
accelerated atherosclerosis

Weill-Marchesani syndrome
Anterior dislocation (March)
Microspherophakia
Brachydactyly
 Cataract

Snowflake cataract Oil drop cataract Sunflower cataract Christmas tree cataract
Diabetes mellitus Galactosemia Wilson's Myotonic Dystrophy
Sorbitol pathway defect Only reversible Chalcosis CTG repeat - Chr 19
Only cortical cataract cataract (Due to retained "Can't terminate grip"
(everything else is post foreign body)
subcap. cataract)

Congenital Cataract
Complicated Cataract 1. Uveitis
Breadcrumb appearance 2. Glaucoma
Polychromatic lusture 3. Retinitis pigmentosa

Glassblower's cataract : IR radiation

Blue dot cataract Lamellar cataract
Shield like cataract : Atopic dermatitis
Most common MC congenital cataract
NF-2 : Posterioir sub-capsular cataract
congenital Cataract causing vision loss

Senile Cataract
Most common cause of cataract
Usually one eye is affected earlier f/b other Immature senile cataract

It could be either soft type (cortical) or hard type

(nuclear)
Mature senile cataract
Cortical cataracts are more common (Cuneiform >
(aka RIPE cataract)
Cupular) and can be further divided as immature or
mature (complete opacification)

Morgagnian Cataract
In hyper-mature cortical cataract (aka Morgagnian)
showing subluxation of lens
entire cortex is liquefied causing subluxation of lens.

Gradual progressive painless DOV : Cataract, POAG GTCS

Sudden painful red eye + DOV : Uveitis, PACG Glaucoma : Topical steroids
Sudden painless DOV : Retinal cause Cataract : Systemic steroids
Floaters : Vitreous cause
Metamorphopsia : Macular cause Topiramate : 2° Open angle glaucoma
 Cataract Surgeries
Conventional : Limbal incision (7-8 mm)

A
SICS : Sclero-Corneal tunnel (5-7 mm)
Phaco-emulsification : Clear corneal tunnel (3-3.5 mm)
MICS (micro incision): < 2mm
FLACS (femto laser assisted cataract surgery) : Nd Glass laser

Complications of Cataract Surgery

Posterioir capsular opacification Rigid IOL : PMMA
Foldable IOL : Silicon, acrylate, hydrogel
aka After cataract
m/c delayed complication
Treatment : Posterioir capsulotomy Power of IOL calculation
using Nd Yag laser Holladay
Hoffer Q
SRK T
Erwin Gass Syndrome
CME after cataract
If myopic / LASER : Haigis L

Endopthalmitis
Most dreaded complication
Early onset : Staph epidermidis
Late onset : P. Acnes
Treatment : Intravitreal antibiotics and vitrectomy
Prevention : Cleaning operative site with povodone iodine

Reverse hypopyon
Collection of emulsified silicon oil
in anterior chamber
Complication of vitrectomy
Trauma

Vossius ring Irido - dialysis Iris prolapse Rosette cataract Hyphema

Iris pigment D shaped pupil Could also be a Posterior Anterior
deposited on lens Detachment of iris complication of subcapsular catarct chamber bleed
from ciliary body cataract surgery

Sympathetic opthalmia (Panuveitis)

Penetrating trauma to Cilliary body
Purtscher's Retinopathy
Multiple cotton wool spots
Granulomatous pan-uveitis
h/o head rauma
Cause : Immune privilege
Also seen with fat embolism or
Prevention : Enucleation of affected eye
pancreatitis
Treatment : Steroids

Other important cause of Pan Uveitis

Vogt Kanayagi Harada syndrome
Vision loss
Hearing loss
Skin changes (vitiligo, alopecia)

E-Nucleation : Eye ball + Optic Nerve

Sympathetic opthalmia
Retinoblastoma
Pan-opthalmitis

E-Visceration : Sclera left behind

E-Xenteration : All orbital contents removed

Mucor mycosis
Metastasis`
EOM Actions
SIN - RAD LR⁶ S0⁴ 0³

3 ADduction
6 ABduction
3 Elevation Intorsion (SIN) ADduction RAD
Recti adduct
3 Depression Extorsion ADduction

4 Intorsion (SIN) Depression ABduction

3 Extorsion Elevation ABduction

3rd Cranial nerve palsy 4th cranial nerve palsy 6th CN palsy
Only 4 and 6 functional Head tilt in image Isolated LR palsy
SO4 + LR6 (down and out) SO palsy (Cautious for MLF syndrome question)
LPS affected : Ptosis

Causes of oculomotor nerve palsy Internuclear Opthalmoplegia

PCOM aneurysm Ipsilateral PPRF generates the horizontal eye movements.
Aneurysm compresses outer The PPRF has two outputs.
parasympathetic (O - P) fibres. Ipsilateral 6th cranial nerve nucleus.
Causes pupillary dilatation
Contralateral MLF which supplies the contralateral 3rd CN
Vascular diseases (eg. Diabetes) Lesion of contralateral MLF ➡️ c/l adduction absent in horizontal gaze
Affects the inner part of nerve fibres
first : Ptosis and diplopia
Center for horizontal gaze : PPRF
Outer Parasympathetic fibres are
Center for vertical gaze : Rostral interstitial
spared (pupil sparing) nucleus of Cajal

Park's 3 step test

A patient presents with left hypertropia which increases on right tilt and right gaze.

Left hypertropia Superioir rectus elevates and left is

Works only with Hyper-tropia
Contralateral tilt : Rectus already elevated
If hypo-tropia in question, make
Contralateral gaze : Superioir Hence, right Superioir rectus palsy
it opposite side hypertropia

A patient presents with left-sided head tilt which on straightening leads to right
Ipsilateral gaze : Inferior IGI
hypotropia. This increases on dextroversion and right head tilt. Paralysis
Ipsilateral tilt : Oblique ITO of which of the following muscles is involved?

Right hypotropia - Left hypertropia Right hypotropia, hence

Contralateral tilt : Rectus right Superioir rectus palsy
Contralateral gaze : Superioir
 Squint
Tropia : Manifested squint Yolk muscles : Muscles in opposite eyes which
Phoria : Latent squint help in same gaze
Herring's law : Equal innervation to yolk
Esotropia muscles
Inward squint Sherrington's law : Relaxation of antagonist
m/c type of squint muscles (on same eye)
Associated with hypermetropia (accomodative squint)
Seen in retinoblastoma (Leucocoria > Esotropia)

Exotropia
Outward squint
Associated with myopia Hess Chart

Concomitant squint In-concomitant squint

Primary deviation is equal to Secondary deviation is more
Secondary deviation than primary deviation
1. Accomodative esotropia (m/c) 1. Paralytic squint : Negative FDT
t/t : Spectacles 2. Restrictive squint : Positive FDT
2. Essential infantile esoteopia :
Large angle deviation
t/t : Occlusion of normal eye to
prevent Amblyopia

Occlusion therapy Formula : (Age : 1)

(Normal eye occlusion : deviated eye occlusion)
Cover test
Cover - Confirm (tropia)
Forced duction test When normal eye covered, squint eye moves to
Positive : Can't move ➡️ Restricitve pick up fixation
Negative : Can move ➡️ Paralytic
Cover un-cover test
For latent squint
Squint eye when covered (loses fixation) and
moves
Hirscheberg Corneal light reflex test When uncovered, moves back to pick up fixation
DOOM : Deflection opposite to movement

Maddox Rod test

Converts point
source of light to a
linear source

Worth 4 dot test Prism bar test

Pupillary margin : 15°-30°

Multiply by 15°
Deflection opp to reflection
 Lacrimal Glands

Congenital dacrocystitis
Superior lacrimal canal
NLD obstruction causing inflammation
Lacrimal sac
Lacrimal punctum of the lacrimal sac (obstructed at valve of Hasner)

Inferior lacrimal canal Management

Lacrimal gland
Nasolacrimal duct Less than 9 months : Massage and antibiotics
9 months - 4 years : Syringing/probing
Nostril
Excretory lacrimal ducts > 4 years : DCR

mc tumor of lacrimal gland : Pleomorphic adenoma

mc carcinoma of lacrimal gland : Adenoid cystic carcinoma

Tests for dry eye

> 15 mm is normal

Eyelids

Chalazion Stye
Meibomian gland affected Also called as hordeolum
Painless Painful Eyelid Coloboma
Chronic granulomatous involvement Due to infection in a blocked gland Eyelids not fused
Risk of "Sebaceous gland carcinoma" Internal hordeolum : meibomian gland Can lead to exposure
involved keratitis
Upper eyelid usually involved
External hordeolum : gland of Moll/
gland of Zeiss / hair follicle involved
Lower eyelid mostly involved

Iris Coloboma
Basal cell carcinoma Associated with
CHARGE syndrome
Most common eyelid tumor
85-90%
lower eyelid involved Distichiasis Madarosis Trichiasis
Extra layer of Loss of eyebrow Inward curling of
eyelashes or eyelashes cilia (trachoma)

Loss of eyebrow Loss of eyelash

Leprosy chronic blepharitis
Myxedema
 Hutchinson's triad Congenital rubella
(for congenital syphilis) syndrome
Cataract
Hutchinson's teeth
Cardiac abnormalities (PDA)
Interstitial keratitis
SNHL
(inflammation of cornea)
SNHL Microcephaly
Blueberry muffin rash

Hutchinson's sign
Involvement of nasociliary nerve is
herpes zoster opthalmicus : bad prognosis

Posterior
Posterior Lens zonules lens capsule
chamber
Vitreous cavity

Iris
Macula
Cornea

Anterior chamber

Pupil
Optic nerve

Sclera
Anterior lens Lens Retina
capsule
CHAPTER 5
ORTHOPEDICS
 Basics

Articular cartilage
Epiphysis
(Proximal) Stages of fracture healing
Metaphysis Spongy bone 1. Hematoma formation 2. Soft callus formation
Epiphyseal line
Marrow cavity
Red bone marrow
Fibrocartilage
Endosteum
Compact bone Hematoma Soft Callus

New blood vessels

Compact bone
micro-movements stimulate
Medullary cavity callus formation
Diaphysis Yellow bone marrow
3. Hard callus formation 4. Bone remodeling
Periosteum

Spongy bone
Nutrient artery
Hard Callus

Metaphysis

Epiphysis
(Distal)
Articular cartilage

Disorders of fracture healing

Mal-union Non-union
When a bone heals but 9 months elapsed since injury &
not in anatomic position the fracture show no healing progress for 3 months
Fractures that undergo mal-union "MISC" Fractures that undergo non-union "FLUTS"
M Mal-union F Femur neck
I Inter trochanteric femur # L LCH, Lunate
S SCH U Ulna (lower 1/3)
C Colles', Clavicular T Tibia (lower 1/3)
S Scaphoid (Most prone for non union)

Non union with no callus formation : Atrophic non union

(t/t : Sclerotic bone excision + grafting )
Non union with callus formation : Hypertrophic non union
(t/t : Stabilisation )
 Fractures of Upper Limb

around shoulder (Clavicular fracture, Shoulder dislocation)

Fractures of shaft of humerus (Holstein lewis fracture) - Radial nerve injury, Hanging slab

around elbow (LCH, SCH, elbow dislocation)

Fractures of forearm (Galleazi, Monteggia, Greenstick, Nightstick)

Fractures around wrist (Colles, Smith, Barton's, Chauffeur's)

Fractures of carpals & metacarpals (Scaphoid fracture, Bennet, Rolando, Boxer's,

Scapho-lunate disjunction)

Fractures around Shoulder

Clavicular fracture Shoulder Dislocation
Overall most common fracture in adults Most common joint dislocation
Most common fracture during delivery of baby Anterior dislocation is more common in shoulder (for
M/c site : Junction of medial 2/3 and outer 1/3 other joints posterior dislocation is more common)
Undergoes mal-union (outer fragment pulled down due Posterior dislocation is more common in epileptics
to weight of arm while inner fragment pulled up by SCM) (light bulb sign seen with posterior dislocation)
Management : Figure of 8 bandage Tests for shoulder dislocation :
1. Dugas test (touch opposite shoulder)
2. Callaway's test (measuring girth of shoulder)
Outer 1/3 SCM 3. Hamilton ruler test

Inner 2/3

Weight of arm Callaway's Hamilton

Dugas test
test Ruler test

Bankart and Hill-Sachs lesion:

Both are seen secondary to anterior
shoulder dislocation
1. Bankart lesion is a tear in Glenoid
Labrum.
2. Hill-Sachs lesion is a dent in the
head of humerus

Figure of 8 bandage
Kocher's technique for t/t of shoulder dislocation
"TEAM"
Traction
External rotation
Adduction
Medial rotation Traction + ER Adduction MR
 Fractures around Elbow
Supracondylar humerus # 3 point relationship of elbow
3 point relationship maintained The three-point relationship is maintained in
Malunion "MISC" a supracondylar fracture of the humerus,
Closed reduction + K wire done but disturbed in an elbow dislocation.
Nerves injured : Fish tail
AIN > Medial > Radial > Ulnar sign
"AMRU"
Olecranon
Signs seen in SCH #
Medial
1. Gunstock deformity Lat. epicondyle
2. Fish tail sign epicondyle
Gartland classification
(dorsal displacement is m/c)

Lateral condylar humerus #

3 point relationship affected
Intra-articular fracture : Non union "FLUTS"
Management : Open reduction + Internal fixation (ORIF)
Cubitus valgus deformity (medial epicondyle grows more)
Tardy ulnar nerve palsy (ulnar nerve streteched due to
cubitus valgus deformity)

Cubitus Varus Normal Cubitus VaLgus

MiLCH Type 1 MiLCH Type 2 (Gun stock deformity) (Tardy ulnar nerve palsy)
(Doesn't involve trochlea) (Involves trochlea) Seen with SCH # Seen with LCH #
"2rochlea"

Fractures of forearm

Galeazzi : Radius inferior Greenstick Fracture

GRIMUS Monteggia : Ulna superior Unicortical fracture of
radius/ulna (break in the
continuity of only one cortex)
Most common fracture in
pediatric age group (because
children have flexible bones)
Not a complete fracture
Green stick #

Night-stick Fracture
Ulnar fracture with minimal
displacement (not involving
Galleazi Fracture Monteggia Fracture radius)
GRImus : Distal radius # GRImus : Proximal ulna # Occurs due to direct trauma to
Intra-articular fracture PIN injured (posterior forearm in defensive stance
ORIF needed interosseus nerve - branch
of radial nerve)
 Fractures around wrist

Colles' Cast
aka Hand shaking cast
Fracture of radius near wrist Position of hand "UP"
1. Ulnar deviation
2. Palmar flexion

Intra-articular Displacement of the radius

(dorsal/ventral)

Doesn't involve Involves radial

radial styloid styloid

Barton's # Chauffeur #

Colles' # "CD" Smith #

Dorsal displacement of Volar (palm side)
the radius displacement of the
Dinner fork deformity radius
Colles' Cast used in Garden spade deformity
management Reverse Colles' cast
used in management

Chauffeur #
In the early 20th century,
chauffeurs often sustained
this injury when the crank-
handle of a car backfired
and struck the back of
their wrist

FOOSH fractures Torus/Buckle fracture

Falling onto an outstretched hand fractures
Involves distal radius and ulna
1. Colle's # (m/c FOOSH fracture in adults) Incomplete bone fracture where
2. Torus/buckle # (m/c FOOSH fracture in children) the bone does't break but bulges
3. Scaphoid # (soft bones in children)
4. SCH # Similar to greenstick fracture
5. Clavicular #
Fractures of Carpals/Metacarpals

Scaphoid Fracture Base of thumb #

Undergoes Nonunion "FLUTS"
Risk of Avascular necrosis of
proximal portion after fracture
ORIF using Herbert screw Bennett
fracture
Glass holding cast used Rolando
fracture
Cast position: "DR"
1. Dorsiflexion
2. Radial deviation

Scaphoid Fracture
1. Bennet : Single oblique fracture at
the base of thumb
2. Rolando : Comminuted fracture that
typically breaks into three parts

Glass holding cast Ronaldo scores

Thumb covered here unlike a hattrick
Blood supply
Colles' cast of proximal
part is cut-off
in case of #

Boxer's #
Fracture of the 5th metacarpal
Herbert Screw (commonly seen with boxers)

Scapho-Lunate disjunction
Disruption or injury to the scapholunate ligament
Results in instability between the scaphoid and lunate bones .
It is the most common form of carpal instability.

Terry Thomas Sign

Widening of the scapholunate interval (>3 mm).
Fractures of Lower Limb

Fractures of Pelvis (open book, Malgaigne, bucket handle)

around hip joint (hip dislocation, femur neck #, intertrochanteric #)

Fracture of Femoral shaft

Lower end of Femur - M/c location for osteomyelitis, GCT & osteosarcoma

around knee (Patellar #, Cozen's #, sports injuries)

Fractures around ankle joint (Pott, Cotton, Aviator, Pilon, Bumper)

Fractures of foot (Choupart, Lis-Franc, Jones, Pseudo Jones)

Pelvic Fractures

Open book fracture Malgaigne fracture Bucket Handle fracture

Malgaigne - Aligned
 Hip dislocation
Dislocation of hip

Posterior Dislocation Anterior Dislocation

Shenton's line
Line along
More common Apparent limb lengthening 1. Superior pubic ramus (inferior border)
Apparent limb shortening FABER position "B in A" 2. Neck of femur (infero medial border)
FADIR position (Flexion + Abd + ER)
Femoral nerve damaged Disrupted in:
(Flexion + Add + IR)
1. Dislocation of hip
Sciatic nerve damaged
2. Femur #
3. DDH
FADIR also seen with TB arthritis
With all other conditions it will be FABER (eg. Synovitis, septic arthritis)

Hip fractures
Femoral neck fracture Inter-trochanteric fracture
Femoral head fracture Intra-capsular fracture Extra-capsular fracture
More risk of AVN (avascular Mal-union is more common
Femoral neck
fracture necrosis) "MISC"
Hence, non union is more Mx : Dynamic hip screw or
common FLUTS Intramedullary nailing
Mx : ORIF (hemi arthroplasty
if ORIF not posible)
Mx in >70yrs : Complete
Intertrochanteric fracture arthroplasty aka Total hip
replacement

Subtrochanteric fracture
Dynamic hip screw

Hemi-arthroplasty

Summary of femur fractures

1. Intra-capsular # : ORIF (or arthroplasty)
2. Inter-trochanteric # : Dynamic hip screw
or Intramedullary nailing
3. Shaft of femur # : Intramdedullary nailing Intra-medullary nailing
4. Lower end of femur # : Plating

Complete arthroplasty
Shaft of femur fracture
Initial management : Immobilisation of fracture
In adults : Thomas splint is used
In pediatric patients (< 2 yr old) : Gallow's or Bryant's traction
In pediatric patients (> 2 yr old) : Hip spica is used

Definitive management :
In adults : Intra-medullary nailing
In lower end of femur # : Plating is done

Thomas Splint Hip Spica

Shaft of femur Intra medullary Gallow's traction Bryant's traction

fracture nailing

Fractures around knee

Patellar Fracture Cozen's Fracture

Sticky
Gum

RUM

Treatment : Tension band wiring Fracture of proximal tibia

(Converts distractive forces to Seen in children 3-6yrs of age
compressive force) Leads to a late valgus
deformity known as Cozen
Phenomenon

Genu Valgum Genu Varum

"Knock-knee" "Bow-legged"
 Sports Injuries
Ligaments around knee joint
Cruciate Ligaments

ACL PCL
Anterior cruciate Posterior femur to Anterior femur to
ligament Posterior cruciate anterior tibia posterior tibia
ligament
Prevents anterior Prevents posterior
dislocation dislocation
Lateral Medial
meniscus meniscus More commonly
injured

Medial collateral
Lateral collateral
ligament ligament Tests for ACL tear

Lachman test
Provocative test, done
at 20-30° flexion
Best test for diagnosing
ACL tear

Anterior drawer test

Provocative test,
done at 90° flexion
More painful
(hence not preferred)
MRI of knee ligaments (IOC for sports injuries)
Gold standard : Arthroscopy

Meniscus
Responsible for rotational motion of the knee Tests for meniscus tear
1. Medial meniscus is more easily injured
2. Lateral meniscus covers more surface area

Thesally's Mc Murray Apley's

test test grinding test

Collateral Ligaments Valgus Varus

Responsible for stability of the knee force force
1. Medial collateral Ligament is tested using Valgus stress test
2. Lateral collateral Ligament is tested using Varus stress test
fibuLA is LAteral
Other tests : Pivot shift test, Dial test
Fractures around ankle joint

Pott's fracture Aviator

(Bimalleolar) (Talus neck #)
Fracture of medial and lateral melleolus Risk of Avascular necrosis

Cotton's fracture Pilon fracture

(Tri-malleolar) C is 3 (Distal tibial #)

Stress Fractures
Normal bone subjected to chronic and repetitive stress
Resorption > Replacement
IOC : MRI (small cortical breaches can be visualised)
Seen in military men, dancers, runners
Fractures include :
1. Runner's fracture (fibula lower end)
2. March fracture (2nd metatarsal)
Runner's #
3. Dancer's fracture/aka Jone's fracture
(5th metatarsal)

Pseudo-jones Fracture
Avulsion by peroneus brevis tendon

Dancer's March #
(Jones) #

Peroneus
brevis

5th Metacarpal : Boxer's Fracture

5th Metatarsal : Dancer's fracture
 Fractures of foot
Calcaneal fracture

Choupart Fracture Lis-franc Fracture

Angle of Bohler Angle of Glissane
Inter-tarsal fracture Tarsal meta-tarsal fracture
decreases increases
"Chauraahe ka fracture" "Cross cultural - French"
Bohler - Behind

Fractures of spine

C¹ Fracture (Jefferson fracture)

Burst fracture of Atlas
Classified into stable and unstable based on
transverse ligament
Unstable fracture : Displacement > 6.9cm
(transverse ligament is ruptured)
Stable fracture : Transverse ligament intact

C² Fracture (Hangman fracture)

Traumatic spondylo-listhesis of axis
Occurs due to hyper-extension
Seen in hanging

C⁷ Fracture (Clay Shoveller fracture)

Spinous process of C7 fractured
Occurs due to abrupt neck flexion along
with contraction of lower neck muscles CR7 - Shovelling

IVD Prolapse
Screening test : Straight leg raising test aka Lasegue test
IOC : MRI

L⁴

L⁵
S¹
Lasegue test
aka Straight leg raising test
Tension at sciatic nerve root assessed
M/c at level L⁴-L⁵
Exiting roots of L⁴ and traversing roots of L⁵ affected
 Complications of fracture
Acute compartment syndrome Fat embolism syndrome
M/c cause in adults is tibial fracture
Pain is the first symptom (on a scale 10/10) with
h/o cast application within a day
Paralysis and pulselessness are late signs
Treatment : Fasciotomy
Complications :
1. Crush syndrome : Necrosed muscles release toxins
(acidic) which causes RTA on reperfusion (urinary
alkalization done to prevent this)
2. Volkmann's Ischemic Contracture: Permanent
flexion deformity due to muscle necrosis and fibrosis.

Important classifications
Salter Harris classification Gustillo Anderson classification
For growth plate injuries For open fractures

Type 1 S Slipping of epiphysis (eg. SCFE)

Type 2 A Above (eg. SCH#)
Type 1 : Clean
Type 3 L Low (eg. Tillaux #)
Type 2 : Moderately contaminated
Type 4 T Total - above and below (eg. LCH #)
Type 3 : Contaminated
Type 5 ER Crush injury
3a : Soft tissue injury
3b : Loss of skin
3c : Vascular injury (C : see into it)

Emergency management of open fractures

1. Antibiotics coverage
2. Splinting
3. Reduction (internal fixation not done)
4. Debridement of wound
 Orthopedic Tumors
Bone tumors

Epiphyseal Diaphyseal Metaphyseal

ECG Check for nocturnal pain
Epiphyseal Chondroblastom & GCT

Check age Present Absent

Osteoid Osteoma Ewing's Sarcoma

< 20 years 20 - 40 years
Nocturnal pain Onion peel
(relieved on NSAIDS) appearance on h/p
Chondroblastoma Giant Cell Tumor Nidus produces PG-E2 PAS positive
Child < 20 yrs aka Osteoclastoma T/t : CT guided t(11:22) translocation
aka Codman's tumor Benign but Agressive tumor radiofrequemcy Homer wright pseudo
(Codman's triangle seen Females > Males ablation rosettes
with osteo-sarcoma) Soap bubble app. Most radio sensitive
Chicken wire Distal end of femur (m/c site) bone tumor
calcifications on h/e Treatment : Ext curettage + T/t : Radiotherpy +
Treatment : Ext bone grafting Chemotherapy
curettage + bone On histopathology
grafting Giant cells and Mononuclear cells
Giant cells (multinucleate) : not
neoplastic
Mononuclear cells : neoplastic

Chondroblastoma
Homer Wright
(epiphyseal tumor)
pseudorosettes
Soap bubble app. Giant cells and
mononuclear cells

Bone Cysts Osteo-Sarcoma Osteo-Chondroma

Bone forming tumor Cartilage cap overlying bony stalk
Permeative, ill defined lesion Self resolving (stops at bone
Simple Bone Cyst Aneurysmal Bone Cyst Lifts the periosteum maturation, after 20yrs of age)
Fallen leaf / trap door Soap bubble appearance (Codman's Triangle) Malignant degeneration :
sign on X ray d/d : GCT Cortical destruction cartilage cap > 2cm / spread to
Treatment : Intra Treatment : Ext curettage Sunburst periosteal reaction surrounding tissue
lesional steroids + bone grafting Most radio-resistant Can become chondro-sarcoma
(t/t : Surgical excision) (aka flat bone tumor)

Trap door/ Soap bubble app (but doesn't Sunburst reaction

fallen leaf sign involve epiphysis) (lifts the periosteum)
 Miscellaneous bone tumors
Enchondroma Fibrous Dysplasia

Benign cartilaginous tumor (arises from cartilage Shepherd crook deformity

that has failed to transform into bone during
Benign bone tumor
development)
Normal bone is replaced by fibrous tissue,
Associated with 2 syndromes
leading to weak, deformed, and brittle bones
Characteristic : Shepherd crook femur
On h/e : Chinese letter app.
Ollier's Syndrome Mafucci Syndrome
(also app. of C. diptheria on microscope)
Multiple enchondromas HeMAngiomas on hand
It can be mono-ostotic (affects a single bone)
or poly-ostotic (affects multiple bones)
Polyostotic FD is associated with 2 syndromes

Mazabroud Syndrome McCune Albright Syndrome

Intramuscular myxoma Cafe au lait spots
Precocious puberty
(endocrine hyperfunction)
Polyostotic FD

Treatment Summary - Tumors

1. Surgical excision 5. Extended curettage &
Osteo-sarcoma (most radioresistant) bone grafting
Chondro-sarcoma (for everything else)
Chondroblastoma
2. Intra-lesional steroids
GCT
Simple bone cyst
Aneurysmal bone cyst
Enchondroma
3. Radiotherapy + Chemo
Fibrous dysplasia
Ewing's Sarcoma (most radiosensitive)

4. Radiofrequency ablation
Osteoid osteoma
Osteomyelitis
Infection of bone is known as osteomyelitis
M/c involved part of bone is metaphysis (most vascular)
Osteomyelitis can be acute/chronic

Acute osteomyelitis
< 1 month
Most common cause is Staph aureus Ring Sequestrum
Acute osteomyelitis in Sickle cell Anaemia is caused Chronic osteomyelitis due to
by Salmonella Broadie's Abscess pin-tract infections with
Sub-acute osteomyelitis of tibia external fixators

Chronic osteomyelitis
> 1 month
Persistent infection leads to
necrosis of bone tissue, forming
sequestrum (dead bone)
surrounded by granulation tissue
Involucrum
and fibrotic tissue.
Cloaca
Formation of involucrum (new
bone around the infected area). Sequestrum
Sinus
Sinus tract formation and chronic
Infected
drainage are common. granulation
On x-ray it's only visible after new tissue
bone formation (2 weeks)
For early diagnosis : MRI X-ray of chronic osteomyelitis

Necrosis of bones
Avascular necrosis Osteochodritis dessicans
Death of bone due to lack of Bone inside cartilage undergoes
blood supply necrosis due to lack of blood flow
h/o long term steroid use/ SCA/ Could be due to stress/genetics
trauma
Important examples :
1. Hip joint
2. Scaphoid
3. Talus

Crescent sign
More frequently associated
with neck of femur fracture
Pediatric Disorders

Developmental Dysplasia of Hip (DDH)

Abnormal development of the femoral head (ball)
and acetabulum (socket).
Causes an unstable hip joint
More common in females Treatment
Screening tests : < 6 months: Pavlik harness
6 months to 2 years: Closed reduction f/b hip spica cast
Older children (or failed non-surgical methods): Open reduction
Barlow's test Ortolani test

On ADduction, hip On ABduction, hip

dislocates relocates
"Barlow BAD test" "Ortolani good test" Pavlik Harness Hip spica cast

Congenital Talipes Equinovarus (CTEV)

Commonly known as clubfoot
Congenital deformity of the foot & ankle
Abnormal positioning and shape of the foot
C Cavus (high arch of the foot)
T Talipes (ankle involvement)
E Equinus (plantarflexion at the ankle)
V Varus (inversion of the heel and forefoot)

More common in males

Screening based on physical examination
Kite's angle (talo-calcaneal angle) used to assess
severity.
Management : Ponseti's method (gold standard)
Surgical Treatment indicated for severe, rigid
deformities or failed non-surgical methods Dennis-Brown splint

Perthe's dis
Avascular necrosis of the femoral head, leading to
its collapse and subsequent regeneration over time
Children aged 4-10 years are affected
More common in males
Typically unilateral
Features : Pain, limp, limited hip motion
Management : Observation & Activity Modification
(self resolving)
 Klien's line : A line drawn through neck cuts the epiphysis.
Slipped Capital Femoral Epiphysis (SCFE)
Growth plate (physis) of the proximal femur
becomes weakened, causing the femoral head to slip
relative to the femoral neck.
Adolescents affected, 10-16 yrs
Obesity is a major risk factor
Presenting features : Pain, limp, or restricted motion Trethowan sign
if Klien's line doesn't intersect the epiphysis: SCFE

Congenital Coxa Vara (CCV)

Neck shaft angle < 120°
Fair-banks triangle (triangular-
shaped ossification defect)
120-130°
Shortening of the limb and < 120°
altered hip mechanics.
Treatment : Valgus Osteotomy Normal Coxa vara

Scoliosis
Scoliosis is an abnormal lateral curvature of the spine

Adam's forward bending test Cobb's angle

Done to rule out postural scoliosis Angle > 10° is diagnostic of scoliosis

Braces used for scoliosis correction

Milwaukee Brace Boston brace Charleston brace "Minerva cast" for

Best brace for scoliosis Need to be worn for 24 hours Need to worn only scoliosis correction
Need to be worn for 24 hours overnight
 Miscellaneous conditions - Upper limb

Carpal tunnel Syndrome De Quervain's tenosynovitis

Median nerve compressed in flexor retinaculum Radial styloid tenosynovitis
(Flexor retinaculum aka transverse carpal ligament) Two tendons involved :
1. Abductor pollicis longus (AbPL) Ab pee le
2. Extensor pollicis brevis (ExPB) Ex bhi pee rhi

Most specific test : Darkan's test (Compression of flex. ret)

Features : Ape thumb deformity, hand of Benediction
Spared : Palmar cutaneous branch (Supplies lateral 3.5
fingers palmar side)

Phalen's test Tinel's test Finkelstein test

hold for 1 min, Tap the flexor Provocative test
elicits pain retinaculum

Tennis elbow Golfer's elbow

Lateral epicondylitis Medial epicondylitis
Tendon involved :
ECRB > ECRL

Sachin Tendulkar is short- brevis

(he had tennis elbow)

hit medially in hit laterally in

Cosen's test Counter Brace golf tennis
Provocative test Used for management
 Thoracic Outlet Obstruction
Important Fingers
Compression of neurovascular structures passing
through the thoracic outlet (a space bounded by the
first rib, clavicle, and surrounding muscles) Game keeper thumb Trigger finger
Compression of the brachial plexus (most common).
Pain, numbness, and tingling in the arm, hand, or shoulder
(ulnar distribution).
Special tests : Roos test, Adson test, Wright test

Avulsion of ulnar collateral

Nodule on a flexor
ligament
tendon
Persistent flexion of
If add policis is trapped it's
known as Steiner lesion one finger

Roos test
Elevated arm abduction stress test (EAAST) Baseball finger Jersey finger
"Sun RISES in EAST"

aka Mallet finger aka Rugby finger

Extensor tendon Flexor tendon
ruptured ruptured
Adson's test Wright test
"Flex your Jersey"
On deep inhalation Checking pulse in
Radial pulse disappears overarm abduction
"Adson - Inhalation"

Infective tenosynovitis
Infection of the synovial sheath surrounding a tendon,
typically in the hand or wrist.
It is a medical emergency requiring prompt diagnosis Prayer sign Popeye sign
and treatment to prevent permanent damage. Stiff hand syndrome Rupture of long head of
Kanavel's criteria used to diagnose (Diabetic cheiro-arthropathy) biceps brachii

Tenderness along the course of the flexor tendon

Fusiform or symmetrical swelling of the finger Painful arc Syndrome

Pain with passive range of motion aka Swimmer's shoulder
A flexed posture of the finger aka shoulder impingement
syndrome
Pain on mid abduction
(60-120°)
Miscellaneous conditions - Lower limb

Fixed flexion deformity of hip Osteo-chondrosis

Tightness of the hip flexor muscles Self-limiting developmental disorders
(primarily the iliopsoas muscle) Abnormal endochondral ossification.
Diagnosed using Thomas Test Commonly affects growing children and
On flexing one leg, the other leg folds
adolescents
Some important named osteochondrosis are
1. Kohler's : Navicular
2. Keenbox : Lunate
3. Sever's : Calcaneus
4. Osgood Schlater : Tibial tuberosity
5. Perthe's : Femoral head

Thomas Test

Ilio-Tibial band contracture

Housemaid's knee Clergyman's knee

Pre-patellar bursitis Infra-patellar bursitis

Ober's test
Tightness or contracture of the iliotibial
Jumper's knee
(IT) band and the tensor fasciae latae
Patellar Tendonitis
(TFL) muscle is assessed.

Instruments

Bone cutter Bone nibbler Osteotome Bone and plate

holding forceps
CHAPTER 6
GENERAL RADIOLOGY
Thumb rules in Radiology

CT scan USG

Air Calcium Fluids Gall bladder

Pneumo-thorax Intra-cranial calcification Cysts Cholelithiasis
Pneumo-peritoneum Renal/Salivary gland Pleural effusion Cholecystitis
Pneumo-mediastinum stones (not gall stones) Pericardial effusion
Intestinal obs. Bone cortex - bone Ascites
fractures (except stress #) eFAST
Others
Osteoid osteoma (for other
bone tumors it's MRI)
Foreign body
Head trauma and stroke

HRCT
(High resolution CT)

Lung Parenchyma Para Nasal Sinuses

Interstitial lung disease Sinusitis
COVID 19 Tumor and polyps
Bronchiectasis
MRI

Nervous tissue Bone marrow edema

Pan coast tumor Bone tumors
(involves brachial plexus) (except osteoid osteoma)
Post. mediastinal mass Stress fracture
Acute osteomyelitis
Sacro-ileitis CT - Angiogram
Others
Cartilage - Osteochondroma R/o pulm. emboli Any vascular pathology
Ligaments - All sports injuries
CTPA (CT - pulmonary Note : Initial inv. is
Soft tissue - Sarcomas
angiography) usually doppler USG
Foreign body
H/o child playing alone
Presents with acute respiratory distress Coin in esophagus vs trachea
M/c foreign body : Peanut
Investigations :
Initial inv : X-ray
IOC : NCCT
MRI is contraindicated (could be a metallic object) "T"
"O"

Foreign body on NCCT

Hyperdense
Streaking artefact EsOphagus Trachea

Counting Ribs on CXR

Identify the rib marked
2
3
4

5 →
Posterior Anterior
6

Count using the posterior ribs

1st rib is not usually visible (hence, the first rib noticed
will be the 2nd rib)
Ribs 10 and 11 are also not usually visible
CT axial section at T4-T5

Ascending aorta

Superior vena cava Right and left Pulmonary artery

Right and left bronchus Descending aorta

Pulmonary artery bifurcation

Tracheal bifurcation
Ascending and descending aorta
Superior vena cava
Esophagus (posterior to trachea, adjacent to descending aorta)

Relative position of heart chambers

PA

RA LV
Right
ventricle

Most anterior : Right ventricle

Most posterior : Left atrium
Radiation
Type of radiation Nuclear medicine
Tc-99m : Bone scan
Ionising Non ionising F-18 FDG : PET scans
X-rays (Radiography, CT scans) Ultrasound (sound waves)
Gamma rays (PET scans, radiotherapy) MRI (magnetic fields)
Radiation Units
Gray (Gy) : Energy
Radiotherapy absorbed per kg of
External Beam Radiotherapy (EBRT) - linear accelerators (LINAC machine) tissue
Brachytherapy - internal radiation (e.g., prostate, cervical cancer) Sievert (Sv) : Biological
Radionuclide Therapy effect of radiation
Iodine 131 : Radio-ablation of thyroid (Note : Iodine 123 used for diagnosis) Roentgen (R) : Ionization
Cobalt 60 : Used in teletherapy of air
Iridium 192 : Used in brachytherapy Becquerel (Bq) : Rate of
radioactive decay

Radiation Effects on the Body ALARA principle

A. Acute Radiation Syndrome (ARS) As Low As Reasonably Achievable
Threshold Dose : > 1 Gy Time: Reduce exposure duration
Symptoms: Distance: Increase distance from source
Hematopoietic Syndrome (1-6 Gy): Bone marrow suppression Shielding: Use lead aprons, thyroid
Gastrointestinal Syndrome (6-10 Gy): Nausea, diarrhea, death shields, and barriers
Neurovascular Syndrome (>50 Gy): Seizures, coma, death
Minimum thickness of lead aprons : 0.5 mm
B. Chronic Effects
Malignancy (leukemia, thyroid, breast cancer)
Cataracts
Infertility (gonadal damage)

Bragg Peak
Seen in Proton & heavy ion therapy
Sensitivity to radiation Protons and heavy ions travel through tissue
with minimal interaction until they reach a
Most radio sensitive Most radio resistant certain depth, where they release a large burst
Actively dividing cells Quiescent cells of energy (Bragg Peak)
(Bergonie's law) Organ : Vaginal epithelium Used for deep-seated tumors (brain, spine,
Organ : Gonads Tissue : CNS (doesn't divide) pediatric cancers)
(Ovaries > Testes) Part of eye : Sclera Reduces radiation exposure to normal tissues
Tissue : Haematopoetic stem Tumors :
cells (in bone marrow) HCC
Part of eye : Lens (Cataract is RCC
deterministic for radiation) Pancreatic ca.
Osteosarcoma
Tumors :
Melanoma
Wilm's tumor
Ewing's sarcoma
Lymphoma/Leukemia
Multiple myeloma
Seminoma
Evomoz notes
Microbiology
PSM
Dermatology
Obs & Gynaecology
Pediatrics
CHAPTER 7
MICROBIOLOGY
 Mechanism of Toxins
(Binding of toxins → ADP ribosylation)

Mechanism of Toxins

Inhibition of Activates cyclic Inhibits

protein synthesis nucleotides neuro-transmitter
(blocks either) causes Secretory diarrhea by release
activating either by blocking SNARE
protein

EF - 2 60 S cAMP cGMP
Crucial in translation of Ribosome Cholera Heat stable
C
A Anthrax toxin of ETEC
1. C. diptheria 1. Shigella (Shiga toxin) L Labile toxin of ETEC G-ground (more
stable on ground)
2. Pseudomonas 2. EHEC (Shiga like toxin) P Pertussis

ETEC is MCC of traveller's diarrhea

EPEC : Pathogenic (Effacement of intestinal cells)
ETEC : Toxicogenic (Traveller's Diarrhea)
EIEC : Invasive (Dysentry)
EHEC : Hemorrhagic (0157 : H7, HUS)
EAEC : Aggregative (Persistent diarrhoea, stacked GABA/Glycine Ach AB
brick appearance) 1. Tetanospasmin Botulinum toxin
(Pre -Synaptic) lock jaw Canned food
EHEC 0157:H7 causes HUS 2. Strychnine Honey (infant
(Post synaptic ) botulism)
Preformed spores in
Hemolytic uremic Sx TTP wound botulism
Clinical syndrome in Seen in adults
children with h/o Triad same as HUS
gastroenteritis Associated with
AMS and fever Strychnine seeds
Toxin damages the
Cause is mutation (nux vomica)
endothelium and
causes thrombosis. in ADAM TS 13 Even one seed is poisonous
Triad of μAHA, gene Post mortem caloricity
thrombocytopenia & 90 % mortality
renal injury Treatment is
Only supportive Plasmapheresis
treatment
Important differential
is TTP
Attachment at a site other
than antigen binding site
Causes widespread cytokine
Cholera toxin release.
Activates CAMP Shock like presentation
GM 1 ganglisode receptor Retained tampon/ nasal gauge piece
Zona occludens affected
1. Staph. aureus
2. Strep. pyogenes
Bacteria - basics

Outer layer of LPS (eNdotoxin)

Peptidoglycan PG in GP Bacterial adhesion Conjugation

Locomotion

GRAM POSITIVE GRAM NEGATIVE

Thick Peptidoglycan layer Thin Peptidoglycan layer Capsule (K)
Teichoic acid present Lipopolysaccharides present Flagella (H)
LPS (O)
No lipo-polysaccharides (endotoxins)
Retain crystal violet dye Can't retain crystal violet dye
Resistance to mechanical Susceptible to mechanical Fimbriae (F)
disruption and anionic disruption and anionic
detergents (thick PG layer) detergents

Proteins Lipo-polysaccharide
More antigenic, potent (comp of cell wall)
Heat labile Less antigenic, less potent
Do not produce fever Heat stable
eg Pseudomonas, Diptheria Usually produce fever
eg. Shiga toxin, ETEC
Listeria is only GP org that Kirby Bauer disc diffusion
produces endotoxin (for antibiotic susceptibility)
Mueller-Hinton agar used

Condenser focuses the light

Eye piece has magnification of 10X
(Multiply 10 for overall magnification)
1. Low power : 10X (scanning)
2. High power : 40X
3. Oil Immersion : 100X Electron Microscope
 Gram Positive Cocci

Catalase Positive Staph.

Gram positive cocci
Catalase Negative Strep .

Catalase test
Chronic granulomatous disease
S Staph aureus, Serratia Pigmented Deficiency of NADPH oxidase
P Pseudomonas colonies
NADPH oxidase converts O² to
A Aspergillus superoxide (ROS) which kills catalase
C Cryptococcus, Candida Fungi positive org.
E Enterobacter 2 tests are done for CGD
Cat in Space 1. Nitro blue tetrazoleum (NBT)
If catalase is present then
2. Di hydro Rhodamine (DHR)
bubbles formed

Bubbles
Lancefield Classification of Strep

Alpha : Optochin
Streptococcus
Beta : Bacitracin
Gamma : Growth in 6.5 % NaCl
Hemolysis

Partial hemolysis Complete hemolysis No hemolysis

Green Clear Grows in bile

Bacitracin sensitivity
Optochin sensitivity and Growth in 6.5% NaCl
and PYR status and
Bile solubility PYR status

Strep. Strep.
Agalactiae Pyogenes
Group B Group A

Strep. Strep.
Strep. Bovis Enterococcus
Viridans Pneumonia
Normal oropharynx flora Grows in bile esculite agar
Endocarditis in Ca.colon

Causes sub-acute 1. Antibody against Streptolysin O exotoxin aka

endocarditis (m/c
Group B : Babies
Early onset neonatal sepsis ASO Ab (Degrades cell membrane)
community acquired)
Strep. Mutans causes
2. Superantigen
Dental carries CAMP test 3. Scarlett fever (peds)
Enhancement of 4. Rheumatic fever
hemolysis by S. Aureus 5. Acute glomerulo-nephritis
6. Erysipelas (raised erythematous lesion)
7. Impetigo (Honey crusting) - can also be caused
by Staph
8. Cellulitis and Necrotising fascitis
Reverse CAMP test shown by C.Perfringens 9. m/c cause of tonsilitis in developed countries
Rx : Amoxiclav
 Sterile vegetations

Warty Large friable Small vegetations Small vegetations

vegetations vegetations (only one side) (both sides)
Invading chordae SLE : LSE
tendinae
NBTE Libman Sach's
(Marantic endocarditis) endocarditis
Paraneoplastic syndrome (SLE/RA)
with GI adenocarcinoma

Ring abscess

Rheumatic heart Infective

disease endocarditis

Acute Rheumatic fever Infective endocarditis

Immunologic reaction to strep Duke's Criteria
Staph aureus is MCC for
antigens Acute IE Major criteria
GABHS (Strep Pyogenes) Hospital acquired (Nosocomial) a.) Blood culture positive
Seen in children IV Drug abusers 1 aerobic and 1 anaerobic
drawn 12 hrs apart (2
Strep. Viridans is MCC for anaerobic for atypical)
J Joint involvement (polyarthritis) Community acquired IE Single positive culture for
O Myocarditis Coxiella Burnetti
N Nodules (subcutaneous) Prosthetic valve associated IE b.) Imaging positive
E Erythema Marginatum Early (< 1 year) : CONS (Staph Epidermidis) 1. Echocardiogram evidence
S Sydenham's Chorea Late (> 1 year) : Streptococcus 2. PET or SPECT CT
3. Cardiac CT
Sub-Acute IE
HACEK group of organisms Minor criteria
Strep Viridans Predisposing heart condition or
IVDU
Fever > 38° C
H-Haemophilus parainfluenzae
Vascular phenomenon : Emboli,
A-Actinobacillus actinomycetemcomitans
Aschoff bodies Antischkow cells infarcts, Janeway's lesions,
C-Cardiobacterium hominis
(caterpiller cells) Cerebral hemorrhages,
E-Eikenella corrodens
K-Kingella kingae Conjuctival hemorrhage
slow growing gram negative bacterias, Immunologic phenomenon :
residing in oropharynx. Osler's nodes, Roth Spots, RF
Microbiological evidence

Erythema Marginatum

Roth Spots Janeway lesion Osler's Node

Retinal Non tender Tender
hemorrhages Vascular Immunologic
Immunologic phenomenon phenomenon
phenomenon
Ouch - Osler
 Strep. Pneumonia
Diplococci - Lanceolate shaped
Polysaccharide capsule (Quellung reaction )
MCC pneumonia, meningitis, otitis media,
sinusitis
Carrom coin colonies (aka Draughtsman
colonies)

Gram Positive Bacilli

Ba Bacillus
Bacillus C Clostridium
Aerobic, hence more at surface C C. Diptheria
Polypeptide capsule
Li Listeria
M'Fadyean test (stains the capsule)
Medussa head colonies
PLET: B.Anthrax Anthrax disease
MYPA: B.Cereus Zoonotic disease from cattles/sheep
aka Malignant pustule, wool sorter's
disease, rag picker disease
Cutaneous/Pulmonary disease
Category A bioterrorism agent

Inverted fir tree

Frosted glass colonies Bamboo shaped appearance appearance Early food poisioning
(B.anthrax) (B.anthrax) (B.anthrax)
Milk products : S.aureus
Chinese food : B. Cereus

C. Diptheria Clostridium
K tellurite agar : Differential
Obligate anaerobe
Loeffler serum slope : Enrichment Spore forming (terminal spores)
Albert's stain used
Chinese letter appearance C. Perfringens
(also seen in Fibrous dysplasia)
Greyish white Bull's neck
pseudomembrane appearance

Pseudomembranous pharyngitis
Membrane bleeds on touch and Gas gangrene
not removed easily Nagler test Presence of air/crepitus
Metachromatic Toxin dissemination may cause
myocarditis or arrythmia Alpha toxin of C. Perf Alpha toxin of C. Perf
Granules
Rx : Erythromycin Toxin inhibits protein synthesis by Breaks down egg yolk Breaks down phospholipase
↓
or Penicillin Albert's stain inhibiting EF-2 T/t : Anti gas gangrene serum along with
(Blue -green stain) Elec gel precipitation test done
debridement and antibiotics
for toxin detection

C. Difficile
Accordion sign
H/o antibiotic use
Listeria (Cephalosporin, Ampicillin,
Clindamycin)
Survives refrigeration (motile at 25°C and non motile at room temp) Toxin B : Cytotoxin that forms a
Tumbling motility (actin mediated) : Propels from one cell to another pseudomembrane
Only gram (+) bacteria to produce endotoxin Diagnosis : detection of
Tumbles from
Causes Meningitis in extreme of ages "cell to cell" toxin/org. in stool + Glutamate
DOC : Ampicillin dehydrogenase assay
Treatment : Vancomycin or
Fidaxomicin (both oral) Pseudomembrane
 Filamentous Gram Positive Bacteria
Nocardia Actinomyces
Aerobic (No Car) An-aerobic
"Mimics TB" : Acid Normal Oral, GI, GU tract flora
fast and pulmonary Facial abscess : yellow sulphur
infection in granules 🟡
Immunocopromised Actinomycetoma of leg 🦶🏻
Rx : TMP SMX Rx : Penicillin

Anthrax C.Tetani C.Botulinum

Gram negative cocci

Gonorrhea
Transport : Stuart - Amy
Neisseria Culture : Thayer Martin
Meningitidis

Features of N.Meningitidis
Maltose fermentation
Capsule
Vaccine present

Waterhouse Friedrichson Fitz Hugh Curtis Syndrome

Syndrome Intracellular diplococci
Seen with N. Gonorrhea
Treatment within WBCs
Seen with N. Meningitidis Peri-hepatic adhesions
Ceftriaxone
Meningitis Also seen with Chlamydia
b/l Adrenal haemorrhage
Petechial rash

MCC of urethritis : N.Gonorrhea

Prophylaxis of Gonococcal meningitis
DOC : Ciprofloxacin MCC of non gonococal urethritis : Chlamydia
Both cause Neonatal conjuctivitis
Ceftriaxone can also be used
In pregnancy or < 18yrs : Ceftriaxone preferred Gonorrhea and Chlamydia often show co-infection
over ciprofloxacin (fluoroquinolones cause DOC for Gonorrhea : Ceftriaxone
tendon rupture in children and teratogenic in DOC for Chlamydia : Doxycycline CD
preg.) Azithromycin in pregnancy
(tetracycline are teratogenic )
 Gram negative Curved-Rods
V. Cholera H. Pylori
Rice water diarrhea Positive urea breath test Reiter Syndrome
Darting motility 1. Salmonella
Urease produces ammonia → alkaline
Transport : Cary Blaire 2. Shigella
environment (makes it survive strong acids) SSCC
media (Carrying) 3. Chlamydia
Antrum of stomach (Type B chronic gastritis)
Culture : TCBS 4. Campylobacter
T/t : ACP (Amoxicillin + Clarithromycin + PPI)
Metronidazole instead of Amoxicillin in
V. Parahemolyticus penicillin allergy
Green colonies on TCBS MALT lymphoma, gastric adenocarcinoma
Capsulated organism Protective in esophageal carcinoma
Hemolysis on Wagatsuma agar Keratoderma Circinate
(Kanagawa phen.) 🇯🇵 blenorrhagicum balanitis
Peritrichous flagella (all other aka reactive Arthritis
vibrio have monotrichous) Campylobacter Triad of arthritis,
Para has peri conjuctivitis and urethritis
Grows in Skirrow media
"Hot camp fire" 42°C
Classical vs El Tor V.Cholera Darting motility (like Vibrio)
El Tor variant causes Antecedent to
Hemolysis 1. Reiter Syndrome
VP Test (+) (reactive arthritis)
Group 5 phage sensitive 2. GBS
Chick erythrocyte
agglutination

Gram negative Bacilli

Mc Conkey agar : Lactose fermentation
Cystic fibrosis Peptone
MC infection : Pseudomonas Lactose
MC in young : S. Aureus Agar
Most specific : Burkholdderia Neutral Red
Most mortality : Burkholderia Taurocholate

Dysentery Cystic fibrosis

Enterobacter is a catalase positive organism

Burkholderia E Coli Klebsiella

Whitmore's disease (melioidosis) MCC of UTI Intestinal microbiome
Fever + cough + hemoptysis (like TB) CLED media preferred Causes pneumonia in
Resistance to 1st and 2nd gen for culture in UTI alcoholics
cephalosporins (eg. Cefotetan) (allows other organisms Dark red currant jelly
to grow as well) sputum

Yersinia Proteus
Y. Pestes causes plague Swarming motility
Y. Enterocolitica causes Urease positive,
bloody diarrhea and predisposes to Struvite
Psuedo appendicitis stone (Mg-NH⁴-PO⁴) IMVC test
Diene's phenomenon To differentiate E coli from Klebsiella
Different strains swarm differently E coli : IM (+)
Similar strains have no line in between while different strains Klebsiella : VC (+)
will have one
 Salmonella Shigella Pseudomonas
Flagellated (Salmon swims) Not flagellated Blue-green colonies
Endotoxin (Vi in S.typhi) "tyVi" Endotoxin : Shiga (60S) Catalase positive organism
Hematogenous spread HUS Exotoxin inactivates EF-2 (also seen with Diptheria)
Typhoid fever : Pulse fever Bacillary dystentry
dissociation Very high fever 1. Echthyma gangrenosum : Necrotic cutaneous lesion
in immunocompromised
Osteomyelitis of nails in SCA Only cell to cell spread
2. Malignant otitis externa : Granulation tissue in
MCC of osteomyelitis of nails
chronic diabetic patient (Tc99 scan)
generally : S.Aureus
3. Burns : m/c infection in burn patients
4. Cystic fibrosis
5. MCC of bacterial ulcer in contact lens users
Salmonella typhoid testing 6. Hot tub folliculitis
B Blood culture : 1st week 7. Scromboid fish poisoning (flushing due to histamine)
A Antibodies titre : 2nd week Ecthyma contagiosum is a zoonotic
S Stool : 3rd week disease caused by parapox virus
U Urine : 4th week

H antigen : > 160

O antigen : > 80
by 2nd week Bartonella
Need to increase 4 fold between 2nd and 4th week Bartonella henslae
Cat scratch disease : enlarged
O antigen denotes acute infection (only shown by S.typhi) axillary LN (stellate granuloma)
Bacillary angiomatosis in HIV ➡️

Bartonella quintana
Trench fever / quintan fever / 5 days fever
(each episode lasts for 5 days)
Fever + "Shin pain"
T/t : Doxycycline

Gram negative coccoid rods

H influenza
Bordatella Pertussis (whooping cough) DOC : Azithromycin
Brucella (brucellosis with unpasteurised dairy)

H.Influenza H.Aegypticus
Grows on chocolate agar because Causes Brazilian Purpuric fever
needs 2 factors
Factor 5 : NAD
Factor 10 : Hematin (HemaTEN)

Fever + Purulent Conjuctivitis +

Satelitism Purpura
Factor 10 (hemaTEN) present in blood Occurs in epidemic forms
Factor 5 produced by S.Aureus with
1. Acute epiglottitis (thumb sign) RBC hemolysis
2. Meningitis / otitis media / pneumonia H.Influenza grows around S.Aureus

DOC for mucosal infections : Amoxi-Clav

DOC for meningitis : Ceftriaxone
 Mycoplasma
No cell wall (Beta lactams ineffective) Colonies
Diene staining (Diene phenomenon shown by Proteus) M.furfur
Cold agglutination reaction (Cold without a coat) Mycoplasma
Eaton/PPLO agar
Appearance
Fried egg colonies
Hairy cell Leukemia
Causes Atypical pneumonia
Oligodendroglioma

Spirochetes
Primary Syphillis Tertiary Syphillis
Treponema Painless hard chancre 1. Skin Gummas
Causative org. of Syphillis 2. Tabes Dorsalis
Secondary Syphillis 3. Argyl Rob. pupil (ARP)
Corkscrew motility (screw-cock syphillis)
1. Rash involving palms and soles 4. Aortic dissection
Treatment for Syphillis : Penicillin G
2. Condyloma lata
IOC : VDRL
3. Alopecia (scarring/non scarring)
Most specific test : FTA Absorption
All types of rash can be seen
(fluorescent treponemal Ab absorption)
except vesiculo bullous rash
In low resource setting : Dark field microscopy Buschke Ollendorf sign (deep
False positive on VDRL : P -VDRL dermal tenderness)
P Pregnancy Rash involving palms
V Viral infection Ca Cox A (HFMD)
D Drugs R RMSF
R Rheumatic fever S Syphillis (2°)
L Lupus, Leprosy

Lyme's Disease
Caused by B.Burdgoferi
b/l facial nerve palsy
BorreLia Erythema migrans 🎯
Vector: Ixodes tick (hard)
Causative org. of Lyme's dis and Relapsing fever
A key lime pie to face
Lashing motility (L - lashing lyme)
Relapsing fever
Caused by B.Recurrentis
Epidemic RF : Louse
Endemic RF : Soft tick

LeptospiRAT
Transmitted by RAT urine
Causes Weil's disease (Entero Hemorrhagic fever) MAT : Leptospirosis (Microscopic agg test)
fever + abd. pain + hematuria SAT : Brucellosis (Standard agg test)
Seen in post-disaster phase CAT : Mycoplasma (Cold agg test)
EMJH media
MAT (Macroscopic agg. test)

Jarish Herxheimer reaction

Flu-like symptoms after starting antibiotics for spirochaete infections
Due to host immune response on sudden release of bacterial antigens
 Ricketssial Diseases
Louse
R Prowazekii : Epidemic typhus (Louse) Love is epidemic Flea 3 pair of legs
R Typhi : Endemic typhus (Flea) Flent Small fleas : chiggers
"Endemic typhus aka Murine typhus" (Chiggerosis)
FLENT, Bubonic plague
"Relapsing Epidemic in trench"
Xenopsylla Cheopis

Hard tick Soft tick

SCUTUM absent
R Ricketsii : RMSF RRR Hard tick for all Capitulum not visible
5 nymphal stages
R Conorii : Indian tick typhus Curry (5 looks like S : Soft)
R Africae : African tick typhus Causes endemic relapsing fever
Ehlrichia (monocytes) and Anaplasma (granulocytes) GAME
Has a head hard head
Lyme's dis
Babesiosis
KFD

Mite

R Tsutsugamushi : Scrub typhus (Trombiculid Mite) Takes a lot of might

R Akari : R. Pox Akar like chicken pox

Coxiella : Q fever (Inhalation)

"Hairy and no head
compared to hard tick"

Weil Felix test Eschar at site of bite Trans-ovarial transmission

Serological diagnosis of ricketssial infection. Scrub typhus Only females (vectors) carry the
Heterophile antibody test : Uses strains of "proteus" R pox infection and males are spared
Indian tick typhus Scrub typhus
Test positive after 10-20 days of infection
Test is negative for R.pox R Pox
Generalized painless
Indian tick typhus
False positives : Proteus infections lymphadenopathy
RMSF
OX K (+) : Scrub Typhus Scrub typhus
R pox
OX 2 (+) and OX 19 (+) : For others

Treatment
DOC for all Ricketssial diseases : Tetracyclines (Doxycycline)
In pregnancy : Azithromycin (Tetracyclines are contrindicated in pregnancy)
Culture Media Motility
Mannitol salt, Ludlams : S. Aureus Tumbling : LIsteria
Bile esculide : Enterococcus (not enterobacter) Darting : Cholera, Campylobacter
Thayer-Martin : Neisseria Swarming : Proteus
Bordet-Genghou/Regan-Lowe : Bordatella Corkscrew : Syphillis
Tellurite / Loeffler serum slope : C Diptheria Lashing : Borrelia
LJ/ Middlebrook : TB Falling leaf : Giardia
BCYE : Legionella Quivering/twitching : Trichomonas
EMB, CLED : E Coli EC
EMJH : Leptospira
TCBS : Cholera
Ashdown : Burkholderia
PLET : B. Anthrax
MYPA : B. Cereus
PALCAM : Listeria
Skirrow : Campylobacter
Eaton : Mycoplasma
Selenite F : Shigella, Salmonella
Cetrimide : Pseudomonas
Cefoxitin : C. Difficile

Culture media are autoclaved except LJ and LSS

(inspissation at 85 degrees for 3 days)
Bacterial Skin lesions

Erysipelas Cellulitis
Erythematous and raised Infiltrative Impetigo
Honey crusting
Well defined lesion Poorly defined lesion
MCC by GABHS (Pyogenes) Can be caused both Strep or Staph
MCC by GABHS (Pyogenes)

Gas gangrene
C. Perfringens
Crepitus present
Air on imaging
Ritter's Syndrome Bullous Impetigo
SSSS (Staphylococcal scalded skin syndrome) Caused by Staph. only
Multiple T is multiple S
Epidermal exfoliative
Staphylococcal exotoxin causes epidermal thinning exotoxin
Thin blisters that collapse (Nikolsky +)
Non scarring
Seen in children (umbilical stump)
Oral mucosa not involved
Differential: SJS (oral mucosa involved)

Fornier's gangrene
Polymicrobial

Folliculitis Furuncle Carbuncle

Infection of hair follicles Tender Multiple hair follicles
MCC by Staph Aureus Collection of pus involved
Can complicate to form Single hair follicle Commonly seen at Meleney's Gangrene
involved nape of neck Orange lesion at
furuncle or carbuncle
H/o DM surgical wound site
Cell wall synthesis inhibitors

Cross linking of peptidoglycans

S/e of Vancomycin
NOT RED
Nephrotoxic Peptidoglycan
Ototoxic
Thrombophlebitis
Red Man Sx (histamine)

Peptide Part Glycan Part

Glycine
Penta-peptide NAM - NAG Beta Lactams
chain
Inhibits transpeptidase
Vacomycin Cycloserine
Inhibits Inhibits penta-
transglycosylase peptide (d-ALA)

BP transporter Cell Membrane

Bacitracin
Topical drug in MRSA

Precursors Muramic Acid (forms NAM) NAM - NAG

Fosfomycin
Used in UTI

Beta Lactams
Penicillinase sensitive penicillins
Penicillin G, V
Ampicillin (DOC for Listeria, safe in renal failure)
Amoxicillin

Penicillinase resistant penicillins

C Cloxacillin (DOC for mastitis) Beta lactamase : Enzyme mediated
O Oxacillin destruction of beta lactams eg. Penicillinase
N Nafcilin (safe in renal failure)
D Dicloxacillin Beta lactamase inhibitors
1. Clavulanic acid (Amoxi + Clav)
M Methicillin
2. Tazobactam (Piperacillin + Taz)
Anti-Pseudomonal
Piperacillin pseudo-piper

Cephalosporins
Organisms that escape cephalosporin class 1-4
1st : Cefazolin fa 1
2nd : Cefoxitin ox 2 L Listeria (DOC : Ampicillin)
3rd : Ceftriaxone tri A Atypicals - Chlamydia, Mycoplasma (DOC : Macrolides)
M MRSA (DOC : Vancomycin) 5th gen cephalosporins can be used
4th : Cefepime PIME 4
E Enterococci
5th : Ceftraroline ROLINE 5

Carbapenems
Cilastatin prevents metabolism of imipenem in renal tubules
Imipenem Cilastatin, Seizures S/E : Seizures
Meropenem

Monobactams All beta lactams show cross allergy except

Aztreonam monobactams (Aztreonam)
 Protein synthesis inhibitors
Ribosome

30 S 50 S
buy AT 30 CCELS at 50

AminO²glycosides Chloramphenicol
(mycins) Not much in use (s/e of bone marrow supression)
No effect against anaerobes (need oxygen to function)
S/e : Nephrotoxic and Ototoxic Clindamycin
DOC for anaerobes above diaphragm
1. Gentamicin (Chemical labyrinthectomy in Meniere's)
Safe in pregnancy and renal failure Klinda safe
2. Neomycin (used to clear gut flora in Hepatic enceph.)
3. Amikacin
4. Streptomycin (DOC for Plague, Tularemia) Erythromycin
5. Tobramycin (Macrolides) thromycins
CYP inhibitors and QT prolong (along with Flqn)
Prokinetics (motilin receptor binding) : CHPS
Tetracyclines DOC for Atypical Pneumonia (Legionella, Mycoplasma)
DOC for Diptheria and Pertussis
Broad spectrum anti-biotics
Teratogenic (contraindicated in pregnancy) 1. Azithromycin
1. Doxycycline (DOC for Ricketsia, Cholera, Chlamydia) 2. Clarithromycin
2. Minocycline (s/e : Black thyroid) 3. Erythromycin (ass. with CHPS, contraindicated in preg.)
3. Demelocycline (s/e: Diabetes insipidus DImelocyclne)
4. Tigecycline (not effective against pseudomonas) Linezolid Streptogramins
DOC for VRSA in lungs Useful in VRSA
Serotonin Syndrome 1. Quinpristine
(with antidepressants) 2. Dalfopristin
Other s/e : Neuropathy
Agranulocytosis.

Other mechanisms
Fluoroquinolones TMP-SMX
(DNA Gyrase inhibitors) FG Antimetabolites
CYP inhibition and QT prolong. (along with macrolides) Sulfonamides, Dapsone : block
Can cause tendon rupture (contraindicated in children) Dihydropteroate synthase
DOC for Meningococcus (Rx and Ppx) TMP : block Dihydropteroate reductase
DOC for Anthrax, UTI, Traveller's diarrhea Individually static
1. Ciprofloxacin TMP SMX (1:5) : Cotrimoxazole (cidal)
2. Levofloxacin (max bio availability) Ratio becomes 1:20 in plasma
3. Ofloxacin Kernicterus in newborn (if taken in preg.)
4. Pe-floxacin P PCP, Coccidian parasites, Nocardia,
5. Mox-ifloxacin M Safe in renal failure Burkholderia
6. Tova-floxacin T

Metronidazole Daptomycin
DNA integrity (via free radicals) Membrane integrity
DOC for anaerobes below diaphragm Overall DOC for VRSA (in Lungs its Linezolid)
Most protozoans (giardia, trichomonas, entamoeba) Streptogramins and 5th gen Cephalosporin (ROLIN)
are also useful in VRSA
 Syphilis, Actinomyces : Penicillin
Listeria : Ampicillin
Mastitis : Cloxacillin
SSI : Cefazolin (1st gen ceph.)
Anerobes : Above diaphragm Clindamycin, Below Diaphragm Metronidazole
Neisseria, Lyme disease, Enteric fever : Ceftriaxone (3rd gen ceph.)
Pseudomonas : Cephalosporins (3rd/4th/5th)
Enterobacter, Acinetobacter : Meropenem
C.difficile, MRSA : Vancomycin (Fidaxomicin for C.dif)
Plague,Tularemia : Streptomycin
Ricketsia, Cholera : Doxycycline
Atypical pneumonia (Legionella, Mycoplasma, Chlamydia) Pertussis, Diphtheria : Macrolides
Nocardia, PCP, Burkholderia, Cyclospora, Isospora : TMP-SMX
Meningococcal (Rx and prophylaxis), Anthrax, UTI, Travelers diarrhea : Fluoroquinolones

Resistance mechanism
Enzyme : Aminoglycoside, Beta lactams, Chloramphenicol ABC
Altered Target : MRSA/VRSA, Linezolid, Macrolides Pneumonia drugs
Efflux Pump : Tetracyclines Cyclic pumps

CIDAL drugs BeVaFA

Drugs safe in Pregnancy Beta lactams and Vancomycin : Time dependent
P Penicillins Fluoroquinolones + Aminoglyosides : Conc dependent
C Clindamycin Klinda safe
M Macrolides (except Erythromycin)

Drugs not effective against

Drugs safe in renal failure Mycoplasma : Cell wall inhibitors
From 50 S : Clindamycin Klinda Safe Anaerobes : Aminoglycosides
From 30 S : Tigecycline, Doxycycline Salmonella : Aminoglycosides
From Penicillins : Nafcillin, Ampicillin Pseudomonas : Vancomycin
From Cephalosporins : Ceftriaxone, Cefoperazone MRSA : Beta lactams (except 5th gen Ceph.)
From Fluoroquinolones : PMT Drugs
Rifampicin

Important Side effects Disulfiram like reaction

Imipenem + Cilastatin : Seizures C Cefoperazone, Chlorpropamide (OHA)
Fluoroquinolones : Tendon rupture in children, seizures G Griseofulvin (anti-fungal)
Macrolides and Fqs : CYP inhibitor and QT prolongation M Metronidazole
Erythromycin : CHPS in newborn P Procarbazine (anti cancer drug)
Tetracyclines : Teratogenic
DImeclocycline : Diabetes Insipidus
Minocycline : Black Thyroid
Vancomycin : NOT RED
TMP SMX : Kernicterus in newborn
Linezolid : Serotonin Sx, agranulocytosis
Cefoperazone : Hemarthrosis (pts on anticoagulation)
 Mycology
Yeast : Cryptococcus
Yeast like : Candida
Mold : Mucor, Rhizopus, Aspergillus, Absida
Dimorphic : HSBC PP
H Histoplasma
S Sporotrichosis
B Blastomyces
C Coccidiodes
P Para-coccidioides Beta Glucan test
P Penicillum Beta Glucan is a component of Fungal cell wall
Culture (cold) : Mold form Beta Glucan test is negative for
H/p (heat) : Yeast form 1. Cryptococcus
2. Zygomycetes (Mucor and Rhizopus)
Echinocandins (inhibit cell wall formation) are hence not
effective against the said fungi and DOC for them is Amp B
Candida
Galactomannan
MCC of opportunistic mycosis It is a biomarker for Aspergillus
Oral and esophageal thrush in immunocopromised
Diaper rash
Disseminated candidiasis in neutropenic
Aspergillus vs Mucor

Budding yeasts and Germ tube formation

pseudohyphae at 20°C at room temp (37°C) Aspergillus : Acute, Septate Mucor
only with C.Albicans
Acute angle branching of Non septate
septate hyphae Obtuse angle branching
Catalase (+) : chronic Mucormycosis in
granulomatous disease Immunocopromised
ABPA : hypersensitivity T/t : Amp. B
C.Krusei
reaction to aspergillus Posaconazole is an
(Resistant to Fluconazole) A
T/t : Voriconazole alternative

Chrom-Agar

Cryptococcus neoformans

Pneumocystic Jirovecci

India ink stain

Mucicarmine stain is
an alternative

Diffuse b/l GGO Crushed ping pong app. Encapsulated yeast

(Gomori meth. silver stain Acquired through inhalation (found in pigeon droppings)
on BAL sample) Disseminated to meninges : Meningitis (in HIV)
Yeast like fungus IOC : Latex agglutination test
Opportunistic infection in HIV (CD⁴ < 200) Culture : Bird Seed agar (Pigeon droppings)
Rx/ Ppx : TMP SMX (cotrimoxazole) t/t : Amp B + Flucytosine
Sporotrichosis Chromoblastomycosis
aka Rose gardener disease h/o walking bare foot (traumatic inoculation)
Dermal + Sub cutaneous Lymphatics involved Subcutaneous and doesn't invade underlying tissue
h/o thorn pick Caused by dematiaecious fungi (Produces brown color)
Dimorphic fungus (yeast in body and conidia in soil)
t/t : Itraconazole

Conidia form (in soil) Copper penny bodies

aka Medlar/Sclerotic bodies
Warty lesios

Nodulo-ulcerative lesions
(along lymphatics)
Asteroid body

Draining sinus
on foot !

Black Yellow
Eu-mycetoma Actinomycetoma
aka Madura foot Actinomyces (Bacteria)
Slow and progressive Rapid
Poor response to More sinuses
medication Early bone invasion
Surgical management Good response to
needed medication (Penicillin)

Differential : Botyromycosis
Caused by Staph.Aureus
Presents with draining sinuses

Penicillosis Histoplasmosis
(Talaromycosis) Immitates TB
Seen in Immunocopromised patients ( HIV ) Caseating Granulomas
c/f : fever, wt. loss, lymphadenopathy Chronic lung disease that seems
Characteristic red pigment and a powder like mould like TB
t/t : Amp. B
 Dermatophtoses (aka Ringworm)

Annular rash
Central clearing
Blue under Wood's lamp

Trichophyton
Tri : all 3 Pencil shaped macroconidia
Skin Endothrix Microconidia +++
Hair Black dots
Nails

Microsporum
Hair is microscopic Ectothrix Spindle shaped macroconidia
Skin Grey patch Microconidia present but less
Hair

Epidermophyton Club shaped macroconidia

Skin
Nails Microconidia absent

Tenia Capitis
Cause scarring Alopecia (DLT)

Kerion Favus
Boggy, tender swelling Crusting and Scutula
Seen in children present
Associated with LN (+) T. Schoenleni is MCC
T. Mentagrophyte is MCC Hair perforation test done
Hair perforation test done for T mentagrophyte
for T mentagrophyte
Men are Ken Favorite Shoe

8
 EchinoCandins
Inhibits cell wall synthesis
Terbinafine Cidal drugs
Inhibits squalene epoxidase Useful in Candidiasis
DOC for Onychomycosis
(Nail lacquer)
Cidal drug
Polyenes
Makes pore in cell membrane
1. Amp. B (Cryptococcus, Mucor, Kala Azar)
2. Nystatin C
S/e of Amphotericin B
1. Nephrotoxicity
2. RTA type 1
Azoles 3. Hypokalemia
Inhibits ergosterol synthesis Flucytosine 4. BM supression
1. Clotrimazole Inhibits nucleic acid synthesis
2. Fluconazole (ppx for cryptococcal meningitis) Used along with Amp B in
3. Voriconazole (aspergillus) transient visual changes Cryptococcal Meningitis
4. Itraconazole (sporothrix, blastomyces, histoplasmosis)
5. Ketoconazole
6. Sertraconazole anti-pruritic and anti-inflammatory action
7. Isavuconazole and Posaconazole (azoles used for Mucor)
PARASITOLOGY - HELMINTHS

Cestodes (tapeworms)
Body cavity absent (flat)
Segmented (tape)
Hooks and suckers present
DOC : Praziquantel

Taenia H.Nana H. Diminuata

aka intestinal tapeworm aka Dwarf tapeworm Rat tapeworm
1. T. Solium : Pigs Not bile stained Eggs bigger than H.Nana
2. T.Saginata : Cattle No intermediate host
Larva causes (humans are only host)
neurocysticercosis No symptoms
(asymptomatic infection)
Na Na 🙂‍↔️

D. Latum E. Granulosus
aka fish tapeworm Hydatid cysts (liver > Lungs)
Operculum present Eggshell calcifications
Has 3 hosts : Cyclops, fish, humans PAIR done
Involves ileum [B¹² deficiency] FNAC or biopsy Contraindicated
(anaphylaxis)

Hydatid Cyst
Neurocysticercosis
Caused by larval form : Cysticercosis cellulosae
Cystic CNS lesions + Seizures
Starry sky appearance (MRI)
DOC : Albendazole Multiseptate (honeycomb) cysts
Steroids are always started prior to
albendazole to avoid inflammation due to
larval antigens on death of larvae.

d/d : Tubeculoma
Lipid lactate peak present
in Tuberculoma Detached membrane (waterlily sign)
Seizure in NCC
Meningitis in Tuberculoma

Calcified cyst (no treatment needed)

 Nematodes (roundworms)
Cylindrical with body cavity
Complete alimentary canal
Separate sexes
DOC : Albendazole

Has an albumin coat

More circular, floats

Enterobius Trichuris Ascaris Ascaris

vermicularis Trichura (Fertilised) (Non Fertilised)
aka Pinworm aka Whipworm Largest nematodes
Not bile stained Barrel shaped m/c human helminth
Peri - anal pruritis Causes Rectal prolapse Man is natural host (no intermediate host)
Diagnosis : NIH swab Eggs contain the infective "Rhabditiform larva"
or Scotch tape
Pin 📌 enters
Egg has
blastomeres

Hookworm Strongyloides
Non bile stained Rhabditiform larva
Cause microcytic anemia Smallest nematode
2 species Ovoviviparous org
1. Necator Americanus (New World) (eggs hatch immediately)
2. Anc duodenale (Old world) DOC : Ivermectin

Not BILE stained Autoinfection

N Necator Americanus C Cryptosporidium
E Enterobius Vermicularis H H Nana
H H. Nana E Enterobius
A Anc. Duodenale S Strongyloides
Hookworm Pinworms and H. Nana T T Solium

Cutaneous larva migrans Blastomeres Yolk Granules,

D Shaped radial striations
M/c organism : Ancylostoma brazilense

Eggs that SINK in salt solution

S Strongyloides
A Ascaris (unfertilised)
T Tinea,
 Trematodes (leaf like)
Only anal opening
Only suckers
Anal Suckers
Primary intermediate : snail
Definitive host : Man
DOC : Praziquantel

S. Mansoni
Lateral spine tedhi mansi
Other trematodes Schistosoma
Causes portal fibrosis
Infective form is Meta-cercaria Infective form is Cercaria Involves inferior
Feco oral transmission Skin transmission mesenteric plexus
Hermaphrodites Separate sexes
Operculated eggs Spines
Secondary intermediates present No secondary intermediate S.Japonicum
No spine
Causes portal fibrosis
Involves superior
mesenteric plexus
Fresh aquatic vegetation Crab Fish
Fasciola Hepatica Paragonimus Clonorchis S.Haematobium
Affects intra-hepatic aka Oriental Lung Causes Terminal spine
billiary system Fluke cholangiocarcinoma terminal cancer
Rusty sputum on Cause peripheral
eating uncooked calcification of bladder
(fetal skull app.)
crab.
Sq. cell ca of bladder

Katayama fever
Portal fibrosis by S. Mansoni
or S. Japonicum

Coccidian Parasites
Causes infection in HIV pt.
Prolonged diarrhea Oocysts stain with ZN stain
Abdominal pain (Kinyoun's method)
Vomiting 1. Carbolfuscin CAMe
2. Acid (decolouriser)
Cryptosporidium 3. Methylene blue (counter stain)
Spherical
Smallest (4-8μm), hence Crypto
Oocysts are immediately infectious and cause auto-infection
DOC : Nitazoxanide Nita Ambani cryptocurrency

Cyclospora
Spherical
8-10 μm
TMP SMX
DOC : TMP SMX 1. PCP (Jirovecci) - treatment and ppx
2. Nocardia
Cyto-isospora 3. Cyclospora and cystoisospora
Oval (can be identified) 4. Bordtella pertussis
DOC : TMP SMX
 Microfilariae

A. Wuchereria bancrofti
Lymphatic
filariasis B. Brugia malayi

C.Loa loa
D. Onchocerca volvulus
E. Mansonella perstans

Lymphatic filariasis
Sheathed microfilariae
IOC: Peripheral blood smear (thin) 10pm - 2am LBW
DEC Provocation test ⬇️
Transmission assessment survey, done for filariasis Loa loa : Line
Brugia malayi : 2 nuclei
DOC: DEC
Wuchereria : No nuclei

Malarial Parasites
Plasmodium Vivax Plasmodium falciparum Plasmodium malariae

Trophozoite Schizont Accole form Banana Band form

(Relapses) Multiple rings gametocytes
in one RBC
Primaquine DOC
for Schizonts
Shiff : Vivax
James : Ovale O James Maurier : Falciparum Zeimann : Malariae

Sporozoites enter skin

Go to liver
Hepatic Schziont (asexually multiplying protozoans)
or Hypnozoites (latent stage)
Hepatic Schizonts rupture releasing Merozoites
which infect blood cells

Trophozoite (ring form) inside RBCs

Erythrocytic Schizonts (relapses)
Mosquito bite: Sporozoite (Skin)
Gametocytes : Taken up by mosquito Transfusion: Trophozoite
Fertilisation in mosquito Placental transfer: Merozoites (Mera baccha)
 Anopheles Aedes Culex Mansonia
Tiger mosquito Nuisance mosquito With Pistia plant
Sophisticated
(Day biters) (cules cause nuisance) Brugia Malayi
Clean water Artificial water collections zoo Dirty water (Brugian filariasis)
Adult at 45° angle Adults parallel and have stripes 10 km (big wings)
Spotted wings like tiger Hunchback at rest
5 km range 100 m range tiger can't go far Eggs in cluster
Single eggs (A) Single eggs (A) Larva at angle
Parallel larva Larva at angle (has siphon tube) (has siphon tube)

6 Diseases under
NVBDCP
1. Malaria
Tiger likes 2. Dengue
Can fly far
DRY Zika Chicken India, Japan and Nile 3. Chikungunya
4. Filariasis
1. Malaria 1. Dengue 1. W. Bancrofti 5. JE
2. Rift Valley fever 2. Japanese encephalitis 6. Kala Azar
3. Yellow fever 3. West Nile fever
4. Zika
5. Chikungunya

For P. Vivax
Card test
Chloroquine : 3 days optiMAL
Entire country, P falciparum:
HRP - 2 ag : P Falciparum
Sulfadoxine pyrimithamine + Artesunate
Aldolase or LDH : P Vivax/Ovale
North eastern states, P falciparum
Lumifantrine + Artemether
In pregnancy
Primaquine is contraindicated Peripheral smear stain : JSB Stain
1st trimester for Falciparum : Quinine Thin : Species identification
Thick: Presence of parasites
Fluorescent stain: Acridine orange
Primaquine
1 microscope: 25k population
Prevents relapse (kills Schizonts)
Most important measure of malaria control : API < 1
C/I in pregnancy
Can cause severe hemolysis in patients with
Best indicator of operational efficiency: ABER
G6PD deficiency Best during outbreak : Slide Positivity rate
Absence of duffy Ag : Protective

Prophylaxis (4 weeks) No incidence in 3 years : Category 0

Doxycycline OD API <1 : Category 1 (Elimination) 1 is 1
Mefloquine Weekly
API 1-2 : Category 2 (Pre elimination) 1-2 is 2
API > 2 : Category 3 (Intensified control phase) > 2 is 3

Complicated malaria API > 2 : Insecticide treated nets Deltamethrin

IV Quinine/Artesunate API > 5 : Long lasting Insecticide treated nets
 Integrated vector management for mosquitoes

Anti Larval Anti Adult Protection Legislative

Done in urban areas Done in rural areas control
from bites

1. Biological control 1. Space sprays (API < 2) Mosquito nets

(Gambusia/Guupy) (Malathion/Pyrethrum) Repellants
2. Chemical control 2. Residual sprays (API > 2) Screening
(Paris green, Abate) DDT (2 rounds)
3. Environmental control ⬇️
(source reduction) Malathion (3 rounds)
⬇️
Deltamethrin (2 rounds)

Leishmaniasis
Caused by protozoan : L . Donovani
M/c type is cutaneous leishmaniasis : skin sore

Visceral leishmaniasis is aka Kala azar (UP, Bihar, WB, Jharkhand)

Kala azar : PUO, HSM

Mucosal leishmaniasis is least common

PKDL (Post kala azar dermal leishmaniasis) d/d for leprosy

Tests for Kala Azar

Rk39 Ag Test : Rapid test
Napier’s aldehyde test
Montenegro test : Skin test Negro Kala
Culture : NNN Media
Gold standard : Demonstration of Amastigotes
in bone marrow (Kinetoplasts are seen)

DOC: Liposomal Amp B

2nd line : Miltefosine

PKDL
d/d for leprosy
DOC : Miltefosine
Sandfly
Hairy wings
lives in cracks and crevices of walls
Diseases caused : Kala azar, oriental sore, oraya fever
Insecticide : DDT
 Miscellaneous Parasites
Entamoeba Toxoplasmosis
Causes intestinal amoebiasis Obligate intracellular parasite
Foul smelling + Blood and mucus Cats and cattles are 1° host
Flask shaped ulcer is typical All other animals are 2° host
Invades liver
DoC : Metronidazole Fecal oocysts (infective)
Tachyzoites : can cross placenta
(Cong. Toxo)
Acanthamoeba Bradyzoites : Cat meat
Microscopic, free-living amoeba
Contact lens "Mis-use" In adults only affects
Acanthamoeba cause 2 diseases: Immunocopromised (HIV)
1. Acanthamoeba keratitis
Sabin fieldman dye test
2. Chronic Granulomatous Amebic
Early antibody detection against
Encephalitis (GAE)
toxoplasma
DOC : PHMB Easy and highly sensitive

Frenkel test
Giardia
Skin test
Secretory diarrhea in Immunocopromised
Not very reliable
Affects duodenum and jejenum (malabsorption)
Foul smelling + Fatty stools
2 nuclei
4 pair flagella Trpanosoma
Both cyst and T. Brucei : African sleeping sickness
trophozoite are (tse tse fly)
infective T. Cruzi : Chaga's disease
(can cause Achalasia cardia)

Trichomoniasis
Mona : One nucleus Trichinella Spiralis
5 flagellae aka Pork worm
Causes cervicitis Diarrheal disease
(strawberry cervix) Causes muscle invasion myalgia +
t/t : Metronidazole periorbital edema

Scabies
Ectoparasite
Female parasite burrows into stratum corneum
Life cycle has 4 stages and takes 15 days
Larvae has 3 pair of legs

Naegleria Fowleri
aka Brain eating amoeba
B.Coli Rapidly fatal meningo-encephalitis
Largest protozoan (Primary amoebic meningoenceph.)
Only ciliate known to parasitize humans Enters through nose (swimming in
Two types of nuclei : Micro and macro contaminated pools)
Intestinal infection Affects immuno-competent
Death within 20 days
Anti-parasite drugs
Cestodes, Trematodes : Praziquantel (except, echinococcus, fasciola)
Nematodes : Albendazole (except strongyloides)
Filariasis : DEC (except onchocerca)
Coccidian Parasites : TMP SMX (except cryptosporidium)

Fasciola (Liver flukes) : Triclobendazole

Echinococcus (Hydatid) : Albendazole
Strongyloides, Onchocerca : Ivermectin
Cryptosporidum : Nitazoxanide
 DNA Viruses
Icosahedral symmetry
20 faces
12 vertices

AP is a non
enveloped
state
Parvo

Herpes
Adenovirus
EBV / CMV / VZV No "parvah" for Parvo because smallest,
Acute hemorrhagic hence is single and without envelope
cystitis Aplastic crisis in SCA
Pox Pure red cell aplasia
Erythema infectiosum (5th disease),
Hep B slapped cheek app.
Papova
Most common infectious cause of
Non immune hydrops

Papilloma (HPV) Other DNA viruses

Chicken pox is not a pox virus but Herpes virus, aka VZV / HHV 3
Polyoma (BK and JC) replicate in nucleus
Herpes Zoster is just another name for shingles
Other DNA viruses have
Molluscum contagiosum is a pox virus
BK virus : Graft nephropathy Icosahedral symmetry
JC virus : PML (Progressive
multifocal Leukoencephalopathy)

(Pox Virus) (HPV) (HSV)

Henderson Patterson body Molluscum

Koilocyte Tzank Smear showing
Lendrum's Phloxine Contagiosum
HPV is the most common STI. multinucleate giant cells
Tartarazine stain is used Central Genital warts : condyloma acuminata Show margination and moulding
umbilication Cervical cancer HSV 1 : Above diaphragm
Pseudo Koebner Prophylaxis : Gardasil 9 HSV 2 : Below diaphragm (painful
phenomenon 6, 11, 16, 18, 31, 33, 45, 52, 58
genital herpes, neonatal meningitis)
(auto-inoculation) L¹ protein : Vaccines
E⁶, E⁷ protein : Oncogenes
E⁶ - p⁵³
E⁷ - Rb

(CMV) Intra-Nuclear inclusions

Basophilic owl eye
HSV : Lipschultz bodies
(Eosinophilic in "Red Sternberg cells)
Yellow fever : Torres bodies
MC infection after organ transplant
Periventricular rash in congenital CMV
Cowdry A : HSV, Yellow fever (HAY)
Serpentine ulcers in CMV Esophagitis
Cowdry B : Adenovirus, Polio (BAP)
Pizza pie appearance in CMV retinitis
Treatment : Ganciclovir
Foscarnet in Ganciclovir resistant CMV Intra-Nuclear + Intra Cytoplasmic inclusions
CMV
Measles (Warthin Finkeldey)
 Varicella zoster virus
aka Herpes zoster virus (HHV 3)

Chicken pox Shingles Ramsay Hunt Syndrome

(Varicella) (Herpes Zoster) (Reactivation of VZV in geniculate ganglion of CN 7)
Fluid filled, pruritic lesions Lesions along dermatomal Bell's palsy + Erosions in pinna and EAC
Starts on trunk (chest and face) distribution (U/L)
and then to peripheries MC area is Thoracic dermatome Herpes zoster opthalmicus
Spares hand and soles Reactivation of VZV (stays Involvement of V1, opthalmic branch of
dormant in DRG) trigeminal nerve.
m/c complication : Post herepetic Leads to corneal anesthasia (loss of
neuralgia corneal blink reflex)
Hutchinson sign : Tip of nose involved (bad
prognosis)

Ebstein Bar Virus

Enters B cells via CD-21 and immortalises them
leading to malignancies :
1. Hodgkin's lymphoma
2. NHL : DLBCL, Burkitt's
3. Nasopharyngeal carcinoma
4. Ca stomach
5. Oral hairy leukoplakia
Downey cells Paul Bunnel test
Ballerina skirt app. aka Monospot test
In adolescents causes fever + lymphadenopathy of cytotoxic T cells Heterophile agglutination
+ HSM aka Kissing disease (not B cells) test (uses sheep RBC)
Advice to avoid contact sports (can lead to
splenic rupture)

EBV + Ampicillin : Diffuse morbiliform rash (maculo papular rash)

HHV 8 HHV 6
aka Kaposi Sarcoma herpes Virus Roseola infantum (6th disease)
Other diseases caused High fever
1. Multicentric Castleman disease Rash when fever subsides
2. Primary effusion lymphoma Lymhadenopathy (d/d is Kawasaki)
Nagayama spots on palate
Violaceous papules Self limiting
CD⁴ < 200
AIDS defining
RNA Viruses
All are single stranded except Rota (aka Rheo) virus
Single copy of genome except Retro viruses (HIV, HTLV) Measles, Nipah : Paramyxo (MNoP)
Unsegmented except "BIRA" ChikunGunya : toGa
Rubella : Matona (MATA)
B Bunya-viridae (3 segments)
NVBDCP viruses : Flavi (Fly)
I Influenza Virus (8 segments) aka Orthomyxo-virus
R Rota virus (3 + 8 = 11)
A Arena virus (2 players in arena) Enterovirus
Picorna-viridae
Replicate in cytoplasm except "RIM" Polio | Cox A | Cox B
R Retro virus MCC of aseptic meningitis
I Influenza virus They don't cause intestinal infections (named
M Measles so because they replicate in gut)
👁️
Enterovirus 70 : Apollo Conjunctivitis (7 )
Enterovirus 71 : HFMD, Herpangina

Influenza Virus
Orthomyxo-viridae
H and N (Hemagluttinin and Neuraminidas)
Segmented genome (BIRA)
Replicates in nucleus (RIM)
Sheds in repiratory tract a day before and 3-4
days after fever.

HFMD caused by enteroviruses

Herpangina (vesicular pharyngitis)

Para-influenza Virus Rota (Rheo) Virus

Causes Laryngo-tracheo-bronchitis (Croup) Only DS RNA virus
X-ray : Steeple sign (Subglottic narrowing) 11 segments (BIRA)
C/f : Barking cough, inspiratory stridor MCC of infantile diarrhea
Rx : Epinephrine nebulization, Steroids Diagnosis : Ag detection in stool
(no Antibiotics) Rota vaccine : Live oral vaccine, can cause
intussuception.

Rabies Virus
Lyssa - Virus (bullet shaped)
Endemic to India
Negri bodies seen in Purkinje cells
Crimean Congo hemorrhagic fever
Stained with Seller stain
West Nile virus

Slow Viral diseases

Spongiform encephalopathy 1. Crutzfeldt Jacob disease
Caused by prions (protein 2. Kuru
containing infectious agents) 3. Mad cow disease
 Dengue
Incubation period : 10 days Tengue
Dengue fever
Fever of 2-7 days with > 2 of the following and Breteau index:
no plasma leakage Done for Aedes mosquito in general
Headache No. of containers / No. of houses checked
Myalgia
Retro-orbital pain
Arthralgia
Thrombocytopenia
Tourniquet test
Plasma leakage (Hct ↑by > 20%) BP cuff inflated midway between systolic
Dengue hemorrhagic fever and diastolic pressure
Plasma leakage along with Dengue fever Left for 5 mins
> 10 petechiae per square inch is positive
DHF 1 : Positive tourniquet test
DHF 2: Spontaneous bleeding, abdominal pain
DHF 3 : Circulatory failure (Hypotension, cold clammy)
DHF 4 : Shock (undetectable BP)

Hct ↑
Confirmed dengue fever
(Any one of the following)
< 5 days : Dengue NS1, viral nucleic acid in PC
After 5 days : IgM antibody in ELISA
After 15 days : IgG antibodies (Seroconversion)
Isolation of dengue virus (Viral culture)

Management
1. IV crystalloids
2. Platelet : < 10000/ bleeding
Dengue fever : Home management
DF in pregnancy, infants, old age,
comorbidities : Hospitalise
DHF 1 and 2 : Hospitalise
White islands in sea of red Blanching of rash on application
DHF 3 and 4 : Tertiary care
Seen when fever subsides of pressure
(critical period)
Criteria for discharge
Platelet count > 50,000 Antibody dependent enhancement
No fever >2 days (without use of antipyretics)
Dengue antibodies from prior infection
No resp. distress/ascites
increase severity of subsequent infection.
Return of appetite, good urine output
Seen with type 2 dengue

Chikungunya
aka Break bone fever
Arthralgia may persist > month
Leukopenia Family : ToGa-viridae
Can have maculopapular rash

Chik sign
 Japanese Encephalitis

Presentation
Acute onset of fever <7 days
Change in mental status and/or
new onset of seizures

Culex Dead end host

mosquito
Vector Confirmation
Ardeid birds India Japan Nile IgM antibody in serum or CSF
Reservoir Virus isolation from brain tissue
Antigen detection by immunofluroscence
Nucleic acid detection by PCR
Pigs
Amplifier
Can be vaccinated to
reduce transmission

Hepatitis
Only Hep B is dsDNA (others are ssRNA) Hepatitis B
Hep B - Hepadna Virus
Hep A and Hep E are non enveloped HBsAg (Australian Ag/ Epidemiological marker) : First to rise
HBsAg (-)
M/c vertical transfer : Hep B ( >90% if HBeAg+ )
M/c blood transf. associated : Hep B
IVDU : Hep C
Anti HBs (+) Anti HBs (-)
Acute hepatitis in children : Hep A
Vaccinated (no anti HBc) Window Period (anti HBc IgM) WM
Acute hepatitis in adults : Hep E
Recovered (anti HBc IgG) Remote infection (anti HBc IgG)
Hep E in pregnancy : 20% mortality

Ideal titres of anti HbS in vaccinated: > 10 mIU/ml

Associations of Hep B
PAN (Immune complex deposition) Pb
Membranous Glomerulonephritis

Associations of Hep C
Cryoglobulinemia (Immune complex deposition)
Lichen Planus

Hepatitis C If HBeAg absent but HBV DNA > 2000 : Pre-core mutant

Anti HCV antibodies : Can't determine if

active or recovered
Hepatitis D
HCV RNA : If positive then active
Anti HDV + Acute Hep B : Co-Infection
Anti HDV + Chronic Hep B : Super-Infection
High risk of Cirrhosis in super infection
 HIV AIDS
Envelope proteins
NACP Targets
RNA virus (Retroviridae)
1. 90% PLHIV know their status
GP 120 : Attachment to CD4
December 1 2. 90% on ART
GP 41 : Fusion and entry
3. 90% are virally supressed
Strains of HIV Capsid protein
Based on envelope gene : HIV 1 and HIV 2 P24 : Used in testing (acute HIV) Drugs against
HIV 1 is more common (MC : Strain M, Type C) GP 120 : Fostemsavir
HIV 2 is less pathogenic, seen in Africa Co-receptors CD4 : IBALIzumab
Donated blood screened for both CCR-5 on macrophages
CCR-5 mutation provides immunity GP 41 : Enfuviritide
CXCR-4 on T cells CCR 5 : Maraviroc

Disease course
Viral load increases initially after infection,
some patients can have acute HIV Syndrome.
The viral load then drops to a steady state Acute HIV Syndrome
untill progression to AIIDS Fever + Maculopapular rash
This time is around 10 years Virus is transmissible
HLA B27, HLA B57 : Progression is very slow Diagnosis : P-24 Antigen
HLA B35 : Rapid progression

Investigation
Initial investigations
1. Antibodies against HIV 1/2 : ELISA (preferred),
Western Blot (m/c done in India)
2. P 24 antigen (antibodies negative in window period)
3. DNA PCR when Ab assays are indeterminate

RT PCR is done for viral load assessment

(not an initial investigation)

Screening : ERS Battery Infant Diagnosis

1. ELISA Screening : Dried blood spot test (DNA PCR)
2. Rapid test (various methods) Confirmatory : RT PCR done at 6 weeks
3. Spot blood test (dried) : also used in infant HIV diagnosis (Antibody testing can detect maternal
antibodies)
ANC screening : Can opt out

Transmission
Max risk of transmission : Blood transfusion (ERS performed, discarded if any 1/3 positive)
Sentinel Surveillance
Most common mode : Sexual (screened at STD clinics, TB centres)
Done to find missing
Risk of vertical transmission : Max during Delivery (LSCS is preferred)
⬇️ cases.
Screening of high risk
Most important prognostic factor : Maternal viral load
groups
Newborn of mother on ART : Nevirapine 6 weeks
Doesn't include the
If mother not on ART : Nevirapine + Zidovudine (12 weeks)
regular screening at
Breastfeeding clinics
Not contraindicated
In India : Recommend
In developed nations : Formula feeds
CD4 < 500 TB is m/c opportunistic infection
CAD is m/c cardiac complication
FSGS (collapsing variant)
Distal sensory neuropathy

Oral candidiasis Oral hairy leukoplakia Kaposi Sarcoma

aka Oral thrush Sides of tongue Violaceous papules
Can be rubbed off EBV infection H/P : Spindle cells
Can't be rubbed off Asso. with HHV 8

CD4 < 200

Pneumocystic Pneumonia (PCP) Histoplasmosis PML HAND

T/t : TMP SMX Multinucleated giant Prog. multifocal HIV ass
Add steroids when SPO² < 70 cells containing leukoencephalopathy neurocognitive
Prophylaxis : CD4 < 350 multiple budding yeast Assymetric disorder
Stop when CD4 > 350 for 6 months forms demyleniating dis. Symmetric white
Immitates TB JC virus Mater lesions

CD4 < 100

Cryptococcal Meningitis Candida esophagitis HSV esophagitis CMV esophagitis

T/t : Amp B + Flucytosine (2 wks) + aka Esophageal thrush Punched out lesions Basophilic owl eye
Fluconazole (6 months) Shaggy esophagus Serpiginous ulcers
Ppx : Fluconazole when CD4 < 100 White spots seen on esophagus

d/d : HIV ass.

enteropathy
Diarrhea > 1 month
No associated
infection

Bacillary angiomatosis Coccidian parasites Toxoplasmosis Primary CNS Lymphoma

Bartonella Henslae Nitazoxanide for crypto Ring enhancing lesions Periventricular
Warthin Starry Stain TMP SMX for others Not ring enhancing (Solid)
CD4 < 50 Pizza and Big-mac AIDS defining conditions
Neoplasms
1. Kaposi Sarcoma
2. Primary CNS Lymphoma (NHL)
3. Invasive Carcinoma of Cervix

Infections
1. Candidiasis (except oral)
2. Cryptococcal meningitis
CMV retinitis MAC pneumonia 3. Mycobacterium avium complex
Pizza pie appearance Involves middle lobe pneumonia
DOC : Ganciclovir 4. Invasive toxoplasmosis
Resistant : Foscarnet 5. Disseminated histoplasma

Entry inhibitors NRTI

Rock and Tide Small name more drugs
1. Maraviroc (oral) : CCR5 1. Abacavir (heart attack)
2. Enfuviritide (s/c) : GP41 2. Emticitabine (pigmentation in palms and soles)
(fusion of virus with T cell inhibited) 3. Lamivudine (safest)
4. Tenofovir (nephrotoxic) Tea no!
5. Zidovudine (BM supression and hepatotoxic)
6. Didanosine (pancreatitis) Dadaji got pancreatitis

NNRTI
Large name less drugs

Integrase inhibitors 1. Nevirapine

Inte"GRA"se → GRA-virs 2. Efavirenz (teratogenic, vivid dreams)
1. Dolutegravir (oral)
First line drug for HIV
Post exposure prophylaxis
Started ASAP (within 72 hrs max)
Protease Inhibitors 3 drugs - 4 weeks
Protein in Navy DLT - 50 300 300
1. Ritonavir 1. Dolutegravir (50)
2. Atazanavir 2. Lamivudine (300)
3. Indinavir (hyperbilirubinemia and 3. Tenofovir (300)
RENAL stones - lucent on CT)
DLT is also 1st line ART in adults
CYP-3a4 inhibitors
In children / renal failure : ALE
Strongest is Ritonavir (Ritonavir
boosting) 1. Abacavir
Causes lipodystrophy syndrome 2. Lamivudine
(Atazanavir has minimum) 3. Efavirenz

Anti-Influenza drugs Drugs used in both

1. Remdesivir (RNA dep RNA polymerase inhibitor) RRR HIV and Hep B
2. Oseltamivir (neuraminidase inhibitor) 1. Lamivudine
3. Amantadine (uncoating inhibitor) Aman uncoats 2. Emticitabibe LET
3. Tenofovir
Anti-herpes virus drugs
1. Acyclovir : HSV 1/2, VZV
2. Ganciclovir : CMV
3. Foscarnet : Resistance to Acyclovir or Ganciclovir
 Childhood Infections
Measles Rubella
aka Rubeola aka German Measles
RNA paramyxovirus. Post auricular LN
Droplet spread, with a SAR ≥ of 90%. Maculopapular rash starting from face
Infectious 4 days before and 5 days after Fourcheimer spots
the appearance of the rash.
Prodrome of conjunctivitis, photophobia,
coryza and cough Roseola Infantum
Rash starts from retro auricular region. 6th disease - HHV 6
Koplik spots and Warthin–Finkeldey giant High fever
cells are pathognomonic Rash when fever
Complications of measles subsides
- Most common : Otitis media Nagayama spots on
- MCC of death : Pneumonia palate
- Delayed complication : SSPE
Self limiting

Scarlett fever 1st disease : Measles

Strep Pyogenes (Group A strep) - 2nd disease : Scarlett fever
exotoxin mediated disease 3rd disease : Rubella
aka Second disease 4th disease : Duke's disease
Rash within 24–48 hours of URTI. 5th disease : Erythema Infectiosum
Rash blanches on pressure. 6th disease : Roseola infantum
The tongue papillae are swollen giving
the tongue a strawberry appearance Sandpaper rash
D/d : Kawasaki disease Pastia lines
Pertussis
Paroxysm of cough followed by
apnea
Parvovirus B19 DOC : Azithromycin
aka Erythema Infectiosum (5th disease) Contacts : Erythromycin
Transmission by respiratory route (also (irrespective of immune status)
transmissible in blood and blood products)
Erythrotropism - targets only RBC lines
(transient aplastic crisis) Mumps
Aplastic crisis in hemolytic anemias and Children - Meningoencephalitis
immunocompromised Adult males - Orchitis

Polio-virus
RNA virus - Picornaviridae
AFP surveillance
Three serotypes - types 1, 2, and 3 (type 2,3 eradicated)
Every case of AFP in any child under
Ages 6 months to 5 years mc affected
15 years is to be reported.
Feco-oral transmission
2 fecal samples are transported to
Humans are the only known reservoir for the polioviruses.
the laboratory within 3 days.
This is done in a process known as
Most cases are subclinical.
the reverse cold chain.
It can present as non-paralytic polio (aseptic meningitis) or
Done by surveillance medical officer
paralytic polio (LMN paralysis).
It is asymmetric paralysis - tibialis anterior mc affected
Death usually occurs due to respiratory paralysis.
Congenital TORCH infections

Congenital CMV Congenital Zika virus

Most common congenital infection Microcephaly
Only 10% cases are symptomatic Grey white junction calcification
Max transmission in 3rd trimester
(most severe in 1st trimester)
Features :
-Microcephaly
-Periventricular calcification
-Blueberry muffin rash
Long term side effect : SNHL
IOC : PCR (Urine > Blood)
Congenital Varicella
Cicatrical skin rash
Congenital Toxoplasmosis Limb hypoplasia
Prevention : VZIG to mother (5 days before
Cats are source of infection and 2 days after delivery)
Most severe in 1st trimester
Features :
-Chorioretinitis (m/c)
-Hydro-Cephalus CCC.
-Parenchymal calcifications
Congenital HSV
Diagnosis : Fetal IgM/IgA detection
From maternal genital tract
(vaginal delivery contraindicated
with active HSV ulcer)
Congenital Rubella Syndrome Encephalitis in neonate

aka German Measles

Matanoviridae family
Characteristic Blueberry muffin rash
Features : Congenital Parvovirus
-SNHL
Non immune hydrops
-Bilateral Cataract
Pure red cell aplasia
-PDA > PS (Most specific)

Congenital Syphillis
Snuffles (nasal discharge) rash and HSM
Late presentation : Hutchinson triad
-SNHL
-Hutchinson teeth
Interstitial keratitis
 Tuberculosis

Primary TB
1st focus of infection : Ghon's focus
Ghon's Complex : Ghon's focus + LN Ranke
Complex
Ranke's Complex : Calcified Ghon's complex

Primary focus is sub-pleural and around

horizontal fissure. Ghon's
focus Consolidation around
Horizontal fissure

Post Primary TB TB Sequelae

Tree in bud appearance Milliary TB Fibrosis

Seen in active post primary TB Bilateral lung involvement Bronchiectasis
Due to endobronchial spread Due to hematogenous spread Cavity
Can be primary or post primary

Dermat. manifestations of TB
Hallmark of TB lymph nodes
Conglomeration (matted lymph nodes)
Peripheral ring enhancement (due to central
caseous necrosis)

Named TB foci
Lupus Vulgaris Scrofuloderma
Simon focus : Apex of lungs (Simon was Apex ruler) M/c skin manifestation M/c skin manifestation
in adults in children
Puhl focus : Supra-cavicular (Pull up) Central Scarring aka Cold abscess
Assman focus : Infra-clavicular (Ass is down)
Lupus Pernio : Sarcoidosis
Simmond : Liver
Rich : Meningial (Brain is rich with knowledge) Central clearing : Tinea
Weigert : Pulmonary vein (Vein-gert) Central crusting : Kala Azar

MC focus in congenital TB : Liver Lichen Scrofulosorum : Diascopy : Apple

Hypersensitivity reaction jelly nodules
against TB antigen
 Orthopedic manifestations of TB

Mortar and pestle app. Pott's Spine

(TB Hip) Para - discal involvement
D/d mets (Involve vertebral body)
Stage 1: Synovitis (apparent lengthening)
T/t : Middle path regime (ATT, if
Stage 2: Early Arthritis (apparent shortening)
no improvement then Sx)
Stage 3: Advanced Arthritis (true shortening)
Stage 4: Advanced Arthritis with Sequele MC site in TB spine : Dorsal Spine
(mortar pestle app.) Least common site in spine : Facet joints

Earliest bone to be affected : Acetabulum

(leads to femoral head dislocation)

Phemister triad : Osteopenia + Erosion +

Joint space reduction
Babcock's triangle : Frequent site of TB
lesions in femur

Ward's triangle : Osteoporosis Psoas Abscess

Fairbank triangle : Congenital coxa vara
Treatment : Open drainage of the abscess

Gastro-Intestinal TB Genito urinary TB

Sterile pyuria (pus present but no e-coli)
String sign of Cantor Most sensitive investment: IVP (IV pyelogram)
Ileo-cecal junction involved IOC : CT urethrography
Also seen in Chron's disease Earliest finding on IVP is moth eaten calyces
Vit B12 def (iron fist bro)

CNS TB
Basilar exudates + Vasculitis + Hydrocephalus

Thimble Bladder Putty Kidney

TB Meningitis Small and contracted Calcified kidney, U/L
Cobweb bladder Autonephrectomy
ADA ↑ Urinary urgency is the Seen in end stage GU TB
Lymphocyte ↑ 1st symptom

Basilar exudates Hydrocephalus Cardiac manifestation in TB : Chronic constrictive pericarditis

 CBNAAT Treatment Status
Diagnostic ALGORITHM Done for all now Cured : Negative sputum at completion (last
CBNAAT takes 1-2 hrs month) and one instance prior
Presumptive TB
Checks Rif sensitivity
(any one)
Fever/cough for > 2 weeks Completed : Last month sputum sample not
In Rif sensitive available (but one prior negative sample)
Haemoptysis
Start ATT : 2HRZE + 4HRE
Significant weight loss
In Rif resistant Failed : Sputum positive after 5 months of t/t
Abn CXR
MDR TB regime
In Rif indeterminate
2nd CBNAAT
Smear CXR If still indeterminate then
examination liquid culture or LPA

Do CBNAAT for all scenarios

Both smear and CXR negative but high Sputum Sample
clinical suspicion : Liquid Culture (BACTEC) 2 samples (Spot and morning)
Tested within 24 hrs

IGRA (quantiferon gold) : Blood test

Pediatrics TB diagnosis LPA : For drug sensitivity
Direct CBNAAT on presumptive cases
If sputum not available : CXR and TST
(If CXR suggestive then CBNAAT on
gastric aspirate)

Isoniazid Rifampicin Ethambutol

Inhibits mycolic acid synthesis Inhibits RNA polymerase Eye-tham-butol
Activated by catalse-peroxidase enzyme Max cidal action Inhibits Arabinoglycan (cell wall)
of mycobacterium (Coded by Kat-G) Safe in renal failure (secreted in bile) Only static drug (others are cidal)
Kat-G mutation : INH resistance Orange urine/ secretions Causes optic neuritis
B⁶ deficiency) : Sideroblastic anemia Enzyme inducer (OCP failure, replace Contraindicated in <6 yrs
Adverse effects : Inhibitor (enzyme) warfarin with Heparin) Causes gout (CANT LEAP)
Neuropathy Mutation in rpoB gene leads to resistance
Hepato-toxic (Detected by gene Xpert)
Isoniazid metabolism
ATT in HIV
INH Start ATT first
Metabolised by acetylation Pyrazinamide
Start ART in 2 weeks
Intracellular bacteria only
Slow Fast (irrespective of CD4 count)
acetylation acetylation
Causes gout (CANT LEAP)
Neuropathy Hepatotoxic Most hepatotoxic
Rifabutin used instead of Rifampicin
(Euphoria, Avoided in pregnancy
(no enzyme induction)
memory loss) Z > H > R (Zehar)

MDR TB : INH + Rifampicin resistance

TB Prophylaxis < 2 years
XDR TB : MDR TB + Fluoroquinolones + Bedaquiline + Linezolid INH
Household contacts
(6 months)
Anti TNF (ACE I Goli)
First line for MDR TB : BPLM 1. Bedaquiline > 2 years
Dialysis patients
2. Pretomanid Rifapentin+INH
Silicosis (3 months)
3. Linezolid
4. Moxifloxacin
TB in preg : 2HRE + 7HR (9 months, no Z)
ATP Sythase inhibitor : Bedaquiline (QT prolongation)
In MDR/XDR TB : Suggest MTP
Mycolic acid synth inhibitor : Pretomanid
NTEP GOALS 2025
TB Death < 90 %
TB incidence < 80 % aka NIKSHAY POSHAN Yojna
Catastrophic costs : Zero Direct transfer of Rs. 500/month
Across treatment period
World TB day : 24th March
NTEP high priority districts
TB-HIV > 10%
Designated Microscopy centre
1 in 1 Lakh population
Tuberculosis Unit
Nodal point for TB in sub-district
DOTS 99 District TB Centre
ICT (information and
communication tech.) State TB Cell
based adherence system.
Central TB Division
For improving compliance
 Leprosy
aka Hansen's disease
Classic presentation : Hypopigmented/erythematous macules and Sensory impairment
Virulence factor of M.Leprae : PGL 1
M. Leprae grows in cooler tissues like peripheral nerves, skin anterior chamber of eye.
Route of infection : Inhalation

Tender and thickened peripheral nerves (GAN thickness can be seen)

First to be affected : Sensory (hot-cold differentiation)
Glove, stocking pattern of sensory loss : Repeated painless injuries
M/c peripheral nerve affected : Ulnar > Posterior tibial
M/c nerve for biopsy : Radial cutaneous nerve of arm > Sural nerve
M/c cranial nerve involved : Facial nerve (exposure keratitis is MCC of blindness in leprosy)
M/c ocular condition : Anterior uveitis

Tuberculoid Borderline Borderline Borderline Lerpomatous

Single, well demarcated Tuberculoid Borderline Lepromatous Leprosy
raised lesion Satelite lesions Annular / Inverted Saucer Ill defined lesions 100s of ill defined lesions
m/c in India

Less number of lesions More number of lesions

Well defined lesions with Ill defined lesions
raised margins More nerves involved
More CMI Less CMI
Single thickened nerve Slit skin smear positive
Slit skin smear negative Sensations present
Anesthetic lesions Foam macrophages and Grenz
Tuberculoid granulomas zones (clear spaces)

Lucio type
Shiny skin with loss of hair follicles
Diffuse form of leprosy

Lucio phenomenon in Leprosy is

ulcerative type 2 leprae reactions.

Indeterminate type Histoid type

Commonest presentation in children Nodules in lepromatous type
No nerve thickenings Variant of LL with good CMI
Skin smear and lepromin test are normal
Lazarine type
Usually self limiting (can progress to
Nodulo-ulcerative lesions
other forms)
Seen with immunocompromised/HIV
D/d : Pityriasis Alba
 National
leprosy
Eradication 0-5 >5
program 0-1 >1
-ve +ve
Leprosy was eliminated in 2005 6 months 12 months
Elimination level : < 1 /10k population
NIKUSHTH is an online portal
R Rifampicin (600mg oams)
for leprosy patients D Dapsone (100mg daily)
C Clofazamine (300mg oams + 50mg daily)
OAMS : Once a month, supervised

Pink blister used for both pauci and multi bacillary

Most effective is Rifampicin
Clofazimine has a side effects of reddish black
discoloration of skin
Clofazimine induced discolouration

Lepra reactions
TYPE 1 TYPE 2
Strong CMI against M. leprae in aka erythema nodosum leprosum.
tuberculoid type (type 4 In lepromatous types, type 3
hypersensitivity reaction) hypersensitivity reaction.
Within 12 months of onset of MDT New lesions are seen
Pre existing lesions become red, Systemic signs of inflammation are
swollen and tender common (fever, arthralgia, orchitis)
Associated with tender neuritis. DOC : Steroids
T/t : Topical or systemic steroids Most effective: Thalidomide
along with painkillers. (teratogenic, reserved for severe cases) Phocomelia/ flipper baby
due to thalidomide

Tender, raised pre-existing lesion New nodular lesions

 Veneral Diseases
Genital Lesion

Painful Painless

Vesicular Chancroid Hard Chancre Beefy red Painful

eruptions (ulcer + regional LN) (ulcer + regional LN) ulcer inguinal LN
HSV 2 Hemophilus Ducreyi Syhphilitic chancre Granuloma Inguinale Lympho Granuloma
(Donovanosis) Venerum

Tzank cells Du"Cry"i DOC : Penicillin Klebsiella Granulomatis Caused by Chlamydia

(multinucleate cells DOC : Azithromycin White/blue kit (Calymmatobacterium Inginal buboes seen
with inclusions) White/blue kit granulomatis) DOC : Doxycycline and
Red Kit Safety pin shaped Donovan Azithromycin
bodies Black kit
No lymphadenopathy but
pseudo-buboes can be seen
Safety bin bodies (due to Granuloma formation)
1. Yersinia Pestis DOC : Azithromycin
(waYson's test) White/blue kit
2. Donovanosis
(Donovan bodies)

Differential diagnosis of vaginitis

Bacterial vaginosis Trichomoniasis Candida vaginitis
Diagnosis (Gardnerella vaginalis) (trichomonas vaginalis) (candida albicans)

Thin, off-white Thin, yellow-green Thick, cottage

discharge Malodorous cheese discharge
Examination Fishy odor Inflammation Pruritis
No inflammation present Inflammation
(strawberry cervix) present

Amsel's Criteria
1. pH > 4.5
2. Clue cells pH > 4.5 Normal pH (3.8-4.5)
Laboratory findings Motile trichomonads Pseudohyphae
3. Positive whiff test
(amine odor with KOH)

Metronidazole or Metronidazole;
Treatment Fluconazole
clindamycin treat sexual partner
 Syndromic management of STI

Vaginal Discharge
Urethral Discharge
Urethral discharge symptoms
Purulent or mucoid discharge
Genital complaints by sexual partners
Pain or burning while passing urine
KIT 1 Increased frequency of urination KIT 2 Low back ache

Systemic symptoms like malaise, fever *Rule out pregnancy

*Treat symptomatic partners

Cervical Discharge Tab. Secnidazole OD Stat

Tab. Azithromycin OD Stat
Urethral discharge symptoms for Bacterial vaginosis and
for Chlamydia
Genital complaints by sexual partners Trichomoniasis
Tab. Cefixime OD Stat Cervical discharge VS vaginal
Low back ache Cap. Fluconazole OD Stat
for Gonorrhea discharge based on discharge's
*Rule out pregnancy for Candidiasis
Quantity
*Treat symptomatic partners Color
3 conditions treated Rachel Green Odour
so GREAT kit Painful scrotal swelling
Urethral discharge symptoms
Pain and swelling of scrotum

Non herpetic Genital ulcer Herpetic Genital ulcer

Genital ulcers or vesicles
Painful or painless genital ulcer
Painful and recurrent
KIT 3 Burning sensation in genital area
Burning sensation in genital area
Enlarged lymph nodes KIT 5

Inj. Penicillin for Syphilis Tab Acyclovir TDS for 7 days

Tab Azithromycin OD stat
for other ulcers
Peaceful White when
Herpetic lesions are
done in single dose
painful and RED

Allergy makes you BLUE

KIT 4

If Allergic to penicillin Treat ALL SEXUAL PARTNERS for No partner treatment needed
Azithromycin (Single dose) past 3 months
Doxycycline for 15 days

Lower Abdominal pain

Lower Abdominal pain
Inguinal Bubo
Cervical motion tenderness Painful swelling in inguinal
Lower back ache region
KIT 6 Dysmenorrhea, dyspareunia, KIT 7 H/o genital ulcers or discharge
dysuria, tenesmus Systemic symptoms like fever
Menstrual irregularities
Cefixime OD Stat Vaginal discharge Azithromycin stat
Metronidazole 14 days Fever Doxycyline for 21 days
Doxycycline for 14 days

Treat ALL SEXUAL PARTNERS

Ye-LOW Treat MALE PARTNER with KIT 1 Black bubo for past 3 weeks
 Disinfection and Sterilisation
Sterilisation : Spores are killed
Disinfection : Most of microbes are killed such that it won't pose a threat to health

Physical methods of Sterilisation Chemical methods of Sterilisation

1. Radiations (Cold sterilisation) Control : B Pumilis Aldehydes
2. Heat (dry/moist) 2% Glutar-aldehyde (aka Cidex)
Used for scopes and metal instruments.
Ethylene Oxide
Gas
Used in cardiopulmonary machine
Dry Heat Moist Heat
Control : B AtrOpheus (old name GlObigi)
Hot air oven 160 ° C for 2 hrs Hydrogen Peroxide
Glassware aka Plasma Sterilisation
Sharp surgical instruments Used for wound cleaning
Arthroscopes and ureteroscopes
Control : B. Subtilis Subtle hot air

< 100 ° C 100 ° C > 100 ° C

Pasteurisation Tyndallisation Autoclave

Ton-dallisation 121 - 15 - 15
Doesn't kill Coxiella Burnetti
Holder : 63° for 30 mins Intermittent at 100°C Steam under pressure
Flash : 72° for 20 secs for 3 days 121 ° C for 15 mins at 15 psi
Culture media (except LJ & LSS),
"Hold her" for 30 mins at 63 rubber and sutures (except
Steam sterilisation Chromic catgut)
Inspissation Control : B. Stearothermophilus
Intermittent at 85°C for 3 days
LJ media and Loeffler serum slope
Inspi Eighty

Methylene blue reductase test Anatomical wastes

done prior to pasteurisation to check quality of milk. Chemicals/ Microbiology/ Vaccines
Soiled linen / Gauge
Expired cytotoxic drugs

Incinerated 🔥
Levels of disinfection
How level disinfection
Used for general cleansing Red → R → Rubber
Chlorhexidine, quat. ammonium compounds
Doesn't kill TB Bacteria

🦷
Intermediate level disinfection Puncture Proof (for sharps)
sharp white tooth
Used for wound cleansing
Alcohol, phenol, halogens
Sodium hypochlorite is best for blood spills Glass and Implants
Doesn't kill Spores
Blood bag : Yellow (anatomical waste)
Urine bag : Red (rubber)
 Miscellaneous
Antigenic drift : Small mutations accumulated over life in a virus (endemic) drift slightly
Antigenic shift : Reassortment of 2 viral genes in a host cell to form a 3rd (pandemics) shift completely

Bioterrorism agents
Category A : Easy dissemination, high mortality - Anthrax, Plague, KFD, Yellow fever
Category B : Moderately easy to disseminate, low mortality
Category C : Emerging pathogens (high mortality and easy dissemination) - Nipah, Hanta, Corona

Precipitation curve

Prozone Postzone
Excess antibody Excess antigen
CHAPTER 8
PREVENTIVE AND
SOCIAL MEDICINE
Epidemiology - definitions

Agent

Agent
Envir-
Host onment Causative factors.
Risk factors
Env. exposures
Epidemiological triad
Time
Incubation
Disease duration
time in triangle Envir-
Trends
Agent
Host onment
Time Person characteristics Place characteristics
Group and population Biological, physical and
Envir-
Host onment demographics psychosocial environments

Epidemiological triangle Advanced Epidemiological triangle

First case in community: Primary case

First observed case: Index case (observed is index, vowels stick)

Time between primary and secondary case: Serial interval

Time between entry of organism and symptom: Incubation period
Time between entry of organism and max communicability: Generation time

Isolation: For diseased

Quarantine: Healthy individuals (quarantine period = incubation period)
*QP of Yellow fever: 6 days (Yellow has 6 letters)

Health indicators:

1. Virulence (killing power) of disease - Case fatality rate (it's a proportion)

Death
_____ (due to a certain disease)
Affected

2. Communicability of disease - Secondary attack rate

No. of new cases

_______________________ (within 1 incubation period)
No. of susceptible individuals

Father of epidemiology : John Snow

Definition of epidemiology : John Last
We define at last
Epidemic trends

Point source Point source Propagated epidemic Interrupted epidemic

single exposure multiple exposure

Disease control
NVBDCP
CONTROL (National vector born
No more a local health problem disease control program)

ELIMINATION
Interruption of transmission Diseases Eliminated
1. Guinea worm aka Dracunculiasis NTEP
Elimination levels 2. Leprosy (National TB
Leprosy: (< 1 case/10,000 population) 3. Yaws elimination program)
Neonatal tetanus (< 1 case/1000 live births) 4. Neonatal tetanus

NLEP
ERADICATION Diseases Eliminated
(National Leprosy
Removal of organism "globally" 1. Small Pox (8 May, 1980) eradication program)

Disease Surveillance
Disease Surveillance

Passive surveillance Active surveillance Sentinel surveillance

Patients in hospital Disease actively Targeted approach to
searched in community find out missing cases
1. Polio : SMO Done for HIV AIDS
(Surveillance medical officer)
Once in 2 years
2. Malaria : Male MPW
Data collected from 8
3. Kala Azar
high risk groups
4. TB : AASHA
1. Pregnant women
(can be opted out)
2. Female sex workers
Polio (AFP) Surveillance 3. Men having sex with men
Done by SMO (Surveillance medical officer) 4. IV Drug abusers
Children 0-15 years checked for flaccid paralysis 5. Transgenders (Hijra)
2 stool samples (24-48 hrs apart) are sent using 6. Single male migrants
reverse cold chain 7. Long distance truck drivers
8. Inmates at Central prison
Natural course of a disease

Pathologic Lead time Usual time

changes of diagnosis Lead time bias
Patient feels he/she has
Onset of been diseased for longer
duration due to early
Exposure symptoms
diagnosis in lead time

Stage of Stage of Stage of Stage of recovery,

susceptibility subclinical disease clinical disease disability or death

Levels of Prevention
Healthy 18 year Healthy 50 year Diabetic 50 year Dressing of diabetic
old doing yoga old doing yoga old doing yoga foot disease

Primordial Primary Secondary Tertiary

No risk factor prevention Risk factor Disease Disability
prevention prevention prevention

Health education Health promotion Early diagnosis Disability limitation

(lifestyle modification) (Screening) Rehabilitation
Specific protection Treatment Eg.
(vaccination) Crutches
Spectacles
Physiotherapy
Prophylaxis and prevention- Primary
Screening and treatment- Secondary

Vaccines - Primary
Post-exposure prophylaxis - Primary
BCG for ca. of UB - Secondary (treatment)
Contraceptives - Primary
OCP for PCOD - Secondary (treatment)
Physiotherapy for polio - Tertiary
Chemoprophylaxis in contacts - Primary
Mosquito repellants / Nets / DDT - Primary
IFA in pregnancy - Primary
Fetal USG - Secondary (screening)
Seat belt/ helmet : Primary

"Check if the procedure is preventing or treating/screening"

Prospective screening : Primary (screening for others, eg screening of blood in blood bank for HIV)
Prescriptive screening : Secondary (screening for oneslef)
 Epidemiological Studies
1. Descriptive : Formulate a hypothesis (eg. case reports, case series)
2. Analytical : Test that hypothesis
3. Experimental : Confirm the hypothesis
"DAE" (similar to steps of PCR)

Analytical Studies

Population based Individual based

Ecological studies
Cross-sectional studies Case Control studies Cohort studies
(aka aggregation studies)
(aka Prevalence studies) (Retrospective study) (Prospective study)
Uses 2° data (data from records) aka snapshot study
Ecological fallacy seen here "Case ho gaya" Observing a
Uses 1° data kaise hua? cohort
(If a school has high average test
scores, assuming every student in Start with a disease and aka Incidence study
that school is above average look for exposure Starts with exposure and
would be an ecological fallacy) Best study for multiple look for disease
exposures Best study for multiple
Best for rare diseases outcomes
Odds Ratio (ask the person what had Relative risk and
he done to get such a attributable risk is
Also known as cross product ratio
rare disease) calculated
From case control studies "Control the odds"
Odd's ratio is calculated Associated with long
Bias involved are duration of study and
1. Recall bias attrition (drops outs)
2. Selection bias Bias involved are
(selecting a control) 1. Hawthorne bias
3. Berkesonian bias (change in behaviour
(when study sample is while being observed)
from hospital only)
Relative risk Co-Hawth studies

From Cohort study

Retrospective cohort
Incidence in exposed Ie Go from exposure to disease (cohort)
The study is based on data already collected,
Incidence in non exposed Ine hence retrospective.
Eg. Checking records of hospitalised TB patients
(TB is exposure) for those who developed
pericarditis (disease).
Attributable risk Benefit : Saves time
the proportion of a disease that can be attributed to a
particular risk factor
Nested Case Control
Ie - Ine What percentage of Lung Cancer Its a prospective study (case control) done on a
Ie
is due to smoking? defined cohort.
Done for rare/expensive investigations

Population Attributable risk

the proportion of a disease in a population that is caused
by a specific risk factor
If smoking was eliminated, what
Itotal - Ine would be the decrease in lung ca.
Itotal in population.?
 Experimental studies
Blinding
done to remove bias
1. Single blinding : Only patient
Randomised controlled trials (RCT) Non randomised 2. Double blinding : Patient & doctor
3. Triple blinding : Patient, doctor
Randomisation eliminates eg. Field trials, and epidemiologist
selection bias community trials
Randomisation is heart of RCT Blinding doesn't remove confounders
Randomisation also removes
confounders
Eg. Clinical drug trials

Clinical Drug Trials

Stage 1 : Healthy volunteers, safety checked (pharmacokinetics checked)
Stage 2 : Patients (small sample), efficacy checked (max drug failure )
Stage 3 : Patients (large sample, RCT), checked if improvement over existing drug.
Stage 4 : Post marketing trial, for long term adverse effects

Confounders and Effect-modifiers

Confounding
Confounder is related to both risk factor and the disease. Matching is best method to eliminate
Smoking is confounder here in the example known confounders
Solution : Stratifying study into smokers and non smokers Methods to eliminate known +
unknown confounders include :
1. Randomisation
2. Stratification (separate smokers from non
smokers)
3. Restriction (restrict smokers from trial)
4. Stratified randomisation
5. Multivariate analysis/ Statistical modelling

Effect modifier
Effect modifiers increase the strength of association of risk factor with the disease
There is no solution to manage effect modifiers
In the following example, being male is an effect modifier
 Sensitivity and Specificity of a test

"Always make a table and keep disease on top" Screening test : Test with high sensitivity
Confirmatory test : Test with high specificity

Disease (+) Disease (-)

Sensitivity Specificity
a b a
Tested (+) True Positives False Positives PPV = Ability to identify Ability to identify those
a+b those with the disease without the disease
(TP) (FP)
aka true positive rate aka true negative rate
c d
Tested (-) False Negatives True Negatives d
NPV =
(FN) (TN) c+d
PPV NPV
Probability that a Probability that a
person tested positive person tested negative
Sensitivity Specificity
actually has the disease actually doesn't have
a d aka pretest probability the disease
a+c b+d

PPV Prevalence
A B C Sn 1/Fn
Sp 1/Fp

Sensitivity decreases if tests in series & vice versa.

Specificity decreases if tests in parallel & vice versa

"Series of stimuli makes you less sensitive towards it"

Bland Altman analysis

Higher specificity for threshold C (100%) > B > A
Higher sensitivity for threshold A (100%) > B > C Comparing newly developed test
Threshold for perfect test : B with the gold standard

Incidence and Prevalence

Incidence Prevalence -
It's a rate Its a proportion -
New cases /unit time Cases/population × 100
-
Prevalence in a period of time
(Incidence X Duration)
Types of Data

Data

Qualitative Quantitative

Nominal data Ordinal data Interval data Ratio

No order or Order present Order present Order present
meaningful No meaningful Meaningful interval Meaningful interval
interval interval present present
eg. male/female, eg. TNM Staging, No true zero True zero present
urban/rural Likert scale eg. Temperature scales eg. Weight, BP, BMI

Measures of central tendency

1. Mean : Average Skewed data
2. Median : 50th centile
3. Mode : Repeats the max
Positively skewed Negatively skewed
Best measure of central tendency overall : Mean
1, 4, 8, 12, 2000 6, 800, 920, 990
Best for ordinal data : Mode
Mode Mode
Most affected in skewed data : Mean
Least affected in skewed data : Mode Median Median
Most useful in skewed data : Median Mean Mean

Mean follows skew tail (most affected by skewed)

Mode opposite to skew (least affected by skewed)
Standard distribution curve Median stays in between (most useful in skewed)
aka Gauccian curve

Mean = Median = Mode

Graphs

Pie chart Spot Map

Source of cholera in London was identified by

John Snow using this method

Need discrete Bars!!!

Bar Chart (discrete data)

Normal bar chart Multiple bar charts Composite bar chart

Continuous data

Histogram Frequency polygon Ogive

Continuous data Derived from histogram Similar to frequency polygon but
(don't confuse with bar graph) only take cumulative data
"Data that goes on giving is ogive"

Line chart

Shows trends of diseases over time

1. Seasonal trend : AGE in rainy, Heat stroke in summer, etc
2. Cyclical trend : Influenza pandemic occurs every in 7-10 yrs
3. Secular trend : Consistent rise as in NCDs or consistent fall as
in TB/Polio
 Box and Whisker chart
Data divided in 4 quartiles
Median
⬇️

Normal distribution in box and whisker chart

Data interpretation using box and whisker chart Skewed distribution in box and whisker chart

Correlation Coefficient (r)

r = -0.8 r = -0.4 r=0 r = +0.4 r = +0.8

Strong negative Weak negative No Weak positive Strong positive

correlation correlation correlation correlation correlation

Goes downward : Goes downward : Randomly Going upwards : Going upwards :

negative negative scattered positive positive
Concentrated : Dispersed : Dispersed : Concentrated :
strong weak weak strong
Evidence based medicine
Father of evidence based medicine : David Sackett

Systematic Reviews
"Focused question" formulated
Literature is searched through
Meta analysis not compulsory

Meta Analysis
Summarise "quantitative" results
All data collected from systematic
review is analysed and compared.
Results depicted in a Forest Plot

Forrest plot

Forrest plot interpretation

Funnel plot
Publication bias
insignificant result Line of significant result
Insignificant results don't get
no effect
published as frequently as the
(Odds ratio = 1)
significant results.
Significant result can be either Odds ratio >1 (causative)
or <1 (protective) based on the study.
Size of the box denotes weight of the study (more the
sample size, more the weight)
The whiskers denote confidence interval
The shape ♦️ denotes summary from all studies
Alpha and Beta errors

Null hypothesis (H⁰)

First step is to formulate a null hypothesis
For a drug trial, null hypotheesis would be "New drug is not better than existing drugs"
Its considered true as long as it's not proved wrong based on experimental data

Errors
1. Rejecting null hypothesis when it's not proven wrong by data : Alpha error (Alpha researcher overconfident)
2. Accepting null hypothesis even when it's proven wrong by data : Beta error (Beta researcher underconfident)
Alpha error is a more dangerous error (alpha males are more dangerous)

P value
The probability of alpha error in the study
P value must be <0.05 or 5%
Confidence level = (1-P) ; shall be 95%

Power of study
The power of study = 1 - ß error
Can be increased by increasing sample size, precision

Standard error
Deviation : How far away a value is from mean
Variance : Mean of square of deviations of all variables (shows spread of data)
Standard deviation : Squared root of variance
Standard error : SD/√n (difference of sample mean from population mean) n-1
n = sample size
If sample size is large, n can be
used instead of n-1
Standard error
__
√__
SD
n
Confidence Interval
The confidence interval of study = Mean ± 2(SE)
Confidence interval includes 95% of the data in study

__
Standard error of proportion

√P(1-P)
__
n Confidence interval ?
Mean ± 2SE
= Mean ± 2(SD/√n)
= 25 ± 2(10/√400)
= 25 ± 2(1/2)
= 24-26
Precision and Accuracy

Precise Precise Not precise

Not accurate Accurate Not accurate

Precision (reliability) Accuracy (validity)

The consistency and reproducibility of a test. The closeness of test results to the true values.
The absence of random errors in a test. The absence of systematic error or bias in a test.
Higher precision decreases standard deviation

Sampling

Simple random sample

Cluster sampling done to

Check immunisation
coverage

Snowballing done for

Judgement Sampling
IV drug abusers
STI patients
 Tests of significance
What are they asking in question?

Comparing mean of data sets Data is in a tabular format, eg 2X2

T test ANOVA Fischer exact test Chi-square test

2 data sets 3 or more data sets Small sample size Larger sample size
(n < 5)
Small fish

Paired T test Unpaired T test

Data is in before and Two sets of data are
after format independent

A study was conducted to assess the association between smoking status (smoker/non-smoker) and the
development of lung cancer (present/absent) in a group of 200 individuals. The following data was obtained:
Which statistical test would be the most appropriate to evaluate the association between smoking and lung
cancer?

A. Student's t-test
B. Paired t-test
C. Chi-Square test
D. ANOVA

A researcher is studying the association between a particular drug and the occurrence of an adverse effect in a
small sample size. The following 2x2 table represents the data collected:
Which statistical test is most appropriate to determine if there is a significant association between the use of the
drug and the occurrence of the adverse effect?

A) Chi-square test
B) Fischer's exact test
C) T-test
D) McNemar's test

A group of 50 hypertensive patients was started on a new antihypertensive drug. Their systolic blood pressure was
measured before starting the drug and again after 6 weeks of treatment. Which statistical test would be most
appropriate to determine if there is a significant change in the systolic blood pressure of the patients after 6
weeks?

A. Chi-square test
B. Unpaired t-test
C. Paired t-test
D. ANOVA
Health Indices

Individual Health index

Positive health indices Negative health indices

HALE DFLE DALY QALY

(Health adjusted (Disability free (Disability adjusted (Quality adjusted
life expectancy) life expectancy) life years) life years)
LE - (Poor health) aka Years lived with disability Quality years added to
Sullivan's index + life due to a certain
Years of life lost intervention
LE - (Disability)
Measures disease burden Measures cost effectiveness
of intervention

Population Health index

Human development Physical quality of Global Hunger

Index (HDI) life index (PQLI) Index (GHI)
Birth - School - Income 1 dead infant can't Everyone hungry
read or write

1. Life expectancy at birth 1. Infant mortality rate 1. Undernourished people

2. Knowledge (years of schooling) 2. Life expectancy at 1 year 2. Underweight children (<5 yrs)
3. Income (GNI per capita) 3. Literacy rate 3. Children dying before age 5
Demography

Determinants of demography Malthusian Model of growth

Birth
Death
Migration
Marriage
Social mobility

Rule of 70
Used to determine the number of
years it takes for a population to
double
Divide 70 by the population's
growth rate
This theory states that population grows exponentially,
eg. 1% growth rate : 70 years
thus out-growing a society's resources.
2% growth rate : 35 years

DEMOGRAPHIC CYCLE

Demographic Demographic
Trap Bonus

High Early Late Low

stationary expanding expanding stationary

Demographic gap = Birth rate - Death rate

Max Demographic gap = Stage 2
Min Demographic gap = Stage 5
Demographic trap = Stage 2 (Death rate falls, dependancy increases)
Demographic bonus = Stage 3 (Birth rate falls, dependancy decreases)
Developing countries : Stage 1 or 2
Developed countries : Stage 4
India : Stage 3
 POPULATION PYRAMIDS

Important formulae in Demography

1. Crude birth rate

No. of live births during the year

X 1000
Midyear population

2. Crude death rate

No. of deaths during the year

X 1000
Midyear population

3. Annual growth rate

BR -DR
______
10

4. Dependancy ratio
Population (<14, >65)
_________________
Population (14 - 65)
 Important formulae related to fertility

1. Gross fertility rate

No. of live births during the year

X 1000
Midyear female population aged 15 - 49 years
in the same area & year

2. Age specific fertility rate

GFR for a specific age.

No. of live births to women of age x

X 1000
No. of women of age x

3. Total fertility rate

Summation of ASFR for all reproductive age groups, in a particular period

age = 49
ASFR
age = 15

Best indicator to check impact of family planning program

Target TFR : 2.1 "Hum 2 humare 2"

4. Gross reproduction rate

Summation of ASFR for only female child birth.

5. Net reproduction rate

Estimation of how many girl childs will be born to a new born female based on mortality rates and ASFR
Best indicator to check growth of population
Target NRR : 1 (replacement level)

6. Contraceptive Prevalence Rate (CPR)

Percentage of women of reproductive age who are currently using at least one contraception method
Target CPR : > 60%

"Formulae with reproduction in name are

associated with female child birth"
 Mortality rates
1. Infant mortality rate

Infant death Infancy : Upto 1 year of life

× 1000
Live births

Best indicator for health status of country

2. U⁵ mortality rate All have live births as denominator

MMR has 1 lakh, everything else 1000
U⁵ death
× 1000
Live births

Best indicator for Social development

3. Neonatal mortality rate

Neonatal death
× 1000 Neonate : 0-28 days of life
Live births

4. Peri-natal mortality rate

Peri-natal death
× 1000 Perinatal period : 28 weeks POG to 7 days after birth
Live births

5. Still birth rate

Still birth
× 1000 Still birth : >28 weeks POG or > 1000gm
Live births

6. Maternal mortality RATIO

Maternal mortality RATE
Maternal death Has women in reproductive age
× 1 Lakh Still birth : >28 weeks POG or > 1000gm
Live births as denominator
Best indicator for Quality of healthcare services delivery

Other Important formulae

Literacy Rate
>7 yrs (can read/write/understand one language)
Population >7 yrs

Sex Ratio
Female
× 1000 "Female on top"
Male
Food adultrants

Neurolathyrysm
Spastic paralysis of lower limbs in adults
Toxic Bua eats dal
Toxin: BOAA (Beta oxalyl amino alanine)
Need Lathi to stand in Lathyrysm
Adulterant : Khesari Dal (Lathyrus Sativus)

Epidemic dropsy
Non-inflammatory, bilateral swelling of legs, with
Drops (fluid) everywhere in dropsy
diarrhoea, cardiac failure
The songs in Argentina and Mexico
Toxin: Sanguinarine
have the best drops
Adulterant: Argemone Mexicana (oil) in Mustard oil

Endemic ascites
Ascites and jaundice
Toxin: Pyrrolizidine alkaloids (Hepatotoxins) Pyrro - Croto
Adulterant: Crotalaria Seeds (Jhunjhunu) in Millets

Aflatoxicosis
Aspergillus flavus
Aflatoxin : Aspergillus
Aflatoxin in groundnuts, cereal, maize

Food standards

Indian Processed food

Food standards standards

International AGMARK
Food standards Agricultural products
standards
Reference male and female
Common for both male and female Energy requirements for reference male/female
Age : 19-39 yrs
1. Sedentary: 2100 / 1700 kcal
BMI : 18.5 - 22.9
2. Moderate : 2700 / 2100 kcal
Weight/height percentile : 95th
3. Heavy : 3400 / 2700 kcal

Weight
Male : 65 kg
21 - 27 - 34
Female : 55 kg 17 - 21 - 27

Pregnancy: +350 kcal

Lactation (0-6 months) : +600 kcal
Balanced diet
Lactation (6-12months) : +520 kcal
Carbs : 55% of total energy (4kcal/gm)
Fats : 30% of total energy (9 kcal/gm)
Proteins : 15 % of total energy (4 kcal/gm)

Obstetrics and Neonatal Care (ONC)

PHC CHC DH
ESSENTIAL ONC BASIC EMONC COMPREHENSIVE EMONC
1. Registration 1. All drugs 1. C-section and other surgeries
2. ANC 2. Manual vaccum aspiration 2. Blood transfusion
3. Safe delivery 3. Manual removal of placenta
4. PNC and newborn care 4. Newborn resuscitation

Antenatal Visits Postnatal Visits

WHO : 8 ANM : 3-4
Indian govt : 4 HBNC (Aasha) : 7
Ideal : 13-14 HBNC in institutional delivery : 6

Ideal Antenatal Visits Home based neonatal care (HBNC)

Once a month for 7 months = 7 Day 0 (skipped in institutional del)
Twice a month in 8th month = 2 Day 3
Once a week for 9th month = 4-5 Day 7, 14, 21, 28
Total: 7 + 2 + 4 or 5 = 13 or 14 Day 42
 Nutrition related programs

6
beneficiaries

6X6X6
Bi-weekly
strategy 20mg 100μg syrup
6 6 45mg 400μg Weekly
institutional
interventions mechanisms
Weekly
1. Prophylactic IFA tablets
2. Deworming
60mg 500μg Weekly
3. Anemia testing
4. Iron fortified food in public health programmes OD
5. Establishing year round behaviour that prevents anemia
(eg. delayed cord clamping) OD
6. Addressing non nutritional causes of iron def. such as
malaria, haemoglobinopathies and fluorosis.

Ministry of education

ICDS BENEFICIARIES
INTEGRATED CHILD 1. Government primary and upper primary schools
DEVELOPMENT SERVICES 2. Govt. aided Madarsas and maqtabs
Ministry of Woman and child development

BENEFICIARIES
Child : 0-6 yrs National nutrition mission
10-18yr adolescent girls Adresses "SULA"
15-49yr ovulating females Stunting
Pregnant, lactating females
Underweight <2% per year
LBW
Anemia <3% per year

Provides
Ministry of woman and child 1/3 of daily calorie requrement
development 1/2 of daily protein requirement

VILLAGE HEALTH NUTRITION DAY (VHND)

Conducted once a month
At anganwadi centres
Villagers interact with health workers
Maternal and Newborn Health Programs

JANANI SURAKSHA YOJNA JANANI SISHU SURAKSHA

Cash assistance with delivery and post-delivery care. KARYAKRAM (JSSK)
For pregnant women going to a public health
institution for delivery, entire cash entitlement is to be
disbursed to her in one go, at the health institution
Mother and newborn
care (upto 1 yr)
LABOUR ROOM QUALITY IMPROVEMENT INITIATIVE guidelines Ambulance services
from home and also for
To improve quality of care in labour room
referral
To reduce preventable maternal and new-born
Free delivery, drugs,
mortality, morbidity and stillbirths.
diagnostics.

Mother and Child Protection Card along

with Safe Motherhood Booklet
ANC for all pregnant women in their
second or third trimester by a
physician/specialist on 9th of every month
(in govt and private institutions)
Identification of medical conditions and
color coding
Green : No risk factor
Red : High risk pregnancy
Yellow : Diabetic, hypothyroid, STDs
Blue : PIH Post natal care till 6 months
Suman - Six

Child and Adolescent Health Programs

Till 18yrs of age Health Programme

Health Screening and for adolescents
Early Intervention services Age 10-19 years
4 "D" : Defect, Deficiency, Target their
Disease, Development nutrition,
delay reproductive health
In deficiencies : Vit C and & substance abuse,
Vit K not included Rashtriya Kishor among other issues.
Rashtriya Bal Swasthya no CK in SK Swasthya Karyakram
Karyakram

Early Free of cost Saathiya Salah app

Referral Launched under RKSK
screening management
 Other Government Health Programs

NACO Target
90% for
Diagnosed
National TB elimination program Treated NATIONAL VECTOR BORNE
Virally suppressed DISEASE CONTROL PROGRAM
World TB Day : 24th March
🦟
Improved quality of life
2024 theme : Yes ! We can end TB
6 diseases covered
NTEP targets
90% redñ in TB death Anopheles Aedes Culex Sandfly
Malaria Dengue JE Kala Azar
80% redñ in TB incidence Filariasis Chikun.
Reduce catastrophic cost to 0 by 2025

Akshya :
Improve access to quality TB care
Sankalk Early detection
NACO's annual booklet and response
Publishes national AIDS to outbreaks
response status Strengthen
National laboratories
Leprsoy Strengthen
technology to
eradication
INTEGRATED DISEASE collect and
program process data
SURVEILLANCE PROGRAM

5 lakh insurance
Cashless
treatment in
NATIONAL IODINE DEF. govt/private
DISORDER CONTROL PROGRAM hospitals
No limit on
Targets
age/members/
Survey and reduction of
type of illness
Nikushth : Online portal for Leprosy pt. goitre
Iodine fortified in salt PRADHAN MANTRI (PM)
Nikshay : Online portal for TB
Nischay : Urine pregnancy test Consumer level >15ppm JAN AROGYA YOJNA (JAY)
Manufacture level >30ppm

National Initiatives for improving

Quality of Public Health Facilities

KAYAKALP PROGRAM
Promote cleanliness,
hygiene and infection
control in health care
facilities.
MENTAL HEALTH ACT 2017
Decriminalisation of suicide
Child < 3 years not be separated
from mentally ill mother NATIONAL QUALITY
Ujala : 20 W LED bulbs
Free treatment for mental illness
Ujjwala : Safer fuel Fair treatment to mentally ill
ASSURANCE SCHEME
Advance directive for t/t and
Ujja-wala : Human trafficking
nominees.
 NATIONAL PROGRAMME FOR CONTOL OF
BLINDNESS AND VISUAL IMPAIRMENT

Blindness : <3/60 in better eye

can't see 360
Aim of NVBDCP : Blindness <0.3 %
Measure of output : Successful cataract
surgeries causing vision restoration
Reach in approach :

VANDE MATARAM SCHEME

Safe motherhood services
Included under JSY
 Immunisation
Intensified mission indradhanush (12 VPDs)
Birth OPV - 0, BCG, Hep B Delayed immunisation
OPV, Penta, Rota 1 6 PCV 1, IPV 1 Upto 1 year : Everything in birth and 6-10-14
OPV, Penta, Rota 2 10 except OPV (5 years)
OPV, Penta, Rota 3 14 PCV 2, IPV 2 Upto 5 years : MR, Vit A, OPV (JE for 15 years)
Vit A, MR, JE - 1 9- 1yr Booster (PCV) Upto 7 years : DTP (pertussis component)
Vit A, MR, JE - 2 16- 2yrs Boosters (OPV, DTP) Upto 15 years : JE
Vit A - 6 monthly till 5 years of age 5-6yrs Booster (DTP) No limit for Td and TT
10yrs Td
16 yrs Td
Pregnant Td (2 doses in 4 months) Vitamin A
or Start at 9 months with 1 lakh
Td single dose, if had 2 Then 6 monthly 2 lakh (5 years)
doses in last 3 years Total : (2 x 4 x 2) + 1 = 17 lakhs

* JE Vaccine in endemic states only

OPV : 2 💧
Rota : 5 💧 OPV
IM Rota BJ
Vit A
IPV (i/d) ID : 0.1ml BCG (i/d)
MR (s/c) SC : 0.5ml
0.5 ml JE (s/c) Live
IM IM
: 0.5ml

Penta
DTP
PCV
Hep B
IM (anterolateral mid thigh)
JE killed
All IM (anterolateral mid thigh)

Vaccine vial monitor Shake test

For heat sensitive vaccines For freeze sensitive vaccines

Can use do not use

Dil saaf hona chahiye

Heat sensitive vaccines Freeze sensitive vaccines

rBCG > OPV > VZV Hep B > DTP
So hot BrOV! HD

Open Vial Policy Diluents

Measles : Water MW
Reuse of partially used multi dose vials till 28 days BCG : Normal Saline
Not appliacble for Measles, BCG, Rota, COVID, Yellow fever MB CRY JE : PBS (Phosphate Buffered Saline)
 Killed RIP ACE
Rabies
Influenza
Polio (IPV) - Salk
Hep A Hep B vaccine is recombinant
Cholera (Dukoral)
Encephalitis - Japanese (Nakayama Beijing strain)
Nakayama killed his legs in Beijing Olympics

Live
IM BJ except IPV Vaccine with max occurence of adverse effects : MR
All oral vaccines (OPV, Rota Typhoral)
Measles has highest mortality amongst the VPD
Varicella vaccine
Only immunisation done after a disaster
Yellow fever (17 D) Only live vaccine not CI in pregn.

Minimal interval between 2 live vaccines Adverse event following immunisation

Either on same day or 1 month apart MR : TSS, Thrombocytopenia
So that it's doens't affect immune response
Rota : Intussusception
Influenza : GBS
Polysaccharide Pertussis component of DTP : Inconsolable
Pneumococcal vaccine Cry, hypotonic-hyper responsive episodes
Meningococcal vaccine (ACWY) Post Spleenectomy Egg allergy : Yellow fever, Influenza
Hemophilus influenza
Inconsolable cry is not a contra-indication for further
Typhoid Vi
doses of DTP
Contraindication for further doses is Anaphylaxis
Toxoid
Diptheria Adjuvant in DTP : AlOH²
Tetanus Preservative in DTP : Thiomeral
Pertussis Causes inconsolable cry
Tetanus Vaccination
Td vaccine to all
(Skip if) > 3 doses with last booster in
5 years in unclean wound
10 years in clean wound
Polio Vaccination
Immunoglobulin for unlcean wound if < 3 doses or
Salk is killed and Injected, only humorall immunity.
unknown
Sabin oral and provides intestinal immunity along with humoral.
Oral vaccine responsible for VDPV Level of anti-toxin necessary in blood : 0.01
Polio has 3 strains 1 2 and 3 (Presently only strain 1 is circulating)

Rabies Vaccination
Category 1 (licks) : Wound cleaning
Category 2 (intact skin) : Vaccine
Category 3 (bleeding/bats) : Vaccine + Immunoglobulin
Vaccine
1. Essen (IM) 5 days : 0, 3, 7, 14, 28
2. Modified Thai (ID) 4 days : 0, 3, 7, 28
3. Pre-exposure : 3 shots P.R.E 0, 7, 21 or 28
4. Re-exposure : 2 shots R.E 0, 3
Immunoglobulin
Human Rabies Ig : 20 IU/kg
Equine Rabies Ig is cheaper, dose is 40 IU/kg
(more chances of anaphylaxis)
Ig is administered as close to wound as possible
Preferably taken on day of bite (can be administered
within 7 days)
Chlorination of water for disinfection
Cl² + H²O ⇌ HClO + HCl

Disinfecting action : Hypochlorous acid (HClO) Residual chlorine level needed

Contact period needed : 1 hour of residual chlorine Drinking : 0.5 ppm
Post disaster : 0.7 ppm
Breakpoint chlorination : chlorine demand of water is met Swimming pools : 1 ppm
Chlorine added after breakpoint chlorination is residual chlorine

tOluidine : tOtal chlorine

Chloroscope Ortho-toluidine test

Measures residual chlorine Free + Combined Chlorine

Horrock's Apparatus
Measures chlorine demand
6 white cups (water) and 1 black cup (contains chlorine)
Chlorine is added, 1 drop in 1st, 2 drops in 2nd and so on
Residual chlorine reacts with starch iodide to give blue color.
Number of cup showing blue colur : n
Chlorine demand = (n ×2g) for 455L of water

Water contamination

Recent contamination : Fecal streptococci Fluorosis

Remote contamination : C. Perfringens (has capsule, hence resistant)
< 0.5 : Dental cavities
Best test to confirm fecal contamination : Detect coliforms (E-coli) 1.5 : Dental fluorosis dedh - daant
Multiple tube method used to detect coliforms. 3 : Skeletal fluorosis
In drinking water coliform count should be Zero 10 : Crippling Fluorosis Give ₹10 to a cripple

Most undesirable metal in water : Lead Nalgonda technique for removal of fluoride

Diseases related to water

Water borne : Feco oral transmission (Diarrhea, Typhoid) Water required per capita
Water based : Vector stays in water (Schistosomiasis, dracunculiasis) In urban : 150-200 Lt
Water related : Vectors born in water (NVBDCP diseases) In rural : 40 Lt
Water washed : With inadequate water causing poor hygiene (Trachoma, Scabies)
Hardness of water
Temporary hardness : HCO³ of Ca/Mg (escapes off as CO²)
Permanent hardness : Sulphate / Chlorides / Nitrates of Ca/Mg
Max hardness level : 150 ppm Some hardness is needed in water
Zero hardness makes water corrosive
Treatment of hard water
Boiling and lime removes temporary hardness
Soda ash, base exchange resins remove permanent hardness

Air

Katta thermometer Globe thermometer Anemo-meter Wind Vane

Initially designed for Radiant temparature Wind velocity Wind direction
cooling power of air
Now used to measure
low air velocity

AIR POLLUTION
Sulphur dioxide is best indicator of air pollution
Biological air pollution indicator : Lichen
Levels of CO² in air don't indicate pollution
Tropspheric Ozone (ground-level ozone) is a
Sling thermometer
secondary air pollutant
Baro-meter (Psychrometer)
Maximum green house effect : Water vapour > CO²
Air pressure Measure humidity
Soiling index : Smoke (air passed through thin
paper that gets "soiled")
Grit index : Dust

CPCB Air standards

AQI (air quality index) is used
Delhi : Severe (400)

Lichen
(symbiosis of algae and cyanobacteria)
Light, Sound and Miscellaneous
Luminous intensity (brightness) : Candela
Rate of light emission (flux) : Lumen
Total light on surface (illuminance) : Lux
Luminous candle Lux soap on skin SURFACE

Tolerable sound level : < 90 db

TM rupture : 150 db
150 compiled
1. Max hardness of water : 150 ppm
Per capita space in house: 80 sqft
2. Water per capita in urban area : 150 -200 L
Doors + Windows : 2/3 of total floor area
3. TM rupture : 150 db
4. RDA of Iodine in adults : 150 mcg (250 in preg)
0)
s s i (8
A e
hud
cha .
..

SANITARY LANDFILL
aka Controlled tipping
Best method for solid waste disposal
Uses either Trench/Ramp/Area method
Area requirement : 1 acre for 10,000 people

Occupational diseases
1. Bysinnosis: Cotton dust (Monday chest tightness)
2. Baggasosis : Sugarcane (thermoactinomyces sacchari)
3. Anthracosis : Coal (can lead to massive pulmonary fibrosis)
4. Silicosis : TB/ most common / mcc of disability / mcc of death (amongst occ. disease)
5. Asbestosis : Lung cancer, mesothelioma (base of lung)
Health Communication
One-way talk : Lecture
Talks series by experts with Q and A : Symposium Series of talks
4-8 experts in front of audience with Q and A : Panel discussion Expert panel
6-12 people (not experts) discussing : Focused group discussion
Practical skills teaching : Workshop
Step by step enactment : Demonstration
Photograph pasting : Flannel graphs (flannel : Khaddi), "Pictures pasted on a stretched piece of Khaddi"

Disaster management

Prepare for the

disaster

Take steps to reduce the

negative consequences of
disaster

MC disease : Gastro-enteritis
MC vitamin deficiency : Vitamin A (fat absorption affected in GI disorders)
MC zoonotic disease : Leptospirosis
Vaccines to health workers : Typhoid/ Cholera/ hepB
Only vaccine which can be given in outbreak : Measles
Most crucial preliminary step : Chlorination of water
Nodal ministry : Ministry of Home affairs
Protocols
CAGE : Alcohol
Stop BANG : OSA (Stop bang fat)
INSPIRE: Child abuse (Inspired to not abuse children)
Spikes : Bad news (yikes)
Gather : Contraceptive plan, Cafeteria approach (gather contraceptive in cafeteria)
Scoff : Eating disorders ( Scoff : To eat something hurriedly)

PHC

Components of PHC "ACE I" Elements of PHC

1. Appropriate tech (Shakir tape, vaccines) Basic treatment
2. Community participation (AASHA workers) Drug availability
3. Equitable distribution
Maternal and child health
4. Inter-sectoral coordination
Vaccination (immunisation)
Prevention of endemic diseases
4 essential As of healthcare
1. Available Nutrition
2. Accessible Sanitation
3. Affordable Education
4. Acceptable

Planning cycle
1. Analyse the health situation : How much do I know?
2. Set objective and goals : NEET PG 2025
3. Assessment of resources : Marrow, Cerebellum, Prepladder, BTR
4. Prioritise : BTR
5. Formulate a plan : Follow Mam's plan
6. Program and implement : Start studying
7. Monitor : Grand tests
8. Evaluate : GT Review Community Health Centre (CHC)
A 30 bedded Hospital
Referral unit for 4 PHCs

Primary Health Centre (PHC)

Referral unit for 4-6 SC
4-6 bedded
MO in - charge
14 paramedical staff

Sub Centre (SC)

Most peripheral contact point of community
with Primary Health Care system;
One MPW(M) and MPW(F)

Village Level
Village level appointed health workers
ASHA, Anganwadi, Dai, local health worker
Acts - Ministry of Labour

Employees' State Insurance (ESI) act -1948 Factory act -1948

1. Sickness benefit Age < 14 years not allowed
70% salary for 3 months 7+3=10 500 ft³ per capita space
2. Extended sickness benefit (extended time) For 1000 workers 1 safety officer
80% salary for 2 years 8+2=10 48 hours per week

3. Enhanced sickness benefit (Enhance : body modification) Factory act not applicable to
Full wage for 1 week in vasectomy 1 tube 1 week Defence
Full wage for 2 weeks in tubecomy 2 tubes 2 weeks Mining
Railway
Split of premium Eateries
4% of salary
Employee pays 0.75 %
Employer pays 3.25 %

Split of coverage ESI not applicable to

Government pays : 1/8 Defence
ESI pays : 7/8 Mining
Railway

Maternity benefit : 6 months 100% pay

Funeral benefit : ₹ 15,000

School health
1 class : 40 students
Each child >10 sqft space
Class of 40, 60 pee, 100 poop
1 urinal for 60 kids
1 latrine for 100 kids
Door and windows, 25 percent of floor area
Minus type desks

Large windows
CHAPTER 9
DERMATOLOGY
 Layers of epidermis

Come Corneum
Stratum corneum Dead keratinocytes
Lets Lucidum
Stratum lucidum Go Granulosum
Sun Spinosum
Lamellar granules
Stratum Burn Basale
granulosum

S. Corneum
Keratinocyte Acellular (dead cells)
Flattened keratinocytes
Langerhans cells
No nucleus
Stratum
spinosum
S. Lucidum
Only present in palms and soles

S. Granulosum
Melanocyte
1. Keratohyaline granules produce filligrin
Merkel cell (defect causes Ichthyosis)
Stratum basale 2. Lamellar (Odland) bodies form a water
barrier (defect causes asteatotic eczema)
Sensory neuron
Dermis
"Dense irregular"
connective tissue
S. Spinosum
Thickest layer
Spinous process (Acanthocytes)
Desmoglein protein binds the
Desmoglein broken down acanthocytes
causes Acantholysis
APCs of epidermis, Langerhan's cells are
present in this layer.

Acanthocytes Seen in
Langerhan's cell
histocytosis

Desmoglein Birbeck Granules

Acantholytic cell (tennis racket shaped)

S. Basale (2 M)
1. Merkel cell : Touch receptor (slow
Primary acantholysis Secondary acantholysis adapting sensory)
Desmoglein broken down Ballooning of Keratinocytes 2. Melanocytes : Has dendritic processes
1. Pemphigus vulgaris (tzank cells) that supply keratinocytes
2. SSSS 1. HSV 1/2
2. Varicella Infections Epidermal melanin unit : 1 : 36
3. Darrier's disease
Epidermal turnover time : 28 + 28 = 56 days
4. Haley Haley disease
 Psoriasis
m/c type : Psoriasis vulgaris
Associated with Psoriatic arthropathy (DIP joint inv)
Scalp, trunk and extensor surfaces involved mostly
hyperkeratinisation of
epidermis and leaky
dermal vessels

Hyper + Parakeratosis

Agranulosis

Erythematous papulosquam. Psoriatic nails

Pustules of Kogoj
rash with silvery scales Irregular pitting
(Hallmark of Psoriasis) Oil drop sign
Sub-ungual Rete ridges
"Regular nail pitting seen in hyperkeratotis
Alopecia areata" Salmon patches

Parakeratosis + Hyperkeratotis
Grattage test
Munro's microabscess (stratum corneum)
Scrap the lesion Stratum Granulosum absent (Agranulosis)
with a glass slide Pustules of Kogoj (stratum spinosum)
Petechial spots seen Rete ridges (elongation of epidermis into dermis)
(Auspitz sign)
Auspitz Sign :
pinpoint bleeding under the
Koebner's Phenomenon
skin's surface (Grattage test)
aka Isomorphic Phenomenon
Shown by LVP (Lichen Planus. Vitiligo, Psoriasis)
Pseudo-Koebner's shown by viral warts
Reverse Koebner's shown by Psoriasis
Types of Psoriasis

Chronic Plaque Guttate Pustular

psoriasis Psoriasis Psoriasis

Most common type h/o URTI h/o sudden steroids withdrawal

Involves extensor surfaces and scalp DOC : Macrolides DOC : Acitretin (Teratogenic : washout period of 3 years)
Management :
1. < 10% BSA : Topical steroids Pustular psoriasis in preg. : Impetigo herpetiformis
2. > 10% BSA : Methotrexate (DOC) DOC : Systemic Steroids (only indication of systemic
or Narrow Band UVB Inverse Psoriasis steroids in psoriasis management)
3. Gockerman Regime : Coal tar
(5hrs/day) + NB UVB
Follows a different pattern of distribution to chronic
plaque psoriasis.
It affects ‘Intertriginous’ areas - points where skin
touches/rubs together.
Scaling is absent in this type
Areas affected include the axilla, groin and genital area,
inframammary folds and gluteal cleft.
 Lichen Planus
Cause is multifactorial
(asso with Hep C and malignancies)
Females > Males
Oral lichen planus is the most common form.
Bilaterally symmetric lesions
Wickham's striae (Pathognomic)

Nail and Scalp involvement Wickham's striae: whitish lines, visible

within the lesion in a lace like pattern
Oral white patch
Planar (flat toped lesions)
Purple (violaceous)
Pruritic

Removed Not removed

Candida 1. Lichen Planus (rule out Hep C)
2. Oral hairy leukoplakia (EBV)

Pterigium of nails
1st line : Topical steroids
2nd like : Oral steroids
3rd line : Methotrexate

lichen plano pilaris

Scarring Alopecia

Lichen Nitidus

Hyperkeratotis without Parakeratosis : Orthokeratosis

Ortho bro listening to LP
Hypergranulosis (Wickham's striae)
S. Basale degeneration : Max Joseph Space
Apoptotic cells : Civatte Bodies

Nodular lesions Hyper-granulosis

Claw catching a ball sign

Psoriasis Lichen Planus

1. Hyperkeratosis with 1. Hyperkeratosis without
parakeratosis parakeratosis (Orthokeratosis)
2. Munro's microabscess 2. Apoptotic Civatte bodies
3. Agranulosis 3. Hypergranulosis
4. Pustules of Kogoj 4. Max Joseph space
5. Rete ridges
Other Papulo-Squamous disorders
Pityriasis Rosea Pityriasis versicolor

Meatball on spaghetti
app. on KOH mount
Christmas tree pattern Herald patch

Starts with a mother lesion known as Herald Patch Hypo + Hyperpigmented lesions
Collarette (cigarette paper like) scales Fungal infection by M.Furfur
Christmas tree pattern Culture : SDA + Olive oil (lipophilic)
HHV 6/7 Fried egg colonies
Spares palm and soles on KOH mount : meatball on spaghetti 🍝 appearance
Reassure (spontaneous recovery) on wood lamp : Yellow

Christmas tree patterns Fried egg patterns

1. Colonies : M.furfur, Mycoplasma
1. Rash : P.Rosea
2. Appearance : Hairy cell Leukemia,
2. Cataract : Myotonic dystrophy
oligodendroglioma
3. Neurologic Urinary bladder

Ichthyosis

Ichthyosis

Ichthyosis X linked Lamellar

Vulgaris Ichthyosis Ichthyosis

Fishnet pattern over limbs Fishnet pattern Baby born with membrane
Antibodies against filligrin protein only over trunk (Colloidon baby)
in str. granulosum Membrane sheds off f/b
fishnet in trunk
 Bullous Disorders
Bullous lesion

Vesico-bullous disorders Mechano-bullous disorders

bullous lesion + h/o trauma EB Congenita : Newborn
Epidermolysis Bullosa EB Aquisita : Old age

EB Simplex Junctional EB Dystrophic EB

Keratin 5/14 Basement Dermis affected
Epidermal Dermal In epidermis membrane Laminin 322
tense bullae (Pemphigoid) Heals without scarring BP-180 Type 7 collagen
flaccid bullae, rupture easily

Chronic bullous disease of childhood Associated with celiac disease

Bullous pemphigoid
Linear IgA disease Dermatitis herpetiformis
Tense bullae + Pruritis (eosinophilia) Peri-oral/Peri-genital string of pearls Pruritis on extensor surfaces
IgG and C³ deposited at dermo- appearance IgA deposition in picket fence
epidermal junction Linear IgA deposition on IF fashion on IF
BPAg (Bullous Pemphigoid antigen) DOC : Dapsone DOC : Dapsone
Steroid pulse treatment
d/d : Zn deficiency which causes
Acrodermatitis enteropathica
(Peri oral/genital lesions + Diarrhoea)

St. Granulosum St. spinosum Other conditions showing

(Subcorneal split) (Suprabasal split) positive Nikolsky
No oral involvement Oral involvement 1. SSSS (Ritter's Syndrome)
Pemphigus foliaceous Pemphigus vulgaris 2. SJS and TEN Pseudo Nikolsky Sign
DSG - 1 involved DSG - 3 involved Flaccid bulla
Vulga3is Nikolsky sign (+)

Drug induced pemphigus

Occurs 1 year after taking the drug
Common drugs implicated are "PCR"
1. Penicillamine
2. Captopril
3. Rifampicin

Fishnet pattern on IF Suprabasal split

Rx of pemphigus vulgaris
IgG/C³ deposition Row of tombstones appearance
Pulse steroid treatment
 Pigmentation Disorders
Pigmentation disorders

Hyper pigmentation Hypo pigmentation

disorders disorders

Epidermal Dermal
Brown lesions Slate gray/blue (due to Tyndall effect)
On wood's lamp : Accentuation No accentuation on wood's lamp
Since it's blue, aka ceruloderma
[also a s/e of Amiodarone]

Melasma/Chloasma Chik's sign Becker's nevus

Increased estrogen/progesterone Seen in chikungunya Epidermal (brown)
stimulate melanocytes to cause nevus at back
hyperpigmentation. "becker - back"
1. Chloasma (mask of pregnancy) Associated with
GLOW in pregnancy - Chlo hypertrichosis
2. Melasma (photosensitive) seen
in non pregnant.

Mongolian spots Nevus of OTA Nevus of ITO

Seen in infants Ota : eye 👁️ 🧱
Ito - at back
Lumbo-sacral region No Hypertrichosis
Benign, reassure parents

White forlock Contact leukoderma Nevus anemicus

aka Chemical Leukoderma Due to vasoconstriction
1. Hydroquinone : Rubber in slippers α receptor dysfunction
2. PTBP (para tert. butyl phenol) : Bindi
3. Parabutyl Catechol : Hair dye
Heterochromia iridis Islands of sparing

Wardenburg Piebaldism
Syndrome (NCC migration defect)
AD transmission
Mutation in C Kit gene
Erythemas

Erythema Erythema
Nodosum Marginatum
Tender nodules on skin due to Transient lesions asso. with ARF
inflammation of s/c fat mARFginatum
Asso. with
1. Drugs : Sulfa drugs
2. Sarcoidosis (Lofgren sx)
3. IBD
4. TB
5. Behcet Sx

Erythema Migrans
Single and large target lesion on trunk
Earliest manifestation of lyme's disease
Borrelia migrates with lashing motility

Erythema
Multiforme
Typical target lesions on hand
Associated with
Infections Drugs
1. HSV (m/c) 1. NSAIDS
2. Mycoplasma 2. Chloroquine

Chloroquine also causes

Bull's eye maculopathy

Atypical target lesions

seen with SJS/TEN
Erythema gratum ripens
Para neoplastic syndrome associated
with adenocarcinoma
 Acne Vulgaris
Pathophysiology
1. Excess sebum production Most common trigger for acne is puberty.
2. Follicular plugging with sebum and keratinocytes During puberty, surges in androgens stimulate sebum
3. Colonization of follicles by an anaerobe Cutibacterium production and hyperproliferation of keratinocytes
acnes (formerly Propionibacterium acnes)
4. Release of inflammatory mediators

Comedones
Characteristic of acne

Treatment
1. Comedones: Topical retinoid (tretinoin)
2. Mild inflammatory acne: Topical retinoid + (Topical Benzoyl peroxide / Topical antibiotics)
3. Moderate acne: Oral antibiotic + topical therapy
4. Severe acne: Oral isotretinoin
5. Nodulo-Cystic acne (Acne conglobata): Intralesional triamcinolone

Rosacea
h/o triggers : emotional states, spicy food
Flushing
Telengiectasia
Nasolabial folds (+) d/d is Malar rash of SLE

Nasolabial folds involved Nasolabial folds spared

Rosacea Malar/butterfly rash of SLE

 Sweat Glands

Sweat glands

Apocrine Eccrine
Axilla, groin Everywhere else
Ass. with hair follicles (Causes miliaria when blocked)
Causes Fox Fordyce disease Fordyce spots seen on lips
when blocked Overgrowth of ectopic sebaceous glands
**Unrelated Fox Fordyce disease

1. Miliaria crystillina : Non inflamed

2. Miliaria rubra : Itchy, red
3. Miliaria profunda : Deep, large
papules/pustules

Hiradenitis Suppurata
Acanthosis Nigricans
Complication of fox fordyce dis.
aka inverse acne Marker of
Obesity and smoking are risk factors Insulin resistance/PCOD/T²DM
Treatment : Surgical Metabolic sx. , Obesity
GI adenoma
sinuses + induration

Ca2+ ATPase channel disorders

Associated with Desmoglein dysfunction
Example of primary acantholysis

Ca2+ ATPase channel disorders

Darrier's disease Hailey Hailey disease

2A2 2C1

Crop grains/ ronds V shaped nail lesion Raised erythematous H/P : Dilapidated brick wall
plaques in axilla appearance
A looks like V : 2A2

2 see 1 (2C1) hailey comet

break a brick wall

Longitudinal lines in nail

Alopecia
Hair Loss

Scarring Non Scarring

1. Discoid Lupus erythematosus 1. Tenogen effluvium (tension/stress/child birth)
2. Lichen planus 2. Anagen effluvium (chemotherapy)
3. Tinea Capitis 3. Trichotillomania (accessible areas)
4. Alopecia areata
5. Trichotillomania
2° Syphilis causes both scarring and non scarring
6. Androgenic alopecia

Alopecia areata Androgenic Alopecia

Autoimmune condition
Asso. with Type 1 DM, Hashimoto thyroiditis
"Going bald overnight"
Nails : Regular pitting
Exclamatory mark sign !
Male pattern Female pattern
aka Hamilton aka Ludwig
pattern hair loss pattern hair loss

TOC :
1. Minoxidil
No inflammation Lymphocytes around hair bulb 2. Finasteride
No scarring Swarm of bees appearance

Stages of hair growth

Trichotillomania
Shedding: Exogen
Psychiatric condition
(Impulse control disorder)
Hair loss from accessible
areas

90% hair in this Proximal hair

phase shaft keratinised. "ACT"
Clubbing

State of latency : Kenogen

Nails

Half and Half nails Terry's nail Muehrcke's nails

Seen in renal failure Seen in heart failure Seen in hypoalbuminemia
2 kidneys 2 zones Terry : Three (reversible with albumin infusion)

Koilonychia (Spoon shaped)

Seen in iron deficiency anemia

Wood's Lamp

Tinea Capitis : Blue - Green

Pityriasis versicolor : Yellow
Erythrasma : Brilliant coral red
Vitiligo : Bright white (milky)
Tuberous Sclerosis : Pale white

Uses UV-A light

Barium Silicate + NiO filter
Erythrasma
365 nm 365 days in a year Caused by Cornybacterium Minutissimum
 Dermatitis
Dermatitis

Atopic Contact
dermatitis dermatitis
aka Eczema aka Irritant dermatitis
Associated with high serum IgE levels More common in incidence over atopic
Family h/o atopy such as asthma or allergic dermatitis
rhinitis Can occur in anyone exposed to the irritant
Onset < 2 yr of age (mostly seen in children) Common irritants : Poison ivy, sumac, oak
Involves predominantly flexural aspect
Involves forehead and cheeks in < 4 yr

Patch test
For allergic dermatitis
Read at 48 hrs and 96 hours

Hives (Urticaria)
A skin rash triggered by a reaction to food, medicine or other irritants (allergic)
Can be acute or chronic (> 6 weeks)

Hives Dermographism (seen in chronic urticaria)

Skin Malignancies

BCC (Rodent ulcer) Pautrier's microabscess

Raised pearly nodules Seen in mycosis fungoides (Cutaneous T cell lymphoma)
m/c cutaneous malignancy Epidermotropism : Lymphocytic movement towards epidermis
Good prognosis Cerebriform nuclei
On H/E : true palisading When disseminated in blood : Scezary syndrome
T/t : Exctracorporeal photopheresis

True palisading

Cutaneous horn
Seen in actinic keratitis
Giant melanocytic nevus Hair present on the nevus Premalignant for Sq.cell carcinoma

Melanocytic nevus
Can transform into malignant melaoma Bowen's disease
Intra-epidermal sq.
cell carcinoma
Low potential of
invasive malignancy
Malignant melanoma Undergoes spont.
Most important resolution
prognostic marker is
depth of the melanoma
"Breslow's depth"
Seborrheic keratosis
Para neoplastic
syndrome
aka sign of Leser Trelat
 Neurocutaneous Syndromes

Neurofibromatosis type 1 Neurofibromatosis type 2

Associated tumors Features of melanocyte dysfunction Associated tumors

Meningiomas

Optic glioma Lisch nodules Early-onset

bilateral cataract Bilateral vestibular schwannoma
Axillary and inguinal
freckling Spinal tumors
(e.g., ependymomas)
Multiple café au lait
Pheochromocytoma spots Skin nodules
(e.g., schwannomas)

Bone involvement
Multiple neurofibromas (e.g. scoliosis,
bone dysplasia)

Tuberous sclerosis
Skin Brain

Hamartoma
Giant cell astrocytoma
Seizures
Intellectual disabilitiy
Adenoma sebaceum
Heart
Ash-leaf spots
(3 or more)

Cardiac
rhabdomyomas

Shagreen patch
Kidney

Renal angiomyolipoma

Renal cysts

Renal cell carcinoma

Ungual fibroma

Sturge Weber Syndrome

CNS

Leptomeningeal vascular
malformations, leading to:

Seizures All neurocutaneous syndromes show

Intellectual disability AD transmission
except
Sturge Weber Syndrome
Glaucoma

Stroke-like episodes
Port-wine stain (e.g., hemianopia,
(nevus flammeus) hemiparesis)
CHAPTER 10
OBS. & GYNAEC.
 Mullerian Anomalies
Initial Investigation : USG
IOC : 3D USG > MRI
Gold standard : Laparoscopy + Hysteroscopy (Diagostic + Therapeutic)

Presentation : Recurrent 2nd trimester pregnancy loss

D/d : Cervical incompetence

Mullerian anomalies

Diagnosed on HSG Need 3D USG or MRI

Bi-sep 💪🏻
Arcuate Didelphys Unicornuate Bicornuate Septate

Best reproductive Best reproductive Max assoc. with T/t : Metroplasty Most common
outcome outcome after renal anomaly (Straussman) mullerian anomaly
Not considered an arcuate Asso. with infertility
anomaly but a uterine Transverse lie not (worst outcome)
variant. possible T/t : Hysteroscopic
septum resection

Cervical incompetence
2 or more second trimester painless abortions. Purse string sutures
Pre-pregnancy diagnosis: No. 8 Hegar's dilator passes without resistance

Management in pregnancy
Uterocervical length < 25mm (only cervical Insufficiency): Only progesterone
>2 painless preg loss in T² : Prophylactic cerclage
1 painless preg loss in T² : USG in 18-24 weeks, if <25mm then prophylactic cerclage

Pre-pregnancy cerclage: Lash and Lash cerclage (Trans abdominal)

Cervical Insufficiency
1. T/Y shaped cervix 1. Shirodkar
2. Funneling of OS > 1cm 2. Mc Donald's
3. Utero-cervical length < 25mm 3. Worm's method
Removed at 37 weeks of pregnancy
 Reproductive Physiology
Follicular phase : Estrogen dominated
Granulosa cells produce estrogen (under FSH)
(from androstenedione produced by theca cells)
Endometrium starts proliferating (aka Proliferative phase)
Estrogen production gradually increases till 14th day
Estrogen peak (200pg/ml for 50 hrs) leads to LH surge ➡️ Ovulation

Luteal phase : Progesterone dominated

Corpus Luteum produces progesterone (under LH)
Basal body temperature increases
Endometrial gland thickening (aka Secretory phase)

Menstrual Phase
When progesterone decreases due to involution of corpus luteum

FSH LH

Granulosa
cell Theca
(aromatase) cell
Estrogen
"EFG"
androgen
precursor ovary

(LH/FSH increased in PCOS)

An-ovulation
MCC of female infertility is anovulation due to PCOS
1. Initial investigation : USG - follicular monitoring
2. Best method : Serum progesterone on day 21 of cycle
(increased if ovulation has occurred)
3. Gold standard : Endometrial biopsy on day 21 of cycle
(secretory and thick if ovulation has occurred)

Ovarian Reserve
Maximum follicles in fetal stage Fetal : Max oocytes (Oogenesis starts)
Gradually decreases across life Birth : 1 million oocytes
Granulosa cells produce Inhibin and AMH (used as Puberty : 4 lakh oocytes (1st meiotic div)
proxy markers for ovarian reserve) Arrested in Diplotene stage of prophase 1
1. FSH > 40 (low Inhibin) F - Fourty Fertilisation : 2nd meiotic div
2. AMH < 1 A-1 Menopause : 400 oocytes

Spermatogonia ➡️ 1° spermatocyte (2n) ➡️ 2° spermatocyte (n) ➡️ Spermatids (n)

Spermiogenesis : Spermatids ➡️ Sperms

Sperms get stored and mature at Epididymis

Seminal vesicles : Major portion of semen (alkaline, fructose)

Prostatic : Secretions are acidic

Capacitation of sperms occur in the female genital tract and take 6-8 hours
Acrosomal reaction occurs on binding to zona pellucida (needs Ca2+), for
penetration of sperms
Zona reaction : Change in egg protein that prevents other sperms to enter
 Barr body (Lyon's Hypothesis)
Out of the two X chromosomes in females, only one
is active and the other forms a Barr body.
Number of Barr body = (X - 1)
Females have 1 (samples from buccal mucosa)
Davidson body : Barr body present as inclusion in
neutrophils of females.

1. Normal males : No Barr body

2. Klinefelter : 1 Barr body (Pseudo Barr body)
3. Turner : No Barr body

Reproductive Anatomy

Ovarian Fallopian Tube

Uterus Cardinal Ligament
ligament
aka Mackenrodt ligament
Round ligament
Prevents prolapse, along with uterosacral
and pubo-cervical ligament

Suspensory ligament Round Ligament

(with ovarian artery and vein)
Maintains angle of anteversion in
pregnant uterus
Ovary Homologous to gubernaculum testes
Utero- Broad ligament in males
sacral Cervix (has remnants of Wollfian duct : PEG)
ligament

Cardinal ligament
(with uterine artery and vein)

Normally uterus is ante-verted and ante-flexed

Uterus is retroverted in almost 25%

Lowest part of cervix on palpation

In normal uterus In retroverted uterus
↓ ↓
Anterior lip of Ext OS or
Ante-version Ante-flexion cervix posterior lip
Cervix with Vagina Cervix with Uterus
At external OS At internal OS
Maintained by round
ligament in pregnant
uterus

Longest part
Fertilisation site m/c site of tubal ligation
M/c ectopic
 Female sterilisation

It's done free of cost in India

Most common site of ligation : Isthumus
MCC of failure : Round ligament ligation Fallope Ring applicator Veeres needle
Consent of spouse : Not needed (Creates pneumo-peritoneum)
45° angle of insertion
CO² (<2 L, 20mm Hg)

Stump buried in Most commonly done Crushed Fimbriectomy

broad ligament Surgically reversible
Pelvis
1
2,3
4,5

Pelvic inlet : S¹
Plane of max pelvic dimension : S² - S³
Plane of least pelvic dimension : S⁴ - S⁵

Antero-posterioir Transverse diameter

Between sacral prom. and pubic symphysis At right angle to obstetric conjugate
True ➡️ Obstetric ➡️ Diagonal Normal value : 13 cm
Diagonal conjugate (can be measured clinically) : 13 cm Contracted pelvis if : < 12 cm
Obstetric conjugate is least : 11.5 cm
Contratced pelvis if OC < 10 cm

Contracted pelvis
inlet
AP dia. (obstetric conj.) < 10cm
Transverese diameter < 12cm
Inter spinous distance < 8 cm

Inter ischial distance < 8 cm

Gynecoid pelvis Platypelloid Android Pelvis AnthroPoid Pelvis

pelvis

Most common type Least common type Most common AP diameter >
(in females) (in females) male pelvis transverse diameter
Round shaped Oval shaped Heart shaped Face to pubes
DTA seen here delivery seen here
 Infertility
1 year of regular intercourse for age < 30yrs
More than 30 yrs : 6 months
Initial investigation : Male sperm analysis
MCC of male infertility : Oligo-spermia (sperm count < 16 million/ml)

FSH and LH
Oligospermia : Reduced sperm count
Azoospermia : No sperms at all

Low High Normal

1. Most important is morphology : 4%
Hypogonadotropic Testicular failure Obstructive 2. Concentration : 16 million/ml
Hypogonadism 3. Progressive motility : 32%
MCC of azoospermia Cystic fibrosis
Kallman Syndrome 1. Orchitis in mumps Congeital absence of MCP : 4 - 16 - 32
Assoiciated with anosmia 2. Varicocele vas deferns

Amenorrhea

Uterus present Uterus absent

Serum FSH
Karyotype XY Karyotype XX
MRKH Syndrome
High Low Normal (Mullerian agenesis)
(Gonadal dysgenesis) 1. Kallman Sx (anosmia) PCOS
Ovaries present
2. Sheehan Sx Withdrawal bleed with
Lower 1/3 of vagina
3. Anorexia nervosa progesterone
present
(BMI <18.5) MCC of female infertility

Androgen Insensitivity Sx
Karyotype XO Karyotype XY (aka testicular feminisation sx)
Turner Sx Swyer's Sx Androgen in excess and peripherally converted to estrogen
Short stature, Streak ovaries SRY gene affected Flawless skin, pubic and axillary hair absent
Webbed neck, shield chest No testes Good breasts (estrogen)
Widely spaced nipples No AMH : Uterus develops Undescended testes (high chance of gonadoblastoma)
Peripheral lymphedema at
Perfect female is a male
birth
Bicuspid aortic valve

Leydig cells : testosterone Crypto-menorrhea

Development of
Male pseudo-hermaphrodites Cyclical pain abdomen

Wolffian duct
Forms DHT : male Imperforate hymen
external genitalia Bluish bulge at Vagina
Axillary and pubic hair Testes absent Testes present T/t : cruciate incision
Swyer's Sx
Sertoli cells : AMH Transverse
Cause regression of vaginal septum
Perfect female Not perfect female
Mullerian duct Hematocolpus :
AIS 5 α reductase def
No testes : Uterus is present Blood in vagina
CAH - 17αOH def Hematometra :
Blood in uterus
 Contraceptives

IUDs Barrier method OCPs

1st gen : Lippe's loop 1. Condoms (male and female)
2nd gen : Copper containing 2. Cervical diaphragm
3rd gen : Hormonal (Not under NFWP) 3. Vaginal Sponge
Spermicidal agent : Nonoxyl 9
Disrupt cell membrane of sperm

Mala N : free of cost

Mala D : not free
Copper T 380 A Multiload 375 Hormonal OCP
M/c used IUD 5 years 1. LNG : 0.15 mg
Has copper in arms also Male condom Female condom 2. Ethinylestradiol : 0.03 mg
380 : Surface area of Cu More effective than Has 2 rings 3. Ferrous fumarate : 7 pills
10 years (effective till 12 years) female condom Polyurethane 0.15, 0.03
Can be used twice
within 24 hours

Progestasert Mirena Chhaya

Non hormonal OCP
Progesterone IUD LNG IUD
65 μg/day 5 years Previous name : Saheli
Cervical Vaginal sponge
Preferred in females Non steroidal, contains
diaphragm (Today)
having menorrhagia Ormiloxofene (Centchroman)
1 year 24 hours Developed in CDRI Lucknow
Menorrhagia : Mirena

Miscellaneous Contraceptives

Progestone only pill

Contraception of choice
during lactation (estrogen
interferes with lactogenesis)

Antara (DMPA) ESSURE device 1. Makes the cervical

NORPLANT
mucus thick
Depot medroxyprogesterone LNG subdermal implants Hysteroscopically put in
2. Decreases tubal
acetate Effective for 5 years Fallopian tube
motility
Depot injection: 150 mg IM Immediate reversal on Causes fibrosis
3. Main mechanism is still
Contraception for 3 months removal Effective after 3 months
inhibiting ovulation.
Useful in patients with
1. Seizures
2. Sickle cell anemia

Pearl's indexOBG
Accidental pregnancy
_________________
100 woman years
Transdermal patch Nuva ring
 Emergency Contraceptives

Most effective emergency contraceptive :

Copper IUD (within 5 days)

Levonorgestrel
1.5 mg : single dose
0.75 mg : 2 doses 12 hours apart Other drugs that can be used as emergency contraception:
1. Mifepristone
2. OCP - Yuzpee regimen
3. Centchroman - 60 mg × 2

Ulipristal Drugs that can't be used as emergency contraception.

Single dose 30mg, upto 5 days 1. Danazol
Most effective hormonal contraceptive 2. Misoprostol
Not provided by government of India

OCPs
Estrogen or progesterone or a combination of both.
MOA : Primary mechanism in both is inhibition of ovulation
Estrogen suppresses GnRH and FSH
Progesterone suppresses LH Protective in CEO Risk factor for
Additionally progesterone makes the cervical mucus thick 1. Colorectal cancer 1. Breast cancer
(prevents penetration of sperms) 2. Endometrial cancer 2. Cervical cancer
3. Ovarian cancer 3. Hepatic adenoma

Non contraceptive uses

1. PCOS
2. Dysmenorrhoea Absolute Contrainidcations
3. Endometriosis
(WHO - 4)
4. Uterine fibroid
5. Dysfunctional uterine bleeding (DUB) Thromboembolism / DVT / Stroke
Heart disease (Valvular/Ischemic)
Hypertension
Newer generation OCPs
Breast cancer
Based on type of Progesterone Hepatic adenoma
2nd gen : Less side effect - Norgestrel/LNG
3rd gen : Less androgenic - Norgestimate Pregnancy or breast feeding
4th gen : Anti-androgenic (in PCOS) - Drospirenone
All generations will have risk of thrombosis

Contraception of Choice
1. Woman on anticoagulation for DVT : IUD (OCPs are CI)
2. Molar pregnancy : OCPs
3. Post partum/ Breastfeeding : POPs > IUD
4. Reversible : Norplant
Early pregnancy ultrasound "GYED 4.5"

Gestational sac Yolk sac Embryo Double bleb sign

Confirms intra-uterine preg. Fetal heart sounds (+) Amniotic and Yolk sac

TVS : 4.5 weeks TVS : 5.5 weeks TVS : 6.5 weeks TVS : 7 weeks
For TAS add 1 week

Gestational sac Crown Rump Length

Intra decidual sign Double decidual sac sign

Earliest sign on USG 1. Decudua capsularis
First sign of pregnancy 2. Decidua parietalis

Decudua paritalis

Decudua basalis Most accurate method to estimate

gestational age in 1st trimester
Decudua capsularis GA in weeks : CRL (in mm) + 6.5
GA in days : CRL (in mm) + 42

Normal G sac is implanted eccentrically

Pseudosac is implanted in midline

Leopold Manoeuvres

Fundal grip Lateral/ umbilical 1st pelvic 2nd pelvic

Determine presenting part Determine fetal aka Pawlik For fetal attitude and descent
Hard and ballotable mass at back Only manoeuvre where
Engagement
fundus : Breech examiner faces towards
and mobility of
patient feet
presenting part
 Aneuploidy Screening

1st trimester
Nuchal translucency scan
<3mm is normal
If increased then could be Aneuploidy or CVS defect

Dual marker
HCG and PAPP
Nuchal translucency
HCG high and PAPP low suggestive of Down's sx
<3mm is normal

2nd trimester
Anomaly scan
Entire fetus checked using USG for anomalies
Nuchal skin fold thickness is checked here
(not nuchal translucency) Summary of triple screen
1. hCG is High : Down's
Triple marker 2. Everything low : Edwards
HCG, AFP and Unconjugated Estriol HAE 3. AFP high : NTDs

Quadruple marker
Triple marker + Inhibin A HAE - I am

Non invasive prenatal testing (NIPT)

Screening test (99% accuracy)
Only maternal blood needed
Can't be used to confirm diagnosis

Confirmatory test

Chorionic Villous Sampling Amniocentesis Cordocentesis

10-13 weeks 15-20 weeks 18-20 weeks
Trophoblasts are taken for Amniocytes and fetal dermal Fetal blood cells are taken
sampling fibroblasts are taken for sampling from umbilical cord
Can lead to limb reduction Most commonly done
defects
 Physiological changes in pregnancy

Increases Decreases Constant

1. BT and CT remain constant
Blood volume increased Haemoglobin and Hematocrit
RBC and WBC count increase decreased (hemodilution) 2. EF remain constant
(increased production) Platelet count decreased 3. All other lung volumes except
All clotting factors and fibrinogen (hemodilution) (IC, TV, MV and FRC)
increased (hypercoagulable state) Factor 11 and 13 decreased 4. Free T3, T4 and TSH
except factor 11 and 13 Protein C/S decreased
(anticoagulant activity decreased)

Total proteins increased

Vaginal pH decreased (more acidic,
Thyroid in pregnancy
SHBG and TBG increased
lactobacilli increased) α Subunit of HCG is like TSH,
ESR increased therefore T³ and T⁴ production
increases
Cardiac activity increased Peripheral vascular resistance and TBG also increased
(Cardiac output, heart rate, BP decreased (vasodilation) (binds the extra T³ and T⁴)
stroke volume) "Free T³ & T⁴" remains constant

Respiratory activity increased FRC of lung decreases (diaphragm If patient is on Levothyroxine, dose
(Tidal volume, Insp. capacity, pushed up) has to be increased because TBG is
minute ventilation) increased.

Renal activity increased Serum urea and creatinine

(Renal blood flow, GFR) decreased (renal activity increased)

Pathologies in pregnancy
Anemia in pregnancy Heart diseases in preg.
Hb : < 11 g/dl Mammary soufle : Continuous murmur in 2nd-4th ICS (normal in pregnancy)
MCC : Physiological > IDA Abnormal murmur : Any pansystolic or diastolic murmur
Prophylaxis for all MC heart disease : MS due to RHD
1. GOI IFA pill : Iron (60 mg) + FA (500 μg) Preferred mode of delivery : NVD + Instruments use
MC time for heart failure : 1. 32-34 weeks
2. Deworming : Albendazole single dose
(400 mg) in 2nd Trimester 2. Intrapartum

Management
Pregnancy not recommended (WHO Grade IV)
> 7g/dl 1. Pulmonarty artery htn
< 34 wks : IFA (BD instead of OD) 2. Ventricular dysfunction (< 30% EF)
> 34 wks : IV iron (iron sucrose) 3. Severe MS
4. Aortic dissection
< 7g/dl 5. Coarctation of aorta
< 34 wks: IV iron (iron sucrose) 6. Eissenmenger's Sign (worst prognosis - 50% mortality)
> 34 wks or < 5g/dl: Blood transfusion 7. H/o Peripartum Cardiomyopathy

Oligo-hydramnios Poly-hydramnios
AFI < 5 or SDP < 2 AFI > 5² or SDP > 2³ GDM
Uterine size is smaller than GA Uterine size is larger than GA PIH
Lesser fetal movements Fetal parts not palpable, FHS muffled
Eclampsia
1. MCC : Undiagnosed rupture of membrane 1. NTDs, Cleft lip, anencephaly (can't swallow)
APLA
2. Renal agenesis in fetus (ACEi/ARB) 2. Gestational DM
3. Posterior urethral valve 3. Omphalocele Liver diseases
4. Twins, trisomy
 Gestational Diabetes Mellitus
Screening done at 24-28 weeks
1. IADPSG screening : Fasting > 92 | 1 hr OGTT > 180 | 2 hr OGTT > 153
2. DIPSI screening : 2 hr OGTT > 140 Overt diabetes (Pre gestational) :
Fasting blood glucose > 126 mg/dl
Management of GDM
Congenital anomalies with Overt diabetes
1st line : Diet control and HbA1c every 3 months
Insulin therapy is preferred over OHA (doesn't cross placenta) Most common : VSD
Metformin crosses placenta, but is safe in pregnancy Most specific CVS anomaly : TGA
Most specific : Caudal regression syndrome

Complications of GDM
Macrosomia (> 4 kg) leads to shoulder dystocia and clavicle fracture
Polyhydramnios
Neonatal hypoglycemia
Neonatal hypocalcemia

Pregnancy Induced hypertension

1. Hypertension (>140/90) after 20 weeks POG in previously normotensive female ➡️ PIH
2. If PIH + Proteinuria ➡️ Pre-eclampsia
3. Pre-eclampsia + Hemolysis + Elevated Liver enzymes + Low Platelets (< 1 lakh) ➡️ HELLP Sx / Severe Pre-eclampsia
4. Presence of Seizures ➡️ Eclampsia HELLP can present without
hypertension or proteinuria

Patho-physiology
Invasion of spiral art. by extra villious trophoblasts
Makes the arteries : Low resistance and high flow systems
Failure in pre-eclampsia

Other Risk factors

Primigravida
Molar/twin/Rh-negative preg
h/o pre-eclampsia
New paternity Smoking is protective

Management

PIH Pre-eclampsia Severe Pre-eclampsia

Anti- hypertensives Definitive management is Admit to labor room
termination of pregnancy MgSO⁴ (Pritchard regime)
at 37 weeks Anti-hypertensives
Anti-hypertensives Cortico-steroids for lung maturation
Deliver at 34 weeks

Termination of pregnancy if
Anti hypertensives in preg. Contraindicated in preg. 1. HELLP
1. Labetalol 1. ACE/ARB : Renal agenesis 2. Eclampsia
2. Methyl-dopa 2. Beta blockers (except 3. Fetal compromise
3. Nifedipine labetalol) : Fetal bradycardia 4. Any other complication
4. Nitroprusside and hypoglycemia
5. Nitroglycerine 3. Diuretics : IUGR
6. Hydralazine
 Liver diseases in pregnancy
Raised liver emzymes

Associated with PIH in late 3rd trimester Infection (fever)

HELLP Viral Heptitis

C/f : Epigastric pain MCC : Hepatitis E
Acute fatty liver of Intrahepatic
Tenesse Criteria pregnancy cholestasis of Preg. aka non A non B enteric
1. Hemolyisis (LDH ⬆️, Bilirubin ⬆️, NH³ ⬆️, Fibrinogen ⬇️ Direct bilirubin ⬆️ hepatitis
Pruritis Feco oral transmission
presence of schistosyctes) Hypoglycemia
Mx: UDCA tablets Can cause fulminant
2. Elevated liver enzymes (AST > 70) Mx : Immediate TOP
Terminate at 37 weeks hepatitis in pregnancy
3. Platelets (< 1 lakh)
HELLP can present without
hypertension or proteinuria

Mx : Immediate TOP

APLA Syndrome
Modified Sydney/ Sapporo criteria
Hyper-coagulable condition, causing thrombosis.
Obstetric criteria
Ischemic stroke
One or more unexplained deaths of a
Amaurosis fugax TIA
morphologically normal fetus at or beyond 10 weeks Migraine
or
Three or more unexplained consecutive spontaneous Pulmonary embolism
Myocardial infarction
abortions before 10 weeks
or Renal insufficiency
Severe pre-eclampsia or placental insufficiency
requiring delivery before 34 weeks Placental
Insufficiency
Pre-eclampsia
Laboratory criteria
Livedo reticularis
Presence of lupus anticoagulant
or
Anticardiolipin antibodies
or Arterial or venous
Anti-β2 glycoprotein antibody thrombosis Ulcers

Treatment
Microglobulin : Multiple myeloma Heparin + Aspirin
Glycoprotein : APLA
2 Transferrin : CSF Rhinorrhea
Anti-coagulation in pregnancy
Till 12 weeks : LMWH (warfarin is teratogenic)
12- 36 weeks : Warfarin
After 36 weeks : LMWH (increased risk of PPH
with Warfarin)
 1st Trimester Bleeding
1st trimester bleeding

Ectopic Pregnancy Molar Pregnancy Abortion

Most common location : Ampulla

Most common cause : PID
Maximum risk : Tubal surgeries Complete mole Partial mole
Measure β HCG and repeat after 48 hours Empty ovum (entirely Paternal) Maternal + Paternal
1. Doubles : Normal Pregnancy Diploid/tetraploid Triploid
2. Decreased : Missed abortion No fetal development Some fetal development
3. Increased but not doubled : Ectopic Uterus increased in size Diagnoed as missed abortion
Management Theca lutein cysts
More medical complications
1. β HCG < 1500 or sac < 3cm :
More risk of choriocarcinoma
Expectant management
2. β HCG < 5000 or sac < 3.5cm :
Mtx single dose IM injection
(repeat β HCG on day 4 and 7)
3. Surgical management if β HCG
> 5000 or sac > 3.5 cm (also for
ruptured ectopic pregnancy)
GESTATIONAL TROPHOBLASTIC DISEASE (GTD)
3 1500 : Expectant
3.5 5000 : Medical MALIGNANT FORM

Criterias GESTATIONAL TROPHOBLASTIC NEOPLASM (GTN)

1. Rubin : Cervix Rubin the cervix
2. Spielsberg : Ovarian Spielberg's movies TROPHOBLASTIC INVASIVE
CHORIOCARCINOMA
3. Studdiform : Abdominal TUMOR MOLE
Studd to the abdomen
EPITHELIAL PLACENTAL SITE
On USG doppler : Ring of fire / Bagel sign

Persistent bleed
Uterine subinvolution
Persistent TL cyst
Mets Mc mets → Lungs
H/P evidence

ß-HCG
Plateau for a month or increase
Detectable > 6months

Treatment
Confined to uterus : Methotrexate
Mets to lungs/adnexa : Methotrexate
Other mets : EMACO regime

OS Open OS closed
Bleeding and pain Spotting

Complete Threatened Missed abortion

Incomplete abortion Inevitable abortion
abortion abortion No symptoms
Uterus < POG Uterus = POG Empty G-sac
Uterus < POG Uterus = POG
Retained product of Fetal Cardiac activity aka blighted ovum
Bleeding has FCA present
conception in uterus absent CRL > 7 (but no FHS)
stopped Bed rest and
progesterone MSD > 25 (but no embryo)
 Pre-term Labor
Requisites
1. Contractions (+) Tests to confirm Amniotic fluid
2. >2cm dilation 1. Ferning
2. Nitrazeneblue test-alkaline
Management 3. Nile blue sulfatase (fetal skin cells)
>34 weeks: GBS prophylaxis ± Steroids
<34 wks: Tocolytic (nifedipine) + GBS prophylaxis + Steroids
<32 wks: add MgSO⁴

Indications for Induction of Labor : PPROM

r/o chorioamnionitis, fetal distress, abruption

Induction of Labor

Modified Bishop's score

B - Bishop's score
I - i(e)ffacement
S - Station
H - Hard/soft (Consistency)
O - Opening (Dilation)
P - Position

Scoring system used to assess labour induction outcomes

A score >6 is considered favorable for IOL

Indications of IOL Contra-indications of IOL

Post-term pregnancy (m/c cause) Distorted pelvis and CPD
Abruption placentae Placenta previa or vasa previa
Premature rupture of membranes Active genital herpes
Rh-isoimmunization Pelvic tumor & carcinoma cervix
Intra-uterine growth restriction (IUGR) Transverse lie or footling breech
Umbilical cord prolapse
Previous classical cesarean or hysterotomy
Previous history of uterine rupture
Previous 3 or more lower transverse CS

274
Doppler in Pregnancy
Indication

IUGR Fetal Anemia Early onset pre-eclampsia

Umbilical artery MCA doppler Uterine artery doppler

doppler Peak Systolic velocity >1.5 mom
in fetal anemia

Normal Absent end Reverse end

diastolic flow diastolic flow

Immediate
<34 weeks >34 weeks termination

Steroids Terminate
For fetal lung
maturation

Signs in Pregnancy
 Stages of Labor
Latent phase
Stage 1 : Onset of labor pain to full dilatation of cervix (10 cm)
Stage 2 : Expulsion of fetus till 5 cm (WHO) and 6 cm (ACOG)
Stage 3 : Expulsion of placenta
Active phase
Stage 4 : 1 hr after delivery

Stage 1
Prolonged latent phase
Recommended Not recommended
Primi para : 20 hours
Delay admission till active labor Routine pelvimetry
Multi para : 14 hours
PV examination every 4h Routine cardiotocography
FHR with doppler/ stethoscope "Early" oxytocin/amniotomy to T/t : Sedation
Respectful maternity care shorten duration of labor • False labor pain would go away
Pain relief Routine vaginal cleaning with • If pain persists, augment using oxytocin
Encourage mobility chlorhexidine
Fluid and food intake Use of IV fluids to shorten
Effective communication and duration of labor Active phase arrest
companionship
No dilation for 4 hrs despite
adequate contraction
4
Stage 2
Recommended Not recommended
To reduce perineal trauma - Routine episiotomy is not
warm compress/ perineal recommended
massage (Ritgen's maneuver) Fundal pressure is not
Encourage the mother to recommended
follow her own urge to push
Birthing position of choice
(lithotomy is not compulsory) Duration of 2nd stage of labor Ritgen's maneuver
Normal : 1 hr (0.5 hr in multipara) This allows to control speed of delivery
Prolonged : 2 hr (1 hr in multipara) and hence reduces perineal trauma
Arrest : 3 hr (2 hr in multipara)

Stage 3
Recommended Not recommended
Active management of third stage of labor Uterine massage (now done to
(AMTSL) examine cause of PPH)
1. Uterotonic administration (Oxytocin 10 IU) Crede's method (fundal pressure
2. Controlled cord traction for placental separation), can
3. Delayed cord clamping (after 1-3 min) lead to uterine inversion
4. Intermittent assessment of uterine tone

Brandt Andrew's Maneuver

One hand puts gentle traction on the cord
while the other presses the anterior
Uterotonics in AMTSL surface of the uterus backward.
Most important step of AMTSL
1. Oxytocin 10 IU : Uterotonic of choice
2. Carbetocin - 100 mcg Early cord clamping done in
3. Misoprostol p/o : If skilled birth 1. Neonatal resuscitation
attendant not present program (birth asphyxia)
4. Methylergometrine : Contraindicated in 2. Rh-iso immunisation
hypertensive females 3. HIV (recommended by NACO)
 Obstructed labor
Good uterine contraction but still no descent
Features
Maternal exhaustion and dehydration
Moulding (+)
Vagina feels hot and dry
Upper uterine segment tender on p/a Schroeder's constriction ring
Groove between upper and lower uterine segment : Bandls ring Incoordinate uterine contractions
due to injudicious use of uterotonics
Causes Ring not felt p/a but felt p/v
CPD (most common cause)
Small pelvis
Big baby (macrosomia)
Deformed pelvis e.g. poliomyelitis
Bandl's contraction ring
Abnormal presentations & position Due to obstructed labor
Progressively moves upwards
Management Ring felt per abdomen but not p/v
Emergency LSCS (can lead to uterine rupture)

Fetal monitoring
Antepartum setting
CTG done
(aka NST here)
⬇️
NST abnormal
⬇️
Repeat NST
⬇️
NST still abnormal Non stress test
⬇️
Modified BPP Manning Score (BPP)
(NST + AFI) B Breathing
⬇️ A AFI
Still abnormal T Tone
⬇️ Ma Movements
BPP N NST (FHR)
(Manning score)

Intra-partum setting
CTG done
↓

Every 30 mins (small box)

1. Fetal heart rate
2. Maternal heart rate (pulse)
3. Uterine contractions
Early Late Variable Sinusoidal
Every 4 Hours
declaration declaration declaration wave
1. Blood pressure
2. Temperature Head Utero- Cord Fetal
3. Vaginal examination compression placental compression anemia
↓ insufficiency
Other values Change position ↓
1. Oxytocin-dose and concentration of mother TOP
2. Urine analysis
3. State of membranes and color of liquor "Early head late UPI"
 Cardinal movements of Labor

(ED FIrE ErE)

Engagement
Descent

Flexion
Internal rotation
Extension

External rotation (restitution)

Expulsion

Transverse Lie
Presenting part : Shoulder
Denominator: Acromion process
Prematurity is the m/c cause (fetus with transverse lie
mostly spontaneously rotate to longitudinal by term)
Most common cause at term : Placenta previa

Features
Height of uterus < Gestational age
Fundal grip and deep pelvic grip are empty

Complications
Maximum chance of cord prolapse Longitudinal lie Transverse lie

Management
1. Attempt ECV
2. LSCS
3. Internal podalic version, for second twin in transverse lie.

External Cephalic version

ECV first attempt
Pre-requisites
Singleton with breech/ transverse lie
(not for knee or footling)
Successful Fails
Reached 36 weeks of gestation
Normal FHR
Wait for ECV 2nd attempt
Membranes intact, adequate liquor
spontaneous (after a week)
No placenta previa
labor

Internal podalic version Successful Fails

Pre-requisites
Second twin in transverse lie (no h/o LSCS) IOL using LSCS
Converts the transverse lie to a breech position oxytocin drip
Done in OT
 Fetal Position

Direct
Occipitoanterior
Right DOA Left Fetal POSITION - refers to the relation of fetal
Occipit anterior Occipitsanterior presenting part (named DENOMINATOR) to the
ROA LOA pelvic inlet.

Left occiput transverse is the most common

fetal position followed by left occiput anterior
in longitudinal lie "LOT common"
In occipito-transverse or occipito-anterior
Fetal position position, vaginal delivery is normal

Right
Occipito- Left Occipito-posterior is an abnormal fetal position
transverse Occipito-transverse (most common malposition)
ROT
LOT Amongst OP position, ROP is more common
than LOP
Right Left
Occipitoposterior Occipitoposterior
ROP Direct LOP
Occipitoposterior
DOP

Occipito-anterior
Occipito-posterior position
Most common fetal malposition
Features : Infraumbilical flattening and fetal heart beat
heard in flanks
More common in primi-gravida
Causes deflexed head (m/c cause of non engagement of
head in primi-gravida) Occipito-posterior
Most common cause : Anthropoid/Android pelvis
Management - wait and watch (rotates itself in 90% cases)

Mechanism of labor in OP position

1. Long arc rotation 135° (becomes DOA)
2. Short arc rotation 45° (becomes DOP) → face to pubis
delivery, associated with more perineal tears
3. Deep transverse arrest : Head gets arrested while
undergoing long arc rotation
4. Persistent OP

Deep transverse arrest (DTA)

Also known as incomplete forward rotation
Fetal head gets arrested while performing long arc rotation
Sagittal suture struck in transverse plane
Results in obstructed labor
More common in Android pelvis (prominent ischial spines)
Treatment : LSCS in primi
Vaccum in multi para (rotation)
 Fetal Presentation

Sub-mento vertical

SOB and SMB both 9.5cm Bi-parietal 9.5 cm

SOB - Complete Flexion - Vertex Engaging diameter
SMB - Complete Extension - Face Also 9.5cm
MV - 14cm 8cm
Bi-temporal
Partial extension - Brow
Smallest diameter
partially extended "bro" of skull
"we SOB flexed"

Complete or incomplete Partial

Any flexion
extension extension

Face Brow
presentation presentation

Face presentation
Complete/incomplete extension of head
Engaging diameter → Submentobregmatic (9.5cm) or
Submentovertical (11.5cm)
Denominator - Chin
Can be of 2 types - Mento posterior and mento anterior
M/c cause - Anencephaly
M/c pelvis - Platypelloid Mento - anterior Mento -posterior
Head can be delivered LSCS has to be done
with flexion (like breech
Delivery by flexion of head : Breech and mento-anterior face
delivery)
presentation
No delivery, LSCS has to be done : "Face anterior is natural"
1. Transverse lie
2. Brow presentation
3. Mento posterior face presentation
Breech presentation
Most common malpresentation
At 28 weeks, 1/4 of babies are in breech → spontaneously rotate,
hence prematurity is the m/c cause of breech
At term, 3-4% breech presentation
M/c breech : Frank breech (extended knee joints)

ECV can be attempted

Vaginal breech delivery attempted in C section for breech considered when
Frank breech Large fetus: 3800 to 4000 g
Facilities for emergency LSCS present Severe IUGR, term weight <2.5kg to 2.8kg
Skilled obstetrician present Incomplete breech presentation
Twins with second twin in breech Oligohydramnios
Hyperextended head (Stargazer breech)
Assisted breech delivery methods
Contracted pelvis
Loveset's
Prior cesarean delivery
Pinard's
Twins, with the first baby in the breech position
Burns and Marshall
Mauriceau–Smellie–Veit
Use of Pipers forceps
"Smellie piper burns and pins Love"

Loveset's maneuver Pinard's maneuver

"Loveset - Offset" "Pin - Knee - rd"
Burn Marshall's maneuver

Piper's forceps - for aftercoming head of breech Mauriceau–Smellie–Veit maneuver

Shoulder dystocia
Call for help
Episiotomy
Suprapubic pressure
Mc-Robert's Maneuver (abduction of thighs)

If failed Mc-Robert's Maneuver

1. Woods corkscrew maneuvre

2. Zavanelli maneuvre (put the head back in and take for LSCS)
3. Rubin's maneuvre
4. Gaskin (all four's position)
5. Cleidotomy (fracture of the clavicle of baby)
Gaskin's Maneuver (all four)
 Post partum haemorrhage 1. > 500 ml in vaginal delivery
2. > 1L in C section

Primary PPH : Atonic uterus (mcc)

Secondary PPH : Retained D & C contra-indicated
products of conception Postpartum haemorrhage in PPH
Succenturiate placenta ↓
Immediate steps
1. Call for help.
Max chance of
2. Resuscitation Ashermann Syndrome

Abdominal palpation

Uterus atonic (Atonic PPH) Uterus hard and well contracted (Traumatic PPH)

1. Bi manual uterine massage

Exploration Suspicion of uterine
2. Oxytocin infusion
(cervicovaginal inspection) rupture
3. Inj. Methergine
4. Blood transfusion
Haemostatic sutures Emergency laparotomy
on the tear sites
Uterus still atonic
Bi-manual massage

1. Carboprost I.M
2. Misoprostol rectally

Uterine tamponade SURGERY SURGERY

Devascularisation Hysterectomy
1. Condom catheter
2. Bakri baloon 1. First hemostatic sutures are tried
2. If bleeding doesnt stop then
devasclarisation
Hemostatic sutures
B/L uterine
⬇️
B/L utero-ovarian
⬇️
Ant div of Internal
iliac artery
B - Lynch Hayman Cho's

Bakri baloon Condom catheter "U-O-I"

B Lynch : Hay man, Kem Cho !!

Perineal tear

1st degree : Vaginal mucosa

2nd degree : Perineal muscles

Repair in Labor room

3rd degree : Anal sphincter

4th degree : Rectum torn If tear found >24 hrs
⬇️
Repair in OT repair after 6 weeks
Types of Placenta

Bi-lobed placenta Circum marginate Circumvallate

Marginate looks like a
margherita pizza

Battledore Placenta Succenturiate Velamentous cord

Marginal insertion placenta insertion
"So-Cute placenta" (r/o Vasa previa)

(r/o PPH if smaller

lobe is retained)

Substances that cannot cross placenta

Albumin
IgM, IgA (IgG can cross)
PTH and calcitonin
Antepartum Haemorrhage

Antepartum haemorrhage
Tests to determine if
bleeding is fetal or maternal
either Patient and fetus stable 1. APT test : Qualitative APT quality
Unstable mother 2. KB test : Quantitative
Fetal distress 1st step : Resuscitation
Both tests are based on the principal that
DIC 1st inv : P/A examination + USG
"Fetal blood is resistant to alkali"
(P/V is contraindicated because it
could be Vasa previa)
Immediate LSCS

Painless Painful
Bright red bleed Dark red bleed
Soft uterus Tense and
tender uterus

Placenta Previa Vasa Previa Abruptio placenta

Placenta in front of int. OS Vessels in front of int. OS
h/o Trauma or PIH
No fetal distress mostly Fetal distress ++ Fetal distress present
Fundal height = POG Fundal height = POG Fundal height > POG
Malpresentations common CTG : Sinusoidal
APT test on blood : Negative APT test : +ve (fetal blood)
(maternal blood) Diagnosis without bleed : Colour
Diagnosis without bleeding : USG doppler

"Associated with
velamentous cord
insertion"
Couvellaire uterus

Management
< 34 weeks : Steroids
> 34 weeks : IOL (not LSCS)

Management
Management Immediate LSCS
< 37 weeks : Mcafee and Johnson
(conservative mx with bed rest)
> 37 weeks : LSCS
 Rh Iso-immunisation
Fetal Rh antigen can sensitise mother to produce antibodies against it
These antibodies if reaches fetus can cause Hemolytic disease of newborn

Indirect Coomb's tests

(check mother's serum for antibodies)

ICT (+) ICT (-)

Antibodies against Rh produced in mother Mother not yet sensitised
(Make sure fetus is not affected) (Make sure mother doesn't get sensitised)

Sensitisation can happen in mother

MCA doppler Fetal USG
during birth/abortion/trauma
MCA PSV > 1.5 MoM Features of Hydrops
To prevent sensitisation : Anti D Ig
(300μg IM)
> 34 weeks < 34 weeks Routinely administered at 28 weeks
After birth : if baby Rh (+) and DCT (-)
Deliver Repeat after a week (Antibodies absent on RBCs of fetus) to
prevent iso-immunisation in further preg.
No improvement

Direct Coomb's test : Hemolytic anemia in baby

Cordocentesis Indirect Coomb's test : Rh iso-immunisation in mother
Intra-uterine blood transfusion if
Hb < 10 or
Hct < 30 %
Hydrops Fetalis
Fluid in 2 out of 4 compartments
1. Ascites
2. Pleural effusion
3. Anasarca
4. Pericardial effusion

Non-immune hydrops
MCC : CVS anomalies > Parvovirus B¹⁹

Complications after birth

Amniotic fluid embolism Obstetric Neuropathies

Onset during labor or within Most common - Lateral cutaneous nerve of thigh
30 minutes of delivery (Meralgia parasthetica)
Sudden onset shock and DIC Foot drop can be seen due to peroneal nerve injury
No fever

Puerperal fever Peri-partum cardiomyopathy

Temperature > 38° Celsius Type of dilated cardiomyopathy
At two occasions Cardiac failure in last month of pregnancy or within 5 months after delivery
(within 10 days of delivery) No other cause for HF
Left ventricular systolic dysfunction demonstrated
Fever in 1st 24 hrs is not included here
 Types of twins

Dichorionic - Diamniotic Monochorionic - Diamniotic Monochorionic - Monoamniotic

0-4 days 4-8 days 8-12 days

Twin peak sign T sign

>13 days : Conjoint (m/c thoracopagus)

Best time to identify type of twin on USG : 11-14 weeks

Miscellaneous

Pregnancy formula Teratogens

G - No. of conceptions Valproate/Phenytoin : Neural tube defect
Irrespective of viability ACE / ARB : Renal agenesis
Include present pregnancy Lithium : Box shaped heart (ebstein's anomaly)
Misoprostol : Mobius Syndrome
P - No. of past pregnancies >28wks
Isotretinoin : Cleft lip/ Cleft palate
Twins are considered single parity
Alcohol : Smooth philtrum, mental retard
Warfarin : Stippled epiphysis (Chondro-dysplasia punctata)
Methotrexate : Clover leaf skull
Calorie requirement in pregnancy Methimazole : Cutis aplasia
Indomethacin : Premature closure of PDA
Second trimester: +350 Kcal/day Tetracycline : Enamel hypoplasia
Third trimester: +450 Kcal/day
Thalidomide : Phecomalia (flipper baby)
Lactation (0-6m): +600 Kcal/day
Lactation (6-12m): +500 Kcal/day

STEROIDS in pregnancy
<34 weeks
Post VVF repair (Latzko procedure) DOC- Betamethasone 12 mg - 2 doses - 24 hrs
Abstinence : 3 months GOI- Dexamethasone 6 mg - 4 doses - 12 hrs
No pregnancy : 1 year 24mg in 48hrs Beta : Baarah "12mg"

Reduce : RDS, NEC, IVH, neonatal mortality

Distension media in hysteroscopy
Neonatal jaundice- No effect
Monopolar cautery : Glycine/ CO²
Bipolar cautery : Normal saline
Glycine can cause water intoxication syndrome Maximum amniotic fluid: 34 weeks
Major contributor: Fetal Urine
Caudal regression syndrome Phecomalia (flipper baby) Anencephaly
Overt DM (not GDM) Proximal limb defects (frog eye sign)

Amniotic band syndrome

Seen with oligohydramnios
Distal limb defects
Potter sequence (pulmonary hypoplasia)

Gastroschisis Omphalocele
Right of midline On midline
No membrane Membrane present
M/c asso. with other
anomalies

281
 Uterine masses

Uterine fibroids Adenomyosis Endometrial polyps

Assymetric and enlarged uterus Symmetric, tender and
globular uterus

Fibroids are most common benign Endometrium inside myometrium.

uterine tumors Multiparous women > 40 years.
Estrogen dependant tumors Painful symptoms - menorrhagia,
Asymptomatic in most cases dysmenorrhea, dyspareunia.
Large fibroids can present with Symmetrical enlarged uterus
infertility (cornual block) corresponding to 12-14 weeks size.
Hyaline degenration is m/c The uterus is soft and tender on
Indications of myomectomy bimanual examination.
1. Fibroid causing cornual block
Feeding vessel sign
leading to infertility Saline infusion sonography
2. Size > 12 weeks done to distinguish it from a
3. Pedunculated or sub-serosal fibroid
4. Rapidly growing after menopause
(malignant suspicion)
Complications

on MRI : Salt and pepper

Red degeneration Torsion of fibroid appearance
In late pregnancy Seen with sub-serosal or Confirmation is by histopathology
Hemorrhagic infarction of pedunculated fibroids Management
central part of fibroid Focal abdominal pain 1. Hysterectomy is TOC because most
Focal abdominal pain with without fever or patients are multipara > 40 yrs of age.
fever and leucocytosis. leucocytosis 2. Mirena in young females (LNG containing
Treatment is conservative IUD)

Uterine prolapse
Young patient Sling for singles
Fertility preserving Abdominal Sling Surgeries
Shirodkar / Khanna

Old patient old as a Fort

Vagina closed - (No sexual function) Normal Pelvis Uterine prolapse Anterior prolapse Posterior prolapse
Colpo-cleisis
Le-Fort repair Patient is fit for abdominal surgery:
Transabdominal sacral colpopexy (Colpos : Vagina)
Middle aged M-M aka Uterosacral suspension
Middle - Manchester repair Best method for vault prolapse
If family complete then Hysterectomy
Complication : Vault prolapse Patient is not fit for abdominal surgery:
Transvaginal sacrospinous ligament fixation.
During Pregnancy / Post-natal Ring pessaries can be tried when surgery is not
Pessary possibble
Kiegel's exercises
Approach to enlarged ovaries

Large follicles
Small follicles
↓
PCOD
H/o IVF H/o molar
pregnancy

Rotterdam Criteria > 2/3 OHSS

Theca lutein
Clinical Biochem. Radiology
cysts
Hirsuitism Raised > 20 follicles
Oligo-menorrhea testosterone < 10mm in size
Infertility LH / FSH ↑ Most specific is
↑echogenecity OHSS
"More than 20 Complication of ovulation­induction therapy
less than 10" for infertility.
Assocaited with ovarian enlargement with
large follicles + increased capillary
Management for PCOD permeability
It occurs due to over stimulation of
1. Lifestyle modification is enough in mild cases
granulosa cells by hCG.
2. OCP for menstrual abn
3. Metformin for insulin sensitivity.
4. Letrozole > Clomiphene for infertility
Abdominal pain occurs due to ovarian
enlargement and accumulation of peritoneal
fluid.
Increased vascular permeability cause
ascites and result in hemoconcentration.
Hemoconcentration causes
hypercoagulability.
Management is only symptomatic

Theca Leutein cysts

Type of follicular cysts
They typically occur after the first trimester
due to exceptionally high hCG or LH.
(HCG and LH have similar action)
Can be seen GTN, multifetal pregnancy
Asymptomatic condition, surgically managed
only if complications arise.
Carcinoma Endometrium

1a : <50% myometrial Cervical stromal 3a : Serosa, adnexa SA 4a : Bowel, bladder

invasion invasion 3b : Vagina, paramet VP 4b : Distant mets
1b : >50% myometrial Cervical glands 3c : Pelvic & para-aortic LN CP (including Inguinal LN)
invasion not included
SA VP in CP

Management for endometrial carcinoma

1a - Only surgery
1b and 2 : Sx + RT
3 and 4 : Inoperable (brachytherapy)

Manchester points in Brachytherapy Normal endometrial thickness

Ovulatory : < 11 mm
Post menopausal : < 4 mm

Endometrial Hyperplasia
Simple hyperplasia : 1 % r/o carcinoma
Complex hyperplasia : 3 % r/o carcinoma
Simple + Atypia : 8 % r/o carcinoma
Complex + Atypia : 29 % r/o carcinoma

Management for endometrial hyperplasia

Progesterone therapy if no atypia
With atypia in post menopausal - Hysterectomy
With atypia in young - High dose progesterone
Point A : 2 cm X 2 cm (7k-8k Gy)
Point B : 3 cm from A (6k Gy)
236

Corpus cancer syndrome

Obesity + Htn + DM
Endometrial cancer
Carcinoma Cervix Screening
Start at : 21 years
Stop at : 65 years Stains used in Pap smear
1. 95% alcohol (fixative)
Pap smear : 3 yearly
2. Harris Hemotoxylin
Co testing (HPV + PAP smear) : 5 yearly (for age > 30yr)
3. Orange G-6
Immunocompromised : Annually 4. EA - 50
Vaccinated : No change "95% HOE"

Interpretation of pap smear

Grade 1 : Normal
Grade 2 : Inflamma2ory
Grade 3 : CIN 1 - LSIL T/t : Regular screening, Cryoablation
Grade 4 : CIN 2 or 3 - HSIL (pre-malignant) T/t : LEEP / LETZ
Grade 5 : Invasive carcinoma

Government Advanced
setup setup
Colposcopic Biopsy
Cervi-brush
Ayre's spatula If abnormal screening or patient has features of
Liquid based
Koplin's jar cervical carcinoma eg. post-coital bleeding
cytology media
More sensitive

Human Papilloma Virus

HPV HPV Proteins

E⁶ : against P⁵³ 5 and 6 together
E⁷ : against Rb
Low risk High risk L¹ : Capsid protein
(Vaccines designed against L¹) Virus took one L
6,11 16, 18,
Condyloma 31, 33,
acuminata 45, 52, M/c for ca cervix : 16
(Genital warts) 58 Most malignant : 18
Most specific : 18

WHO SAGE guidelines for HPV

Gardasil 4 : 6, 11, 16, 18
vaccination Cervarix : 16, 18
Age 9-20 : 1 or 2 doses Cervavac : 6, 11, 16, 18
Age 21-50 : 2 doses (6 months interval) (Made in Serum institute, India)
Immunocomp. / HIV : 3 doses
0.5 ml IM (male and female)
Most important group is 9-14 years
 Carcinoma Cervix Staging
Within cervix Involves Vagina Beyond Vagina Bowel - bladder
(VP) (V-P in CP)
1a : Microscopic 2a : Upper ⅔ of vagina 3a : Lower ⅓ of vagina 4a : Bowel, bladder
t/t conisation 4b : Distant mets
2b : Parametrium 3b : Pelvic side wall (including Inguinal LN)
1b : b¹ < 2cm Hydronephrosis
b² 2-4cm mc stage of presentation
b³ > 4cm
"B - 2 - 4" 3c : Pelvic and para-aortic LN

Fertility preservation procedure (conisation) can be done till 1B¹

For all other stages its CT + RT

Carcinoma Ovary

1a : U/L ovary 2a : Fallop. tubes or uterus 4a : Pleural effusion

Peritoneal spread
1b : B/L ovaries 2b : Other pelvic str. 4b : Distant mets
1c : Capsule involved (including Inguinal LN)

Ovarian tumors are not radiosensitive and radiotherapy does not form part of
the protocol for treatment of ovarian cancers.

Distribution
Cell type of primary
tumors (%) Epithelial tumors (germinal epithelium)
Most common ovarian tumors
Serous (watery; psammoma bodies) or Mucinous
CA-125 raised
Surface Epithelial
epithelial cells tumors
(~90%) 1. Cystadenoma : Single cyst
2. Cystadenocarcinoma : Complex cyst
3. Endometroid : Resembles endometrium
4. Brenner : Bladder like, coffee-bean nuclei

Germ cell
Oocytes tumors
(~5%)
Germ cell tumors
1. Dysgerminoma : LDH elevated, m/c GCT (Radiosensitive)
2. Yolk Sac tumor : AFP elevated (Schiller Duval)
Granulosa 3. Choriocarcinoma : HCG elevated
cells 4. Teratoma : Mature (dermoid cyst, m/c GCT overall),
Immature (Embryonal carcinoma)
Theca cells
Sex
cord-stromal
tumors Sex cord stromal tumors
Fibroblasts (~3-5%)
1. Granulosa cell tumor : Estrogen excess (Call Exner bodies)
2. Sertoli - Leydig cell tumor : Androgen excess (Reinke crystalloids)
Primitive
gonadal
3. Fibroma : Meig's Syndrome (Pleural effusion + Ascites + Ovarian tumor)
stroma
 Schiller Duval bodies Cyto-Syncitio-trophoblast Inhibin B
Yolk sac tumor Chorio-carcinoma Granulosa cell tumor

Krukenberg: diffuse gastric CA mets bilaterally to ovaries; signet ring cells

Pseudomyxoma peritonei: Mucinous tumor of appendix with mets to ovary

Functional ovarian cyst

Simple unilocular cyst in women
of reproductive age
Size less than 7 cm
Only regular follow up needed
OCP if symptomatic

Ovarian cyst in post-menopausal

Ca-125 to be checked

Carcinoma Vulva
Squamous cell carcinoma is most common - HPV 16
Older females : 55-85 yrs
The most common site of vulvar cancer is Labia Majora > Clitoris > Labia Minora
LN status in groin is best prognostic indicator - Sentinel lymph node biopsy done
Vascular spread is very rare

Types of hysterectomy
Important OBG drugs

Drugs related to prostaglandins Uterotonics

A. Misoprostol (PG E1) A. Syntocin
Uterotonic agent Induction and augmentation
800mcg (mucosal) for MTP AMTSL : 10 IU
PPH : 40 IU
B. Dinoprostone (PG E2) Dinner for 2 MTP : 2nd trimester
Available as gel Complication : Tachysystole
Used for induction of Labor
Never used for PPH B. Methyl-ergometrine
Used for PPH
C. Carboprost (PG F2 alpha) Alpha drug for PPH Contraindicated in htn, heart diseases, twins
Best drug to control PPH
0.25mg IM C. Oxytocin
Max doses 8 (2mg) At low dose increases force and frequency of
contractions
D. Mifepristone : Inhibits progesterone At high doses causes HYPOTENSION
Used for MTP hence never administered as bolus
aka RU-486
200mg mucosal

Magnesium Sulphate Tocolytics

1. Treatment of eclampsia (Pritchard regimen) 1. Ritodrine (ß agonist)
2. Nifedipine (tocolytic of choice)
2. Neuroprotective and membrane stabiliser
3. Terbutaline
(reduces motor endplate sensitivity to Ach)
4. MgS04
3. Tocolytic 5. Indomethacin
6. Atosiban
Pritchard regimen
Loading dose : 14 gm Prit chauda
4gm (20%) IV Selective receptor modulators
10gm (50%) IM - 5gm in each buttock
A. Tamoxifen (SERM)
Maintenance dose : Estrogen antagonist at breast
5gm (IM) in alternate buttock (4 hourly) Agonist at endometrium
(risk of endometrial cancer)
Therapeutic level DOC for luminal A type breast cancers
4-7 meq/L in pre-menopausal patients

Side effects B. Raloxifene (SERM)

Pulmonary edema Used for post menopausal osteoporosis
Anuria No risk of breast/endometrial cancer
All SERMs have higher risk of VTE
Monitoring for toxicity
Deep tendon reflexes lost (1st sign of C. Ulipristal (SPRM)
toxicity, skip the maintenance dose) Best emergency contraceptive
Resp. depression
Cardiac arrest D. Letrozole (Aromatase inhibitor)
Prevents peripheral conversion of
T/t for toxicity : Calcium gluconate androgens to estrogen
No risk of VTE
MTP

1st trimester 2nd trimester Upper limit of MTP

1. Mifepristone 1. Misoprostol
1. Upto 20 weeks for contraception failure
2. Miso + Mife 2. Miso + Mife
(1 RMP needed)
3. Miso + Mtx 3. Dinoprostone
2. Upto 24 weeks for rape/vulnerable women
4. Miso + Tamoxifen 4. Carboprostone
(2 RMPs needed)
Vaccum aspiration Dilation and evac 3. No upper limit for fetal anomalies
Suction and evac. Oxytocin infusion
Dilation and evac. Qualification :
DNB/MS OBG
RMP 25 cases
6 months housejob in OBG
Mild preclampsia : 37 weeks
Severe preclampsia : 34 weeks
Eclampsia/ HELLP : Immediate TOP Consent :
Only patient's consent needed
Rh isoimmunization nonsensitised : 39 weeks Husband's consent not needed
Rh isoimmunization sensitized : 37 weeks
Record maintenance :
Placenta previa : 37 weeks
Can't disclose patient's identity
Abruptio placenta : 34 weeks
Patient's name not recorded.

Absent EDF : 34 weeks

Reversal of EDF : Immediate TOP

MVA
Used for MTP at 7-12
weeks of gestation
660 mm Hg
60 ml capacity
Gynaecological infections
Differential diagnosis of vaginitis
Bacterial vaginosis Trichomoniasis Candida vaginitis
Diagnosis (Gardnerella vaginalis) (trichomonas vaginalis) (candida albicans)

Thin, off-white Thin, yellow-green Thick, cottage

discharge Malodorous cheese discharge
Examination Fishy odor Inflammation Pruritis
No inflammation present Inflammation
(strawberry cervix) present

Amsel's Criteria
pH > 4.5
Clue cells pH > 4.5 Normal pH (3.8-4.5)
Laboratory findings Motile trichomonads Pseudohyphae
Positive whiff test
(amine odor with KOH)

Metronidazole or Metronidazole;
Treatment Fluconazole
clindamycin treat sexual partner

Clue cells Kite shaped organisms Sheesh Kebab sign Cotton ball
Vaginal Epithelial cells Trophozoites of Pseudohyphae of
h/o IUD or Cu-T
studded with bacteriae trichomonas candida
Bacterial vaginosis Trichomoniasis Candidiasis Actinomyces
CHAPTER 11
PEDIATRICS
Definitions

IUGR
< 10th centile intra-uterine size
Abnormal doppler indices

Symmetrical IUGR Asymmetrical IUGR

NO head sparing Head sparing
Congenital infections UPI
Ponderal index > 2 Ponderal index < 2
Poor prognosis Better prognosis

Ponderal Index = Weight

_______________
(Length of femur) ³

Normal value >2

LBW : < 2.5 kg Physiological weight loss

VLBW : < 1.5 kg Preterm : 15 % of TBW, regain by day 15
ELBW : < 1 kg Term : 10 % of TBW, regain by day 10

Upper limit of normal

First urine - 24 hours number 1 in 1 day
First stool - 48 hours number 2 in 2 days

Mortality

Neonatal mortality At risk infants

Prematurity > Asphyxia > Sepsis > Cong. anomalies Birth weight < 2.5kg
Twins
NMR : (Neonatal death / Live births) X 1000 Birth order of 5 or more
Artificial feeding

Under 5 mortality Weight <70% of the expected weight

Failure to gain weight during 3
Pneumonia > diarrhea > injury > malaria successive months
U5MR : (Under 5 death / Live births) X 1000 Children with protein-energy
malnutrition (PEM) and diarrhea
Indicator of social development (according to UN)
Working mother
 Neonatal resuscitation

Birth
Neonatal resuscitation is done for all newborns and
starts before birth. Term
Yes Routine care
Tone
Provide warmth
Cry
Open airway
Bag and mask : HR < 100 Dry
Invasive ventilation : HR < 100 (even after bag and mask) No

Chest compressions : HR < 60 Stimulate

Epinephrine : HR < 60 (even after chest compressions) No

HR < 100 No Labored breathing or

Routine care 30 sec Gasping or apnea? persistent cyanosis?
Suction : Mouth then nose (M ➡️N) Yes Yes
Room temp : 25° C
PPV
(Bag and mask) CPAP
60 sec

Bag and mask ventilation HR < 100

Yes
Start within 1 min, if HR < 100/min
Oxygen saturation - 21 % (Room air) Endo-tracheal
No
Contraindicated in : CDH or TEF intubation

Chest compressions HR < 60

2 thumbs Yes

Lower 1/3 of sternum Start CPR

CC : PPV - 3 : 1

Epinephrine HR < 60

1 : 10,000 IV Yes

Vascular access of choice - Umbilical vein IV epinephrine

APGAR Score

Prognostic score
Done at 1min and 5mins
Appearance
5 components
Min 0 and max 2
Score < 3 indicates need for
Pulse
resuscitation
Grimace R is repiratory effort and not rate

Attitude

Resp. effort
Benign newborn Lesions

Erythema Neonatal Pustular Miliaria Harlequin Cutis

toxicum dermatitis change marmarota
Blocked sweat
↑Eosinophils ↑Neutrophils glands (eccrine) Physiological vascular response

Mongolian Strawberry Neonatal Cradle cap Nipple/Vaginal

spots hemangioma acne (Seborrheic dermatitis) discharge
Dermal Capillary hemangioma Due to maternal in older children Due to maternal
pigmentation (aka Stork bite) androgens rule out LCH estrogens

Congenital adrenal hyperplasia

Aldosterone Testosterone
Increased Testosterone
21-hydroxylase
deficiency 2 1 Virilisation in females
Precoceous puberty in males
11-hydroxylase
deficiency 1 1 Decreased Aldosterone
17-hydroxylase Electrolyte imbalance
deficiency 1 7 Shock in severe cases

21-OH deficiency is most common (ambiguous genitalia + shock in a female child)

Low Cortisol due to enzyme defect : no negative feedback on ACTH ➡️ high ACTH
High ACTH causes hyperplasia of adrenals
Screening for 21-OH deficiency : Serum 17-OH-progesterone levels
Confirmation of diagnosis by serum levels of cortisol, testosterone and aldosterone.
 Neonatal hypothermia
Temperature of < 36.5 ° C in neonates
Measurement : Axilla for 3 mins Kangaroo mother care
Physiological protection by non shivering For all babies
thermiogenesis (brown fat, ETC uncoupling) Started immediately after birth

1. Skin to skin contact

2. Exclusive breastfeeding
37.5 -36.5 °C Normal 3. Support from hospital staff
36.5 - 36 °C Cold stress 4. Early dischage
Moderate
36 - 32 °C hypothermia
Severe
< 32 °C hypothermia

No bateesi in
babies

Neonatal sepsis

MCC of neonatal sepsis : Klebsiella Sepsis Screen ≥ 2 indicates sepsis

Earliest clinical feature : Reduced feeding
Leukopenia (TLC < 5000)
Risk factors : Preterm > ROM for more than 18 hrs > PPV
Neutropenia (ANC < 1800)
Initial investigation : Neonatal Sepsis screen
IOC : Culture Immature neutrophil to
total neutrophil (I/T) ratio > 0.2 Band form

Micro-ESR > 15mm 1st hour

Early onset sepsis Late onset sepsis CRP + ve
Within 72 hrs of birth After 72 hrs of birth
Group B strep is mcc No single organism
From maternal genital tract Community acquired
Presents as pneumonia Presents as meningitis

Neonatal hypoglycemia

Blood glucose : < 40 mg/dl Management

Plasma glucose : < 45 mg/dl If symptomatic → IV dextrose
Sample : Heel prick If asymptomatic, check blood glucose
Earliest clinical feature : Jitteriness

< 20 20-45
20-40 IV dextrose Oral feeds
(IV dextrose if not responding)
Neonatal Jaundice

Pathological Jaundice
Appears < 24 hrs - ABO/Rh incompatibilty
Persists > 14 days - CN Syndrome, Breast milk jaundice Breast - milk jaundice
Serum bilirubin increase by 5 mg/dl/day Pregnediol in "breast milk"
Serum bilirubin > 15 mg/dl inhibits UDP-GT
Jaundice > 14 days
toxic guests Continue breast feeding
Come within 24hrs and
don't leave for 14 days
Breast - feeding jaundice
Insufficient "breatfeeding"
Extra-hepatic biliary atresia Causes dehydration in
Obstructive Jaundice (clay colored stool, urine staining clothes yellow) neonate → Jaundice
Direct bilirubin > 2 mg/dl Counsel on proper breast
Associated with CFC1 gene mutation feeding
Initial investigation : USG
Highest NPV : HIDA scan
Gold standard : Intra - op cholangiogram
Treatment : Kasai's procedure

Unconjugated bilirubinemia Conjugated bilirubinemia

Crigler Najjar Sx Dubin Johnson Sx

UDP -GT severely deficient MRP 2 aka ABCC2
Type 1 : Kernicterus (ATP Binding Casette,
Type 2 : Responds to Phenobarbi2one family C type 2)
Black liver (due to
epinephrine metabolites)
Gilbert Sx
UDP -GT mildly deficient
Jaundice manifests at times Rotor Syndrome
of stress (fever/infection) No black liver

Phototherapy
Structural isomerism is the main mechanism (Bilirubin → Lumirubin)
Other mechanisms are photo-isomerisation and photo oxidation.
Distance : 30-45cm (wooden scale length)
Wavelength of light : 450 nm

Trans cutaneous
bilirubinometer
Screening for neonatal jaundice
HIE (hypoxic ischemic encephalopathy)

Neonatal Seizures
Most common type : Subtle Seizures Best prognosis : Focal clonic
Most common cause : HIE Worst prognosis : Myoclonic
Other causes : Bedside monitor : Amplitude integrated EEG
1. B⁶ def (Glutamine → GABA) Initial investigation : USG ( Rule out IVH)
2. Hypo/hyper natremia IOC : DW MRI (Shows Ischemia)
3. Hypocalcaemia DOC - Phenobarbitone
4. Hypoglycemia (<45)

HIE Patterns

Term infant Pre-term infant

Quadriplegia Choreo- Diplegia

(all 4 limbs) athetoid type (only lower limbs)

1. Scissoring
2. Crouching
3. Toe walking

Parasagittal injury Status Marmarotus Periventricular leucomalacia

Spastic quadriplegia Most common type of HIE Spastic diplegia

Sarnat and Sarnat staging for HIE

HIE 1 HIE 2 HIE 3

Irritable Lethargic Comatose
Moro Moro Moro
exaggerated diminished absent
Mild hypotonia Hypotonia Severe hypotonia
No seizures Seizures No seizures
Poor suck No suck Irregular respiration
 Neonatal Respiratory distress

Respiratory Distress

Pre-term Term Post-term

At birth 1-7 days h/o persistent

oxygen support

Hyaline membrane Apnea of Bronchopulmonary

disease prematurity dysplasia
B/L ground glass Bradycardia > 21% O² for 28 days
↓ Pleural effusion
opacities ↓
Low O² Transient tachypnea
B/L air bronchogram ↓ O² impairs alveolar
White out Apnea development of newborn
appearance of lungs DOC : Caffeine Removal of fluid from
lungs is aided by the
process of labor and
maternal epinephrine
(during labor)
In C-section, there is
retained fluid in lungs
Resolves spont. in few
days

Shake test
Used to test for fetal lung maturity.
Amniotic fluid + 95% ethanol
If bubbles formed then lecithin
present (mature lungs)

Peri - hilar opacities

Other tests for fetal lung maturity Meconium aspiration

1. Lecithin : Sphingomyelin ratio > 2:1 syndrome
2. Nile blue sulphatase test : Orange when Check HR, cry, tone "HRCT"
phosphatidylglycerol present If any-one abnormal then non-
vigorous baby
Non-vigorous babies need PPV
Meconium is green in color due
Respiratory Distress with particular history to biliverdin
Can also cause meconium ileus
(obstruction at ileum)
Scaphoid abdomen h/o sibling death

Congenital Diaphragmatic hernia Neonatal pulmonary alveolar proteinosis

Abnormal protein deposition in alveoli : SP-B
Crazy Pavement pattern on HRCT

Bag and mask ventilation is contraindicated Bowel in thorax

 Silverman Anderson Scoring Downe's Scoring
Lung - X RG CAR

L Lower chest retractions R Retractions

U Upper chest movement G Grunting
N Nasal dilatation C Cyanosis
G Grunt on expiration A Air entry
X Xiphoid retraction R Respiratory rate

(low score is better prog for both)

Neonatal Reflexes

Palmar grasp Rooting ATNR Moro's Parachute

reflex reflex (Ass. tonic neck reflex) reflex reflex
Disappears in 3 Helps in latching Disappear : 6 months Disappear : 6 months Appears after 8
months Disappears in Symm. tonic neck reflex months
1 month develops at 6-9 months Exists for life
Boo!
Mono - play

Abnormal Moro reflex

Persistent moro : Cerebral palsy
Exaggerated moro : HIE -1
Absent moro : Kernicterus, HIE 2 or 3, Down's
Assymetric moro : Erb's Palsy, Clavicle fracture
Landau Symm. tonic
reflex neck reflex
Reflexes that appear after birth
Parachute reflex Appears after 3 months Helps in crawling
Symm. tonic neck reflex Exists for 1 - 2 years On neck extension, UL also
Landau's reflex extend and LL flex
Feeding

Late Term Post term

Moderately preterm
Very preterm 37-40 41-42
Extremely preterm 35-36 weeks weeks
preterm 32-34 weeks
29-31 weeks
28 weeks
weeks

+3 +3 +2 +3

IV fluids OG/NG tube Palladai Breast-feeding

No gastric No coordination spoon
motility between suck Coordination
swallow and breath begins
(for training)

Necrotising Entero-Colitis
Risk factors : Preterm, formula feed, PDA
Breast milk is the most important protective factor

Bell's Staging
Pneuma2sis : 2A
1A Bradycardia, Apnea
Suspcted NEC
1B Bloody stool 🩸 Pneumatosis intestinalis

2A Air in bowel wall

(pneum. intestinalis)
Proven NEC
2B Gas in portal vein

Ball : 3B
3A Acidosis and DIC Complications
3B Pneumo-peritoneum of NEC
Football sign
(pneumoperitoneum)
Indication for surgery
NPO and antibiotics for all
Surgery for 3B
Acute Diarrhea

Acute Diarrhea Dehydration in SAM

Holliday Segar formula
Unreliable:
For daily maintenance fluids Parametres checked Skin turgor
< 10 kg : 100 ml/kg 1. Appearance Mental state
11-20 kg : 1000 ml + 50 ml/kg 2. Thirst Mouth and tongue
"ATES"
>20 kg : 1500 ml + 20 ml/kg 3. Eyes Most reliable
4. Skin pinch Urine output > Thirst

Everything Irritable child Lethargic child

Normal Thirsty Not able to drink water
Eyes sunken Eyes very sunken
Skin pinch > 1 sec Skin pinch >2 secs

No dehydration Some dehydration Severe dehydration

Give ORS whenever
child wants
75ml/kg 100ml/kg
Oral > IV fluids IV fluids
Over 4 hours 30 ml and 70 ml in 1:5 time
Zinc for 14 days (10mg for <6 < 1 yr over 6 hrs
months and 20mg for others) > 1 yr over 3 hrs

Cmposition of ORS

Rehydration solution for

Reduced osmolarity ORS ReSoMal malnourished
Glucose and sodium : 75 each More Glucose and pottasium
Chloride + Citrate : 65 + 10 = 75 Lower Sodium - 45
Pottasium : 20 Added zinc, copper, magnesium

Total : (75 × 3) + 20 245 Overall osmolarity higher

300
1. Potassium : Replace the large potassium losses
2. Citrate : Corrects base-deficit acidosis.
3. Glucose : Promotes the absorption of sodium in the small intestine (SGLT¹)
IMNCI Pneumonia

Signs of Danger signs of

pneumonia pneumonia
1. Chest indrawing 1. Sleepy
2. Fast breathing 2. Starving "S"
3. Stridor
> 1 year : 40/min
4. Saturation < 90
< 1 year : 50/min 5. Cyanosis
< 2 months : 60/min 6. Seizures

Rx Rx
Amoxicillin for 5 days First dose of Amoxicillin
Home care IM gentamicin
Explain danger signs Refer to higher center

Acute Rheumatic fever

Molecular mimicry, Group A strep (S. Pyogenes)

JONES criteria used for diagnosis

J Joint involvement (polyarteritis)

O Myocarditis
N Nodules (subcutaneous)
E Erythema Marginatum
S Sydenham's Chorea

Minor criteria includes

CRP, ESR, Fever, Leukocytosis
Arthralgia
Prolonged PR interval
History of rheumatism

Throat cultures 2 Major criteria

Sydenham chorea
growing GABHS
DOC : Penicillin
OR
(Late finding) OR
Elevated ASO
and
titres 1 Major criterion 2 Minor criteria
Erythema Marginatum

Prophylaxis: Benzathine penicillin (IM 3 weekly)

Without carditis : 5 yrs / till age 21
With carditis : 10 yrs/ till age 21
With carditis + valvular disease : 10 yrs / till age 40
 GI Emergencies
1. Newborn with continuous drooling : Tracheo-esophageal fistula

Coiling of NG tube H type (E)

in stomach Type A Type B Type C Type D Type E
Presents late
Only Proximal Distal Double Isolated
Iohexol/gastrograffin
atresia fistula fistula fistula fistula
study
(no gas in stomach) m/c aka H type

2. 6-8 weeks baby with non-billious emesis : Congenital hypertrophic pyloric stenosis (CHPS)

Visible peristalsis : left to right

Olive shaped mass
Electrolyte abnormality due to loss of gastric fluid
(Reduced Na, K, Cl + met alkalosis)
Paradoxical aciduria (kidney saves K+ and gives up H+)
Management
Initial medical mx for electrolyte correction
String sign on Thickened pylorus on
barium study USG (IOC) Ramsted's pyloro-myotomy (definitive)

3. 2 day old with billious emesis : Small intestinal atresia 4. Lower GI bleed
Lower GI Bleed
1
Painless Painful
2 Meckel's
1 2 Intussuception
3 Diverticulum Red currant jelly stools
True congenital H/o rota virus vaccine
diverticulum
"Rule of 2"
Double bubble sign Triple bubble sign
2% of the population
↓ ↓
2 feet from SI lower end
Duodenal atresia Jejunal atresia 2 inches long
Age of onset : before 2 yrs

Barium enema
5. Failure to pass meconium > 48hrs Diagnostic as well
as therapeutic

Meconium ileus Hirschprung dis.

Ileal obstruction Absent nervous plexus
Associated with NCC migration defect
cystic fibrosis M/c location : Sigmoid colon
Gold std : Punch biopsy Tc⁹⁹ pertechnate scan
Target sign /
Donut sign
On USG
 Cystic Fibrosis
AR transmission (important example)

CF is diagnosed when an individual has both:

1. One clinical presentation of the disease
2. Evidence of CFTR dysfunction.

Clinical Presentation of CF includes:

Positive neonatal screening test
A sibling carrying the diagnosis of cystic fibrosis
One clinical sign of cystic fibrosis

Evidence of CFTR dysfunction:

Elevated chloride concentration in sweat (≥ 60 mmol/L) in at least two independent measurements
At least two CFTR mutations (chromosome 7)
Nasal potential difference measurement (NPD) or intestinal short-circuit current measurement (ICM).

Sweat 60ic
Sweat chloride > 60

Chronic sinusitis
Nasal polyps

Obstructive lung disease Excessively salty sweat

Bronchiectasis
Frequent infections
Pancreatitis
Abnormalities of the liver and bile duct Exocrine pancreatic insuficiency

Nephrolithiasis
Rectal prolapse
Urinary tract infections

Delayed puberty
Male: usually infertile
Female: reduced fertility

Digital clubbing
Osteoporosis
(due to chronic hypoxia)
Frequent fractures
Kyphoscoliosis
1. Meconium ileus
2. Malabsorption/failure to thrive
3. Neonatal obstructive jaundice
Adult VS Fetal Circulation
Adult circulation

Right heart Pulm art Pulm vein Left heart

IVC SVC

Asc. Aorta Desc. Aorta

(upper body) (lower body)

Fetal circulation

1. Ductus arteriosus
Mixed oxygenated and deoxygenated blood

Right heart Pulm art Pulm vein Left heart

High Pulmonary
IVC SVC vascular resistance

2. Foramen ovale Asc. Aorta Desc. Aorta

⅓ of IVC blood without mixing (upper body) (lower body)

5. Ductus Venosus
1. Ductus arteriosus
Placenta 2. Foramen ovale
3. Umbilical artery
4. Umbilical Vein 3. Umbilical Artery
4. Umbilical vein
5. Ductus Venosus
Fate of fetal circulation

1. Ductus arteriosus
Lig. arteriousus

Right heart Pulm art Pulm vein Left heart

IVC SVC Lungs functional

2. Foramen ovale Asc. Aorta Desc. Aorta

Limbus fossa ovalis (upper body) (lower body)

5. Ductus Venosus
Lig. Venosus
Placenta
4. Umbilical Vein 3. Umbilical Artery
Lig. teres hepatis Medial umb. ligament

Closure of DA Closure of DV
Pulmonary vascular resistance gone, low Functionally closed after placenta
pressure in DA removal (3rd stage of labor)
Oxygenated blood from aorta enters DA Anatomical closure in a week
Muscular spasm in DA due to oxygenated Forms ligamentum venosus
blood (functional closure in 10-15 hrs)
Anatomical closure : 10-21 days
Forms ligamentum arteriosus

Prostaglandins
Cause vasodilation, prevent closure of DA Summary
Alprostadil (PGE¹analogue) keeps it patent 1. Ductus Art. : Ligamentum arteriosus
Used in cyanotic heart diseases 2. Ductus Venosus : Ligamentum venosus
3. Foramen Ovale : Limbus fossa ovalis
Indomethacin/ibuprofen
4. Umb vein : Lig. Teres Hepatis
Anti Prostaglandin, used for closure
5. Umb artery : Medial umbilical ligament
of PDA in pre-term babies
Median umbilical ligament : Allantois/Urachus

Closure of foramen ovale

Functional closure on initiation of
breathing
Anatomical closure takes "Months"
Forms fossa ovalis
 Congenital Heart disease : Acyanotic

Acyanotic heart disease

Pulmonary Plethora Normal pulmonary

(Excess blood in lungs due to blood flow
left to right shunt)
Coarctation of Aorta
PDA

Right heart Pulm art Pulm vein Left heart

ASD / VSD /
End. Cushion defect

Brachio - femoral delay

1. PDA Intermittent claudication
Continuous machinery murmur (heard at infra-clavicular fossa) Hypertension (lower perfusion to kidney
Mostly asymptomatic and resolves spontaneously. activates RAAS)
Small/asymptomatic PDA : only monitoring needed,
Indomethacin for closure of PDA in pre-term babies.
Large/ symptomatic PDA : PDA device closure (cath based procedure)

2. VSD
Most common congenital heart disease
Membranous type is more common
Pan-systolic murmur
Small defects dont need t/t (resolve sponaneously by 2 yrs)
Closure needed for large/symptomatic VSDs

Inferior rib notching (Roesler's Sign)

3. ASD 3 sign on X-ray
Wide and fixed split of second heart sound Reverse 3 sign on Barium Swallow
ASD repair via cath based procedure or open heart surgery. Associated with Turner's Sx

4. Endocaridal cushion defect

Gooseneck deformity
Associated with Down's Syndrome
 Congenital Heart disease : Cyanotic
Cyanotic heart disease

PleThora Oligemia
Box and Boots

TAPVC TGA
Total Anomalous Pulmonary Venous Transposition of Great Arteries
Circulation Small vascular pedicel
2nd heart sound wide and fixed split Dependent on septal defect
All chambers have same O² TGA is m/c cyanotic heart disease
saturation in neonates
Dependent on septal defect Rx : Alprostadil (keep DA open),
Rashkind's atrial septostomy
Pulmonary Vein
Figure of 8

Pulmonary
TAPVC
Vena Vena
Cava Vein
Cava

De-oxygenated Oxygenated
Types
blood to Aorta blood to PA Egg on string app.
1. Supracardiac : M/c (Figure of 8)
2. Cardiac (Rt atrium) TGA
3. Infracardiac (inf. VC) most lethal

Tetralogy of Fallot Ebstein's Anomaly

Boot shaped ht. (Couer en sabot) BOX shaped heart (large right atrium)
RVH causes the boot shape Small RV : Oligemia
M/c cyanotic heart disease H/o lithium intake in mother
Himalayan P waves
1. RV outflow obstruction
Boot shaped heart ⬇️ RBBB
2. RV hypertrophy
TOF
3. VSD (Right to left shunting)
4. Over-riding of aorta over
ventricular septum
Severity of Symptoms
Depends upon degree of RV obstruction
In severe TOF, heart failure occurs as soon as PDA Himalayan P waves
closes
Tet spells : When kid cries, there is syncope
Squatting increases peripheral resistance and
Most commons
lessens shunting of blood
Congenital heart dis : VSD
Box shaped heart Cyanotic heart dis : TOF
Treatment
Ebstein's Cyanotic heart dis in neonates : TGA
Treatment for heart failure in symptomatic
Anomaly Surgery : For right outflow tract, VSD.
Growth

Weight Teeth Eruption

Doubles in 4 months Primary teeth in the upper jaw
Becomes 4 times in 2 years erupt earlier
Lower central incisors are an
Becomes 3 times in 1 year exception and also are the first
Becomes 5 times in 3 years to erupt.
Delayed Eruption if no primary
2 in 4 4 in 2 teeth by 13 years.

Height
Height at birth is 50cm Upper segment /
Lower segment
1/2 of adult height in 2 years
U/L is 1 at 7 years of age
Doubles in 4 years
U/L > 1 for kids less than 7 years
U/L in adults is around 0.9

High : Rickets, Achondroplasia,

Head circumference congenital hypothyroidism
At birth 34cm
Low : SED, vertebral anomalies
HC > CC at birth
HC = CC at 1 year
HC < CC after 1 year

HC shouldn't be measured in the

first 24 hours (moulding if
present can give wrong values)

MACROcephaly : > 2 SD Achondroplasia Spondylo-epiphyseal

MICROcephaly : < 3 SD dysplasia

SED and low

at 4 Short Stature
Months : weight doubles
Years : height doubles

1. Constitutional growth delay (m/c) Familial short stature

at 7 yrs Delayed puberty Short stature history in family
US = LS Eventually achieves normal height Sab theek hai still short
Weight : 7 times of birth 2. Hypothyroidism
3. GH def
Breast milk
Antimicrobials in breastmilk:
Breast milk vs Cow milk 1. IgA, IgM, IgG
Less protein, more availability (more whey, less casein) 2. Bifidus factor
More lactose 3. Lactoferrin
More Vit C and Vit D 4. Macrophages
More taurine and cysteine Cys-Taur : Sister 5. B12 Binding protein (haptocorrin)
Less calcium and phosphorus

Colostrum - 1st milk rich in IgG

Foremilk : More water
(quenches thirst)
Hind milk : More protein
(nutrition)

Breast milk deficient in Expressed breast milk

Not in comparison to cow's milk but generally can be stored at
Vit K Room temp - 6 hours
Iron KID Refrigerated - 24 hours
Vit D Frozen (-20 degree C) - 3 months.

Protein energy malnutrition

Kwashiokor Marasmus

Flag sign

Kwashi Orkor Mara-smus

Swollen belly (looks dead 💀)
Protein deficit Total calorie deficit
Edema prominent Voracious appetite
Loss of appetite More common in infants <1 year
Flaky paint Dermatitis
Flag sign
Fatty liver

Macronutrients
1. Fats (∼9 kcal/g)
2. Carbohydrates (4 kcal/g)
3. Protens (∼4 kcal/g)

Energy from saturated fats

should be <10%
 Malnutrition
Criteria for SAM
6-59 months of age
A. Weight-for-height below - 3 SD
B. Visible severe wasting
C. Presence of bipedal edema
D. Mid-upper arm circumference below 11.5cm

SAM workup
Severe edema or low appetite (failed appetite test) or
⬇️Weight for ⬇️Height ⬇️Weight medical complications - Complicated SAM (inpatient)
height for age for age
If the above-mentioned signs are absent -
Acute Chronic Acute + uncomplicated SAM (home management)
malnutrition malnutrition Chronic

Compicated SAM Mx
Vitamin K deficiency 1st week - Stabilisation (infection treated, no iron)
2nd week onwards - Rehabilitation (iron added)
Breastfed infants (breast milk is deficient in
1st 3 days of Stabilisation : treat hypoglycemia,
vitamin K while formula milk is fortified)
hypothermia and dehydration.
Cystic fibrosis (fat malabsorption) Electrolyte correction happens throughout
Billiary atresia (fat malabsorption)
Antibiotics (kill the gut bacteria)

Mild to Moderate malnutrition mx

Zinc deficiency -2 SD to -3 SD
Dwarfism - Diarrhea - Dermatitis Nutritious home cooked food with min 150 kcal/kg/day
Hypogonadism Frequent feeding may be required to achieve the
T-cell immunodeficieny necessary energy intake.
Animal-source foods > Plant source foods
Phytate rich food can cause chronic iron and A slight increase in protein intake (3g/kg/day)
Weight gain is the best measure of treatment efficacy for
zinc deficiency
mild and moderate malnutrition.
Acrodermatitis enteropathica (Congenital
zinc deficiency)

Hypophosphatemic rickets
Aka X-linked dominant rickets Shakir tape
MC genetic cause of rickets (MCC overall is MUAC
nutritional vitamin D def.) Borderline : 11.5-12.5
PHEX gene mutation inhibits phosphate Herpenden callipers <11.5 : Malnourished
reabsorption in the proximal tubule levels Triceps fold thickness Age independent
and hence, causes increased excretion of
phosphate.
It also inhibits renal 1-alpha hydroxylase
leading to reduced 1,25 dihydroxy vitamin D.

Infantometer
Baby's length upto 2 yrs
 Developmental milestones

1 - Boring 2 - Smiles 3 - BOO ! 4 - ROFL

Visual fixation Social smile Palmar grasp disappears Bidextrous grasp - mouthing
Neck holding starts Binocular vision
Recognise mother Laughs and plays
Cooing Pulls to sit, no head lag

6 - Solo play 9 - Toxic GF 10 - FRIENDS 12 - Birthday

Unidextrous grasp Immature pincer grasp Pivot Mature pincer grasp
Monosyllables Bi - syllables (bye bye) Creeps Stands without support
Tripod Sits without support Stands with support Throws ball
Stranger anxiety Crawling Peek-a-boo !! Comes when called
Moro and ATNR 1-2 words
disappears

Enuresis
Child has never been dry - primary
enuresis (Should be by 18 months)
If bedwetting starts after a minimum
period of six months of dryness at
night, it is termed as secondary
enuresis.
15 - Mini me 18 - Domestic mimicry 2 years
Tower of 2 Explores drawer 2 steps up and down Due to delay in maturation, circadian
blocks (mini me) Unzips Parallel play rhythm is impaired leading to enuresis.
Jargon speech Draws lines
Runs and kicks ball
Walk alone Feeds with spoon Asks for food and drink Treatment - Behavioural therapy with
Undresses completely positive reinforcement, bladder
Dry during day
Names body parts alarms.
3 blocks 2 X 3 = 6 blocks Nasal desmopressin for resistant cases

3
o 4+
3 years - tricycle 4 years - hopscotch 5 years
1 step upwards 1 step downstairs Skips
Circle, Tricycle Hops Draws Triangle
Name, age, sex Right left discrimination Can dress and undress
Dresses + undresses Square, cross herself
(can't do buttons) Can say stories and poems Can tie shoe lace
Toilet alone Asks the meaning of words
3 X = 9 blocks
Neuroblastoma vs Nephroblastoma

Neuroblastoma Nephroblastoma
(Wilm's tumor)

Neuro-endocrine tumor (from adrenal medulla) Kidney origin

Most common abdominal malignancy in children Most common renal malignancy in children
N-MYC mutation 2nd m/c abdominal malignancy in children
Associated with opsoclonus-myoclonus syndrome WT 1 gene associated with (WAGR Sx, Denys Drash Sx)
Homer Wright pseudorosettes seen here WT 2 gene associated with (Beckwith Weidman Sx,
Horseshoe kidney)

Overall m/c malignancy in children : ALL

Most common solid tumor in children : Astrocytoma
Evomoz notes
Biochemistry
FMT
Anesthesia
Psychiatry
CHAPTER 12
BIOCHEMISTRY
 Glucose Transporters

SGLT GLUT
Sodium and Glucose co-transport Only Glucose transport
Secondary active transport Facilitated transport
Unilateral Bilateral

SGLT 1 : Intestines 1 intestine GLUT 1 and 3 : Basal uptake in crucial organs

SGLT 2 : Kidneys 2 kidneys (Brain, RBCs, Placenta)
GLUT 2 : Food related Max affinity for glucose : GLUT 3
SGLT 2 inhibitors
(Liver, Pancreas, Small intestine)
OHA : Flozins GLUT 4 : Insulin dependent uptake
Risk of UTI, Euglycemic DKA
(Skeletal muscle and adipose tissue)
Used now in heart failure

Substrates
FED STATE : Every organ uses Glucose
except Heart to prevent lactic acid build up, which can affect ion channels.

FASTING STATE (12-18hrs) : Every organ uses Fatty Acids

except RBCs (only glycolysis) and Brain (fatty acids can't cross BBB)

STARVATION (1-3 days) : Every organ uses Ketone bodies

except RBCs (only glycolysis), Liver (lacks Thiophorase, hence uses AMINO ACIDS).

Basics of Metabolism

Anabolic Pathways Catabolic Pathways

Occurs in Cytoplasm Occurs in Mitochondria
Insulin mediated (LPL active) Glucagon mediated (HSL active)
Sensitive
Enzymes active in dephosphorylated phase Enzymes active in phosphorylated phase
(⬇️ CAMP and Protein Kinase A) (⬆️ CAMP and Protein Kinase A)
1. All synthesis reactions except KB synthesis 1. Gluco-neo-genesis
2. Glycolysis 2. Glycogen-o-lysis
3. FA oxidation
4. KB sythesis and breakdown

Glycogenolysis is an exception, occurs in cytopalsm

HUG pathways
cytoplasm + mitochondria
1. Heme synthesis
2. Urea Cycle
3. Gluconeogenesis
 Trans-Amination
One amino acid to another
Requires Vit B⁶ as cofactor for enzyme amino-transferase
Alanine is the most glucogenic amino acid and forms Cahill cycle

GOT or AST
Oxalo-acetate Aspartate (toAST in OT)
Aspartate transferase or
Glutamate-oxaloacetate transferase

GPT or ALT
Pyruvate L-Alanine
Aspartate transferase or
Glutamate-oxaloacetate transferase
 Glycolysis vs Gluconeogenesis

Glucose
Hexokinase Glucose-6-phosphatase
Glucose-6-phosphate
Phosphohexose isomerase Phosphohexose isomerase
Supported by
PFK 2 Fructose-6-phosphate
Fructose 2,6 Phosphofructokinase-1 Fructose-1,6-bisphosphatase
bisphosphate Rate limiting Step
Fructose-1,6-bisphosphate
Inhibited by
Citrate Aldolase Aldolase

Dihydroxyacetone phosphate Dihydroxyacetone phosphate

Glyceraldehyde-3-phosphate (2)
Inhibited by
Arsenic Glyceraldehyde phosphate dehydrogenase Glyceraldehyde phosphate dehydrogenase
Iodoacetate Produces 2 NADH
1,3-bisphosphoglycerate (2)

Phosphoglycerate kinase Phosphoglycerate kinase

3-phosphoglycerate (2)

Phosphoglycerate mutase Phosphoglycerate mutase

2-phosphoglycerate (2)
Inhibited by
Enolase Enolase
NaF
PEP carboxykinase
Phosphoenolpyruvate (2)
Pyruvate kinase Oxaloacetate (2)
Pyruvate (2) Pyruvate carboxylase

Irreversible Steps Pyruvate carboxylase is present in mitochondria

Pyruvate to Oxalo-acetate reaction occurs in
Glycolysis Gluconeogenesis mitochondria and uses ATP
1. Hexokinase/glucokinase 1. Glucose-6-phosphatase Malate-Aspartate shuttle moves Oxalo-acetate from
2. PFK-1 (RLS) 2. Frucrose 1,6 - bisphosphatase inside mitochondria to cytosol for Gluconeogenesis
3. Pyruvate kinase 3. PEP carboxykinase Malate Aspartate shuttle also moves NADH produced
4. PEP carboxylase (in mitochondria) in cytosol to mitochondria

Gluco-kinase vs Hexokinase Substrates for Gluco-neogenesis

1. Hexokinase present in all tissues (low Km and Vmax, which 1. Alanine most glucogenic amino acid (cAhill cycle, alanine
means more affinity for glucose) to pyruvate)
2. Glucokinase present in Liver and B cells (High Km and Vmax 2. Lactate from muscles get converted to pyruvate
which means it has lesser affinity for glucose) (Cori cycle) core muscles training
High on Glucose 3. All TCA intermediate
4. Odd chain Fatty Acids : PMS FuMO

Energetics of Glycolysis Acetyl Co A the strongest initiator of Gluconeogenesis

but can't be a substrate (link reaction is not reversible)
Anaerobic : 4 - 2 = 2
Aerobic : (5 + 4) - 2 = 7

Glycolysis + link rn + TCA : 7 + 5 + 2(10) = 32 Fasting (0-16hrs) : Glycogenolysis

Fasting (16-48hrs) : Gluconeogenesis
Hexikinase and PFK1 consume 1 ATP each.
Glycogenolysis skips hexokinase (8 ATP from aerobic)
Occurs majorly in Liver and Kidney
Phosphoglycero kinase and Pyruvate kinase produce 2 ATP each
In Prolonged fasting : Kidney
 Link Reaction

Cytoplasm Mitochondria
Thymine Dependent enzymes
PDH complex Be Branched chain KA dehydr.
Lipoic acid A Alpha Keto glutarate dehydr.
Irreversible
(2) Pyruvate (2)CO² + (2)NADH + (2) Acetyl coA dependant P PDH complex
(3 C) (2 C)
T Trans-ketolase in RBC

PDH complex
5 Co-factors : Vit B(1,2,3,5) + Lipoic Acid
PDH complex has 3 components
1. PDH : produces CO2
2. DH lipoic trans acetylase : produces Acetyl coA
E1
3. DH lipoic dehydrogenase : produces NADH
di-hydro-Lipoic
PDH
Products of link reaction and ATP are trans-acetylase
allosteric inhibitors of PDH Complex
1. NADH
2. Acetyl coA di-hydro-Lipoic
3. ATP dehydrogenase

Kreb's Cycle

Kreb's Cycle is an AMPHIBOLIC pathway (catabolic + anabolic) Urea cycle

Breakdown of Acetyl CoA ⬆️
Anabolism of various reaction intermediates Aspartate
FA synthesis
⬆️
Acetyl CoA (citrate synthase) = Citrate
Citrate inhibits RLS of glycolysis
Citrate is allosteric activator of Acetyl CoA carbocylase in FA synthesis

Citrate (Aconitase) = Iso-citrate

Aconitase contains Iron and is inhibited by Fluoro-acetate (in pesticides)

Iso-citrate (Iso-citrate dehydr.) = Alpha Keto Glutarate

Rate limiting step
Alpha Keto glut. combines with NH³ to form Glutamate
(excess ammonia can hence affect Kreb's Cycle) +
From NH3
Urea Cycle
Alpha Keto glut (AKG dehydrogen.) = Succinyl CoA ⬇️
Succinyl CoA + Glycine : Heme synthesis Pathway Glutamate
Succ. CoA (Succ CoA dehydr.) = Succinate
Only substrate level phosphorylation in Kreb's Cycle
Succinate produced from Odd chain FA oxidation, joins TCA here From +
PMS Glycine
Succinate (Succ. dehydr.) ➡️ FuMO (Fumarate - Malate - Oxalo Acetate) ⬇️
Succinate Dehydrogenase is also Complex 2 in ETC Heme Synthesis
Fumarate produced in urea cycle, joins TCA here
 Electron Transport Chain
Complex 1
1. Roten-one
Utilises NADH
2. Phenobarbit-one
Inhibitors one
3. Metform-(in)one

Complex 2
Succinate dehydrogenase
(TCA cycle intermediate)
Utilises FADH
Co-factor : iron
Inhibitors Malonate - MSD
Malonate blocks Succ. Dehydr.
Classic example of Competitive Inhibition

Complex 3
Cytochrome 3ductase (reductase)
aka Cytochrome bc1 complex
Inhibitors An3mycin 1 NADH = 2.5 ATP
1 FADH = 1.5 ATP
Complex 4 Mobile Carriers
Cytochrome C
Cytochrome oxidase
1. Azide Co-enzyme Q
Contains Iron, Copper 2. Cyanide
Inhibitors Ides 3. Hydrogen sulphide
(except carbon dioxide) 4. Carbon monoxide
Uncouplers
Complex 5
Oxidative phosphorylation occurs here Electron transport occurs 1. 2,4 Dinitrophenol
but no ATP production 2. Aspirin overdose
H+ ion transfer across gradient (Chemi-osmosis)
Produces heat (non 3. Brown fat (thermiogeneis)
Has an ATPase enzyme
Inhibitors : shivering thermiogenesis)
1. Atractyloside : Inhibits ATPase
2. Oligomycin : Inhibits movement of H+ ions

Pathways with no ATP production

Uses of NADPH
1. HMP shunt : NADPH production (requires G6PD) Free radical scavenging:
2. RL shunt : 2-3 BPG in RBCs (reduces oxygen affinity) •RBC (hemolysis in G6PD deficiency)
•Lens (transperancy of lens)
3. FA Oxidation - α, Ω, VLCFA
4. Arsenic poisoning Synthesis of steroids and fatty acids:
5. Uronic acid pathway •Liver
•Adipose tissue
6. Uncouplers of ETC •Adrenal cortex
•Gonads

Rossman fold: NADP binding domain

Galactose and Fructose metabolism
Glycemic index
DHAP (to glycolysis)
Fructokinase Aldolase B Glucose, Galactose : 1
Fructose Fructose-1-P
ATP Glyceraldehyde Fibres : 0
Low Glycemic index
Fructose
Fructokinase def : Essential fructosuria (benign)
Sucrose
Aldolase B def : Hereditary fructose intolerance (severe)

Galactokinase Uridyl-transferase
Galactose Galactose-1-P Glucose-1-P
Converts UDP Glucose to
ATP UDP Galactose

Galactokinase def : Type 2 Galactosemia (benign)

Uridyl transferase def : Type 1 Galactosemia (severe)

Galactose if present in excess can form Galactitol - causes oil droplet cataract Oil droplet Cataract
(due to accumulation of Galactitol)

Glycogen Metabolism
Both processes occurs in cytoplasm

Glycogen Synthesis
Glycogen Synthase
+ Branching enzyme
Glucose Glucose 6-P Glucose 1-P UDP Glucose GLYCOGEN
Glucose Insulin

Glycogen-o-lysis

Glycogen Phosphorylase Gllucose 6 Phosphatase

+ debranching enzyme
Glycogen Glucose 1-P Glucose 6-P GLUCOSE
Glucagon Vit B⁶
Epinephrine Calcium
Muscle AMP

Von Gierke Disease 1-4 bonds

M/c glycogen storage disease
1-4 bonds
def of Glucose - 6 - phosphatase
Hypoglycemia (glucose can't be produced) 1-6 bonds
Hyperlipdemia, Hyper-uricemia
Fatty liver, renomegaly 1-4 bonds
1-6 bonds

McArdle's and Her's disease

McArdle's Her's Anderson Vs Cori's Disease
Glycogen phosporylase Glycogen phosporylase ABCD : Anderson Branching, Cori Debranching
absent in muscles absent in liver
Exercise intolerance Hepatomegaly Anderson Disease Cori Disease
Myoglobinuria (due to Hypoglycemia Amylopectin Limit Dextrans
rhabdomyolysis) Growth retardation accumulates accumulate
Second wind phenomenon : Hyperlipidaemia Fatal liver cirrhosis in Hepato-toxic
Revival of exercise tolerance childhood
 Pompe's Disease
I Cell disease
Cardiomyopathy (pump failure)
ACID maltase deficiency (aka lysosomal alpha-glucosidase) Products tagged by Golgi body are destoyed in
Hypotonia lysosomes
When "N-acetyl glucosamine
phosphotransferse" is absent, no tagging hence
Tarui's Disease no destruction
Results in inclusions
Muscle weakness + Hemolytic anemia
Defect in PFK-1

Lysosomal Storage disorders

Fabry's Disease Tay Sach's Disease
My Fabrite activity is Ceramics. We made A Galaxy A Gang of six small Jews eating onions
α- Galactosidase def Maltese cross in urine
GM² gangliosidosis Onion skin bodies
Ceramide accumulation Hexosaminidase A def
XLR transmission Angio- Ashnaki Jews are predisposed
(all others are AR) keratomas no HSM
Onion skin bodies on EM
Vortex keratopathy
Maltese cross in urine
Vortex keraropathy
Neuropathy
Angiokeratomas Neiman Pick's Disease
Pick your big nose with your sphinger with foam

Krabbe's Disease HSM present

Crab gloB is out of this galaxy! Sphingomyelin def Zebra bodies
Foamy macrophages
Globoid bodies
Zebra bodies
β-Galactosidase def
CNS involvement in type A

Thalamic hyperdensity Globoid bodies

Optic atrophy
Neuropathy
Wolman's Meta-chromatic
Leuko dystrophy
Disease Aryl Now, some tiger time
Gaucher's Disease
Acid lipase def Aryl sulphatase def
Oh my Gauch! He broke the bones, We need a bit glu and tissues! Adrenal Calcifications Tigroid app. of brain on MRI
Osteopenia - bones break
Crumpled Tissue
appearance
β-Glucosidase def.
(Alpha is Pompe's)

HSM
Pancytopenia Crumpled tissue app
(Gaucher cells)
Ehrleyn Meyer flask
Pseudo gaucher cells seen in CML
deformity

GM : Ganglioside
Ceramidase defect:
Farber's disease GM2
Hexosaminidase A : Tay sachs
(mimics RA) Hexosaminidase A, B : Sandhoff

Sulfatides GM3 Ceramide trihexoside

MLD Fabry's dis.

Glucocerebroside
Galactocerebroside
Gaucher's
Sphingomyelin
Krabbe's Ceramide
Neiman Picks
 Glycosaminoglycans
Has 2 components
1. Acidic Sugar : Glucuronic acid, Iduronic acid
Glucosamine sulphate and chondroitin
2. Amino Sugar : Glucosamine, Galactosamine
sulphate → used for t/t of Arthritis
Negatively charged
Absorbs water

1. Chondroitin sulphate : Most abundant Iduronate defect

2. Hyaluronic acid : Cell migration (metastases), Wound repair I do wanna Hunt
3. Keratan sulphate : Corneal transperancy keratan cornea 1. Hunter : No corneal clouding, XLR
4. Dermatan sulphate : Sclera, atherogenic (binds with LDL) Sclera athera 2. Hurler : Corneal clouding
5. Heparan sulphate : Negative charge on GBM

Ketone Body Synthesis

In Liver
Fatty acids and amino acids breakdown to form Acetyl CoA
HMG CoA synthase and thiolase: Forms Ketone bodies from Acetyl coA Synthase starving
Thiophorase is absent in Liver, hence can't utilise Ketone bodies
1st ketone body to be synthesised: Aceto Acetate
M/c ketone body to be utilised/tested : B-hydroxy Butyrate

Organs that utilise Ketone bodies

Brain
Heart Rothera test Benedict test
Muscles
For ketone bodies Benedict : Blue reagent
Beta hydroxy Butyrate For reducing sugars
Fruity odour in ketosis is due to Acetone formed from aceto-acetate can't be tested

Only rothera positive : Prolonged starvation

Both positive : DKA

Gerhardt test is another test for Ketones

Lipoproteins
Reverse cholesterol transport:
1. ABCA1 : tangier's disease
2. ABCG1
3. SRB1

Minimum Triglycerides Max cholesterol

Minimum size Deposits in peripheral tissue
Max phospholipids, protein, density Responsible for atherosclerosis
Fastest
Moves and gives Apo-c2 (lipoprotein lipase)
and Apo-E (absorption by liver)
No HDL
aka familial HDL deficiency
Orange tonsils
 Apo C2 Apo E

Triglycerides Taken up by
Liver
FFA
Apo B 48
(eg of RNA editing) Defect in Apo E causes
Chylomicron Remnant Chylomicron
type 3 hyperlipoproteinemia
Formed in intestinal mucosa After breaking down the triglycerides
(palmar xanthomas)
Max Triglycerides (max size) by Apo C2 (lipoprotein lipase)
Excess chylomicrons and VLDLs
Minimum phospholipid,
in blood
proteins. Apo C2 deficiency causes
Has apo-protein : apo-48 Type 1 hyperlipoprotienemia
(excess chylomicrons)

Apo C2

Triglycerides
Apo B 100
FFA

VLDL Remnant If LDL receptors are absent it causes

type 2 hyperlipoprotienemia.
Apo B 100 deficiency seen in
A-beta-lipoproteinemia
Formed by liver (Excess carbs) VLDL
aka Familial hyper cholesterolemia
Absent LDL and VLDL Endogenous triglycerides
Tendon xanthomas, corneal arcus.
MTTP gene defect Has apo-protein : apo-B-100
Familial MI
Acanthocytes in blood
Presents with malabsorption Hepatic overproduction of VLDL
causes type 4 hyperlipoprotienemia

Hyperlipoprotienemias

Familial C² : Cuts and cleaves

Familial MI
2 tendons

3:E
Remnants to beggars
in their palm
 Fatty Acid Metabolism

Fatty Acid Synthesis Fatty Acid Breakdown

Palmitate Fatty Acid (upto 8 C)

Thiokinase + CoA
Inhibits + ATP
Malonyl CoA
Biotin (carboxylation) Fatty acyl CoA
Acetyl CoA carboxylase
Insulin
+ NADPH from HMP shunt Citrate Carnitine Palmitoyl
Glucagon
Transferase - 1
Acetyl CoA
Carnitine Shuttle
ATP Citrate lyase Present on inner membrane Car breaks down

Citrate shuttle
Sit = Fat synthesis Fatty Acyl CoA
Beta Oxidation
Citrate
(from TCA cycle) Acetyl CoA

Palmitate (16 C) is the most commonly produced Thiokinase (aka Fatty Acyl CoA synthase is the
Fatty Acid. only step requiring ATP in FA breakdown.
Long chain fatty acids (> 8 C) are first broken
down in Peroxisomes.
Fatty Acids

Saturated Unsaturated Zellweger Syndrome

Monounsaturated Polyunsaturated Defect in biogenesis of peroxisomes
(mutation of PEX gene)
Omega-6 Omega-3 VLCFA + Phytanic acid accumulation
aka Cerebro-hepato-renal syndrome
Lauric acid Oleic acid Linoleic acid Linolenic acid
Myristic acid (Omega-9) Arachidonic Acid EPA
Palmitic acid DHA Odd chain Fatty Acids
Stearic acid
Lino"teen"ic acid Propionyl CoA + Acetyl CoA formed
La my pa-sta
Propionyl CoA enters Krebs cycle : PMS FuMO
Linoleic : Safflower oil Needs biotin (P to M) and Vit B¹² (M to S)
Linolenic : Flax seeds

Alpha Oxidation of FA
Branched chain FA have Phytanic acid (Methyl group
at Beta position)
These FA undergo alpha Oxidation (no ATP formed)
and need Phytanoyl coA hydroxylase
Occurs in peroxisomes (brain and liver)
Deficiency of Phytanoyl CoA causes Refsums disease
(Retinitis pigmentosa + dry scaly skin) due to Phytanic
acid accumulation.

LCAT deficiency
Lecithin Cholesterol acyl transferase deficiency
MCAD deficiency
Low HDL, high VLDL Hypoglycemia in an infant without ketones
Defective beta oxidation (Omega oxidation occurs)
1. Partial deficiency : Corneal opacities (fish eye disease) Treatment : IV glucose
2. Complete deficiency : Norum's disease Ω - MCAD
 Amino Acids
Basic : Arginine > Lysine > Histidine HLA
Tyrosine
Acidic : Glutamate, Aspartate
Dopamine and Catecholamines
Semi-essential : Arginine Melanin
Thyroxine
Branched chain : Valine, Isoleucine, Leucine VIL
Ketogenic : Leucine, Lysine Tryptophan
Niacin
Aromatic : Tryptophan, Tyrosine, Phenylalanine
Melatonin
Max UV Light : Tryptophan Serotonin
Sulphur containing : Cysteine, Methionine
Arginine
OH containing : Tyrosine, Syrine, Threonine Urea and creatinine
Imino acid : Proline NO

21st and 22nd Amino acid : Selenocysteine (UGA) and Pyrrolysine (UAG) Histidine
Co-translational modification Histamine Require
Vitamin B6
Glutamate
Essential Amino acids GABA
All basic, branched chain and Ketogenic AA : HLA + VIL + LL Glycine
From aromatic : Phenylalanine and Tryptophan Porphyrin
From OH : Threonine Heme
From Sulphur : Methionine Collagen (every 3rd element)
Valine Creatinine (Glycine, Arginine,
Arginine (semi essential) Methionine)

Maple syrup urine disease Reabsorption disorders

Cystinuria : defect in PCT
branched chain
amino acids
COLA
1. Cystine (lost "in" urine)
branched chain 2. Ornithine
keto acids 3. Lysine
4. Arginine

Hartnup's disease
Neutral amino acids not reabsorbed
in intestine
Tryptophan deficiency : Niacin
Enzyme deficient: BCKA dehydrogenase enzyme complex deficiency (Pellagra like dermatitis)
(BCKA decarboxylase in particular) Diagnosis: Excessive neutral amino
Vitamin B1 is needed BeAPT for BCKA dehydrogenase acids in urine.
Accumulation of Branched chain amino acids and keto acids
occurs
Urine odour is of Burnt sugar / Maple syrup odour
Garrod's tetrad
Clinical features Inborn errors of metabolism
1. Mental Retardation
Present in 1/2500 births
2. Ketosis
Tetrad of
3. If untreated, coma & death can occur
4. Has high mortality rate 1. Cystinuria
Rx 2. Albinism
1. Vitamin B1 supplementation 3. Alkaptonuria
2. Dietary restriction of VIL 4. Pentosuria
 Classical Phenylketonuria
Phenyl-alanine hydroxylase def
Melanin absent (fair child)
Mental retardation (↑Phenyl-alanine)
Mousy odour urine (Phenyl-acetate)
Microcephaly if in pregnancy
Screening : Tandem mass spectrometry
Blonde but
not white hair
Malignant Phenylketonuria
Tetra hydro biopterin (BH4) def
Phenylalanine
Phenylalanine hydroxylase BH4
FAH
Fumarate Homogentisic Acid Metabolism Tyrosine Thyroxine
Broken down by
Homogentisate oxidase Tyrosine hydroxylase BH4
Tyrosinase
Alkaptonuria Dopa Melanin
Homogentisate oxidase deficiency B6
Black - urine (ON STANDING)
Dopa Decarboxylase
Accumulation of homogentisate in Albinism
connective tissues known as OCHRONOSIS Dopamine Tyrosinase deficiency
(pigmentation, IV disc calcifications) Hypo-pigmentation of skin,
t/t : Nitisinone
Vitamin C
hair and Iris

Norepinephrine
SAM

Epinephrine

Tyrosinemia
Type 1 : FAH deficiency F - First
aka Hepato-renal tyrosinemia Maple syrup urine disease VIL
Cabbage smell in urine PKU M
Type 1 tyrosinemia
Type 2 : TAT deficiency T - Two
Oculo-cutaneous tyrosinemia
Hawkinsinuria
Corneal ulcers two eyes Carboxylase def. (Requires B⁷)
Isovaleric acidemia
Type 3 : HPD deficiency 4-h
Neonatal tyrosinemia (transient) Trimethyl- aminuria (Choline, Leucine)
Hawkinisinuria - when AD
(Swimming pool urine)

Rx : Nitisinone and avoid Tyrosine in diet

Urea Cycle Kreb-Henseleit cycle/ Ornithine cycle

CPS 1 Carbamoyl Phosphate

NH⁴ + H²O + CO²
Caramoyl phosphate synthase 1

OTC
Carbamoyl Phosphate + Ornithine Citrulline
Ornithine Trans-
Carbamylase

HHH syndrome
Ornithine Citrulline (Ornithine Transporter problem )
Aspartate (from TCA) Hyperornithinemia
Arginase
Urea produced Arginosuccinate synthase Hyperammonemia
Homocitrullinuria
Arginine Arginosuccinate (CPS binds with lysine to form
Arginosuccinate lyase
Fumarate (goes to TCA)
homocitrulline)

NAG produced by Glutamate and Acetyl CoA is allosteric activator for CPS 1
CPS 2 is present in pyrimidine synthesis.

Newborn with hyperammonemia/ high glutamine/

encephalopathy and resp. alkalosis
Citrulline

High Low
Check Argininosuccinate Check Orotic acid
(Excess CPS enters pyrimidine
synthesis and forms orotic acid)
High Low
AS-lyase def. AS-synthase def.
Arg-succinic aciduria Homocitrullinemia High Low
Associated with OTC deficiency CPS deficiency
trichorrhexis nodosa Hyper-ammonemia type 2 (m/c) Hyper-ammonemia type 1

Treatment of urea cycle disorders

1st line is Arginine as it provides Ornithine
Ammonia scavengers - Phenylbutyrate and Benzoate
Structure of Amino Acids

Acidic amino acids have -ve charge

Basic amino acids have +ve charge
In acidic medium : AA are basic (positive)
In basic medium : AA are acidic (negative)

Titration curve
1. Lower pKa: carboxyl end carboxyl-acid
2. Higher pKa : amino end
3. If more functional groups, then more PkAs

Primary structure
Peptide/amide present
No functional capacity Amino acids that can't
Can't be denatured from alpha helix
1. Glycine : Too small (causes bends)
2. Proline : Imino ring
3. Tryptophan : Bulky side chain
Secondary structure 4. Charged amino acids : Aspartate,
Hydrogen bonds present Glutamate, Arginine, Lysine, Histidine
Alpha helix is m/c secondary structure
(Other is Beta-pleated)

Tertiary and Quaternary structures (Monomeric)

Hydrophobic > hydrogen > Ionic
Has disulphide bonds
Has functional capacity
Quaternary structure has multiple sub-units

Primary : Peptide (Polymeric)

Secondary : Hydrogen (H-2)
Tertiary : Hydrophobic
 Vitamins

Thiamine (Vit B1) Niacin (Vit B3)

RBC transketolase NAD/NADP
Thiamine is a co-factor for Functions
Be Branched chain Keto acid dehydr. complex (MSUD) Source of NAD and NADP
A Apha keto glutarate dehydrogenase (Kreb's cycle) Used to treat dyslipidemia
P PDH (Link reaction)
T Transketolase (HMP Shunt) Synthesis
60 mg of Tryptophan → 1 mg of Niacin
Requires B² and B⁶ for synthesis

Deficiency
Deficiency
Beri-Beri
Wet : High output heart failure
Dry : Neuropathy Pellagra
Dermatitis
Wernicke encephalopathy (in alcoholics) Diarrhea
G - Global aphasia Dementia
O - Opthalmoplegia + Nystagmus Death
A - Ataxia
Reversible with B1 supplementation Casal's necklace
If not treated can progress to Korsakoff Psychosis
1. Hartnup's disease (AR condition, can't absorb Tryptophan)
2. Serotonin Syndrome (Carcinoid)
Korsakoff Psychosis 3. Maize diet (low niacin and tryptophan)
Anterograde amnesia (inability to create memories) 4. Vit B⁶ def with Isoniazid
Confabulations (make up false memories)
Personality changes
Non reversible

Tryptophan
Lactic Acidosis
Due to PDH deficiency Aromatic amino acid (max absorption of UV light)
Doesn't form alpha helix due to bulky side chain
Precursor for Serotonin, Melatonin
Needed for synthesis of niacin
Not absorbed in intestine and renal tubules in
Hartnup's disease
Riboflavin (Vit B2)
RBC Glutathione reductase
Carcinoid syndrome
Functions
Excess production of Serotonin (5 Hydroxy Tryptamine)
1. FMN and FAD derived from Vit B2 Signs of Pellagra (tryptophan consumed)
2. Co-factor for Succinate dehydrogenase in TCA Cycle Characterised by triad of Flushing, Diarrhea and Cardiac
involvement.
Diagnosis - Excess 5 hydroxy Indole acetic acid (5-HIAA) in
Deficiency urine ( formed upon metabolism of serotonin )

Corneal neovascularisation
Cheilosis + Magenta tongue
2 eyes and 2 angles of mouth
 Pantothenic Acid (Vit B5) Folate (Vit B9)
Component of Coenzyme A
Deficiency
1. Burning feet syndrome
2. Adrenal insufficiency

FIGLU
PyridoXine (Vit B6)
Xanthenuric acid (assay)
FIGLU is an intermediate in Histidine metabolism
Functions FIGLU assay (in urine) done in Folate deficiency
Levels increased in Folic acid def.
1. All decarboxylation reactions
2. GABA from Glutamate Levels of homocysteine also increased
3. Heme synthesis (ALA synthase)
4. Glycogen Phosphorylase (Glycogenolysis) Functions
5. All transamination reactions
Converts into THF, important co-enzyme for
6. Catecholamines synthesis
methylation reactions (1 carbon transfer)
7. Serotonin synthesis
Synthesis of nirogenous bases in DNA and RNA

Deficiency Deficiency
Seen with Isoniazid or OCP 1. Megaloblastic anemia
1. Sideroblastic anemia (heme synthesis) 2. Homocysteinuria
2. Hypoglycemia (glycogenolysis)
3. Convulsion and neuropathy No neurological manifestations
4. Homocysteinuria (B⁶, B⁹, B¹²) Supplementation of folate can mask the
hematological manifestation of B¹² def but not the
Neurological manifestations.
Only B vitamin not involved in TCA Cycle is B-6
Folate supplementation always done along with B¹²
(folate uses the B¹² stores)

Biotin (Vit B7)

Functions
(Biotin is cofactor for Carboxylation reactions) B-C
1. Pyruvate carboxylase (Gluconeogenesis)
2. Acetyl coA carboxylase (Fatty acid synthesis)
3. Propionyl coA carboxylase (Odd chain FA and branched
chain AA breakdown)

Deficiency
Deficiency is rare (Associated with raw eggs
which has AVIDIN which binds to B⁷)
Presents as : Dermatitis, enteritis, alopecia

Toxicity of B complex vitamins Folate trap

Folate gets trapped in its inactive form in absence of Vit B12
Pyridoxine
Sensory neuropathy
Homocystunuria
Niacin B6, B9, B12 def
1. Prostaglandins mediated flushing (PG D²)
Accelerated atherosclerosis
2. Glucose intolerance
Marfanoid habitus
3. Gout
Ectopia lentis (Infero-nasal)
4. CME
 Cobalamin (Vit B12) Vitamin A
Functions Functions
Regeneration of methionine from Cellular differentiation
homocysteine (also needs B⁶, B⁹) Vision
DNA synthesis
Methyl malonyl coA mutase
(PMS pathway for odd chain FA Deficiency
and branched amino acids) 1. Phrynoderma (toad skin)

Deficiency
1. Megaloblastic anemia
2. Homocysteinuria
3. SACD -Sub acute cord degeneration
4. Prolonged def : irreversible nerve
damage 2. Bitot spots
earliest manifestation of Vit A deficiency
S Spino-cerebellar tract
C Cortico - spinal tract (lateral)
D Dorsal column

Vitamin A excess
1. Teratogenic (hence, avoided in pregnancy)
2. Pseudo-tumor cerebri (aka Idiopathic intracranial htn)

Markers of deficiency Vit A Dosage

1. Increased MMA
< 1 year age : 1 lakh IU
2. Increased homocysteine (along with B⁶ and B⁹) Every 6 months
> 1 year age : 2 lakh IU
3. 2° folate deficiency (folate trap)
Total: 17 lakh IU in 5 years

Risk factors for deficiency

1. Ileal problem (TB, Crohns)
2. D latum (Parasite)
Jejenum
3. Pernicious anemia
4. Vegan diet Iron fist bro
Duodenum Ileum
5. PPI

Vitamin D Vitamin C
Lower calcium absorption Needed for hydroxylation of lysine and proline (collagen)
PTH increases due to low calcium, phosphate is excreted.
PTH causes bone resorption, ALP high (formation follows resorption) Deficiency : Scurvy
Bleeding gums
Deficiency : Rickets Peri-follicular haemorrhage
Cork-screw hair

Metaphyseal
C Cupping
S Splaying
F Fraying

Earliest change : Growth plate widening

Rosary : Round (non tender)

Metaphyseal : White line of Frenkel

Earliest change : Reduced bone density
Rosary : Pointed and tender
 Vitamin K Vitamin E
Co factor for γ-Glutamyl-carboxylase Most potent antioxidant
Activates :
Factor 2, 7, 9, 10
Protein C, S

Competetitive inhibition
Vit E is surface anti oxidant at cell membrane
Warfarin, Dicoumarol ↓
Blocks regeneration of the co-factor Replenished by Vit C
Used as anti-coagulant ↓
Replenished by glutathione
↓
Sources of Vitamin K
Replenished by NADPH

Natural Synthetic
Deficiency
K¹ K² K³ 1. Hemolytic anemia
(Phylloquinone) (Menaquinone) (Menadione) 2. Peripheral neuropathy that mimics B¹² def
Green veggies Intestinal flora Synthetic form
IM injection
1mg @birth to
prevent hemorrhagic
dis of newborn
Because breast milk is
deficient in vitamin K

Heme Synthesis
Rate limiting step : ALA synthase (B⁶ is co-factor)
Inhibited by : Glucose, Heme, INH and OCP (Sideroblastic anemia)

ALA Synthase ALA dehydratase

Succinyl CoA + Glycine ALA Porphobilinogen
Vit B⁶ Amino
From TCA Cycle
Levulinic acid Porphyro-bilinogen deamnase

Acute Intermittent Porphyria

AIP Neuro-visceral type
Acute abdominal pain
Peripheral neuropathy
APH-UCP
Hydroxy-methylbilane
Lead PCT
"Dehydrated lead"
Uro-porphyrinogen

Uro-porphyrinogen decarboxyalse

Soret band at 400nm

Porphyria Cutanea Tarda
Sporadic, m/c type
Cutaneous blisters + Photosensitivity
Hepatic involvement
Asso. with Hep C, HIV 15

Ferrochelatase Proto-porphyrin Copro-porphyrinogen

Heme
Iron
Enzymes
Vmax
Catytic efficiency of
Substrate concentration at which there's saturation of receptors enzyme
Adding more substrate doesn't change the rate

Km Kcat /Km
Substrate concentration at which 1/2 of Vmax is reached Cat on top
It's a reaction specific constant

Competitive Non-Competitive Uncompetitive

Substrate
Substrate
Substrate Inhibitor Substrate binding alters
inhibitor binding site

Enzyme
Enzyme

Different
Inhibitor competes for Inhibitor Inhibitor
binding site
the active site
can't bind binds

Inhibitor

Lineweaver–Burk plots

Kompetition → more Km

No Competition → slower (Vmax ↓)

Un Competition → Everything decreases (Universal)

1/Km 1/Km 1/Km

Vmax const Km const Both decreasing

Can't be non competitive Can't be competitive Universal, hence Un-Competitive
Hence, Competitive Hence, Non-Competitive
 Enzyme Co-factors
Metal Metalloenzymes
Ca Lipase, Lecithinase CaLcium

Fe Succinate deH MSD is Iron man

Zn Carbonic anhydrase, Glutamate dehydrogenase, LDH, ALA dehydratase

Mg Hexokinase, Phosphofructokinase, Glucose-6 phosphatase, Enolase, Glucose Acrodermatitis

pathways
Glutathione synthase Enteropathica
Cu Tyrosinase, Cytoplasmic SOD, Ceruloplasmin (Wilson's), Lysyl oxidase (Menke's Congenital Zinc deficiency
Copper CyTy Kinky hair)
Dermatitis
Mn Arginase, Ribonucleotide reductase, Mitochondrial SOD Alopecia
Diarrhea
Se Glutathione peroxidase, Deiodinase

Mo Xanthine Oxidase, Sulfite Oxidase Mo Xo So

Collagen
Most abundant protein in animals
(Glycine - X - Y)n i.e. every 3rd amino acid is Glycine ALPORT Syndrome
X, Y can be Proline, Hydroxyproline, Lysine, Hydroxylysine Collagen Type IV is defective
28 types of collagen found in body Clinical features are: Hematuria,
SNHL, anterior lenticonus

Epidermolysis bullosa
Collagen Type VII is defective
Clinical features are skin blisters

Osteogenesis Imperfecta
Collagen type 1 disorder
Reduced bone mineral density
Multiple diaphyseal fractures
d/d : Non accidental injury
Post Translational Modifications (PTM) of Collagen (multple metaphyseal fractures)
1. Hydroxylation of proline and lysine residues, to increase H-bonds
Wound Repair
Early : Type 3 collagen
Late : Type 1 collagen

Hydroxylation requires Vitamin C

Hence deficiency of vitamin C leads to poor hydroxylation
Weak collagen leads to easy b ruising and gum bleeding in scurvy.
Ceruloplasmin
Protein that transfers copper
2. Glycosylation ATP 7B and copper needed
Addition of carbohydrate in collagen for production.
Enzyme required is Lysyl oxidase which require Cu (copper) as co-factor. Hence low in both Wilson's
Hence deficiency of Cu leads to weak collagen (Menke's Kinky hair) and Menke's Kinky hair
disease.
 DNA Basics

Chromosome

Chromatin fiber NUCLEOSOME

Histones
"Beads on a
string"
DNA wound on
nucleosomes

Double helix

Mitochondrial DNA
Circular and double stranded DNA
Shows maternal inheritance pattern
Makes up 1% of total DNA pool
Euchromatin Heterochromatin
Codes for 20% of proteins involved
(Actively transcribed (Condensed Junk DNA)
in electron transport chain
during interphase) Inactive
DNA polymerase it uses is GamMa
Active Rich in AT
(no proof-reading, hence high Rich in CG Methylation
chances of mutation) (silencing)

Genetic Code
Stop Codones
1. Unambiguous (Particular code for Particular AA)
2. Degenerate (One AA can be coded by multiple codons) 1. UAG U are gone
3rd position of codon is known as Wobble position (doesn't affect) 2. UGA U go away
3. Non overlapping 3. UAA U are away
4. Universal (except mitochondrial DNA)

Mutations

Point mutations Frame Shift mutation Splice site mutations

Can be either nucleotide Introns are supposed to be spliced,
Silent Mis-sense Non-sense insertion or deletion but here they are translated
UCA : Serine UCA : Serine UCA : Serine
B Beta thalasemia
UCU : Serine CCA : Proline UAA : STOP
G Gauchers
Mutation at Different amino Mutation forms M Marfan's
wobble position acid coded a stop codon
Extrons are expressed
No change in eg. UCA ➡️ CCA No AA formed Important examples Introns if expressed are
protein coded eg. UCA ➡️ UAA 1. DMD
eg. UCA ➡️ UCU background music (BGM)
2. Tay Sach's disease
 DNA Replication
Enzymes for opening the double helix Topoisomerase
DNA (swivel)
1. Helicase : Opens the replication fork
helicase
2. Topoisomerase : Prevents supercoiling
3. SSBP : Prevents re-annealing of strands

DNA helicase defect

1. Werner syndrome
2. Bloom syndrome Single-stranded DNA
binding protein (SSB)

Enzymes for replication

1. Primase : adds RNA primers in 3' - 5' direction
2. Ligase : Joins the okazaki fragments
3. DNA Polymerase

Prokaryotes Eukaryotes
1. DNA Pol 1 : Removal of primers Pol α : Initiates replication, removes primers
2. DNA Pol 2 : DNA repair Pol β : DNA repair
3. DNA Pol 3 : DNA replication Pol γ : Mitochondrial DNA synthesis GamMa
Pol δ : Lagging strand synthesis (Okazaki fragments) Delta : D-late
Pol ε : Leading strand synthesis

Klenow's Fragment

DNA Pol - 1 DNA Pol - 2

Direction of action
Primers added : 3' to 5' Made using : Kornberg enzyme
Primer removal : 5' to 3'
The portion of DNA polymerase-1 that is
responsible for Primer removal is removed.
Replication : 5' to 3'
This can now be used for synthetic DNA
Proof reading : 3' to 5' (done by all DNA polymerases)
replication
DNA Repair defects
1. Nucleotide excision repair : Xeroderma pigmentosa
2. Base excision repair : MUTYH associated polyposis
3. Mismatch repair : HNPCC associated polyposis
4. Non homologous end joining : SCID, Ataxia telengiectasia (ataxic dude scid because non homologous steps)
5. Homologous end joining : BRCA 1/2, Fanconi's anemia

Transcription and Translation

Post transcriptional
modifications
1. Capping at 5' end
2. Poly-adenyl tail at 3' end
3. Splicing of introns

Exception to one gene one protein

RNA Editing Alternate splicing

Apo B-100 (liver) Introns are alternatively
Apo B-48 (intestines) spliced
8 sounds like atE Produces different
proteins
Lac Operon

Bacterias generally depend on Glucose for energy

In absence of glucose + presence of lactose : lac operon gets activated

1. Repressor (blocks transcription) is inactivated by Lactose. double negative is positve

2. CAP (activates cAMP needed for transcription) is inhibited by Glucose.
 Epigenetics
Chemical changes in genome (either activates or deactivates a gene without changing the code)
These changes are reversible and transmissible
Epigenetics includes
1. "DNA" Methylation (methylation mutes, i.e DNA Silencing)
2. "Histone" Acetylation (acetylation activates)
3. "Histone" Deacetylation (deactivates)

Clinical application of epigenetics

Prader Willi Syndrome AngelMan Syndrome

Paternal deletion Maternal deletion
(maternal is silenced) (paternal is silenced)
Or maternal uniparental or Paternal uniparental
disomy (of the silenced disomy (of the silenced
maternal gene) paternal gene)

1. Fat child (hyperphagia due 1. Happy puppets

to high Ghrelin) 2. Gelastic seizures
2. Hypotonic

Other mechanisms of genetic alteration

1. Gene knock in : Gene insertion
2. Gene knock out : Gene removal
3. Gene knock down : Gene supression (aka Post transcriptional gene silencing)

Post transcriptional gene silencing

aka Gene knock down / RNA-interference

Mechanism
1. siRNA (short interfering RNA) and miRNA (micro RNA) are synthesised using DICER
2. siRNA and miRNA form RISC (RNA induced silencing complex)
3. RISC binds with mRNA (messenger RNA) to stop translation
Polymerase Chain Reaction

95°C - Strands separate

DNA Sample Primers Nucleotides

55°C - Primers bind template

Taq polymerase Mix Buffer PCR Tube

"DAE"

72°C - Synthesise new strand

PCR Cycle

Thermal Cycler

1. Denaturation - PCR components heated to 95°C to separate the DNA strands.

2. Annealing - 55°C
3. Extension - 72° C

Types of PCR

1. Quantitative real-time PCR (qPCR): Monitors the amplification of DNA in real time and
provides quantitative info.
2. Reverse Transcriptase PCR (RT-PCR): Measures RNA expression levels
3. Multiplex PCR: Uses different primer pairs to amplify multiple targets simultaneously
4. Nested PCR: Reduces nonspecific binding and increases sensitivity and specificity
Restriction Fragment Length Polymorphism
Molecular biology technique used to identify differences in DNA sequence
Used in DNA fingerprinting and paternity testing (application in forensics)
Makes use of a special type of enzyme known as Restriction Endonucleases (they have endonuclease activity
at palindromic sites)

Individual A Individual B Unknown Sample

DNA isolated and digested with restriction endonuclease

Here, unknown sample could be from individual B

DNA sequencing
DNA sequencing is the process of determining the order of nucleotides in DNA
1. Sanger sequencing : Gold standard
2. Next gen. sequencing : Best method (faster, more sensitive)
Cytogenetics
The study of chromosomes is called cytogenetics
Conventional cytogenetics : Karyotyping
Molecular cytogenetics : FISH and Microarray

Karyotyping FISH

Diagnosis of structural and numerical Pathologists mark DNA with fluorescent

chromosomal abnormalities labels so they can see the areas they're
Inherited genetic abnormalities interested in under a microscope.
Fetal loss and pregnancy-related issues
Best investigation for micro-deletion
Cells are arrested in metaphase using colchicine Diagnosis of translocation and
Carnoy fixative is used amplification
Not useful in diagnosing point mutation

Micro-array
uses Comparative Genome Hybridisation (CGH)

Uses nucleic acid hybridisation with fluorescent probe.

Hence, useful for point mutations as well
 Purine and Pyrimidine

A. De Novo pyrimidine synthesis B. De Novo purine synthesis

Glutamine PRPP
many many
steps steps

Orotate IMP
Forms purine
+ PRPP - CO²
IMP breaks down to form AMP and GMP
UMP AMP and GMP metabolise to form
Forms pyrimidine hypoxanthine and guanine
Hypoxanthine and Guanine metabolise to form
Xanthine and Uric acid (excreted)

C. Purine salvage pathway

Here, free purine bases can be reconverted to their corresponding nucleotides using PRPP

HGPRT
Hypoxanthine IMP
Instead of xanthine
Guanine HGPRT H Hyper-uricemia
GMP
G Gout
Deficiency of HGPRT : Lesch Nyhan Syndrome P Pissed off (Self mutilation )
R Red urine crystals (monosodium urate)
T Tone (dystonia)
CHAPTER 13
FORENSIC MEDICINE &
TOXICOLOGY
Mechanical injuries

Mechanical injuries

Blunt Force Injuries Sharp Force Injuries

Incised Wound
Clean-cut wound caused by a
Tear/split in the skin Skin intact sharp-edged weapon (knife, blade)

Stab/Puncture Wound
Laceration
Superficial skin Sub-cutaneous Deep wound caused by a pointed
(if sharp force : Incision)
injury (epidermal) haemorrhage weapon (knife, spear)
Largest dimension is depth
Abrasion Bruising
Chop Wound
Injury caused by a heavy, sharp
weapon (axe, cleaver)

Laceration Incision
Irregular edges Sharp edges
Crushed floor Clean floor
Tissue bridges (+) No tissue bridges
Bruising (+) or bruising
Defence wounds Hesitation
(on palms) cuts (suicidal)

Laceration that looks

like incision
Bruise
Laceration of bony Also known as Contusion
prominences Hemorrhage beneath the skin due to rupture
of blood vessels
Color changes over time (can help estimate age
of the injury)
Red - Blue - Brown - Green - Yellow "RBBGY"
Normalises in a week
Abrasion Artificial bruise :
Semecarpus seeds (aka Bhilwanol) is used
Associated with vesicles and itching

Graze abrasion Pressure abrasion

Ectopic bruise 6 penny Tram track
m/c abrasion Compressed for a prolonged
(Battle sign) bruise bruise
aka Gravel burn/ period of time
brush burn eg. Ligature marks from Middle cranial fossa Sign of Laathi
Tailing present hanging fracture "Child abuse" injury
Blast Injuries

Primary Secondary Tertiary Quaternary

(Blast wave) (Missiles) (On hitting ground) (Others)

Blast lung

Ruptured tympanic Penetrating

membrane trauma & Burns,
lacerations asphyxiation,
Blunt trauma
and toxic
and fractures
substances

Bowel
perforations

Primary blast injuries : affect air-filled organs (lungs, Tympanic membrane, GI tract)
Blast lung is the most common fatal primary blast injury
Secondary blast injuries : are caused by projectiles and shrapnel, leading to penetrating trauma
Tertiary blast injuries : result from the body being thrown by the blast wind, causing blunt trauma
Quaternary blast injuries : includes burns and traumatic asphyxiation

Heat induced injuries

1. Heat Cramps
Painful muscle cramps (usually in the abdomen, arms, or legs)
Caused by electrolyte loss due to excessive sweating Localised heat injuries
Management : Oral or IV electrolytes
1. Burns
2. Heat Exhaustion Tissue damage caused by dry heat
Excessive electrolyte and water loss (hypovolemia) (flames, hot objects)
No significant alteration in mental status 2. Scalds
3. Heatstroke Injury caused by hot liquids or steam
Body’s thermoregulatory mechanism fails, leading to a core body 3. Sunburn
temperature above 40°C Superficial skin damage caused by
Associated with altered mental status prolonged UV exposure.
Types:
i. Classical (non-exertional) heatstroke: No sweating (seen in elderly,
children or individuals with chronic illness)
ii. Exertional heatstroke: Associated with sweating (individuals doing
intense physical activity in hot environments)
iii.
Heat stroke is a medical emergency
If pulse present : Immediate cooling (f/b IV fluids)
If pulse absent : CPR
 Ballistics

Rifles Shotgun
Rifled Barrel : Spinning Bullet (stable)

Smoothbore Barrel : Unstable Flight

Rifled bores (grooves cut in the barrel) Smooth bore

Rifling increases gyroscopic ability of bullet Uses pellets
Size: CaLibre (distance between opposite Lands) Size of bore : Measured in gauge (Inv prop to size)

Bullet shooting
ahead
Grease Collar
Gun Abrasion Collar

Contact shot : BBT + Cruciate wound

BBT Close shot (<10 cm) : BBT
Flame Smoke Unburnt powder Near shot (30-60 cm) : Only T
(Burning & (Blackening) (Tattooing) Distant shot (>60 cm) : Nothing
singeing) On skin On dermis
Can be wiped Can't be wiped Grease collar and abrasion collar seen with all

Cruciate wound (contact shot) BBT present (close shot) Only tatooing (near shot) Only GC & AC (distant shot)

Entry vs Exit wounds

Entry wound Exit wound

Rat hole appearance
Grease collar and No BBT or GC/AC
abrasion collar present Everted margins "E" Seen with shotgun (near shot)
BBT present based on Larger, irregular For contact and close shot, it's same as rifle
distance Tissue fragments For distant shot : Complete dispersion (no
Inverted margins "in" can be seen central hole)
Types of bullets

Dum Dum bullet Frangible bullet Ricocheted bullet

aka Butterfly bullets or Expanding bullets Breaks into small pieces when it Bullet changes its path and
Produces larger wound hits a hard surface velocity after hitting a target.
Banned for use in war No risk of ricochete Can happen as an accident or
(safer for shooter) intentionally

Yawning vs Tumbling bullet Tracer bullet

Normal bullet shows precession flight (rotation of the bullet around

the center of mass)

This bullet contains a material that

ignites when fired, creating a visible
Yawing : Nose of bullet deviates from the line of flight trail of smoke or fire.
Tumbling : Extreme yawing where the bullet rotates completely Used by to track the trajectory of the
bullets and adjust aim in wars.

Piggy back bullet (Tandem bullet)

Gunshot residue tests
On firing, bullet fails Gunshot residue is composed of lead,
Bullet
to exit muzzle end barium, and antimony from the primer
SEM-EDX is the most reliable method for
detecting GSR
Dermal Nitrate tests are also done to
look for GSRs
Griess test
Walker test
Piggy back bullet Tewari test
Second bullet pushing
the first bullet
Asphyxial deaths
Asphyxial death refers to death resulting from interference
with the process of respiration.
Petechial hemorrhages in head and kneck (aka Tardieu spots)
are characteristic signs of mechanical asphyxia
Tardieu spots

Hanging
Mechanical asphyxia (typically suicidal)
Body suspended by a ligature around the neck
Mechanism of death
a. Carotids and Jugular veins obstructed
b. Airway obstruction
c. Vagal inhibition (stimulation of the carotid sinus
can cause reflex cardiac arrest)

Types of hanging
1. Based on the Position of the Body
Complete Hanging : Entire body is suspended, with Complete Incomplete La facie sympathique
no part touching the ground hanging hanging
Partial Hanging : Part of the body (feet or knees)
touches the ground
2. Based on the Position of the Ligature Knot
Typical Hanging : The knot is placed at the nape of
the neck (midline posterior)
Atypical Hanging : The knot is placed elsewhere
(e.g., lateral or anterior)
Typical hanging
3. Based on death before/after hanging Atypical hanging
Antemortem hanging : Death is due to hanging
Dribbling of saliva (characteristic feature)
Postmortem hanging Strangulation
La facie sympathique - eye on one side remains
Ligature mark is oblique Ligature mark is horizontal
open and pupil dilated (the ligature knot
and non continuous and continuous.
presses the cervical sympathetic Ganglion)
Ligature mark is dry, hard, More likely to show
Postmortem hanging : Person was already dead
and parchment-like fractures of the hyoid
while hanging (mostly staged)
without vital reaction bone and thyroid cartilage.
Have to be differentiated from strangulation
in medico legal cases.

Strangulation
Constriction of the neck by ligature or manual force without suspension of the body.
Mostly homicidal, with horizontal ligature marks and possible hyoid bone fractures "HHH"

Types of strangulation

Throttling Mugging Garroting Bansdola

Using hands to strangulate Using elbow to strangulate (Spanish Windlass)
 Suffocation
Blocking air entry to the lungs
Types of suffocation

Smothering Gagging Burking

Blocking of external air passages Obstruction caused by a gag Combination of smothering
(nose and mouth) device (piece of cloth) and compression of the chest
Characteristic method, named
after William Burke
Rescue methods in choking

Choking Heimlich Maneuver Back thrusts Overlaying

Blockage of the Internal airway Done in adults Done in babies Accidental smothering, often seen
by a foreign body (eg. food) in infants sleeping with adults

Traumatic Asphyxia Café coronary syndrome

Death due to choking that mimics sudden
Asphyxia caused by
cardiac death (death occurs due to asphyxia or
compression of the chest or
reflex cardiac arrest on vagal stimulation)
abdomen, preventing normal
Risk factors : Obese person, alcoholic
respiratory movements
Heimlich maneuver is the primary life-saving
aka Olivier's syndrome,
technique
Perthes' syndrome
Postmortem findings
Post mortem features :
Food bolus in the airway
Craniocervical cyanosis Petechial hemorrhages
Ecchymotic mask
Subconjunctival hemorrhage Heart is normal
Multiple petechiae (Traumatic Asphyxia)

Positional Asphyxia

Occurs when a person is

trapped in a position that
prevents adequate
respiration

Jacknife position
(Positional Asphyxia)
Drowning
Drowning is a form of asphyxial death caused by the entry of fluid into the airways

Types of drowning :
a. Wet Drowning:
Water enters the lungs, causing asphyxia
Accounts for the majority of drowning cases
b. Dry Drowning:
Washerwoman's Hand
Reflex laryngospasm occurs upon water contact with the larynx, preventing water
entry into the lungs. Seen with prolonged
Asphyxia results from airway obstruction immersion in water
Can be seen in both
c. Immersion Syndrome (Cold Shock) :
antemortem and
Reflex cardiac arrest caused by sudden immersion in cold water, without aspiration of postmortem drowning
water
d. Near-Drowning:
Saved from drowning but dies due to complications of drowning

Fresh water vs Salt water drowning

Fresh water drowning Salt water drowning

Rapid absorption of water into circulation Salt water in lungs : draws water from
causes hemodilution and hemolysis blood into alveoli (hemoconcentration)
Electrolyte imbalance : Electrolyte imbalance : High Na, Cl
Low Na, Cl (Hemodilution)
Frothy discharge from
High K (RBC lysis) mouth and nose
Hallmark of wet drowning
Due to fluid aspiration
GettLer's test Hence, only seen in
antemortem drowining
Test used to differentiate fresh water and salt water drowning
Measures Chloride level in Left ventricle compared to right ventricle
Fresh water drowning : Low Cl level
Salt water drowning : High Cl level

Internal organs (in antemortem drowning)

a. Lungs
Emphysema aquosum - Voluminous, edematous, and waterlogged lungs
Paltauf's hemorrhage - Pleural hemorrhages common in lower lobe
b. Stomach
Wydler’s sign - Water, mud, or debris in the stomach (from swallowing water)
c. Diatom test
Cadaveric spasm
Diatoms are microscopic algae found in water
Diatoms present in organs like bone marrow or liver Clutched grass/roots is sign
Indicating aspiration and circulation before the person died of life before drowning
(antemortem drowning)
D/d is Rigor Mortis

Diatoms
Human Identification

Fingerprints Dentition
Study of fingerprints : Dactylography 1. Primary Dentition (Deciduous Teeth)
Types of fingerprints : 20 teeth (10 in each jaw)
a. Arch Between 6 months and 2½ years
b. Loop (m/c type) Dental Formula: 2 : 1 : 2 (incisor : canine : molars)
c. Whorled 2. Permanent Dentition
Special conditions : 32 teeth (16 in each jaw)
Complete loss : Celiac disease, burns After 6 years
Permanent impairment : Leprosy, electrical injury Dental formula : 2 : 1 : 2 : 3 (i : c : premolars : molars)
Increased distance between ridges : Acromegaly, Rickets
3. Mixed Dentition
Alteration of ridge : Scleroderma, Eczema, Acanthosis Nigricans
Period: 6–12 years
SEA 24 teeth constant 6-12-24
Contains both primary and permanent teeth
At age 9 yrs : 12 primary and 12 permanent
At age 10 yrs : 8 primary and 16 permanent
At afe 11 yrs : 4 primary and 20 permanent

1 16
Arch Loop Whorled 32 17

M/c type of
fingerprint

Pelvis Skull

Forehead/orbit/chin
(more rounded)

Everything is larger and wider in female pelvis except Everything is larger and wider in Male skull except
O Obturator foramen F Frontal eminence
S Sacro-iliac joint N Nasal aperture
A Acetabular notch P Parietal eminence

Within pelvis, the best bone for sex determination : Pubis

Inter-membrial index : Hand length : Leg length (used to determine race)

Haase's rule : Used for fetal age estimation

First half (first 5 months) : GA = √(Length in cm)
Second half (last 5 months) : GA = (Length in cm) ÷ 5
Inter-membrial index
Thanatology
Immediate (Early) signs of death:
a. Cessation of Respiration and Circulation: No detectable pulse or breathing
b. Fixed Pupils: Non-reactive to light.

Late signs of death:

Algor Mortis: Cooling of the body
Body temperature decreases 1–1.5°C/hour initially (slows after 12 hours)
If no cooling within 12 hours : Postmortem Caloricity
Heat stroke / Pontine hemorrhage / Sepsis / Strychnine poisoning / Tetanus
Burns are NOT A CAUSE of postmortem caloricity

Rigor Mortis: Stiffening of muscles

Cause : Depletion of ATP (ATP needed for muscle relaxation)
First organ to undergo rigor mortis :
Internal organ : Heart (overall first organ)
External organ : Eyelids
Nysten's rule : Stiffnes is always proximal to distal
Peaks at 12 hours
Disappears after 24 - 48 hours

Livor Mortis (Postmortem Lividity): Settling of blood in dependent areas

Fixation of hypostasis occurs in 6-12 hours
Confirmed using incision test
Specific discolorations:
1. Cherry red : Carbon monoxide poisoning CO = C
2. Brick red : Cyanide poisoning
3. Chocolate : Nitrite
4.
Decomposition: Can be further classfied

No organs preserved Some organs preserved

Putrefaction
Moist Hot and dry
Foul odour
environment environment
Green discoloration (due to sulf-meth-hemoglobin formation)
Earliest internal site : Blood vessels
Adipocere Mummification
Earliest external site : Right iliac fossa (over cecum)
Bloating, skin slippage seen Sweet odour No odour
First organ to be putrified : Trachea & larynx f/b Stomach and Waxy transformation Maximum organ
intestines (due to fat saponification) preservation
Prostate and non-gravid uterus are the last to be putrified Organ preservation (+) Cause : Dehydration of
Not possible in fetal death tissues

Putrefaction Adipocere Mummification

Marbling
Early indicator of putrefaction
Greenish-black discoloration along
Casper's Dictum
superficial veins (Intestinal bacteria A body decomposes quickest in air
enter venous system and form sulf- Decomposition in water takes twice the time and in soil it
meth-hemoglobin ) takes 8 times the time
Occurs 24-48 hours after death
Time taken in Air : Water : Soil = 1 : 2 : 8
 Autopsy

Various methods of autopsy Types of incisions

1. Virchow :
Organs are removed one by one for examination
Time consuming method "vir-slow"
2. Letulle :
All organs are removed en masse (as a single block)
3. Ghon :
Organ systems are removed in groups (eg. heart-lungs,
stomach-intestines, etc)
aka en block
Easier to perform than Letulle
4. Rokitansky :
I shaped Y shaped Modified - Y
Organs are examined in situ (within the body) without
removal "Rokitansky pouch" incision incision shaped incision
Quickest method Used in non- Most Better examination
Done for autopsy in transmissible diseases medico-legal commonly of neck structures
cases used in Essential in cases of
Simpler and medico-legal asphyxial deaths or
faster to autopsies neck trauma
Order of body cavity opening perform (hanging,
Standard Order : Cranial - Thoracic - Abdominal - Pelvic "CTAP" strangulation)
Cranial cavity opened first to prevent distortion of brain structures Has better cosmetic
due to changes in pressure when other cavities are opened results post-autopsy

Order is changed in specific conditions :

a. Poisoning : Abdominal - Thoracic - Cranial (to check undisturbed
stomach contents, which may contain poison)
Special forensic tests
b. Chest Trauma : Thoracic cavity opened first
c. Newborn : Normal order is followed 1. Precipitin test : To determine if the tissue sample is
from human or not.
2. Barberio's test : Looks for semen (uses picric acid)
Tests for newborn deaths 3. Tests for blood
1. Breslau's first life test : a. Teichmann's test : Stains hemin crystals "He-man"
b. Takayama test : Stains hemochromogen
Remove the lungs carefully
c. Spectroscopic test : Best test for blood
Place the lungs in a water-filled container
Observe whether the lungs float or sink
FLoat : Live born (has breathed)
Sink : Stillborn (never breathed)
False positive : If putrefaction has occured in dead fetus
2. Breslau's second life test :
Stomach and intestines put inside water
A cut is made in them inside water to see if air/amniotic fluid/or
any other fluid comes out
Presence of air or substances : Live birth
Absence of air or substances: Stillbirth

Barberio's test

Autopsy findings in death due to

"starvation"
1. Collapsed lung
2. Atrophied liver
3. Hypothermia
4. Distended Gall bladder (no release of bile)
Takayama test
(Pink feathery crystals)
Important autopsy images

Post Mortem eye signs

Kerwokian Sign Tache Noir Corneal opacification

Filigree burns
Earliest post mortem 3-6 hrs post mortem 6 hours post
Also seen in ochronosis
In lightning injury
eye sign mortem
Tram track app. (alkaptonuria) aka litchenberg flower,
arborisation burn

Puppe's rule Gastric ulcers on Autopsy

Tells the sequence of skull fracture 1. Wischnewsky ulcer : Hypothermia "Vaishnodevi is cold"
2. Curling ulcer : Burns "Curl when burn"
Fractures that 3. Cushing ulcer : Head injury
occur late don't 4. Cameron ulcer : Hiatal hernia
cross the
previous fracture
line Wischnewsky spots
here A> B > C

Cardiac Tamponade on autopsy Paradoxical undressing

Seen in hypothermia
Autopsy photograph showing a large People experienced to prolonged cold experience a
clot within the pericardium feeling of heat just before death
Reason : Vasodilation of extremely constricted blood
vessels just prior to death

Chicken fat clot

Clot formed postmortem
Doesn't have any RBC
Perversions
Common Paraphilic Disorders Other Paraphilic Interests
1. Exhibitionism: 1. Frotteurism:
Deriving sexual gratification from exposing one’s Sexual arousal from rubbing against a non-
genitals to unsuspecting strangers consenting person
Often driven by a need for shock or attention 2. Necrophilia:
2. Voyeurism: Sexual attraction to or engagement with corpses
Sexual arousal from observing unsuspecting 3. Zoophilia:
individuals who are naked, undressing, or engaging Sexual attraction to animals
in sexual activities 4. Transvestic Disorder:
aka Peeping tom Sexual arousal from dressing in clothing of the
3. Pedophilia: opposite gender, often accompanied by distress
Sexual attraction toward prepubescent children aka Eonism
Considered a severe disorder with significant 5. Urophilia/Scatophilia:
societal and legal implications Arousal related to urine or feces
4. Sadism:
Sexual pleasure derived from inflicting pain,
suffering, or humiliation on others Excessive sexual desire
5. Masochism: Male : Satyrysm (aka Don Juanism)
Sexual gratification from experiencing pain, Female : Nymphomania
humiliation, or suffering
May be consensual (e.g., BDSM)

Torture methods

Telefono El- Planton Parrot porch Saw Horse Cattle proding

Felanga/bastinado Wet submarine Hog flying

(Dry submarine - Plastic bag used)

Declarations
Tokyo, Istanbul Protocol, Hamburg declaration : Torture banned
Hongkong : Elderly abuse
Ottawa : Child abuse
Venice : Terminal illness "place to visit for terminally I'll"
Oslo : Abortion "O-slow down abortion rates"
Helsinki and Nuremberg code : Human experimentation
Sydney : Brain death "Australians are brain dead"
Geneva : Hippocratic oath
Malta : Doctor's role in hunger strike "no MALT"
Toxicology
Corrosive poisoning Anoxic poisoning
Acid : Coagulative necrosis (doesn't penetrate very deep)
ALkali : Liquefactive necrosis (Can penetrate deep and cause perforation ) Carbon Monoxide poisoning
Causes anemic anoxia (reduced
oxygen-carrying capacity of the
blood due to altered
hemoglobin)
Characteristic cherry red
postmortem lividity
Causes softening of basal
ganglia (seen on autopsy)
H²SO⁴ poisoning Boric acid poisoning Treatment : Hyperbaric oxygen
H²SO⁴ aka oil of Vitriol The "boiled lobster" rash is
Causes blackening of tissues a characteristic symptom of
(except teeth) boric acid poisoning
Black/blotting paper stomach
mucosa

Cherry red postmortem lividity

Cyanide poisoning
Causes histo-toxic anoxia
(inability of tissues to utilize
Phenolic (aka Carbolic) acid poisoning Nitric acid poisoning oxygen due to enzymatic or
Green urine (Carboluria) due to PCT Yellow staining of mitochondrial dysfunction)
necrosis. tissue due to protein Blocks ETC - IV "ides"
Causes miosis and ochronosis (gray-blue nitration are Characteristic brick red
discoloration of tissues) diagnostic postmortem lividity
Leathery stomach : Stomach becomes (xanthoproteic Hydroxocobalamin (vitamin B12)
leathery because of thickening of the reaction) is first line managament for
mucous membrane Methemoglobinemia cyanide toxicity
Hence it's the only acid poisoning for can occur in severe Lille's kit used for treatment
which gastric lavage can be done. cases

Cardiac poisons

Aconite Digitalis purpurea White Oleander Yellow Oleander

aka Monk's Hood or Meetha Zeher Xanthopsia (yellow vision) is (Nerium oleander) (Thevetia peruviana)
Causes AV block a classical symptom. Both are ornamental plants
Roots are most toxic ECG shows scooped ST
White oleander : Leaves are toxic
Ideal homicidal agent depression and bradycardia
(contain nerrin, oleandrin)
Characteristic feature : Hippus Digibind is the specific
Yellow oleander : All parts are toxic
(alternate miosis and mydriasis) antidote
(contain Thevetin)
Treatment : Atropine
Toxicity from Na⁺/K⁺-ATPase inhibition
 Toxicology - Heavy metal poisoning

Arsenic poisoning Mercury poisoning

Acrodynia
Source : Contaminated fish/ dental amalgams
MOA : Inhibits pyruvate dehydrogenase Acute features :
Acute features : N & V, abdominal pain
Cholera like rice water stools
Garlic odor in breath 🧄 Chronic features :
Coarse tremors (aka Danbury tremors, Hatter shakes, Glass blower shakes)
Chronic features : Erethism (neurological disorder) : Personality disturbance, insomina, memory loss
Hyperpigmentation (rain drop Acrodynia : Painful pink rashes (mostly at extremities) - hence aka Pink disease
pigmentation) Treatment : DMSA (or BAL)
Hyperkeratosis
Mees lines (white lines on nails)
Peripheral neuropathy Lead poisoning
Other characteristic features :
Common source in adults : Inhalational
a. Red velvety stomach mucosa on autopsy
(from lead based paints)
b. Found in bones/nails/exhumed bodies
"Ash-in-ic" MOA : Interferes with heme synthesis and
Special tests : Marsch test, Reinsh test deposits in bones
Treatment : DMSA (or BAL) Acute features :
N & V, abdominal pain
Chronic features :
CNS: Irritability, learning disabilities, memory Clapton's / Burtonian lines
(Not specific and can be seen
loss (in children)
with Fe/Hg/Cu)
Hematologic: Microcytic hypochromic anemia
with basophilic stippling.
Burton's line : blue-black line on gums
Mees Lines Rain drop pigmentation Treatment : DMSA (or BAL)

Thalium poisoning Cadmium poisoning

MOA : Mimics Potassium, "Itai Itai disease"
disrupting cellular function Itai Itai means "ouch ouch"
Acute features : Chronic cadmium toxicity
N & V, abdominal pain causes bone pain due to
Chronic features : Osteomalacia
Alopecia (hair loss within 2 Osteoporosis
weeks)
Proteinuria and lung
Painful peripheral
Alopecia damage also seen in chronic
neuropathy
Treatment : Prussian blue (within 2 weeks) poisoning
(binds thallium in the gut) Treatment : EDTA

Summary
Ideal homicidal agents Arsenic : Garlic breath, Mees lines, neuropathy T/t: DMSA
Cheap and easily available Mercury : Tremors, Acrodynia, memory loss (DMSA is a
Colourless, odourless & tasteless (can be Lead : Abdominal colic, Anaemia, Burton's line derivative of BAL)

added in food/drink without any suspicion)

Highly toxic Thallium : Alopecia, painful paraesthesia (t/t : Prussian blue)
Features resembling some disease Cadmium : Osteoporosis (t/t : EDTA)
Shouldn't be detected by chemical tests
No specific postmortem changes
Examples include Garlic breath also seen with : Phosphorus poisoning
Arsenic Phosphorus is of two types :
White/yellow phosphorus : Rodenticides (more toxic)
Thallium
Red phosphorus : Match-sticks (less toxic)
Aconite
Acute poisoning : Garlic breath, phosphorescent vomit
Cyanide
Chronic poisoning : Phossy Jaw (Painful necrosis of the jawbone)
Toxicology - Snakes

Elapidae (Cobra, Krait) Viperidae (Russell's viper)

Neurotoxic (Descending paralysis) Vasculotoxic
Earliest manifestations : Ptosis Damages blood vessels, causing
necrosis, cellulitis, and coagulopathy
Cobras

Russell's Viper
Common cobra King cobra
"Has V on it's body"
Spectacles + hood Only hood
"King doesn't wear spectacles"

Hydrophidae (Sea snake)

Kraits
Myotoxic (causes muscle necrosis)
Found in sea (marine snakes)
Most venomous snakes

Common Krait Banded krait

"B/w is common and
boring"

Venomous Non venomous

snakes snakes
Scorpion
Red scorpions are more poisonous than
black scorpions
Scorpion poison causes Autonomic storm
DOC : Prazosin (sympathetic blocker)

Spanish Fly
Produces Cantharidin which can cause
Priapism (prolonged erection, >4 hrs) if
ingested.
Toxicology - Poisonous seeds

Abrus precatorius Semicarpus (Bhillwanol)

Contains the toxin Abrin aka Marking nut
aBRus : Black Red Causes artificial bruise

Croton Strychnine (Nux vomica)

aka Jamal-gota Toxin : Brucine
Poison : Crotin Crushed seed is poisonous
Causes skin irritation (even one)
Uncrushed seeds are not
poisonous
Ricinus (Castor) Causes post synaptic
All parts are toxic (except the oil) inhibition of Glycine, GABA
Poison : Ricin (Prevents RNA polymerase) (Pre-synpatic inhibition of glycine
Causes : Bloody diarrhoea and burning and GABA caused by tetanus toxin)
oral mucosa

Toxicology - Important plants

Datura Atropa Belladonna

aka thorn apple aka deadly nightshade
Seeds are Kidney shaped Active chemical : Atropine Parthenium
Active chemical : Hyoscine and Scopolamine (Carrot grass)
and Atropine
Highly invasive weed
Causes airborne contact
Both are anticholinergic toxins (Mydriasis, dry skin)
dermatitis
DOC : physostigmine (crosses BBB)
 Toxicology - Antidotes
Paracetamol : N -acetyl cysteine Heparin : Protamine sulphate
Methanol, Ethylene glycol : Fomepizol Dabigatran : Idarucizumab
BZD : Flumazenil Iron : Desferioxamine (BAL is contraindicated)
TCA : Sodium bicarbonate Arsenic, Mercury, Lead : DMSA (or BAL) "AML"
B - blockers : Glucagon Cadmium : EDTA
Copper : Trientine-zinc, D-penicillamine
Cyanide : Vitamin B12, Lille's kit
Meth-Hb : Methylene blue Organophosphate, Carbamate : Atropine
Datura, Atropine : Physostigmine
Opioid : Naloxone
Digoxin : Digibind

Judicial Courts
Magistrate Courts
Handles less severe criminal cases Examination of Witnesses
Presided over by a Judicial Magistrate 1. Examination-in-Chief (Direct Examination):
Maximum punishment: 7 years imprisonment Conducted by the lawyer of the party who has
called the witness.
Witness gives testimony regarding the facts of the
Sessions Court case.
Handles serious criminal cases (punishable by death or life No leading questions allowed unless the witness
imprisonment) turns hostile (a witness who gives evidence contrary
Highest Criminal Court in a district to the party who called them)
Can impose a death sentence, but it must be confirmed by
the High Court 2. Cross-Examination:
Hears appeals from magistrate courts Conducted by the opposing lawyer
Purpose: Test the credibility, reliability, and
consistency of the witness's testimony
District Court Leading questions are allowed (e.g., “Isn’t it true
Handles civil cases only that you saw the accused leaving the scene?”)
Highest Civil Court in a district
3. Re-Examination:
High Court (Highest Court in State): Conducted by the lawyer who conducted the
Appeals from Sessions/District Courts and writ jurisdiction examination-in-chief
Confirms death penalties imposed by Sessions Courts Purpose: Clarify any ambiguities arising during cross-
examination.
New facts cannot be introduced unless permitted by
Supreme Court of India (Highest Court in India): the court.
Appeals from High Courts and constitutional matters

Negligence by Medical Professionals

Civil negligence Criminal negligence

Non-intentional act causing harm Gross or reckless negligence causing death or harm
eg. Diagnostic errors eg. Operating under intoxication
Objective of case : Compensation to the victim Objective of case : Punishment for the wrongdoer
Onus of proof : Patient Onus of proof : Doctor
Trial at civil courts or consumer courts Trial at Criminal courts
Punishment : Financial compensation Punishment : Imprisonment, fines, or both

Res ipsa loquitur : Facts speak for themselves

(eg. Piece of gauge left inside body)
New Indian Laws (BNS)
IPC changed to BNS (Bhartiya Nyaya Sanhita)
CrPc changed to BNSS (Bhartiya Nagarik Suraksha Sanhita)
IEA changed to BSA (Bhartiya Sakshya Act)

Criminal responcibilty (20-24) Rape & Sexual offence (63-79)

"Six-ual offences"
Section 20
Pre-MBBS, too innocent Section 63 : Definition of rape
Age < 7 years : No criminal Minimum age for consent is 18 years
responcibilty Rape involves penetration without consent, by force,
coercion, or under deceitful circumstances
Section 21
First year, MBBS tests you Section 64 - 71 : Punishment of rape
For children aged 7 - 12 years, criminal 64 - General punishment (10 years to life)
responsibility is conditional 65 - Rape of minor
The court assess whether the child had < 16 years: 20 years to life imprisonment
sufficient intellectual capacity to < 12 years: 20 years to death penalty
understand the nature of their act 66 - Victim dead or in vegetative state (20 years to life)
67 - Rape by a husband during separation (2-7 years,
Section 22 bailable)
Second year, you have lost your sanity 68 - Rape by person in authority (5-10 years)
69 - Sex using decietful means eg. false promises (10 years)
A person with a mental illness is not
70 - Gang rape
held criminally responsible
> 18 years: 20 years to life imprisonment.
This is based on the McNaughten Rule.
< 18 years: Life imprisonment to death penalty
71 - Repeat offender
Section 23
Third year, friends force you to drink Section 72-73 : Protection of identity of victim
Offense under involuntary intoxication (both punishable with upto 2 years of imprisonment)
is not held criminally responsible
72 - Disclosure of victim's identity
73 - Publishing court proceedings related to sexual offences
Section 24
Fourth year, your're drinking yourself Section 74-79 : Other sexual offences
Offense under voluntary intoxication is 74 - Sexual Assault
held criminally responsible
75 - Sexual Harrasment
76 - Removal of Clothes
77 - Voyeurism
Consent (25-30) 78 - Stalking
"Junior doctors aged 25-30 take consents" 79 - Insult to Modesty of a Woman
Section 25 : For normal procedure
Section 26 : For risky procedure
Section 27 : < 12 years (guardian's consent) Miscellaneous
Section 28 : Consent invalid (under fear or intoxication)
Section 80 : Dowry death
Section 29 : Consent invalid for illegal procedures
Death of woman within 7 years of marriage
Section 30 : In emergencies, consent is implied
Section 114 : Definition of hurt
Section 116 : Definition of grievous hurt
Section 123 : Hurt with poison
Offences affecting life (100-113) Section 124 : Hurt with acid
Section 100 : Culpable Homicide (broader term, includes Section 227 : Definition of perjury (false evidence)
intentional and unintentional acts) Section229 : Punishment for perjury
Section 101 : Murder (Subset of culpable homicide with clear
intent to kill)
Section 103, 105, 106 : Punishments
103 : for murder
105 : for Culpable Homicide (not amounting to murder)
106 : for death due to negligence
 Dying declaration (BSA 26) Magistrate inquest (BNSS 196)
A statement made by a dying person about the cause or Inquests are conducted to determine the cause of death,
circumstances of their impending death (actual death is not whether natural or due to criminal activity.
mandatory; it is the belief of imminent death that matters) Magistrate Inquest is needed in cases of unnatural deaths
Admissible in court under BSA Section 26 a. Dowry death
It is considered truthful since the person believes they are b. Death in police custody
on the verge of death and has no reason to lie - No leading c. Death in psychiatry hospital
questions permitted d. Exhumation (digging a corpse out)
The declarant must be mentally sound
It can be oral or written (patient has to sign or give thumb
impression)
Ideally recorded by judicial magistrate (if magistrate is not
present, doctor or police can even record)

Miscellaneous
POCSO act
The POCSO Act (Protection of Children from Sexual
Offences Act, 2012) provides protection to children from
sexual abuse and exploitation
For children under the age of 18 years
Protection of children from offenses of
a. Sexual assault
b. Sexual harassment
c. Pornography

Signs of child abuse

1. SDH (sub-dural hemorrhage)
2. Retinal haemorrhages
3. Fractures of different healing stages
Mostly metaphyseal fractures aka bucket-handle fractures

Bad newz : Movie about heteropaternal superfecundation

Superfetation Superfecundation
Different menstrual cycles Same menstrual cycle
(different gestational ages) (same gestational age)
Ovulation occurs during Ovulation occurs in the
pregnancy same cycle
Very rare in humans Same or different partners
Possible in humans
CHAPTER 14
ANAESTHASIA
Important instruments

Airway adjuncts Airway devices

Keeps the airway open by
preventing tongue fall

OP
airway

aka Guedel's airway

NP
airway
Laryngeal mask airway
(aka Supraglottic airway devices) Endo-tracheal tube

Easier to insert (used in difficult More secure airway (lower

intubations) risk of aspirations)
Blind procedure (no laryngoscopy) Laryngoscope is needed
Increased risk of aspirations

Laryngoscope

OP airway can cause gag reflex in

conscious patients
Hence NP airway used in conscious McIntosh
patients Curved blade
Used in adults
Measurement of size
From mouth to angle of mandible Straight blade for the larger epiglottis
in pediatric patients
Miller's
Straight blade
Used in pediatrics

McCoy
Has a lever

Left hand
Right side of mouth
Sweep tongue from right to left
Pressure forward and upward
Video Laryngoscopy Upper incisors m/c injured
Best for difficult intubations
 BTR by Dr. Zainab Vora
Endo-tracheal tube

Double lumen ET tube

2 cuffs, 2 ports, 2 tubes
Used for single lung ventilation

Uncuffed Modifications of ET tube

Used in pediatric age group
To avoid sub-glottic stenosis
Position to insert ET tube
To confirm intubation
ETCO² on capnography
Oral surgeries PNS surgeries
pnS - South

Intubation stylet Flexion at C spine

Bougie Flexible and metallic Extension at A-O joint
Used as guidewire to insert ET tube Used to alter the shape of ET tube
Vowels stick

Laryngeal mask airway

First generation LMA Second generation LMA Intubating LMA I-Gel LMA
Only one tube for Two tubes Can be used to intubate Takes up heat from body
ventilation One for ventilation and and expands to seal
one for gastric aspiration

LMA Proseal is the most

commonly used LMA
Oxygen delivery systems

Nasal prongs Hudson's mask Venturi mask

40% 60% 60%

5 L/min 10 L/min 15 L/min

Fixed O²
Bernoulli's principle

Non
High flow nasal C- PAP
rebreathing
cannula (NIV)
mask

85% 100% 100%

15 L/min 60 L/min No limit

Gas cylinders Diameter index safety system

B/w is oxygen
Nitrous oxide - blue For pipelines
Blue and white - N²O with oxygen Intermediate pressure systems
Mixed - Air
All grey - CO² White - Oxygen
Blue - N²O
Pressure - 2000 Psi for all (750 for N²O) Black - Air
Yellow - Vaccum

Pin index safety system

Yellow vaccum
cleaner
Air - (1,5)
O² - Two atoms (2,5)
N²O - Three atoms (3,5)

CO² - (1,6)
Entonox -7
 BTR by Dr. Zainab Vora Anaesthesia
Needle Gauge

14 Orangutan - Largest
16
17 Wait for 1 year
18 Green signal at 18
20
22
24 Yellow - sevoflurane - kids
26

Measured in gauge
Gauge is inversely related to diameter
Minimum 18 gauge needle to be used
in ATLS - 96ml/min

Foley's and NG tube

NG tube insertion
Measure size - NEX in adults and NEMU in kids

GORY
from PB

Fowler's position (aka beach chair position)

Measured in French (Fr)

French is directly proportional to
diameter
External diameter is considered here
Females - 14 Fr
Males - 16 Fr Fowler's position is also used in various
French are extrovert neurosurgeries
Female- 14 Risk of air embolism
37
 Anaesthesia BTR by Dr. Zainab Vora
Central Line

3 ports

Central venous catheter Chemo port

For chemotherapy

>3 ports

Swan Ganz catheter

PCWP measurement Internal Jugular vein - Safest
Core temperature can be measured Subclavian vein - Risk of pneumothorax
Temp at lower end of Femoral vein - Line related sepsis, thrombosis
esophagus is m/c used for
core body temperature

Monitoring of Anesthesia

Electromyography

Bispectral Index Ulnar Nerve (adductor policis tested)

Intra-op depth of anaesthesia measurement Facial nerve (orbicularis oculi)
BIS of 40-60 is ideal Train of Four (0.5 sec apart)
> 0.9
Central Neuraxial Anesthesia

Skin and subcutaneous tissue

Stripes
Wings
Supraspinous ligament
Interspinous ligament
Tuhoy Needle

Ligamentum flavum
Epidural space is a negative pressure space
Epidural Anesthesia (loss of resistance is felt)
Dura mater Continuous anesthesia can be given
Arachnoid membrane
Post neuraxial shivering
Spinal Anesthasia
More with epidural than spinal anesthasia
The most efficient way to prevent is by
avoiding cold epidural and intravenous fluids.
IV Meperidine is the DOC for it.
Tramadol is also useful in post anesthasia
No wings shivering.
Special tip

Spinal cord extent

Post-dural-puncture Headache At birth : L3 (upper border) like collagen in
Onset 12-72hrs and last for 1-2 weeks. Adults : L1 (Lower border) would healing
Aggravated by sitting and relieved by lying down.
Risk factors : Young, pregnant, female, large needle
Level at which LP done
Prevention by smaller needle
Mx : Caffeine and analgesics Lumbar Puncture done at L3-L4 in adults
Refractory : Epidural blood patch Posterior superior Iliac crest is the landmark
Early ambulation doesn't increase risk of PDPH In children at level L4-L5

Regional Anesthesia

Anterior ethmoidal Naso - ciliary nerve

Infra-Orbital nerve block
nerve block block
 Anaesthesia BTR by Dr. Zainab Vora
Inhalational Anaesthetics

"Hollow"thane
Sevo PIL hepatitis Desi - Pungent, Potent

Sevoflurane Isoflurane Halothane Desflurane

Sweet smelling Liver transplant AI Hepatitis Specialised surgeries
Induction in children Coronary steal Only used in Special TEC-6 vaporiser
Cardiac surgery phenomenon asthmatics Pungent smell (can't be
Toxic compound-A (bronchodilator) used to induce)
(nephrotoxic)

MAC - Minimum alveolar concentration

It's ED⁵⁰ for anaesthetics
Min dose at which there is immobilisation
Inversely related to potency of the inhalational agent HIDden potential
Desflurane > Isoflurane > Halothane Halothane > Isoflurane > Desflurane

Blood/gas coefficient
Indicates time needed for induction
More BG - More time needed (more in blood)
Less BG - Less time needed (more in alveoli)
Xenon has the lowest BG coefficient (quickest induction and recovery)
Halothane > Isoflurane > Desflurane

Nitrous Oxide
Minimum potency But used due to its second gas and concentration effect
Second gas effect : Better uptake of secondary gases because of N²O
Concentration effect : Gets absorbed in blood quicker and hence more partial pressure O² in alveoli
Fills empty cavities : Because it vaporises so easily, it can get accumulated in body cavities, hence
avoided in closed space surgeries (ear surgeries, pneumothorax)
Diffusion hypoxia : During recovery, rapid elimination causes a reduction in the partial pressure of
oxygen leading to hypoxia (Pre-oxygenation with 100% O² needed)
Maximium incidence of PONV with Nitrous oxide
 BTR by Dr. Zainab Vora Anaesthesia
IV Anaesthetics

Propofol
DOC for TIVA (Total IV Anesthesia) Cardiac surgery
DOC for - daycare/specialised sx Inhalational : Sevoflurane
DOC in porphyria patients IV agent : Etomidate
Contains egg (C/I in egg allergy) NDMR : Vecuronium
Painful injection
Anti-emetic properties
Asthma
Inhalational : Halothane
Ketamine IV agent : Ketamine

NMDA antagonist at Phencyclidine site

Dissociative anesthesia Neurosurgery
No pain after recovery Inhalational : Desflurane
DOC in shock - ↑ ICP, ↑IOP IV agent : Thiopentone
DOC in asthma
Has addictive potential (Schedule X)
Increased salivation Day care anaesthasia
C/I in hypertensive/ glaucoma/ epileptics
IV agent : Propofol
Inhalational : Sevoflurane
Etomidate NDMR : Rocuronium

DOC in cardiac surgeries

S/e : Adrenal supression
Heart for my "date"

Thiopentone
DOC in seizures (neuroprotective)
DOC in hyperthyroidism

Local Anesthetics

Na channel blockers (inactivated state)

Lignocaine aka lidocaine is an intermediate acting LA (DOC in Bier's block)
Cardiotoxic - Bupivacaine (not used for Bier's block)
LA toxicity : CNS + CVS effects (DOC : 20% Intra-lipid)
41
 BTR by Dr. Zainab Vora Anaesthesia
Muscle Relaxants

Non Depolarising muscle relaxants Depolarising muscle relaxant

Curare drugs Succinylcholine (aka Suxamethonium)
Competitive antagonist of It has a rapid-onset (30–60secs) and short
acetylcholine duration of action
Reversal is via Neostigmine Rapid hydrolysis by plasma cholinesterase
(aka pseudocholinesterase)
Vecuronium - Most cardio stable
Rocuronium - Day care anesthasia
Atracurium and Cis-atracurium
} Reversal by
Sugammadex
Because of fast onset and recovery, it's the
muscle relaxant of choice in Rapid sequence
intubation (RSI)
safe in renal and liver failure
Increases gastric pressure and can cause
Pancuronium - Longest acting
hyperkalemia (hence Rocuronium is used in
Can cause post op paralytic ileus and urine retention RSI now)
Causes post op Muscle pain
Post op rigidity due to - Fentanyl (opioid)
Neostigmine
Used for reversal of NDMR
Acetylcholine esterase inhibitor (indirectly acting
cholinergic)
Decreased breakdown of acetylcholine at the motor
endplate - more Ach

Hoffman elimination
Atracurium and Cis-atracurium
Spontaneous non-enzymatic degradation
Safe in Liver and Renal failure
By product - Laudanosine (Seizures)

Malignant Hyperthermia

Genetic predisposition Presentation

Mutation of ryanodine receptor (Ryr 1 gene), Rigidity and muscle spasm (masseter spasm)
located on chr 19. High fever and sweating
Ryr 1 is responsible for calcium release from the Increased metabolism : EtCO² increases (step
sarcoplasmic reticulum. ladder pattern on capnography)
Mutated Ryr-1 releases too much calcium on Muscle damage : ↑ K+ (hyperkalemia)
certain triggers causing spastic contractions
Management
Trigger
Dantrolene Sodium + 100 % O²
Inhalational anesthetics 41
Discontinue causative agent
Succinylcholine (DMR) Electrolyte correction
 Anaesthesia BTR by Dr. Zainab Vora
Capnography

Surest sign of endotracheal intubation

Step-ladder pattern - Malignant hyperthermia
Shark fin pattern (bronchospasm)
COPD, asthma
Sudden loss of waveform
ETT disconnected, dislodged, kinked or
obstructed.

Hypoventilation

CPR assessment
Attempt to maintain minimum of 10 mmHg Hyperventilation

Mapleson Circuits

Adults - Mapleson A, D Pediatrics - Mapleson E, F

A - APL adjacent (spontaneous) E - Ayre's T tube
D - APL distant (controlled) F - Jackson Reece
Spontaneous ventilation in children

Soda Lime
Active ingredient that absorbs CO² is CaOH² (80%)
If NaOH - Soda lime, If BaOH² - BARALYME
Small amount of KOH present.
End product - CaCO³ + NaOH (soidum hydroxide is
regenerated)

Bane's circuit (co-axial) Sevoflurane reacts with soda Lime to

Tube within tube
Modification of type D produce Toxic compound -A
 Anaesthesia BTR by Dr. Zainab Vora
One liners
Pre-op drug DOC to reduce anxiety : Midazolam
Pre-op drug DOC to reduce secretions : Glycopyrrolate
Pre-op Antibiotic time : 3omins - 1hr before incision (Cefazolin)
MC nerve injured intra-op : Ulnar nerve
MC intra-ophthalmic complication : Corneal abrasion
Post op Vision loss mcc : Ischemic optic neuropathy
Max PONV with : Nitrous Oxide
PONV DOC : Ondansetron (5HT³ inhibitor)
MCC of intra-op anaphylaxis: Antibiotics

Mallampatti Grading
Difficult intubation

PUSH
2 3 4
1 Pillars of tonsils
Uvula
Soft palate
Hard palate

Entire uvula - 1 floor -4

ASA Grading
1 - Healthy
2 - Mild disease (under control)
3 - Disease not under control Well controlled diabetes - ASA 2
4 - Constant risk of death Diabetes with HbA1c of 9 - ASA 3
5 - Won't survive without the procedure
6 - Brain dead (organ donation)

Pre-op drugs discontinuation

Clopidogrel : 7 days
Warfarin : 5 days Aspirin can be continued in
Aspirin : 3 days
1. Percutaneous coronary intervention (PCI)
LMWH : 1 day 7 -5-3-1
2. Coronary artery disease (CAD)
UFH : 4 hrs
3. Stroke in the past 9 months

Lithium : 2 days (12-24 hrs half life)

Anti-depressants : 3 weeks TCA - 3 weeks

ACE I / ARB / OHA / Insulin : Skip morning dose

 BTR by Dr. Zainab Vora Anaesthesia
Basic life support

1st step
Verify scene safety Recovery position
Check for responsiveness When normal pulse
Call the emergency services and breathing
present

2nd step
Check for breathing
Check the pulse (Carotid pulse for 10 secs) Rescue breathing
When pulse present but no breathing
3rd step (If no breathing + no pulse) 10 breath/min
Keep checking pulse every 2 mins
Start CPR
30 :2 (Compression : Breath)
100-120 compressions/min
5-6 cm depth (1/3 of AP diameter)
Allow complete recoil

If AED arrives
Put AED and follow automated
instructions
Continue CPR till ROSC or untill ALS
providers arrive

ACLS

1st step Shockable rhythm Non Shockable

Shock Epinephrine ASAP
Start CPR
Continue CPR for 2 mins Continue CPR for 2 mins
Oxygen
Epinephrine every 3-5 mins Epinephrine every 3-5 mins
Attach defibrillator
Shock Continue CPR for 2 mins
Continue CPR for 2 mins Repeat
2nd step Repeat
Amiodarone/Lidocaine can Pulseless
Check if rhythm is
be used electrical
shockable or not
activity

V fib
Asystole

V tach No role of Amiodarone

or Lidocaine here
CHAPTER 15
PSYCHIATRY
 Disorders of PERCEPTION

Hallucination Illusion
No stimulus Stimulus present
Percieved in outer Thinking of a "rope
objective spcae to be a snake"

Pseudo-hallucination occurs in inner subjective space (can be seen in

Narcolepsy
normal people)
Reflex hallucination aka Synesthesia seen with LSD (can hear colors) Reduced hypocretin
Sleepy during the day (sleep attacks)
Hallucinations associated with Narcolepsy : Cataplexy (sudden loss of tone)
Hypnagogic hallucination : While "GO"ing to sleep DOC : Modafinil
Hypnapompic hallucination : While waking up

Psychotic vs Neurotic hallucinations :

Auditory hallucinations are mostly psychotic (eg. Schizophrenia)
Visual hallucinations are mostly neurotic (medical cause)

Healthy thought
Disorders of THOUGHT Constant
Organised
Continuous

STREAM of thought disorder FORM of thought disorder

1. Flight of ideas : Moves from Characteristic of SCHIZOPHRENIA
one topic to another 1. Derailment : No association
2. Pressure of speech : Have to 2. Neologism : Makes new words
say a lot in a short span 3. Incoherence : Word salad
Flight of thoughts and pressure of 4. Clang words : Rhymes
speech seen in MANIA
3. Thought block : Depression Palilalia :Repeats last word of sentence
Logoclonia : Repeats last syllable
Circumstantiality : Beating around the bush
Prolixity : Adding masala Echo-lalia : Repeats last word of doctor
Perseverance : Same responce to everything Echo-praxia : Repeats the activity of the doctor

CONTENT of thought disorders POSSESSION of thought disorders

Seen with DELUSIONS Seen with OCD, IMPULSE, PHOBIA
1. Persecution :M/c delusion
Thought insertion : Someone putting thoughts in my head
2. Folie A deux : Shared delusions
Thought withdrawal : Someone taking away my thoughts
(only treat the primary patient)
Thought broadcast : Others can hear what am saying
3. De Clerembault : Erotomania
4. Othello : Morbid Jealousy
5. Cotard : Nihilistic delusion
 Delusions of mis-identification

CAPGRAS syndrome FREGOLI syndrome

CRAP! Shez not my mother! Strangers appear like family members
Known person replaced by a Strangers are "wearing masks" and
stranger coming

Grades of INSIGHT

GRADE 1 : Complete denial

GRADE 2 : Somewhat agrees but denies at the same time
GRADE 3 : Agrees but blames on external factors
GRADE 4 : Agrees but doesn't apply this knowledge for future experinces (intellectual insight)
GRADE 5 : Agrees and wants to modify future behaviour (emotional Insight)

Memory
Immediate memory : attention and concentration

ATTENTION CONCENTRATION
Ability to focus without Sustained attention
getting distracted Serial 7 substraction test
"Digit Span test" - Digit
forward or backward
"Attention Span"

Recent memory : 24 hour recall test

Remote memory : Old memories tested

Personality tests

Objective : Minnesota multiphasic personality inventory

Subjective : Rochart's ink blot, Thematic appreciation test

Rochart's ink blot Thematic appreciation test

 Theories

Sigmund Freud's structural model of mind

Id : Pleasure
Super-ego : Morality
Ego : Reality (decides between Id and superego)

Topographical model of mind

Conscious
Pre-consciouus
Unconscious

Pavlov's experiment (classical conditioning)

Example of Operant conditioning (reinforecemnt or punishment)

Reinforcement done for desired positive behaviour (can be positive or negative)

Positive reinforcement > Negative reinforcement

Punishment done for negative behaviour

Discontinuation eventually eliminates behaviour.

Maslow's hierarchy of needs

Basic needs : (Roti kapda makaan) + (Safety)
Psychological needs : (Intimate relationships, friends) + (Prestige and feeling of accomplishment)
Self fulfillment needs : Creativity

Freud's Psycho-Sexual stages of development

Oral (0-18 months) Latency (6yrs - Puberty)
Pleasure centers on the mouth - sucking, biting, chewing Dormant sexual feelings
Child grows intellectual and social skills
Anal (18-36 months)
Pleasure focuses on bowel and bladder elimination Genital (Puberty)
Coping with demands for control Maturation of sexual interests
OCD is a disorder of anal stage of development
Phallic (3-6 years)
Pleasure zone is the genitals
Coping with incestuous sexual feelings (Oedipus complex)

Classical Psycho-analysis
Free association (therapist lets the patient talk freely)
Abreaction : Repressed memories come out when talking freely

Catharsis is when Repressed memories come out involuntarily in other forms eg. Music or painting 21
Parapraxis is slip of tongue
 Defence Mechanisms

IMMATURE defence mechanisms NARCISSITIC defence mechanisms

Regression in milestones Denial DPS
Acting out Projection : Attributing own feelings on otehers
RAP
Passive agression Splitting : Black or white (seen with borderline PD)

MATURE defence mechanisms NEUROTIC defence mechanisms

Sublimation : Sublime into another activity Repression : Unconsciously forget
Altruism : Do other good activities Intellectualisation
Anticipation : Prepare well SAASH Seen with "OCD"
Supression : Only voluntary defence mechanism, 1. Dispacement : Displace someone's anger on someone else
aka Pseudo-defence mechanism 2. Undoing : Trying to catch up DURI
Humor 3. Reaction formation : "Dear !"
4. Isolation of affect : No emotions

Personality Disorders

Cluster A personality Cluster B personality Cluster C personality

Paranoid (suspicious) Anti social (criminal and hostile) Avoidant (sensitive to crticism, timid)
Schizoid (loves to stay alone) Conduct disorder if <18yrs OCPD (perfectionism, ego syntonic)
Schizotypal (magical thinking) Borderline (impulsive, suicidal OCD is ego-dystonic
female, bad relationships) Dependant (need support)
a/w splitting
Histrionic (attention seeking)
Narcissitic OCD
> 2 weeks
Disorder of thought possession
Urges that are repetetive and unwanted
Cause marked anxiety and distress
T/t : Exposure and responce prevention
Eating Disorders

Anorexia Nervosa Bullemia Nervosa

Low BMI (<18.5) and doesn't eat Normal to high BMI and compensatory behavior
Has body dysmorphia No body dysmorphia
Associated complications are related to starvation Associated complications are related to vomiting
(refeeding syndrome, amenorrhea, osteoporsis) (Russel's sign, tooth decay, Mallory Weiss tear
Rx : Nutritional rehabilitation + CBT hypochloremic + hypokalemic met alkalosis)
Refractory : Anti-psychotics Rx : CBT
Refractory : SSRI

Most common eating disorder is binge eating disorder

Russel's sign
(d/d Gottron papules
seen in Dermatomyositis)
 Somatoform Disorders

Un-intentional Intentional
1. Illness anxiety disorder : Obsessed with a 1. Malingering : Has a secondary gain
"diagnosis" (aka hypochondriasis) 2. Factitious disorder (aka Manchausen's)
2. Somatic symptom disorder : Obsessed
with a "symptom"
3. Functional neurological disorder (ACR) :
La Belle indiference

Schizophrenia

DSM 5 criteria Timeline of psychotic dis.

Two or more symptoms for > 1 month and one Breif psychotic episode : < 1 month
must be amongst the reds Schizophreniform : 1-6 months
Hallucination Schizophrenia : > 6 months
Delsuion
Disorganised speech (formal thought)
Delusion : > 1 month
Catatonia (DOC for catatonia : Lorazepam)
Negative symptoms
Schizo-affective : Schizophrenia with
Overall mood disturbance shall be >6 months
concurrent mood disorders + atleast 2
weeks of psychosis without mood
symptoms
Good prognostic factors
Sudden onset in old lady with depression
and family history of depression.

Positive symptoms are good prognosis 10% of schizophrenia

(because can be treated) patients die by suicide
(Alternatives are bad prognosis)

4 A's of Bleuler
Bleuler coined the term Schizophrenia and described
the primary symptoms
Association problems (formal thought disorder)
Autism (social withdrawal)
Ambivalence (can't take decision)
Affect problems
 Anti-psychotics

Theory for psychosis !

DOPAMINE pathways
Excess dopamine in brain
Typical antipsychotics are hence D² blockers Meso-limbic pathway : Positive symptoms (excess D)
(S/e Extra pyramidal symptoms, hyperprolactinemia) Meso-cortical pathway : Negative symptoms (deficient D)
Nigro-striatal pathway : EPS (deficient D)
Atypical antipsychotics work via other mechanisms
Tubulo-infundibular pathway : Hyperprolactinemia
(eg. Serotonin blocker), hence lesser side effects and
(deficient D)
acts on both positive and negative symptoms.

Typical antipsychotics Atypical antipsychotics

Strong D² blocker Weak D² blocker Clozapine

Haloperidol Chlorpromazine 5HT²a antagonist
(Highest risk of EPS) (s/e vortex keratopathy and DOC for TRS (treatment resistant schizo)
cholestatic jaundice) Agranulocytosis (dose independent)
Thioridazine
Sialorrhea (m/c side effect)
Penfluoridol
Max risk of lipodystrophy syndrome
Akathisia m/c (Propranolol) if C/I then BZD Can cause Myocarditis
Acute dystonia - within hours (Benzhexol or promethazine - Anticholinergic)
Tardive dyskinesia - in years (Valbenazine - VMAT blocker)
Drug induced Parkinsonism (Benzhexol or promethazine - Anticholinergic)
Malignant Neuroleptic Syndrome (Dantrolene Sodium)

Depot injection (for non compliance) using Z

track technique
Ziprasidone causes weight loss and QT prolong (Zara is QT with LBW)
DOC for psychosis in PD : Pimvanserin
Clozapine and Olanazapine cause metabolic syndrome
Aripiprazole is an antipsychotic that's D2 agonist (Not PPI)
Risperidone causes max hyperprolactinemia (Rizz-peridone)
ACUTE DYSTONIA
Penfluridol is longest acting (Pen writes long)
Quetapine causes cataract

Oculo-gyric crisis Torticollis

Depression

Criteria for diagnosis Beck's cognitive triad

Corrected in CBT
Sadness along with > 4/8 of SIGECAPS
Hopelessness can
Sleep (increased or decreased) lead to suicidality
Interest deficit (anhedonia)
Guilt I'm bad
Energy deficit
Worthless
Concentration deficit
Appetite eficit
Psychomotor (retardation or agitation) Future Everyone
Suicidality is bad is bad

Hopeless Helpless
 Atypical depression Post partum blues vs depression
Blues resolve within 10 days while PPD
Mood gets better when stimulated M/c type of depression doesn't
Hypersomnia Rx : CBT + SSRI SIGECAPS >4/8 in PPD
Hyperphagia Reassure for blues while antidepressants for
Leaden paralysis (heaviness in PPD (Zuranalone)
arms and legs)
Post partum Psychosis
Anti-psychotics and antidepressants

Anti-depressants

Theories for cause of depression !

Old theory : Decrease in mono-amines (5HT > NE > DA) causes depression
Latest theory : Decrease in BDNF (Brain derived neurotrophic factor) which is responsible for neuroplasticity.

MAO - A (Serotonin, NE, Dopamine, Tyramine)

Typical Anti-depressants MAO - B (Dopamine)
act by increasing serotonin (5HT)
MAO A is needed for metabolism of Tyramine, inhibition can
Reputake inhibitors (TCA, SNRI, SSRI)
MAO-A inhibitors eg Phenelzine, Moclebemide
🧀
cause cheese reaction (hypertensive crisis)
(DOC : Phentolamine)

Non selective Selective

Inhibit reputake of both Serotonin and NE Only inhibits reuptake of Serotonin

Tri Cyclic antidepressants (TCA) SSRI

Anti-cholinergic effect (Dry mouth) TCA - amine DOC for mild-moderate depression
Postural hypotension (α¹ inhibited) Imipr-amine DOC for most neurotic disorders
Sedation (H¹ inhibited) Desipr-amine Flu sit sir
Toxicity : Seizures, Clomipr-amine Flu-oxetine Citalopram
arrythmia, met acidosis Amine-tryptiline Flu-voxamine Es-citalopram
Nor-tryptiline Paroxetine Sertraline
T/t of TCA toxicity : NaHCO³
Dapoxetine
Indicated when QRS > 100 ms
Corrects acidosis and arrythmia
Am-ox-apine 🐂
(TCA with antipsychotic activity) Adverse effects of SSRI
M/c acute SE is nausea and vomiting
SNRI M/c long term SE : Sexual side effects
Du ven severely depressed (anorgasmia, premature ej.)
Lesser side effects than TCA
Duloxetine Premature ej. can be treated with Dapoxetine
DOC for Severe depression
Venlaflaxine Discontinuation syndrome, flu like symptoms
when antidepressants are stopped (least with
fluoxetine)

Atypical Anti-depressants Antidepressant of choice in pregnancy : Sertraline (SSRI)

Works by various mechanisms
Most teratogenic : Paroxetine
Bupropion (anti smoking, low sexual side effects, TCA used in nocturnal enuresis : Imipramine
minimum weight gain) TCA for neuropathic pain : Amitryptaline
Mirtazapine (least sexual side effects) TCA for cocaine dependence : Desipramine
Trazadone (causes priapism) DOC for insomnia in blind : Tasimelteon
Zuranolone (approved for Post Partum Depression)
Brexanalone Fluoxetine takes 4-6 weeks to show effect
Esketamine Anti smoking drugs : Varenceline (partial agonist at
nicotinic receptors), Bupropion (NDRI)
Buspirone : anti-anxiety drug
 Bipolar disorder

Criteria for MANIA

> 1 week (unless hospitalised) Lithium
Marked functional impairment Half life of 24 hours
Psychotic features may or may not be present Takes 4-5 days to show effect (steady
state)
Criteria for hypo-MANIA
≥ 4 days (consecutive) Absorbed by ENaC (toxicity in cases of
No functional impairment
starvation/dehydration/diuretics)
No psychotic features

Narrow therapeutic index

Mania with or without depression is Bipolar 1 Therapeutic levels : 0.8-1.2
Hypomania + Depression is Bipolar 2 Prophylactic levels : 0.5-0.8
Toxicity : >1.5
If 2 years of fluctuating mood with hypomania and sadness Measurement : 12 hours after last dose
(not depression) : Cyclothymia

S/e : Leukocytosis, increased urination,

> 4 mood episodes in a year : Rapid cycle BPD
fine tremors, hyperPTH
Toxicity : Diarrhea, Ataxia, Tremors
Management of mood disorders
DOC in acute mania : Lithium + Atypical anti-psychotics If taken in pregnancy : Box shaped heart
DOC for prophylaxis of mania : Lithium (Ebstein's anomaly)
Mood stabiliser with anti-suicidal properties : Lithium
DOC in rapid cyclers : Valproate Fine termors : Side effect (it's fine)
Effective in depression : Lithium and Lamotrigine Coarse tremors : Toxicity
DOC in pregnancy : Only anti-psychotics (Lithium is
teratogenic) Treatment for toxicity : Hemodialysis

Anxiety disorders

Panic attack Adjustment disorder

Isolated event Mild stressor (breakup, divorce)
Feeling of "impending doom" < 6 months
T/t : BZD (ECG done in all to rule out organic causes)
Acute stress disorder vs PTSD
Panic disorder Life threatening event
> 1 month Flashbacks
"Persistent concern" about having another attack ASD < 1 month, PTSD > 1 month
May be associated with Agoraphobia (fear of places EMDR is useful
from which escape is dificult) TOC : CBT
Rx : BZD
Phobia
General anxiety disorder > 6 months
> 6 months Out of proportion fear
Excessive anxiety about everything in general TOC : SSRI
Childhood Psychiatry

ADHD (2 X 6 = 12) Selective mutism

≥ 6 months Child doesn't talk to selective people
At 2 settings and onset before 12 years Onset < 5 years
Earlier known as minimal brain damage
Higher occurence of alcoholism and anti-social PD Oppositional defiant disorder
1st line : CBT Anger and irritability towards authority figures
> 6 years : Stimulants (Methylphenidate, amphetamines)
< 6 years : Atomoxetine Disruptive mood dysregulation
disorder
Always angry child
Autism Spectrum disorder
Temper outbursts
Decreased eye contact (impaired social interaction)
Onset < 10 years
Repetitive movements
IQ can be normal (Asperger Syndrome)
Intermittent explosive disorder is an
Reduced IQ (regression of milestones)
IMPULSE disorder in adults
1. Rett Syndrome (MECP 2 gene, XLD)
2. Heller's Syndrome

Tourette Syndrome
Motor and vocal tics present (not necessary to be
concurrent)
Psychiatric cause (no organic problem)

Nocturnal enuresis
Bed wetting >5 years of age
1st line : Bell and pad (Operant conditioning)
Refractory : Desmopressin
TCA that can be used : Imipramine

Mental healthcare act 2017

Decriminalization of suicide
Restriction on use of ECT Muscle relaxant used in ECT is Succinylcholine
Advance directive (on how to treat/ not treat) and anaesthetic used is Methohexital
Nominated representative to take decisions (no anti-epileptic property)
Voluntary admission (30 days)

Delirium vs Dementia
Delirium is acute and has a fluctuating course. Patient is disoriented (seen in hospitalised patients)
Dementia has a chronic course

MMSE (Folstein's test) done for delirium assessment

< 24/30 indicates delirium
Alcohol
Legal limit : 30 mg/dl Alcoholic hepatitis
Excitement : 50-150 mg/dl AST > ALT In alcoholic hepatitis
Critical level : 150 mg/dl Carbohydrate deficit transferrin > GGT : Best marker
In-coordination : 150-250 mg/dl Mallory-Denk bodies seen
Coma : 250mg/dl

Methanol poisoning
"M" in alcohol
Snow field vision
Mellanby effect : Better kick while drinking
Hooch tragedy
Marchiafava Bignami : Corpus Callosum
Putamen necrosis (MP)
demyelination on long term drinking
Morbid jealousy
Ethylene glycol poisoning
McEwen sign : Mydriasis on high doses
aka Anti-freeze/ brake fluid
Wernicke's encephalopathy : Thiamine def
PCT necrosis due to oxalic acid formation
(Korsakoff Psychosis if untreated)

T/t : Fomepizole + Ethanol

Alcohol withdrawal
1. Earliest : tremors (< 24hrs)
2. Alcoholic hallucinosis : Visual hallucinations +
Intact orientation (12-24 hrs)
Alcohol detection tests
3. GTCS : 24-48 hrs
4. Delirium tremens : Hallucinations + Loss of Windmark formula : To detect conc. of
orientation (48-72 hrs) alcohol in blood
Henry Gas law : In breath analyser
DOC : BZD (Lorazepam) + Thiamine Max conc. of alcohol : Urine
BZD safe in liver failure : Lorazepam , Oxazepam,
Temezepam (LOT)

Anti craving : Naltrexone > Acamprosate

Opioids

Heroin (aka brown sugar/ smack/ dope)

Chasing the dragon
is abused
Heating and puff inhalation
Depressant (depressed mental status,
resp depression, constipation)
Miosis Speedballing : Cocaine + Heroine
Hot Shot : Heroine + Strychnine
Opioid withdrawal (aka Cold turkey due to Micky Finn : Chloral hydrate
appearance of goose bumps on skin)
Lacrimation
Diarrhoea
Cholinergic + Anticholinergic
Mydriasis
manifestations
Toxicity DOC : Naloxone Opioid withdrawal
Withdrawal : Methadone SSRI toxicity
 Substance Abuse
Phencyclidine (Angel dust) Cocaine (Snow, white lady, coke, crack)
Hallucinogen Stimulant
Dissociation (Ketamine is a phencyclidine) Tachycardia , hypertension
Amnesia Mydriasis
Magnan bugs (tactile hallucination)
LSD (acid, paper) Nasal septum perforation
Hallucinogen Black teeth
Bad trips, flashbacks
Synesthesia
Amphetamine (ecstasy, crystal meth, ice)
Stimulant
Cannabis (weed, grass) Paranoid hallucinatory syndrome
Mydriasis
Hallucinogen

Bhang/ Majoon : Leaf Mydriasis Miosis

Ganja : Flower top
Toxicity Toxicity
Charas/Hasish : Stem resin (Most potent)
Cocaine OP
Amphetamine (MDMA) Opioids
Smell of burnt rope
Alcohol (McEwan) Nicotine
Increased appetite + Conjuctival injection
Withdrawal Carbolic acid
Amotivational syndrome
Opioid withdrawal poisoning
RUN AMOK (homicide f/b suicide)

M/c abused substance

India : Tobacco > Alcohol
World : Cannabis

Psychiatric Emergencies
CNS + CVS : TCA toxicity (DOC : NaHCO3)
MAO (-) + Cheese/wine : Cheese reaction (DOC : Phentolamine)
AMS + Fever + Muscle rigidity {h/o antipsychotic drug intake} : NMS (t/t : Dantrolene Sodium)
AMS + Clonus, anti-depressants + bupropion/tramadol/St. John's Wort/ Linezolid : Serotonin Sx
Evomoz notes
Int. Medicine
Gen. Physiology
Gen. Pharmacology
Gen. Pathology
CHAPTER 16
INTEGRATED
NEUROLOGY
 Sensory Receptors

Merkel Disk receptors

Epidermis →
Epidermis (Edges)
Merkel Braille
Braille

Meissner's Corpuscle
Most numerous
Non-hairy skin only
Fast moving touch, two point Miss Pacman
discrimination is fast

Paccinian Corpuscle
Largest receptor
High frequency vibration

Ruffini Corpuscle
Skin stretch, pressure Rough Knee
Maximum in joint capsule joints

Erlanger Grasser Classification

Conduction velocity and

Diameter

C fibres aka Type 4 (Lloyd and Hunt)

Cold sensation and Fast pain : A delta (mediated by Glutamate) ColD Delta
Warm, burning and freezing pain : Type C (mediated by Substance P) Burns and freezes slowly
Local anaesthetic sensitivity : A > B > C (Gamma and delta > Alpha and Beta) GOD!
Pressure : A > B > C Return to basics under pressure
Hypoxia : B > A > C BACO !
 Sleep Physiology
Status

Awake Asleep
Eyes open : Beta waves
Eyes Closed : Alpha waves

NREM (75%) REM (25%)

Beta waves
Muscles relax
HR and RR increased
(increased sympathetic
Stage 1 Stage 2 Stage 3 outflow)
Shortest stage of Longest stage of Deep sleep Memories are processed
sleep cycle (5%) sleep cycle (45%) Delta waves PGO (ponto-genicular
Theta waves 2 things Associated with ocular waves)
(memory formation) 1. K complexes 1. Sleep walking Night Mares (have memory
thoughta : memory 2. Sleep Spindles 2. Noct. Enuresis of dream) MRE REM
Bruxism 2=B 3. Night terrors

Good BAT Dance

max frequency
max focus

normal focus
(eyes open)

Eyes closed

N1 sleep
(memory formation)
Awake person REM NREM
EYE (+) EYE (+) EYE (-)
N3 sleep
Muscles (+) Muscles (-) Muscles (+)
Deep sleep
lowest frequency Muscles relaxed

REM decreased : Elderly quality of sleep bad in elderly N3 (deep sleep)

REM increased : Depression sleeping too much reduced in both
REM latency decreased : Narcolpesy
 Neurotransmitter Changes
Acetylcholine
Produced at : Basal nucleus of Meynert
Decreased in Alzheimer's
Increased in Parkinson's (compared to Dopamine)

Dopamine
Produced at : Substantia Nigra
Increased in Psychosis (Schizophrenia) and Huntington's
Decreased in Parkinson's and Depression

GABA
Produced at : Nucleus Accumbens
Decreased in Anxiety

Norepinephrine
Produced at : Locus Ceruleus
Decreased in Depression
Inreased in Anxiety

Serotonin
Produced at : Raphe nuclei
Decreased in Depression and Anxiety

Dementia
Alzheimer's
Most common cause of Dementia
(2nd m/c is Vascular dementia - early executive dysfunction)

Early : Short-term memory loss, spatial disorientation Neurofibrillary tangles Hirano bodies
(temporal and parietal lobe involved early)
Flame shaped basophilic structures Eosinophilic rod like structure
Late: Personality changes (frontal lobe involved late) Made of TAU proteins (Tau Tangles) Made up of actin
Non specific Non specific
Apo E2 is good prognosis 2 good to be true
Apo E4 is bad prognosis
Bielchowsky Stain
Mild disease : Donepezil, Rivastigmine, Galantamine (AchE Silver-stain
inhibitor) Stains Neuritic plaques

Severe: Memantine (NMDA inhibitor)

Pick's Disease (frontotemporal dementia)

Early personality changes Pick 's body
Knife like atrophy of Frontal lobe Tau protein + Ubiquitin
Tau proteins + Ubiquitin deposited as "Pick's Bodies"
 Lewy body dementia Normal pressure hydrocephalus
Visual hallucinations Wet-wacky-wobbly Hakim's triad
Spontaneous parkinsonism 1. Urinary incont,
REM disorder 2. Dementia
Alpha - Synuclein deposition 3. Ataxia
Shuffling gait with preserved arm swing
(magnetic gait)
B/l dilated lateral ventricles

Prion's disease
Lewy body Rapidly progressive
α- Synuclein Myoclonus
Infective proteins in CSF
Lewy body dementia is the Periodic sharp waves on EEG
Spongiform
connecting link between
Alzheimer's and Parkinsonism Pulvinar/hockey stick sign encephalopathy
Seen in Variant CJD

Parkinsonism aka Paralysis Agitans

Tremor + rigidity Treatment

Micrographia 1. Syndopa Long term use leads to "on-off phenomenon"
Mask like facies Levidopa + Carbidopa (on : dyskinesia, off : akinesia)
Autonomic features DOC in elderly DOC : Amantadine (s/e : Livido reticularis)
Postural instability
2. Dopamine Agonists
Shuffling gait
Pramipexole, Ropinirole, Rotigotine, Bromocriptine
Dementia and Depression S/e : Pathological gambling (DOC : Atomoxetine)
are late features
3. MAO-B inhibitors
Good responce to dopamine Selegiline, Rasagiline
(MAO - A inhibitors used for depression)
Diagnosis
UK brain bank criteria

Parkinson + syndromes Poor response to dopamine

Progressive supra- Lewy body Multi system atrophy Cortico basal

nuclear palsy dementia (MSA) - C degeneration
Impaired downward gaze Dementia Autonomic features Alien limb phenomenon
Humming Bird sign Visual hallucinations Hot cross bun sign in pons Assymetric bradykinesia

All are Syn-nuclein-o-pathies except PSP which is Taupathy

Taupathies : Alzheimer's, Pick's disease, Down's Sx, PSP, SSPE (Measles complication)
 Approach to headache

Headache

Unilateral Bilateral

Pulsatile Paroxysms (5-200 secs) MALE (repetitive headache)

Aura present Triggered by chewing/touch Excruciating pain
4-72 hrs Trigeminal Neuralgia Cluster headache
Migraine DOC : Carbamazepine DOC : 100 % O² + Sumatriptan
d/d : SUNCT Ppx : Verapamil
First line : NSAIDS
d/d : Paroxysmal hemicrania
DOC : Triptans (5HT1B/1D +) Short-lasting, Unilateral, Neuralgiform headache
attacks with Conjunctival injection and Tearing
Triptans C/I in CAD, CVA Seen in
Prophylaxis : Propranolol females
Newer drugs : Responds to
1. Lasmiditan migraine direct antagonist indomethacin
2. CGRP (-) : Erenumab, Galanezumab

Indication for prophylaxis

Migraine : > 4 attacks in one month
Tension headache : > 15 days a month
Tension Pseudo-tumor
headache Cerebri
M/c headache aka Idiopathic
Band like tightness intracranial htn
DOC : NSAIDS
Dull aching headache
Ppx : TCA
Papilledema
6th CN palsy
T Tetracycline
O Obesity
A Vit A
D Danazol

Rx
Weight loss
Acetazolamide
(For refractory)
Repeated LP
Optic fenestration
Demyelinating disorders
Optic nerve involvement

Unilateral Bilateral
Multiple sclerosis
20-40 yrs
Most common : Relapsing remitting type
IOC : CE MRI (Mcdonald's Criteria)
McDonald criteria : Dissemination in time and space ADEM Neuromyelitis
Charcot triad SIN (Acute dissem. Optica
1. Scanning speech (Devic's disease)
encephalo myelitis)
2. Intentional tremors
3. Nystagmus < 20 years 20 - 40 years
h/o viral infection Anti aquaporin 4 Antibodies
Llhermite sign : Shock like sensation on
Long segment spinal Long segment spinal cord
flexion of neck Lower-my-neck
cord involvement involvement
Uthoff phenomenon: Exacerbation of
symptoms on hot water bath tub se uthooff 1. Area prostema Sx
Short segment spinal cord involvement 2. Diencephalon Sx
3. Acute myelitis
4. B/L Optic neuritis

Osmotic Demyelination Syndrome

Rapid electrolyte correction
Quadriplegia and mutism
Pons are m/c affected (aka Central pontine demyelinosis)
 Acute Flaccid Paralysis
H/o GI or Respiratory infection
MCC of ascending paralysis
is hypokalemia

Truncal paralysis Bilateral ascending paralysis

Bowel bladder involved No sensory loss
Sensory level Autonomic features
Conduction velocities reduced, distal latencies

Transverse myelitis Guillian Barre Sx

IgG antibodies are involved
Saltatory conduction affected
(around nodes of Ranvier)

1. AIDP : anti GM1 antibodies

2. AMAN : anti GD1A antibodies
3. AMSAN (AMAN and AMSAN are Axonal types)
Q
4. Miller Fischer Sx : Opthalmoplegia, anti GQ1b antibodies

Long segment spinal Management : IVIG + Plasmapheresis

cord hyperintensity No role of steroids

Epilepsy Syndromes
Juvenile myoclonic Lennox Gastaut
West syndrome Absence seiz.
epilepsy Syndrome

Developmental delay Transient LOC Seen in adolescents Multiple seizure types

Salaam spells No loss of postural control Dropping things / falling in Low IQ
Hypsarrythmia 3 Hz spike and slow wave early morning < 2.5 Hz spike and wave
(mountain waves ) on EEG T/t : Ethosuximide or Valproate 3-6 Hz spike and wave T/t : Topiramate / Valproate
DOC : ACTH DOC : Valproate New drug : Rufinamide
Vigabatrin is DOC when ass.
with tuberous-sclerosis

Rule of 3
Absence seizures : 3 Hz When to stop Anti-epileptic therapy
Less than 3 : LGS (L = less) Seizure free after 2 years (normal EEG and MRI)
Greater than 3 : JME If EEG/MRI abnormal then continue life-long
 Anti-epileptics
DOC focal seizure : Carbamazepine Risk of SIADH, SJS
DOC focal seizure in elderly : Lamotrigine Risk of SJS, Hemophagocytic Lymphocytosis
DOC trigeminal neuralgia : Carbamazepine
DOC typical absence sz : Ethosuximide (Ca2+ channel blocker)
DOC atypical absence sz : Valproate
DOC infantile spasm : ACTH
DOC infantile spasm in TSC : Vigabatrin S/e : visual field contraction
DOC neonatal sz : Phenobarbitone
DOC febrile sz : Diazepam (Rectal) Phenytoin/valproate/Leviteracetam
DOC status epilepticus : Lorazepam → Midazolam infusion / Phenobarb coma
BZD approved in LGS : Clobazam GA with IV propofol
DOC GTCS/JME/ LGS : Valproate
DOC in pregnancy : Lamotrigine, Leviteracetam (if seizures controlled well with valproate then continue it)
Valproate and Vigabatrin are GABA transaminase inhibitors (Inhibit metabolism of GABA)

Carbamazepine Valproate
BZD : Increase frequency of
DOC for focal seizures V Vomiting GABA opening
Used for peripheral neuropathy A Alopecia Barbiturates : Increase duration
(DOC for trigeminal neuralgia) L Liver damage Barbi-durates
Enzyme inducer P PCOD
S/E : Agranulocytosis, Ataxia, SIADH, SJS Retigabine : K+ channel opener
R Rash
(doesn't act on GABA) RK
Oxcarbamazepine has lesser SJS but more SIADH O Obesity
Tiagabine : GABA reuptake
A Anorexia
inhibitor
T Teratogenic (max teratogenic)
Phenytoin E Edema
Cy-P450 induction Beta Carboline : Inverse agonist at BZD
Hirsuitism, enlarged gums
Yellow brown skin Gabapentin and PreGabalin
Low Vitamin D : hypocalcaemia Along with carbamazepine, used for
Low Folate : Megaloblastic anemia peripheral neuropathy.
Insulin resistance (avoid in DM) DOC for Restless leg syndrome
Teratogenic (fetal hydantoin syndrome) Post herepetic neuralgia
With Carbamazepine : Induce each
other's metabolism
Topiramate
With Valproate : Liver failure
Dual mechanism (GABA
With OCP : OCP failure
agonist + NA channel blocker)
With Warfarin : R/o bleeding
Renal sTOnes
(switch to heparin)
Glaucoma
 Stroke

NCCT

Thrombolysis
Alteplase (0.9 mg/kg)
Hemorrhage No hemorrhage If neurological status declines ,
cryo-precipitate administered
Within 4.5 hours : Thrombolysis
Putamen bleed Contraindications
4.5 - 6 hours : CT angiography
M/c cause of ICH
Intra-arterial thrombolysis if thrombus + penumbra 1. BP : > 185/110mm Hg
Seen with Htn
2. Recent MI or head injury
3. Bleeding diathesis
4. Major surgery : 2 weeks Sx = 2
5. GI bleed : 3 weeks GIT = 3

Edema > 1/3 of MCA territory is also a

contraindication for thrombolysis

Stroke localisation
ACA Stroke
Lower limb involved
Urine incontinence
P
Personality changes P
MCA Stroke mcc of hemiplagia
Face and upper limb involved MM
A
Dominant side - Superioir division : Broca's Aphasia
Dominant side - Inferior division : Wernicke's Aphasia
Non-dominant side : NO aphasia

PCA Stroke
C/L hemi-anopia
Anton Syndrome (denial of blindness) Parietal lobe stroke
Alexia (can't read) without agraphia (can write) Hemi-spatial neglect (Non dominant side)

Thalamic stroke (Dejerine Roussy Syndrome)

C/L Hemi-Sensory loss
Agonizing pain in affected areas
aka Thalamic pain syndrome

Occipital lobe lesion

Stereognosis Graphesthasia Simultagnosia

Identify an object Ability to recognise Inability to perceive
by touching tracings on skin multiple objects together
Pro-sopagnosia
Inbility to perceive known faces
CHAPTER 17
INTEGRATED CVS
 Action Potential
Action potential

Myocyte action potential Pacemaker action potential

Corresponds to QT interval

Phase 1 (K efflux) Phase 0

Phase 3
Phase 2 (Ca L type slow channels vs K efflux) Ca channel (L Type) K efflux
0 mV
Phase 3 (K efflux continues)
Phase 0
(Na influx) Efective refractory period Phase 4
Na and K Funny currents
200 msec
Phase 4 (dominated by K efflux) Ca influx (T Type)
-85 mV
1. Adenosine lowers HR by slowing phase 4 (DOC for PSVT)
2. Catecholamines increase HR by hasting phase 4

Class 1 Class 2 Class 3 Class 4

Blocks Na channels Beta blockers Blocks K channels Blocks Ca channels
Slow down phase 4 Slow down the action Non DHPs : Slows heart rate
Reduces oxygen potential (QT prolong) and force of contraction
demand A (Verapamil, Diltiazem)
Amiodarone
I DHPs are used as anti
Ibutilide
D hypertensives
Dofetilide
1A 1B 1C S Sotalol (not a β blocker)
K channel K channel No action on
blocker opener K channel Side effects of Amiodarone
Queen proclaimed 1. Lignocaine No PROoF Please Pigmentation (ceruloderma) and photosensitivity
Diso's pyramid 2. Phenytoin 1. Propafenone Check Corneal deposits
1. Quinidine 2. Flecanaide LFT Hepatotoxic
2. Procainamide DOC for ischemic
C/I in ischemic PFT Pulmonary fibrosis
3. Disopyramide arrythmias and
arrythmias TFT Thyrotoxic
digitalis toxicity
Slow down the
action potential Shortens QT
(QT prolong) interval

Adenosine
1. Shortest acting anti-arrythmic
2. DOC for PSVT (stable)
3. Inhibited by Caffeine and theophylline
1a 1c

1b 3
 ECG

PR interval : 0.2 secs

QRS : 0.1 secs
2-1-4
QT : 0.4 secs

Wave at J point

Osborn wave Epsilon wave

Hypothermia ARVD (Arrythmogenic RV dyscrasia)
Familial condition
F/h/o sudden cardiac death

Delta (δ) wave

Heart Rate Corrected QT interval WPW syndrome
Buzzet's formula : Abnormal pathway : Bundle
300/large squares
QT of Kent
<3 squares : Tachy _______
QTc = _______
√RR interval Reduced PR (faster path)
>5 squares : Brady
Increased QRS (normal QRS
superimposed on abnormal)
Patient can be asymptomatic
Tall p waves Prevalence decreases with age
P pulmonale TOC : Radiofrequency ablation of abnormal path
Right atrial hypertrophy DOC : Flecainide
In emergency : IV Procainamide
Bifid p wave Rate lowering drugs are avoided (accessory pathway is not affected)
P mitrale
Left atrial hypertrophy

1st degree
Increased PR

Axis deviation
2nd degree type 1
"Check 1 foot" (Wankenbach)
Normal breakup
Check lead 1 and aVf
2nd degree type 2
1. Both positive : Normal (Mobitz)
2. 1 + and aVf - : Left axis deviation Bad breakup (ghosted)
3. 1 - and aVf + : Right axis deviation
3rd degree
4. Both negative : Extreme axis deviation
P and Q not related
Eg. Stoke's Adam Sx
Pacemaker needed for
2nd degree type 2
3rd degree
Sick sinus syndrome
(bradycardia + irregular rhythm in elderly)

Bundle branch block

"bundle of 6 sticks"
Normal LAD RAD Check V1 and V6
1. W and M : WilliaM (Left)
2. M and W : MarroW (Right)
Tachyarrythmias
Tachyarrythmias

Narrow complex Wide complex

Atrial fibrillation Atrial flutter (sawtooth pattern) PSVT

Cardioversion : 200 J Cardioversion : 25-50 J Cardioversion in unstable
DOC : Esmolol/ Ibutilide DOC : Esmolol/ Ibutilide 1st line stable : Carotid sinus
Lignocaine is C/I massage (vagal)
2nd line stable : IV Adenosine
Non DHP can be used
(Verapamil and Diltiazem)

Ventricular fibrillation Ventricular tachycardia Torsades de pointes

Defibrillation (1st line in unstable) Defibrillation (1st line in unstable) aka Long QT syndrome
DOC in unstable : Lignocaine DOC in unstable : Lignocaine DOC : MgSO4
In stable : IV Amiodarone In stable : IV Amiodarone

Special beats in Ventricular arrythmias

1. Capture beats Risk of stroke in AF
Normal QRS due to SAN signal
CHA²DS²VASc score
2. Fusion beats CHF Vascular diseases
SAN signal and Ventricular signal fuse to form a tall QRS
Hypertension Age > 65
Age > 75 Sex category :
DM Female
Causes of Long QT syndrome Stroke

Syndromes Total : 9
1. Romano Ward : No SNHL 0 : no anticoagulation
2. Jerwell Lange Nelson : SNHL present 1 : Aspirin
≥ 2 : Dual anticoagulation
Drugs
1. Anti-arrythmics 1A and 3
2. Antibiotics : Fqs and Macrolides
3. Ziprasidone
4. Chloroquine
Special case ECGs

Hyperkalemia Hypokalemia

Peaked T waves

Everything prolonged (except QT)

ST Elevation Flattened T waves
P waves lost U waves Underkalemia
Peaked P waves (Pseudo P pulmonale)
Sine wave QT prolongation

Treatment of Hyperkalemia Digitalis toxicity

Calcium gluconate/Calcium chloride
(Not Calcium Carbonate) Scooped ST depression
Insulin Flat T waves
Salbutamol QT shortening (quick conduction)
PR increased (better contraction)

ST Elevation
1. Hyperkalemia
2. STEMI
3. Acute pericarditis (concave up, global)
4. Prinzmetal angina (transient)
5. Takotsubo cardiomyopathy (mimics STEMI entirely)
6. Vent aneurysm
7. Brugada Syndrome (V1 - V3)

STEMI Acute Pericarditis

Peaked T waves

ST elevation
(convex elevation aka Pardee sign)

Q wave (always pathological)

Takotsubo Cardiomyopathy
Inverted T waves
Mid ventricular
narrowing of left
ventricle
Brugada Sx Hypokinesis of mid
ventricle (apex : normal)
Coving ST elevation Octopus Jar
Congenital cause of ST Broken heart syndrome/
elevation stress cardiomyopathy
Sodium channel defect
Even cardiac biomarkers are elevated.
V1 -V3
Diffferentiated from STEMI only on angiography
Angina
ECG and Troponins are normal (except Prinzmetal angina which has transient ST elevation)
ROSE questionnaire used for assessment.

Angina

Low perfusion Coronary artery vasospasm

Stable angina Unstable angina Prinzmetal Angina

Pain on exertion Pain on rest (Beta blockers are
Mx : Beta blockers Mx : MONA contraindicated)
Fibrinolysis is c/I Mx : CCB

Newer anti-anginal drugs

1. Ranolazine : Late Na channel blocker
2. Ivabradine : Inhibits funny channels
3. NiKOrandil : Pottasium channel opener
4. Trimetazidine : pFOX inhibitor (anti-metabolic drug)
5. Fasudil : Rho-kinase inhibitor Fasu rho rha

Myocardial Infarction
ECG and Troponins are abnormal.

Myocardial Infarction

Anterior
NSTEMI STEMI Aneurysms
Sub endocardial infarct Trans-mural infarct Free wall rupture
ST depression ST elevation
Posterior
Conduction blocks

Cardiac Biomarkers
Earliest : Myoglobin (non specific) Re-perfusion therapy in STEMI
Best after 1 day : Troponins (stays in blood for a week) To catch lab for PCI (< 90 mins)
Best for re-infarction : Serial trop-I
HFABP (heart FA binding proteins) : New marker, earliest to rise If hospital doesn't have PCI, get out of that
hospital within 30 mins

Transfer to PCI hospital within 120 mins

Dressler's Syndrome If not possible to transfer then fibrinolytics
Pericarditis (auto-iimune) after 3-4 weeks of MI within 30 mins
AI reaction against the necrotic tissue in heart
DOC : Aspirin
 Coronary Circulation

Anterior Posterior
aortic sinus aortic sinus

RCA LCA
Conus
AV groove Anterior MI : LAD
branch
Lateral MI : LCX

PDA LAD Inferior MI : RCA

Posterior Left Anterior Posterior MI : PDA
descending artery descending
(Decides dominance) (widow's artery)
Supplies Posterioir LV wall Supplies Anterior LV wall
Posterior 1/3 of septum Anterior 2/3 of septum

Right Marginal artery

Left Circumflex (LCX)
(Acute)
↓
Venous Drainage Left Marginal artery
Everything drains into Coronary Sinus (obtuse)
except Anterior Cardiac vein (ACV)

Posterior

Lateral

Septal
Anterior

Lateral
wall MI

Inferior wall MI
JVP

Atrial
contraction
A
Venous
Tricuspid
filling
valve
closure V Tricuspid regurgitation TS/PS/PAH/TOF Complete heart block
C Large V wave Large A wave Cannon A wave
"it's a cannon event"
Y
Emptying
into vent.

X
Atrial Cardiac tamponade Constrictive Pericarditis
relaxation Prominent X descent (TAX) Prominent X
Tamponade
Loss of Y descent and Y descent X descent

Cardiac tamponade Constrictive Pericarditis Pulsus paradoxus

Beck's triad Kussmaul's sign (paradoxical On inspiration, venous return
1. Hypotension increase in JVP on inspiration) increases
2. Raised JVP Pulsus Paradoxus ↓
3. Muffled heart sounds Pericardial knock RV pushes IV septa towards LV,
Pulsus Paradoxus Low voltage ECG stroke volume of LV decreases
Ewart's sign (intra-scapular dullness) 1. Cardiac tamponade
Electrical alternans on ECG 2. Const. Pericarditis
3. Pulm. Emboli
4. Pregnancy
5. Asthma

Pulse types

Dicrotic notch

Normal Pulse Hypokinetic Pulse Hyperkinetic Pulse

Dicrotic notch due to Low stroke volume High stroke volume
closure of aortic valve eg. AS eg. Wet Beri Beri, AR
Waterhammer/
Collapsing pulse
Seen with AR and other
High output states

Pulsis Bisfiriens Bigeminal Pulse Pulsus Alterans

Outflow tract obstruction Seen with Arrythmias Seen with LVF
eg. HOCM
 Heart Sounds and Murmurs
Systole Diastole

Closure of bicuspid Closure of aortic and

and tricuspid valves semilunar valves
Loud S1 in early MS S2 is split (more blood in Vent. Gallop Atrial Gallop
(mobile valve) RV during inspiration, Any high output Due to stiffening
Soft S1 in later takes more time to close) state
stages when valve Paradoxical split in AS
becomes immobile

Continouous-machinery murmur
PDA Murmurs

Systolic Diastolic
ARMS

Crescendo - decrescendo Mid systolic click Holosytsolic

Aortic Stenosis MVP
Ejection systolic murmur Late systolic murmur

Blowing murmur Harsh sounding

MR/TR VSD
MR : Radiates to axilla
TR : Tricuspid area
Other Systolic Murmurs
1. Still's Murmur : Benign flow murmur
in pediatrics age Still baby
2. Caravallo's : Early systolic murmur on
inspiration in TR Ca-right-vallo

Other Diastolic Murmurs

1. Austin flint : Seen in AR
2. Graham Steel : PR in PAH
Early Diastolic, decrescendo Opening Snap
3. Carey coomb : ARF
AR MS

Dynamic Auscultation
All Murmurs decrease with decreasing pre-load except MVP and HOCM
All Murmurs decrease with decreasing after-load except MVP, HOCM and AS
Right sided Murmurs - increase on taking deep breath (Caravallo sign in TR)

370
Cardiac Physiology

Mary's Law
BP inversely related to HR Baro-receptors
Sense change in blood pressure
Bainbridge reflex Present in Aortic arch (aortic Chemo-receptors

Brain asks heart to form a bridge when bodies/ carotid sinus) AB

too much water (blood) Most sensitive to pulse pressure
Increased VR leads to increased HR
Chemo-receptors Baro-receptors
Sense change in concentration
Bazold Jarisch reflex
🫑
Give capsicum or serotonin to heart,
of gases
Present in Carotid Body
it stops working Most sensitive to pCO²
Bradycardia, hypotension and
apnea when LV receptors come in
contact of serotonin or capsaicin.
Vagal C fibres mediate it
Fick's law
Cushing Reflex Measures cardiac output
🤕
After head injury , resp. regulatory
mechanisms go bad
Bradycardia, hypertension and
irregular respiration

J receptor reflex
Juxta Pulmonary capillaries, get irritated
due to blood in CHF
Apnea f/b rapid breathing
Hypotension and bradycardia

Cardiac Pathology
DCM
Most common cardiomyopathy
Mutation in titin (largest
protein in humans)
Alcohol, ischemic Ninja star appearance
Peripartum (within 5 months)
TTC Stain
Normal tissue : Red
Damaged tissue : White
HOCM (releases LDH)
Mutation in beta-myosin
Banana shaped septum 🍌
Seen in athletes
Sudden cardiac death
on ECHO : Systolic anterior Myofibril disarray
motion of wall
CHAPTER 18
INTEGRATED
HEMATOLOGY
Basics of Hematology
Inside Bone Marrow

Low platelets are not a

contraindication for
Core BM
BMA biopsy
needle
Salah's Klima's
needle needle

Preferred site for BMA

Adults : PSIS
Child : Tibia

RBC lineage

Reticulocytes
Have a reticulum of RNA, hence
named such
Stained with Supra-vital stain
(stains RNA)
Normal : 0.5 -2%
Increased in hemolytic anemias

Corrected retic count

Pt. Hb
= Retic count X
Target Hb (taken as 15)
1st cells to show Hb on electron microscope : Pro-erythroblast
1st cells to show Hb on light microscope : Polychromatophilic erythroblast
RBC Shapes and disorders

Megaloblastic Anemia

"No
Central
MCV > 100fl Segmented neutrophils Cabot ring
pallor"
> 5 in 5% or
Hereditary > 6 in even 1 cell
Hereditary spherocytosis
eliptocytosis Membrane disorder H/o vegan diet (B12 def), fast food diet (folate def)
Membrane disorder Ankyrin mutation, AD condition Fine basophilic stippling
Spectrin mutation Low surface area, raised MCHC Low retic count
Other causes : AIHA (m/c), G⁶PD def
Increased osmotic fragility
EMA binding test HEMA is fragile
T/t : Spleenectomy after puberty Sideroblastic Anemia

Ringed Pearl's/Prussian
Acanthocytes (Spur cells) Echinocytes (Burr cells) sideroblasts blue stain
Irregular spines Regular spines
Abetalipoproteinemia Renal failure, Burns Defect in heme synthesis
Anaemia in liver disease Pyruvate kinase def a. X linked : ALA synthase def.
Vit E def. b. Pb poisoning (blocks ALA Dehydratase
and Ferrochelatase)
c. B6 deficiency
Coarse basophilic stippling
"heme synthesis has a long course"

Sickle cells G6PD deficiency

aka Drepanocytes drape silk saree
Autospleenectomy Dog bites
(Howel Jolly bodies seen in asplenia) Howel Jolly bodies

Bite cells (Heinz body)

aka Degmatocytes Denatured RNA

NADPH not formed (anti-oxidant action)

Intravascular+ Extravascular hemolysis
Target sign 🎯 Teardrop cells 😿 Supravital stain (stains denatured RNA)
aka Codocytes aka dacrocytes
Seen in "HALT" Seen in myelopthsis
1. Hemoglobin C (bone marrow infiltration)
2. Aspleenia Granuloma, mets, Auto-immune hemolytic anemia
3. Liver dis. myelofibrosis
Positive direct coomb's test
4. Thalassemia
Warm AIHA is m/c in SLE, CLL, Drug
(opsonisation by IgG) Garam 🔥
Cold AIHA in Mycoplasma, EBV
Helmet cells aka (complement activation by IgM) ❄️
Helmet cells 🪖 "Schistocytes"
AIHA in CLL : Evan's Syndrome

Seen in MAHA Paroxysmal Cold Haemoglobinuria

Microangiopathic : HUS, TTP, HELLP IgG Abs
Macroangiopathic : Prosthetic mitral valve Bind to RBCs at 37° C but causes hemolysis at 30° C
 Microcytic Anemia
Iron deficiency Anemia
S Sideroblastic TIBC increased Top IDA bottom chronic
Everything else decreased
I IDA
T Thalassemia AOCD
A AOCD Hepcidin prevents iron absorption
Ferritin is high (has iron stores) Iron deficiency Anemia
TIBC low
Poikilocytes
Anisocytosis (RDW increased)
Sideroblastic Anemia
Heme not formed, everything is high

Thalassemia

Alpha Thalassemia Beta Thalassemia

4 alleles on Splicing defect in
Chromosome 16 4² = 16 chromosome 11 (2 alleles)

1 allele 2 allele 3 allele 4 allele

deletion deletion deletion deletion
α Thalassemia α Thalassemia Hb H disease Hb Barts
minima minor Severe Anemia Intra-uterine death
Asymptomatic Mild Anemia β⁴ Hb formed Bart no birth
Golf ball inclusions
in HbH disease

NESTROF test
Bedside screening test for thalassemia
In Thalassemia and SCA, RBCs have
lower osmotic fragility (do not lyse) 1 abnormal allele Both severely
Both abnormal alleles
and other is normal abnormal or absent
β Thal minor β Thal intermedia β Thal major
aka β thal trait aka non transfusion aka transfusion
Normal HbA² increased dependant thal dependant thal or
SCA / Thal Mild anaemia Moderate anaemia Cooley's Anaemia
Mild HSM Severe anaemia
Jaundice and HSM

IDA vs Thalassemia Minor

Mentzer index
MCV/RBC count
Low in Tha-less-emia (< 13)
> 13 in IDA ← RBCs lyse in hypotonic saline

RDW
Increased in IDA
Hair on end app. Chipmunk facies
Low in Tha-less-emia
Lyse early Due to extra-medullary hematopoiesis
HPLC
Lyse late
Confirmatory test for thalassemia
HbA² increased in thal minor
HbF increased in thal major
 Hemolytic Anemia
Hemolysis
LDH raised
Retic count increased

Intra-vascular Extra-vascular
In blood vessels In liver and spleen
Hemoglobinuria Hepato-spleenomegaly
Low haptoglobin Jaundice
(binds to free hemoglobin)

PNH MAHA
CD 55 and CD 59 (MIRL) prevents complement mediated destruction 1. Microangiopathic :
In PNH there is inactivation of CD 55,59 (PIGA gene mutation) HUS, TTP, HELLP
Reduced pH at night, causes complement mediated lysis of RBCs in 2. Macroangiopathic :
blood (IVH) Prosthetic mitral valve
Associated with both Pancytopenia and Leukemia (rare)
Associated with thrombosis and Budd Chiari syndrome (MCC of death)
IOC : Flow cytometry
Rx : Eculizumab (C5 -) Prophylaxis for encapsualted organisms

Normal PNH

Hemoglobinopathies RBC membrane Enzymatic AIHA

Thalassemia Spherocytosis (Ankyrin) G6PD def Warm AIHA
Sickle cell anemia Elliptocytosis (Spectrin) Puruvate kinase def Cold AIHA
HbC disease Paroxysmal Cold
Hb-uria

Hb Electrophoresis
HbA1 α²β² 90% adult Hb
Normal adult HbA2 α²δ² 2-5% adult Hb
Normal newborn (HbF) α²γ² More affinity to O² Raised in thal minor

Sickle cell trait (risk of Medullary RCC)

Sickle cell anemia

Drugs used in SCA
Hemoglobin C trait 1. Glutamic acid (replacement)
Hemoglobin C disease 2. Hydroxyurea
3. Vuxelotor
Hemoglobin C trait in SCA
4. Crizanlizumab
prevents 'creasing" of RBC)

Mis-sense mutations
1. Sickle cell anemia : Glutamate replaced by Valine "Glutamate go, Valine welcome"
2. Hemoglobin C : Glutamate replaced by lysine Ly"C"ine
 WBCs lineage

Myeloblast Pro Myelocyte Meta Band/Stab Mature

Myelocyte Myelocyte form neutrophil
Auer rods seen D shaped Kidney shaped
Increased in APML nucleus nucleus

Approach to Leukemia
Leukemia

Chronic Acute

CLL CML ALL AML

Lymphoid Myeloid Child Adult
(convent girl) (garden party)

PAS (+) Auer Rods, MPO (+) Sudan Black (+)

MC leukemia in adults and MASSIVE spleenomegaly T cell ALL : HSM or M0 : Undifferentiated
western countries. Blasts < 20 % Mediastinal mass M1 : Immature
13q deletion Philadelphia chromosome : B cell ALL : Bone marrow M2 : Chloroma , m/c, t(8:21)
Not associated with radiation Translocation (9:22) infiltration (pancytopenia) M3 : APML, DIC, t(15:17), t/t ATRA
Smudge cells on h/p (artefact) Ph (BCR:ABL) - 210 kD T - tissue M4 : Inv 16, gum infiltration
IOC for all NHL : Flow cytometry Causes activation of JAK-STAT B- bone marrow M5 : Gum infiltration
Criteria for diagnosis : pathway : Excess proliferation M6 : Erythroblastic
1. Lymphocytes in blood > 5000 Good prognosis in ALL M7 : Ass. with Down Sx, Dry tap
Pseudo-Gaucher cells seen
2. Lymphocytes in BM > 30% 1. Pre B cell
IOC for CML : FISH for 9:22
3. CD 5 and CD 23 (+) 2+3 = 5 2. L1
translocation detection Sweet Syndrome
3. Hyperdiploidy
Treatment : Tyrosine kinase Red painful plaques (febrile
4. t (12:21)
Syndromes associated with CLL inhibitors ( Imatinib, Dasatinib) neutrophilic dermatoses)
Ladies Being hyper at age Commonly seen in AML
1. Richter Sx : CLL/SLL ➡️ DLBCL
12, 21 is good prognosis Other causes : IBD, SLE
tumor got richer Juvenile CML
2. Evan's Sx : AIHA, TTP in CLL Doesn't have 9:22 translocation
everyone RBC, WBC, platelets Poor prognosis in ALL Differentiation Syndrome
Ass. with Noonan Sx, NF 1
1. Age <1 or >10 S/e of ATRA for APML
2. t(9:22) - 190kD Fever + b/l lung infiltrates
3. T cell type (brain DOC : Steroids
/testes/mediastinum)
LAP Score
(Leukocyte Alkaline
Phosphatase Score)
Done on left shift of WBC lineage
Increased in Leukemoid reaction
Decreased in CML, PNH
 Approach to Pancytopenia
Pancytopenia

HSM (+) HSM (-)

Dragging sensation in abdomen

Hyper-cellular marrow Dry Tap Hyper-cellular marrow Dry Tap

Myelodysplasia Aplastic Anaemia
Leukemia

Myelopthisis Hairy cell leukemia

Bone marrow infiltration BRAF mutation
Pawn ball Pseudo Pelger
Metastases, Granuloma TRAP (+)
megakaryocyte heut cells
or myelofibrosis Markers :
Tear drop cells 1. Annexin A1 (most sp. and sn.) Primary MDS seen in Fat cells in bone marrow
(dacrocytes) 2. CD 11c, 25, 103 elderly, develops slowly.
Congenital apalstic anaemia :
Annexin V is marker for apoptosis Therapy related MDS
Fanconi's Anaemia
seen after chemo/radio
Affects Red pulp of spleen MCC of Agranulocytosis :
and has a poor prognosis.
MAC (mycobac. avium Drug toxicity
Risk of AML
← complex) infections are seen Pure red cell aplasia :
Parvovirus B19
Hairy cells Fried egg app.

Approach to Hodgkin Lymphoma

Hodgkin's Lymphoma
15 x 2 = 30

Nodular lymphocyte Classical

predominant CD 15 (+) 30 (+)
CD 20 (+) 45 (+) EBV (+)
BCL 6 (+) PAX 5 (most specific)
EBV (-)

Nodular Sclerosis Mixed Cellularity Lymphocyte rich Lymphocyte depleted

Lacunar RS cell Mixed background Mono-nuclear RS cell Mummified RS Cell
Most common overall Classical RS cell Lymphocytic background Rarest
(eosinophilic) Best prognosis Worst prognosis
M/c in INDIA rich is good prognosis
mixed population
L and H type RS cell
Popcorn cells
Rare
Very good prognosis
Predominant - popcorn
 Approach to NHL
C myc Cyc D1 IgH BCL-2 Check CD 5 and CD 23

8≈B
t( 11:18) Marginal (takes margins) Both CD 5 (+) and Both
Burkitt positive CD 23 (-) negative
Lymphoma Mantle Marginal
SLL/CLL
8 : 14 t( 11:14) Mantle (ends with El : Eleven) Cyclin D1 Ass. with
13q deletion
8 : 22 SOX 11 MALTOMA and
2:8 Cleaved other inflammatory
buttock cells conditions
Except 8:21 t( 14:18) Follicular (fo → follicular, fourteen)
(M2 AML)
CD 10 (+) : Actively dividing cells

BCL- 6 (+) BCL- 2 (+)

Follicular
Best prognosis
2 good to be true

CLL/SLL Mantle DLBCL Marginal Multiple

Burkitt myeloma DLBCL Burkitt's
Follicular Most common NHL Most agressive (Ki67 : 100%)
Aggresive tumor C-Myc
Ass. with EBV Endemic type : Jaw swelling,
CD -3 (+) Three is T associated with EBV (Africa)
Sporadic type : Abdominal mass
Cutaneous T cell lymphoma
(Mycoises fungoides)
Cerebriform nuclei Background : Tumor cells
Pautriers microabscess Stars : Macrophages
Disseminated : Sezary Sx Starry sky appearance
(extracorporeal photopheresis is t/t)

Treatment of NHL
1 2 4 ABVD regime
Anthracycline
3 Bleomycin
Vinblastine
Dacarbazine

Ann Arbor staging

Used for both Hodgkin's Lymphoma and NHL
 Multiple Myeloma
Increased number of plasma cells, produce excess antibodies (IgG > IgA)
Type of plasma cell dyscrasia
Presents with bone destruction without regeneration
(hence calcium high but ALP low)
On imaging there's no radiotracer uptake (uptake occurs only at areas
of bone formation)

Diagnosis
On serum protein electrophoresis : M spike pattern seen due to X ray of skull showing punched out
raised gamma proteins (antibodies) osteolytic lesions in MM
Serum β² microglobulin : Serum marker that indicates poor prognosis
On bone marrow aspirate :
1. Flame cells (abnormal plasma cells)
2. Russel body (in cytoplasm) : Cells with many
Russel bodies are known as Mott cells
(or Mulberry cells due to the appearance)
3. Dutcher body (in nucleus)

On peripheral blood smear : Rouleux formation

(Immunoglobulins increase viscosity of blood)
In urine : Bence Jones Protein
(due to amyloid light chain deposition)

CRAB SLIM criteria

Rouleux formation

MM defining biomarkers

Renal failure in multiple myeloma :

Hypercalcemia is mcc
Light chain deposition is 2nd mcc

"M spike" pattern on

Waldenstorm Macroglobulinemia Serum Protein Electropheresis
Another plasma cell dyscrasia
d/d for multiple myeloma (M spike and flame cells)
Hyperviscosity due to raised IgM
Not osteolytic, hence calcium levels are normal
Associated with hepatitis C
 Myeloproliferative Disorders
Associated with JAK-2 mutation
Can be classified based on which component of blood is affected

RBC, WBC and Platelets ⬆️ Only platelets ⬆️ Everything decreased

Polycythemia Vera Essential thrombocytosis Myelofibrosis

m/c myeloprolif. disorder Erythromelalgia is asso. Enlarged spleen is asso.
Aquagenic pruritis is asso. Staghorn megakaryocytes Bone marrow fibrosis
JAK 2 mutation 95% JAK 2 mutation 30-50 % JAK 2 mutation 30-50 %
MCC of death : Thrombosis
T/t : Ruxolitinib (JAK 2 Inhibitor)

Ruxolitinib
Jak 2

Erythromelalgia (redness, itchy

and inflammed skin of hands)
Rose (Rux) doesn't let Jack on the door
cause she had aquagenic pruritis

Overview of Hemostasis

Hemostasis is maintained in the body via three mechanisms :

1. Vascular spasm
Damaged blood vessels constrict
Injury or damage
2. Platelet plug formation
Circulating platelets gather at the site of endothelial injury
Platelets adhere to damaged endothelium to form plateletplug Vessel contracts
(primary hemostasis)

3. Blood Coagulation Platelet plug

Clots form upon the conversion of fibrinogen to fibrin (secondary
hemostasis).
Series of steps involved known as coagulation cascade
Fibrin clot
 Mechanism of Platelet plug (1° Hemostasis)
1. Injury to endothelium
Endothelin released (potent vasoconstrictor)
Endothelin acts in paracrine fashion
Transient vasoconstriction in surrounding tissues
(first responce)

2. Exposure of VWF
VWF is present inside endothelial cells bound to Platelets
sub-endothelial collagen.
GP1b
When endothelial cells are damaged, this VWF is (magnet)
exposed to platelets VWF

3. Platelet adhesion (to VWF)

Platelets bind to exposed VWF using GP1b
After binding platelets release : Calcium, ADP, TXA²
CAT

4. Platelet activation ADP activates GP2b/3a GP2b/3a

ADP released binds to P2Y12 of other platelets to Fibrinogen
activate them (inhibited by Clopidogrel, Ticagreor)
Activated platelets express GP2b/3a on their
surface (needed for aggregation)

4. Platelet aggregation P2Y12

Fibrinogen binds to GP2b/3a and links platelets ADP
TXA² is a pro-aggregant : Slows down blood flow and
helps in aggregation (blocked by Aspirin)
Prostaglandin I² and Nitrous Oxide are anti-aggregants
Anti-Platelet Drugs

GP1b deficiency GP2b/3a deficiency 1. TXA2 inhibitor (Aspirin)

Platelet adhesion defect Platelet aggregation defect
Side effects
Bernard Soulier syndrome Glanzman Thromboasthenia
(Abnormal ristocetin aggregation) Increases uric acid
Reye's syndrome
GP1b : 1st (adhesion) HAGMA (acidic drug)
GP2b/3a : 2nd (aggregation) Peptic ulcer (inhibits Prostaglandins)
Reye's syndrome in children
(Microvesicular steatosis)
Von Willebrand disease
Platelet adhesion defect Hence, only indication of Aspirin in
Type 1 : Reduced quantity (AD transmission) m/c pediatrics is Kawasaki's disease
Type 2 : Reduced quality (AD transmission)
Type 3 : Factor 8 absent (AR transmission) 2. P2Y12 inhibitor

Prasugrel Reversible Irreversible

10 times more potent than clopidpgrel Tica-grelor Clopidogrel
Its a prodrug and converted to active form by CYP³A⁴ and CYP²B⁶ Can-grelor Prasugrel
Contraindicated in CVA strokes, because it's associated with severe bleeds.

Ticlopidine (P2Y12 inhibitor)

Not used anymore - risk of pancytopenia as s/e 3. GP2b/3a inhibitor
Epti-fib-atide
Abciximab (GP2b/3a inhibitor)
Tiro-fib-an
Monoclona Antibody (novel drug)
Safe in renal failure Fibrinogen in between
Coagulation cascade (2° Hemostasis)

Extrinsic Pathway Intrinsic Pathway

Internal damage (to tissues) Intrinsic damage (to endothelium)
Tissue factor involved Factor 12-11-9 get activated
Factor 7 gets activated Tested using aPTT
Tested using PT (prothrombin time) T Twelve
E Eleven
CR-7 does PT outside
N Nine

Common pathway
Factor 10 activated
Factor 5-2-1 activated
Factor 1 is fibrinogen which gets
activated to form fibrin
Fibrin forms a mesh which stabilises
the platelet plug

Factor 13
Stabilises the fibrin meshwork
Deficiency can cause coagulopathy
with normal PT and aPTT

tPA
Plasminogen (tissue plasminogen
Plasmin
activator)
Breaks down
fibrin

Thrombolytics Anti-Thrombolytics
Activate tPA Blocks tpA
Indicated in Pulmonary embolism, Indicated in trauma, menorrhagia
ischemic cerebral stroke and MI 1. EACA : ε amino caproic acid
S Streptokinase 2. Tranexamic acid
U Urokinase
R Reteplase
A Alteplase
T Tenecteplase
Anticoagulants
Anticoagulant drugs

PARENTERAL ORAL

Direct Thrombin Heparin

Inhibitors
1. Bivalirudin
2. Argatroban Unfractionated heparin Low molecular weight heparin
3. Melagatran Administered IV or SC Administered only SC
Safe in renal failure Can't be used in renal failure
S/e : Heparin induced Lesser SE and hence does't need
thrombocytopenia (HIT) : monitoring
antibodies against platelet factor 4 Eg. Enoxaparin, dalteparin
Hence monitoring of platelets Anticoagulant of choice in
required 1. Pregnancy
Unfractionated HIT amongst kidneys 2. Cancer associated
thromboembolism

Antidote for heparin : Protamine Sulphate

NOAC Warfarin and

(novel oral anticoagulants) Dicoumarol
Blocks Vit-K eporeductase
(Vit K needed for factors 2,7,9,10)
Takes 4-5 days to start effect
DABIGATRAN Xa Inhibitors
PT-INR done for monitoring
(Direct thrombin inhibitor) 1. Rivora-Xa-BAN (reversible)
Rare complication of purple toe
2. Api-Xa-BAN
DOC for HIT (Heparin induced syndrome
3. Edo-Xa-BAn
thrombocytopenia) (warfarin blocks protein C/S as well)
4. Betri-Xa-BAN
Doesn't require monitoring To prevent purple toe sx, warfarin is
Antidote : Idarizumab Antidote : Ande-Xa-nate alpha combined with heparin
Warfarin preferred anticoagulant in
Atrial fibrillation
Antidote : Vit K / FFP

Purple toe syndrome

 Approach to bleeding disorders

Bleeding disorders

Platelet disorder Coagulation disorder

Petechieae Ecchymosis
Purpura Hemarthrosis
BT ⬆️ (bleeding into joints)
CT ⬆️

Platelet count normal Platelet count decreased

1. Bernard Soulier Sx 1. Immune thrombocytopenic
2. Glanzman Thromboasthenia purpura (ITP) : Auto-antibodies
against platelets
2. Aplastic anemia

Platelet count < 20,000 : Spontaneous bleeding

PT raised aPTT raised Both normal Both raised

1. Factor 7 def. Factor 13 def. 1. DIC
2. Vit K def (early) 2. Factor 10 def
Child Adult 3. Afibrinogenemia
1. APLA
2. Acquired hemophila

X linked hemophilia AR hemophilia

Hem A : Factor 8 Hem C : Factor 11 DIC
Hem B : Factor 9 (aka Disseminated intravascular coagulation
Christmas factor) Uncontrolled activation of fibrinogen due to
exposure of blood to high levels of tissue factor
Factor 9 not present in cryoprecipitate
(eg. Sepsis, amniotic fluid embolism, major sx)
Hence cryoprecipitate won't be useful in hemophila B
Body tries to breakdown the thrombus formed
b looks like inverted 9 Extensive Thrombosis + Thrombolysis
9 is "na" present in cryoprecipitate
This consumes platelets and clotting factors
Because of thrombolysis
1. D Dimer ⬆️
ITP
2. Anti-thrombin ⬇️
Immune thrombocytopenic Purpura
3. Thrombin anti-thrombin complex ⬆️
Auto-immune destruction of platelets Complications
Asso. with SLE, HIV, Hep B 1. MAHA
Generally mild features 2. Spontaneous bleeding (low platelets)
Treatment for relpase : Glucocorticoids Most sensitive test : Fibrinogen degradation
Definitive t/t : Spleenectomy + Vaccination product (FDP test)
against encapsulated organisms "HMP"
Blood Grouping
Blood group name = Antigen present on surface (serum has antibodies for other antigens)
1. A(+) : Antigens (A, D), Antibodies (Anti B)
2. A(-) : Antigens (A), Antibodies (Anti B, Anti D) Rh factor is aka D antigen
3. B(+) : Antigens (B, D), Antibodies (Anti A)
4. AB(+) : Antigens (A, B, D), No antibodies H antigen is an RBC antigen present
5. O(+) : Antigen (D) , Antibodies (Anti A, Anti B) in all but Bombay blood group
6. O(-) : No antigens, Antibodies (Anti A, Anti B, Anti D)

Only A antigen : A(-)

A & D antigens : A(+)

Only B antigen : B(-)

B & D antigens : B(+)

H & D antigens : O(+) (H antigen present in all)

NO antigens : Bombay blood group

Resistance to P. Vivax and P. Knowlesi

Duffy antigen

Resistance to P. Falciparum
Sickle cell trait
Thallasemia
HbF
G6PD deficiency
 Transfusion Medicine

Whole blood storage Massive Transfusion

1. CPD (Citrate Phosphate Dextrose) : 3 weeks
More than 10 units of whole blood transfused
2. CPDA (CPD + Adenine) : 5 weeks
within 24 hours
3. SAGM (Saline Adenosine Glucose Mannitol) : 7 weeks
Complications of massive transfusion are
SAGM is most commonly used (42 days) 1. Hypocalcemia : Citrate binds calcium
2. Hypokalemia > Hyperkalemia : Donor RBCs
Stored at 2-6° C
take in K+
Once opened has to be transfused within 4 hours
3. Metabolic acidosis due to citrate f/b alkalosis
4. Hypothermia
MCC of death : Dilutional coagulopathy
Platelet storage
Stored at 22-24 ° C (AC room)
Can only be stored for 5 days in platelet agitator
Once opened has to be transfused within 30 mins

FFP , Cryoprecipitate
Acellular component of blood (least chance of
transmitting viral infections)
Stored at -30 ° C
Can be stored for upto 1 year
Once opened has to be transfused within 30 mins Platelet agitator
Prevents clumping

Complications of blood transfusion

Anaphylaxis in transfusion patients
1. Febrile transfusion reaction is common with IgA deficiency
Most common transfusion related complication
Occurs due to donor WBCs
Fever/Chills/Malaise
Only supportive treatment needed

2. Allergic reaction
Urticaria, pruritis, hives
Mx : Anti-histamines Leukofilter
Filters out WBCs
3. ABO incompatibility Lowers incidence of febrile
aka Hemolytic transfusion reaction transfusion reactions
Pain at IV site , shock, dark urine along with fever and chills Reduces CMV transmission
Mx : STOP the transfusion, IV fluids as well

4. TRALI (transfusion related acute lung injury)

Dyspnea + b/l chest infiltrates
Occurs 1-6 hours after transfusion (occurs due to donor HLA antibodies)
2nd mcc of death related to transfusion
Mx : STOP the transfusion and airway management

4. TACO (transfusion asso. Circulatory overload)

Dyspnea + raised JVP
MCC of transfusion related deaths
Mx : Slower infusion, diuretics
CHAPTER 19
INTEGRATED
RENAL
 Renal Physiology
Clearance is the amount of blood that is cleared of a certain substance in unit time.

Conc in urine
____________ X Rate of urine (ml/min)
Conc in plasma
Counter Current
Clearance > GFR : PAH (secreted)
Clearance = GFR : Inulin (passes unchanged)
Clearance < GFR : Glucose/Sodium/bicarbonate (absorbed) Multiplier Exchanger
Loop of henle Vasa recta
Clearance of Inulin is a proxy for GFR (maintains it)
(establishes the
Clearance of PAH is a proxy for RPF (renal plasma flow) counter current)

Regulation of glomerular blood fllow

1. Afferent arteriolar constriction :
Reduces RPF and GFR
Prostaglandins dilate afferent arteriole
2. "Severe" efferent arteriolar constriction :
Hence, NSAIDs cause constriction (Reduce GFR)
Reduces RPF and GFR
3. "Moderate" efferent arteriolar constriction :
Reduces RPF but increases GFR
(filtration fraction increased)
4. High plasma protein : GFR decreases and RPF
same (filtration fraction decreased) Angiotensin constricts efferent arteriole
5. Low plasma protein : GFR increases and RPF ACE inhibitors/ARBs hence dilate it and reduce GFR
same (filtration fraction increased)
6. Ureter constriction : GFR decreases and RPF
same (filtration fraction decreased)
JG Apparatus

In Shock
Both afferent and efferent are
Macula Densa JG cells Lacis cells
constricted : Low RPF and Low GFR Densa DCT Around Glomerulus :
Filtration fraction is increased Mesangial cells
Afferent arteriole Anti inflammatory
Tubuloglomerular feedback
Chemoreceptors
Baro-receptor
Myogenic Autoregulation Between DCT and thick Modified smooth muscle
ascending loop of LOH cells of afferent arteriole
Increased stretch of arteriole
Activates RAAS if GFR low
causes calcium entry
Calcium causes vasoconstriction
Protects kidney in hypertension Increased sodium Decreased sodium
Adenosine released Prostaglandins released
Aff. arteriole Aff arteriole
constriction vasodilation
(GFR decreased) (GFR increased)
Renal Tubules
Proximal Convulated Tubule
SGLT²
100 % glucose absorption, 70% of NaCl absorption in PCT
Secondary active transport
Inhibitors used for treatment of diabetes (dapaglifozin)

Na - H antiport
H+ pushed into lumen : traps HCO³ and NH³
Essential for HCO³ absorption and ammonia excretion.
Angiotensin is agonist at this receptor

Carbonic anhydrase/ Type 2 RTA

Blocked by acetazolamide "Acid"azolamide
HCO3- lost in urine : RTA type 2 Other causes of Type 2 RTA
Ammonia can't be excreted Wilson's disease
Sodium not absorbed (absorption in distal part : Hypokalemia) Fanconi's disease (Global PCT dysfunction)

Thin Descending Limb of LOH

Only permeable to water
Aquaporin 1 present

Thick Ascending Limb of LOH

Impermeable to water (urine dilutes)

Na+ K+ 2Cl-
Absorption of Na(25%), K, Cl
Causes increased K+ on membrane : forces paracellular
absorption of Mg² and Ca²
Inhibited by Loop diuretics and in Barter syndrome

Loop diuretics
High ceiling diuretics, used in Pulmonary edema
Loss of calcium in urine (loops lose Calcium) : urinary stones
Na+ reabsorption in distal tubes (hypokalemia and alkalosis)
Ototoxic
Sulfa allergy
“Barter in loop”
Can precipitate Gout

Distal Convulated Tubule

Na Cl cotransporter
NaCl absorption
Blocked by Thiazide diuretics and in Gittleman Syndrome

Thiazide diuretics
Increase calcium absorption (preferred in osteoporosis)
First line for CHF, Hypertension, Calcium stones
Sulfa allergy
Citrate combines with calcium, in absence of calcium there is too
much oxalate in urine which precipitate stones.
Na+ reabsorption in distal tubes (hypokalemia and alkalosis)

H+ ATPase / Type 1 RTA PTH receptor

H+ ATPase pushes H+ into lumen PTH acts in DCT
If this H+ ATPase is blocked, it causes type 1 RTA ↑ Calcium absorption and
Increased pH of urine (alkaline urine) ↓ Phosphate absorption
Can cause urinary stones (one : stone)
Associated with autoimmune conditions (SLE, Sjogrens, Type 1 DM)
 Collecting Duct
Na Cl cotransporter
NaCl absorption
Blocked by Thiazide diuretics and in Gittleman Syndrome
“Gillete for thigh”

Thiazide diuretics
Increase calcium absorption (preferred in osteoporosis)
First line for CHF, Hypertension, Calcium stones
Sulfa allergy
Citrate combines with calcium, in absence of calcium there is too
much oxalate in urine which precipitate stones.
Na+ reabsorption in distal tubes (hypokalemia and alkalosis)

Vasopressin (ADH)
Acts on V² receptors (V¹ receptors in vascular smooth muscles)
Principal cells of CT
Aquaporins expressed K+ sparing diuretics (SEAT)
Free water absorption S Spironolactone
Conditions associated with ADH Blocks Na+ channels
E Eplerenone
A Amiloride
Blocks aldosterone
T Triamterene
SIADH Diabetes Insipidus
Excess ADH secreted Insufficient ADH
Low serum sodium but Large amounts of urine
increased urinary sodium Hypovolemic hyponatremia
Euvolemic hyponatremia Treatment: Desmopressin
Causes : Small cell ca. of lungs,
meningitis, CNS surgeries
Treatment : VAPTANS

Aldosterone / Type 4 RTA

Receptor present in intercalated cells (vowels stick)
Express : ENaC and ROMK channels
This causes Na+ absorption and K+ excretion
H+ is also excreted in exchange of Na+
Gain of function of ENaC : Liddle's syndrome "Little ENaC"
Hypo-aldosteronism causes Type 4 RTA (mc RTA)

Renal Tubular Acidosis

Metabolic acidosis due to problem in renal tubules
2 - 1 -4
Low low More

serum K+ serum Ca++ Urine pH

Type 2
Type 1
↓HCO³ absorption ↓H+ secretion Type 4
1. Fanconi's disease 1. Sjogren's
2. Wilson's disease 2. SLE
Hypoaldosteronism
1. Obstructive uropathy All high for 1
All low for rest
 Nephritic Syndromes
Inflammation present, hence Nephritic

Cola colred urine /dysmorphic RBCs/ RBC Casts

Hematuria / oliguria / hypertension

Pharyngitis RPGN
Mesangial proliferation
Complication of PSGN (< 5%)
It is usually immune-mediated
Child Adult
(ANCAs, anti-GBM, ANA).
10-21 days after pharyngitis 3 days after pharyngitis Hence seen in Good Pasture
PSGN Berger's Disease syndrome and Wegner's.
Glomerular proliferation Mesangial proliferation
Sub-epithelial humps IgA in mesangium
C3 and IgG on (aka IgA nephritis)
immunoflorescence MCC of nephritic syndrome

Crescents are made up of

1. Proliferated epithelial cells
2. WBCs
Normal glomeruli Inflammed glomeruli Mesangial proliferation 3. Fibrin
with neutrophils
Nephrotic Syndromes
Proteinuria >3g/day, frothy urine
Destruction of GBM
Maltese cross in urine (also seen in Fabry's disease)

Nephrotic Syndrome

Child Adult Elderly

Minimal Change Membranous
disease Nephropathy
aka Lipoid Nephrosis FSGS MPGN Elders have membranous skin
No changes seen on light <50% of glomeruli Thick GBM Associated with
microscopy involved in parts Hepatitis B/C, adenocarcinoma (lung/colon)
Effacement of foot processes HIV / SCA / Obesity malaria and melanoma.
on electron microscopy Collapsing variant Antibodies against
has worst prognosis Phospolipase A2 receptors
Glomerular tip Sub epithelial Spike and Dome
Type 1 Type 2
variant has on electron microscopy
good prognosis. Tram track Dense deposits
appearance 2 dense

Collapsing Variant

Nodular Glomerulo-sclerosis

aka Kimmelsteil Wislon Disease

PAS (+)
Seen in Diabetic nephropathy
 Deposits on Electron Microscopy

Endothelial cell
GBM

Capillary lumen Foot processes

Epithelial cell

Intra-membranous MPGN type 2 Humps : PSGN

Sub-endothelial MPGN type 1
Sub-epithelial

Spike and domes : Membranous

Mesangial Berger's dis, RPGN

Type 4 collagen disorders

Alport Syndrome
Anterior
Basket weave pattern of basement lenticonus
membrane on EM (α3) (α4) (α5)
Good Pasteur's Thin BM Alport
Type 4 collagen disorder (α5) Syndrome disease syndrome
Can't see aka
Family history present Benign familial
can't pee
hematuria
T/t : Ace inhibitors can't hear a
Definite management is buzzing bee
Anti GBM antibodies
transplantation (doesn't recur) Hematuria SNHL Hematuria + Hemoptysis (Pulmo-renal)
M/c presentation
d/d : MPA, Wegner's, EGPA

Immunofluorescence

1. Linear : Good Pasteur's syndrome (RPGN)

2. Granular IgG: PSGN (kids), Membranous (Elderly)
3. Granular IgA in mesangium : Berger's disease
4. Full house effect : Lupus Nephritis

Granular Linear Full House effect

Renal Failure
Renal failure

AKI CKD
Size maintained Contracted kidney and cortico medullary
differentiation lost
Isosthenuria (constant urine osmolality of 0.010)
AOCD (erythropoeitin def.)
Pre renal Renal Secondary hyperPTH (renal osteodystrophy)
(No perfusion) (Acute tubular necrosis)
Waxy-broad cast
Sodium and urea aew Sodium and urea not
reabsorbed reabsorbed
(tubules are normal) (tubules are impaired)
FeNa < 1% FeNa > 1%
Urine Na < 20 Urine Na > 20
Urine osmolality is high Urine osmolality is low
Urea/creat is >20 (no active secretion)
(normal reabs. of urea) Urea/creat is <10
Waxy broad cast
No casts (no reabs. of urea)
Granular/muddy brown
1. Shock
casts
2. Hepato-renal syndrome
S 1. Sepsis Conditions associated with CKD
I 2. Ischemia 1. Low Vit D synthesis : Low calcium and
secondary hyper PTH
N 3. Nephrotoxins
2. AOCD
3. Hyperkalemia (K+ can't be excreted)
AKI markers
4. NAGMA in early CKD (HCO3 loss)
Kim 1
5. HAGMA in late CKD (can't excrete toxic
TIMP 2
substances)
Cystatin C
6. Water intoxication (MCC of convulsions
NGAL
in CKD)
IGFBP 7
Osteopontin

Granular/Muddy cast
Indications of dialysis
1. Refractory acidosis
2. Refractory hyperkalemia
3. BAL intoxication
(Barbiturates, Alcohol, Lithium)
4. Uremia in ESRD (when GFR < 15)
presents with
Asterexis
Pericarditis
WBC cast Seizures
Pyelonephritis
Hyaline cast
Seen normally in urine Complications of dialysis
Tam Horsfall protein
1. M/c complication : Hypotension
2. Dialysis equilibrium syndrome
(removal of urea reduces blood
osmolality, causing Cerebral
RBC cast
Nephritic Syndrome edema), aka reverse urea effect.
3. Peritonitis in peritoneal dialysis
Acid base imbalance
Check pH

Normal values
1. pH : 7.4
2. CO² : 40 40 divisible by 2 pH > 7.4 pH < 7.4
3. HCO³ : 24 24 divisible by 3 (Alkalolsis) (Acidosis)

“Compensation is always in same

direction as primary change”
CO² < 40 HCO³ > 24 HCO³ < 24 CO² > 40
eg. CO2 increased in resp. acidosis then
HCO3 will increase as compensation (Respiratory (Metabolic (Metabolic (Respiratory
Alkalolsis) Alkalolsis) Acidosis) Acidosis)

Winter's formula
For compensation in Compensation Compensation Compensation Compensation
metabolic acidosis (HCO³ decreased) (CO² increased) (CO² decreased) (HCO³ increased)
CO² = [ 1.5 (HCO³) + 8 ] ± 2
Check Anion Gap

Represents unmeasured anions

12 ± 4 > 16

Normal anion gap High anion gap

met. acidosis met. acidosis
(NAGMA) (HAGMA)
HCO³ is lost causing acidosis Unmeasured anions (acids) in blood
Anion gap maintained by increase 1. Acidic drugs : Salicylates (aspirin) or Isoniazid
in chlorine 2. Lactic acidosis : Sepsis
Hence aka Hyperchloremic acidosis 3. Uric acidosis : Renal failure
4. Keto acidosis : DKA
5. Methanol : Retinotoxic (Hooch tragedy)
Check Urine Anion Gap 6. Ethylene glycol : Ca. oxalate crystals in urine

Salicylates
Initially cause hyperventilation
High urine Normal urine and respiratory alkalosis
anion gap anion gap Later cause HAGMA
Renal tubular acidosis 1. Diarrhea
2. Ureteric diversion

pH 7.12 : Acidosis
↓ Anion gap : (Na+K) - (CL+ HCO³)
High HCO³ : can’t be met acidosis ↓
↓ 145-125
High pCO² : resp acidosis ↓
↓ 20 : high anion gap, hence HAGMA
Resp acidosis with metabolic compensation
CHAPTER 20
INTEGRATED
GI HBP
 GI Motility
GI Motility

Electrical motility Mechanical motility

Basal electrical rhythm (BER) Spike Potential Fed state Fasting state
Generated by interstitial cells of Cajal Potential that causes
-45 to -65 mV contraction Migratory motor compex
BER doesn't cause contraction Only when excited
90-120 mins after food intake
(pre-contraction potential)
Caused by Motilin
Present all the time
(Macrolides : Motilin agonists)
Sweeps through intestine to
Membrane potential

clear residual food

Spike potential aka housekeeping waves
Threshold Speed : 5 cm/min

BER
Segmentation Peristalsis
BER determines contractility (mixing of food) (pushes food forward)
Maximum : Small intestines (Small and fast) Ach and Substance P

(Duodenum > Jejenum > Ileum)

Minimum : Large intestine and Stomach
(Caecum < Stomach < Sigmoid)

VIP and NO

Contraction : Ach and Substance P

Relaxation : VIP and NO

GI reflexes

GIST Negative Positive

(Gastro intestinal stroma tumor) reflexes reflexes

Arises from interstitial cells of Cajal

m/c mesenchymal tumor of abdomen Entero-gastric reflex 1. Gastro-colic reflex
Age : 60 years (sporadic type) 2. Gastro-ileal reflex
Carney Strataka sx (SDH mutation, Inherited GIST) Intestines Gastric
irritation secretions
Gastric Colon / Ileum
Most specific mutation : DOG 1 relaxation
distention
Most sensitive mutation : C KIT (CD 117)
"Cats are sensitive" Seen in infants,
Drug for t/t : Imatinib c/o pooping right after feeding
TOC : Complete resection
 GI Secretions
Maximum secretions : Stomach
Most alkaline : Duodenum (Brunner's glands) PHASES OF GASTRIC ACID PRODUCTION
Most acidic : Stomach 1. Cephalic : Anticipatory release (30%)
2. Gastric : Due to distention (60%)
Maximum K+ concentration : Colon
3. Intestinal (10%)
Maximum K+ amount : Salivary glands

Octreotide is a Mucus producing cells

somatostatin HC0³
analogue used for Trefoil peptide (Mucus stabiliser)
D cells
VIPoma Produce
Acromegaly Somatostatin
Carcinoid sx
Chief cells
Variceal bleeding Produce pepsinogen

Parietal cells
Produce CCK ← I cells Produce HCL, IF
Produce Secretin ← S cells
Produce GIP ← K cells MECHANISM OF ACID PRODUCTION
Vagus nerve
(Release GRP) Somatostatin
Inhibited
G cells Gastrin releasing peptide
from D cells
Chole-cysto-kinin (CCK) Produce Gastrin
Gall bladder contraction
G cells
Pancreatic secretion H Pylori resides (Release Gastrin)
Sphincter of Oddi relaxation in Antrum
In TPN, insufficient CCK leads to GB ECL like cells
stasis and consequent GB stones (Releases histamine)

Secretin Parietal cells activation

Stimulates pancreatic & GB secretions (Produce HCL and IF)
Reduces gastric acid secretion

Glucagon Like Peptide (GLP) Gastrin

aka GIP (Gastric Inhibitory Peptide) Stimulates gastric acid secretion
Endocrine function : Insulin release Most important stimulus : GRP from Vagus
Exocrine function : Reduces gastric secretion Gastrinoma seen with Zollinger Ellison Sx,
GLP analogues : Exenetide, Liraglutide, Semaglutide MEN-1 Syndrome (excess Gastrin secretion)

Pancreatic juice Saliva Stomach

Increasing conc of HCO³- Increasing conc of Na+ High H+ and Cl-

Constant Na+ & K+ Low concentration but
maximum amount of K+
Acid Supression

Histamine (H²) blockers Proton pump inhibitors

Cimetidine Pantoprazole
Famotidine "Dinner for 2" Omeprazole
Nizatidine Lansoprazole

Cimetidine Overall DOC for acid suppression

CYP (-) "Hit and run" drugs : Short half life
Gynaecomastia but effect stays much longer
Side effects :
1. C. difficile infection
2. B¹² def (intrinsic factor needs
acidic env. for activation)
Prostaglandin analogue 3. Acute interstitial nephritis
4. Ca²/Mg² deficiency (Risk of #)
Misoprostol
Most specific t/t for
Omeprazole
NSAID induced ulcers
CYP-2C19 inhibitor
DOC still are PPIs with Clopidogrel : risk of
bleeding (CYP 2C19 needed for
activation of clopidogrel)

Antacids
Ulcero-protective
(forms a protective coat)
Al(OH)³ + Mg(OH)³ CaCO³
1. Sucrafate
Neutralize existing acids in stomach s/e : Milk alkali syndrome 2. Bismuth
Al(OH)³ causes constipation as s/e (due to increased absorption of HCO³)
Mg(OH) causes diarrhoea as s/e Space other drugs by
1. Met alkalosis (due to excess HCO³)
Mug for Diarrhoea 2. Hypercalcemia (excess calcium
120 mins (2 hrs)
absorption in distal nephrons)
3. Acute kidney injury

Specific absorption - Iron

Iron
Duodenum
fist
Jejunum
bro
Ileum
Iron absorbed as Fe³

Iron Folate B¹²

Ferrido-reductase DMT-1
Fe³ to Fe²
Iron absorption occurs in duodenum
Steps of iron absorption :
1. Intestines to mucosal cells (Iron from diet) Intestinal mucus cells
Iron in diet is Fe³ (EAT = 3)
Reduced to Fe² by Ferridoreductase (essential for transport)
Divalent metal transporter - 1 : Transports Fe² (also transports Ca², Hepcidin
Ferro-portin
hence iron prevents calcium absorption) Inhibits
2. Mucosal cells to blood vessels
Ferroportin : Transports iron into blood vessels
Ferroportin is inhibited by Hepcidin (produced by liver in states of Transferred as
chronic inflammation) Transferrin

Various iron forms in body

Stored as
1. Ferritin : Iron stored in tissues/cells "stored in tins" Ferritin
2. Transferrin : While in blood "being transferred"
Specific absorption - Vit B¹²

At mouth
B¹² + Haptocorrin
Haptocorrin
Secreted by salivary glands
Protects B¹² from acid in stomach
Needs to be removed by pancreatic At stomach
enzymes for absorption of B¹² in Haptocorrin protects B¹²
ileum from acidic environment
Intrinsic factor is activated
B¹² + Haptocorrin + IF

Intrinsic factor At small intestine

Produced by parietal cells of Haptocorrin digested by
stomach pancreatic enzymes
Needs HCl for activation (B¹² + IF) absorbed at ileum
Required for B¹² absorption in ileum

Serotonergic Receptors

1. 5HT¹
Calming effect (1 is calm)
5HT - 1A : anxiety and depression
5HT¹ and 5HT²
(Buspirone is agonist at 5HT¹A)
5HT - 1B/D : Triptans for migraine
5HT³
2. 5HT²
Psychosis (Mujhe drugs 2)
5HT- 2A/2C : blocked by atypical
antipsychotics
5HT - 2C causes weight gain (Too fat 2 C) 5HT⁴

3. 5HT³
Emetic (3-E)
Blocked by anti-emetics (Ondansetron)

4. 5HT⁴
Pro-kinetic
Metclopromide is agonist at this receptor
(also Inhibits D² and hence stops vomiting)
Vomiting

Motion vertigo
(labyrinth in inner ear → Cerebellum)

Chemoreceptor trigger zone (CTZ) Vomiting Center

(area postrema) (in Brainstem) Vomiting
Drugs and hormone mediated
DOC : Ondansetron 5HT³ and D² receptors

Nucleus Tractus Solitarius (NTS)

1. Pharyngeal stimulation via CN - 9
2. Gastric mucosa irritation via CN - 10

Treatment for Vomiting

5HT³ blockers D² blockers

"setrons" Can cross BBB Can't cross BBB

Ondansetron, Granisetron
DOC for Metoclopramide Domperidone
1. Post chemo N&V* Also a 5HT⁴ agonist (Used for Levidopa
2. Post op N&V (prokinetic) and hence used induced vomiting)
3. Post RT N&V for gastroparesis
"Don't-peridone"
S/e of EPS, Prolactinemia
Side effects
1. QT prolongation
2. Headache
*Aprepitant
3. Constipation
DOC for Cisplatin induced delayed N&V
NK-1/Substance P Inhibitor

Named sickness

Mountain Morning Motion

Sickness sickness sickness
Hypoxia at high altitudes DOC : Scopolamine
(also known as hyoscine)
transdermal patch
Increased cerebral Hyperventilation
blood flow
Resp. alkalosis
HACE
High alt. cerebral edema Seen during pregnancy
DOC : Doxylamine + Vit B⁶
Headache Doxylamine is an
anti-histaminic drug
DOC : Acetazolamide
Relieves Cerebral edema
Causes met. acidosis
 Constipation and Diarrhoea
Treatment of Diarrhoea Treatment of Constipation
One of the s/e of opioids (Morphine) is constipation Bulk forming : Methylcellulose "cellulose for bulk"
Enkephalinase metabolises opioids Osmotic: Lactulose, PEG (Polyethylene glycol)
Stimulant: Senna (S/e : Melanosis coli), Bisacodyl
Cl- channel activator: Lubiprostone "Lubes the gut"
Enkephalinase inhibitors μ (opioid) agonist cGMP agonist: Linaclotide, Plecanatide
(Enhances opioid action) (Constipation) 5HT-4 agonist: Prucalopride "Poo-karlo"
Peripheral opioid inhibitor: For post-op ileus
Racecadotril Loperamide
Used to treat Diarrhea Used to treat Diarrhea (Alvimopan, Naloxegol, Methylnaltrexone)

Mu Kappa Delta
Physical dependence Antidepressant Melanosis coli
Miosis
Euphoria Dysphoria effects (S/E of Senna)
Resp & Cardiac depression Sedation
Constipation
Sedation

Analgesia shown by all opioid receptors

Approach to Diarrhoea
Diarrhoea

Acute Chronic
(< 1 month) (> 1 month)

Stool osmotic gap

Non - bloody Bloody
diarrhoea diarrhoea

High Low
< 6 hours > 6 hours
1. Staph aureus (dairy) 1. ETEC (traveller's diarrhoea ) OSMOTIC SECRETORY
2. B. Cereus (Chinese food) 2. V. Cholera (rice water stool) Improves on fasting
1. Zollinger Ellison Sx
3. V. Parahemolyticus (shellfish)
2. Carconoid Sx
4. Giardia (malabsorption)
5. Yersinia (RIF pain, Hydrogen breath test 3. VIPoma
imitates appendicitis)
6. C. Difficile (h/o antibiotics)
Negative Positive

Check stool fat LACTOSE

1. SalmOnella (poultry and eggs) (>7% is steatorrhea)
Campylobacter jejuni 2. Shigella (very high fever)
INTOLERANCE

Mimics IBD clinical 3. Campylobacter Jejuni (GBS, Reiter Sx)

4. EHEC - 0157:H7 (HUS) MALABSORPTION
features as well as
5. Amoeba (flask shaped ulcer)
biopsy features 6. Typhoid (longitudinal ulcers)
Diagnosis: Culture/PCR 7. TB (transverse ulcers)
Approach to Malabsorption
Diarrhea (steatorrhoea), weight loss and anaemia
Steatorrhea (m/c feature) - bulky, floating, malodorous stool (difficult to flush)
Weight loss - may be profound
Anaemia : Vit B¹², iron, folate malabsorption

Steatorrhea (malabsorption)

D-Xylose test
measures how well the intestines absorb D-xylose

Normal Abnormal
(intestines are normal) (Intestines not normal)

Pancreatitis Rifaximin trial (for 7 days)

No improvement Diarrhoea improves

MUCOSAL disease SIBO

(small intestinal bacterial
Biopsy of mucosa overgrowth)

Villi Flattening of villi

Crypts
hyperplasia
Crypts
PAS(+) Foamy macrophages in lamina propria

Celiac sprue Whipple's disease

Cell mediated immunity against gliadin Caused by : Tropheryma Whipplei (G+ bacteria)
(present in gluten) Impairs Lymphatic transport, hence causes
HLA - DQ2/DQ8 malabsorption
Duodenum affected (impaired iron absorption) Other features :
Risk of : C Cardiac inv.
1. T cell lymphoma A Arthralgia
2. Dermatitis herpetiformis (T/t : Dapsone) N Neurological inv. (Dementia, oculo masticatory
Screening : myorrhythmia)
1. TTG IgA (tissue trans glutaminase ab) CNS manifestations (m/c is dementia) has poor
2. Anti-gliadin Ab prognosis
Associated with loss of fingerprints Oculo masticatory myorrhythmia is a rhythmic
Differental diagnosis : Tropical sprue eye and jaw movement, characteristic of
(Infective etiology) Whipple's disease.
d/d : Gastric TB (also has foamy macrophages)

Pass the whipped

foam CAN
 Inflammatory Bowel Disease (IBD)
Chronic abdominal pain, diarrhoea and tenderness in abdomen.
Classified into 2 major conditions :

Ulcerative Colitis Crohn's disease

Colitis : Inflammation of colon Disease : Granulomatous condition that involves
Rectum is always involved (starts at rectum) all layers (trans-mural), hence fistula and
Continuous spread from rectum to colon strictures are more common
Only superficial mucosa involved (pseudopolyps) Terminal ileum is m/c site (B¹² def)
Antibody : P-ANCA Skip lesions present
H/p : Crypt abscess Antibody : ASCA (anti saccharomyces cerev. ab)
Earliest imaging : Lead pipe appearance of colon Earliest imaging : Cobblestone appearance
(mucosal granularity & loss of haustrations) (apthous ulcers + serpentine ulcers)
"True Love Witt" classification "Montreal" classification
Smoking and appendectomy are protective Smoking and OCPs are risk factors
Management : Management : Steroids f/b biologicals
(surgery not done for Crohn's)
Mild - Moderate disease Severe disease
(< 6 stools/day) (Perforation/
Toxic megacolon) Ustekinumab
5-ASA Drug useful in both IBDs
(Sulfasalazine/Osalazine) Surgery Also useful in psoriatic arthritis
f/b
(Mucosal procto-colectomy)
Steroids

String sign
Distal ileum structure
(also seen with TB)
Granuloma on h/p
Lead pipe colon Pseudopolyps

Cobblestone app
Apthous + Serpentine ulcers
Crypt abscess

Extra-articular manifestations of IBDs

Extra-articular manifestations of IBD
Episcleritis Uveitis

Responds to treatment Doesn't respond to treatment

"Peripheral manifestations" PSC
"Central manifestations"
Migratory polyarthritis Ank. spond
Peripheral arthritis Axial arthritis (ank spond)
(migratory polyarth.) Pyoderma gangrenosum
Erythema nodosum Primary sclerosing cholangitis Erythema nodosum Pyoderma
Uveitis Gangrenosum
Episcleritis
Pyoderma gangreosum and PSC are associated with P-ANCA (m/c manifestations of UC)
M/c manifestation of Crohn's disease is RENAL STONES
 Irritable Bowel Syndrome (IBS)
ROME (IV) criteria
used for diagnosis of IBS
IBD vs IBS
"1-2-3 : Rome 4" Fecal lactoferrin and calprotectin
1 day/week present in IBD but not in IBS
Associated with 2 or more Related to defecation
of these symptoms Change in stool form
For >3 months Change in stool frequency

Polyposis
Polyps

Non-neoplastic Neoplastic

Adenomatous Polyps

Hyperplastic Hamartomatous
Polyps (m/c) polyp
Noncancerous growths
that develop in the
4 year old 11 year old
digestive tract due to an
overproduction of cells
Juvenile Peutz Zeghers Tubular type Villous type
Serrations in superficial
polyp Poor prognosis
1/3 layer is it's hallmark syndrome R/o ca. colon
Presents as
If serrations throughout STK 11 / LKB-1 gene "villous = villain"
rectal bleed
thickness then rule out SSA Presents as
SMAD 4 gene
(Serrated sessile adenoma) Intusucception (Polyp
acts as a lead point)
100% risk of pancreatic
adenocarcinoma

Juvenile polyp
Cystic spaces within
the polyp
Hyperplastic polyp
Superficial layer Arborising (tree Mucosal
serrations like) pattern Pigmentation

Other syndromes associated with

hamartomatous polyps
1. Cowden Syndrome
PTEN mutation PTEN COWDEN 🎵
R/o BET cancers : Breast, Endometrial, Thyroid
Trichilemmoma is a benign lesion associated
with this syndrome
2. Cronkhite Canada Syndrome
Non hereditary ectodermal dysplasia
Syndromes associated with Ca. Colon

Familial Adenomatous Hereditary nonpolyposis colorectal

Polyposis (FAP) Syndrome cancer (HNPCC) Syndrome
AD transmission aka Lynch Syndrome
Not very common AD transmission
100% chance of colon cancer by puberty More common than FAP sx
Loss of function mutation of various 80% chance of colon cancer by puberty
tumor supressor genes : Mismatch repair defect in genes MLH-1
and MSH 2
APC KRAS p53

Normal Early adenoma Late adenoma Adenocarcinoma Lifetime risk of Cancer

AK -53
APC K-RAS P-53
Chr 5 Chr 12 Chr 17

FAP Sx associated with various conditions like

1. Ampullary cancer of pancreas
(waxing & waning jaundice)
2. Polyposis
"CEOs"
Associated syndromes include

Gardner's Turcot
Syndrome Syndrome
BRAF mutation
Supernumary teeth Medulloblastoma
Osteoma (drop metastasis)
Fibromas Glioblastoma
Congenital multiforme
hypertrophy of
"Turban : Tumors in head"
Retinal pigment

"Garden of tumors"
 Ascites
SAAG (Serum ascites albumin gradient)
= (Serum albumin) - (Ascites albumin)
High SAAG = Hyper

High SAAG (> 1.1) Low SAAG ( < 1.1)

Portal hypertension Rules out portal htn

Check ascitic protein Further evaluation

Frothy urine : Nephrotic Sx
> 2.5 g/dl < 2.5 g/dl Fever, weight loss : TB
Weight loss (elderly) : Malignancy
Liver is working fine and Liver cirrhosis Acute pain : Pancreatitis
cause of portal htn could be (liver can't produce
1. Budd Chiari Sx albumin)
2. Cons. Pericarditis
3. IVC obstruction

Management of ascites Refractory ascites

Ascites that persists even after
Mild (only seen on USG) : Salt restriction
Sodium restriction
Moderate (c/f present) : Furosemide f/b Spironolectone or Eplerenone
Maximum dose of diuretics
(no gynaecomastia with eplerenone)
(400 mg Spironolactone or
Severe (respiratory distress present) : High volume paracentesis
160 mg Furosemide)
(albumin supplementation if >2.5L removed)

Ascitic volume
USG detection : 50-100 ml
Shifting dullness : 500 ml
Fluid thrill : 1500 ml

Complications of Cirrhosis

Hepatic Spontaneous Hepato-renal Hepato-pulmonary

encephalopathy Bacterial Peritonitis syndrome syndrome
Earliest symptom : Altered Portal htn and ascites Example of pre-renal AKI Due to dilated
sleep cycle Ascitic neutrophil : >250/mm³ FENA < 1% capilalries in lungs
Specific sign : Asterexis DOC : Cefotaxime DOC : Terlipressin + Albumin Cirrhosis
(flapping tremors) Albumin infusion enhances Hypoxemia
Triphasic waveform on EEG survival.
(δ waves)
West Haven staging
Kupffer and Ito cells

Vit A storage
Ito cells
(aka Stellate cells) Responcible for
fibrosis in cirrhosis
Space of Disse

Sinusoids
Kupffer cells
Space of Disse (macrophages in Liver)

Ito cells : Space of Disse

"Dito"
Kupffer cells : Walls of sinusoids

Zones of Liver

Zone 1
Portal Vein Central Vein
aka peri-portal zone
Affected first in viral hepatitis

Zone 2
Between zones 1 and 3

Zone 3
Zone 1 Zone 2 Zone 3 aka centri-lobular zone
Affected first in congestion, hypoxia
and intoxication

H/p of Acute VS Chronic hepatitis

Acute Hepatitis Chronic Hepatitis

"ABC"
A : Acute Bridging - necrosis and fibrosis
B : Balooning degeneration In Hep B : Ground glass opacties
C : Councilman bodies (seen in Hep C) In Hep C : Lymphoid aggregates

Balooning Councilman body Groung glass app. Lymphoid agg.

degeneration (single apoptotic cell) Chronic Hep B Chronic Hep C
Acute Hep C
 Alcoholic Liver disease
Most specific marker of alcohol induced liver disease : GGT (gamma-glutamyl transferase)
Liver enzymes raised and AST/ALT > 2
Maddrey score (aka discriminant function) tells about severity and mortality in alc. hepatitis
(> 32 is severe and indication to start steroids)
Mallory Denk bodies are seen on h/p (not specific and seen in various other conditions)
Mallory Denk body

Autoimmune Hepatitis
Lympho-plasmocytic infiltration of portal and peri-portal veins
LKM Antibodies
Type 1 AIH : SMA and ANA autoantibodies involved LKM 1 : AIH-2 and Hep C "1-2-C"
Type 2 AIH : LKM-1 and SLA autoantibodies involved LKM 2 : Drug induced hepatitis
(eg. Minocycline) "Drugs do!"
AI Hepatitis is associated with emperipolesis (eating of one cell by another) LKM 3 : Hep D "3 D"

Emperipolesis is also seen with

1. Interface hepatitis
2. CLL
3. Rosai Doffman Disease
4. Myelodysplastic Sx

Emperipolesis

PBC vs PSC

Primary Billiary Cirrhosis (PBC) Primary sclerosing Cholangitis (PSC)

Florid duct lesions. Onion skin app. Beaded appearance

(granulomatous) on h/p on MRCP/ERCP

Granulomatous inflammation destroying Sclerotic (fibrosed) bile ducts

bile ducts Progressive obstructive jaundice
Fatigue and pruritis with negative MRCP More common in males
AMA Ab (+) - Anti mitochondrial Abs. Associated with IBD (UC > Crohn's )
Young females because associated with P-ANCA

"BC = AMA behen ki gaali"

Wilson's Disease
Problem with copper transport
Copper can't be excreted into bile (low copper in bile and excess copper in urine)
ATP - 7B defect (ATP-7A in Menke's kinky dis) "A - Monkey"
Copper deposited in various tissues
KF-ring : Copper in Descemet's membrane
Initial investigation : Ceruoplasmin levels low (it's a copper containing enzyme)
KF ring
Prognostic index : NAZER
Seen in 90% of patients with
TOC : Zinc (blocks Intestinal absorption of copper) neurological features
Chelating agents : D - penicillamine and Trientine Seen in 50% of patients with
hepatic features

Hereditary Hemochromatosis
Abnormal accumulation of iron in parenchymal organs
Most common inherited liver disease
HFE gene on chromosome 6 "Hemochromato6"
Presenting features :
1. Liver : Jaundice
2. Skin : Pigmentation (increased melanin production stimulated by iron)
3. Pancreas : Diabetes Mellitus (aka Bronze diabetes)
4. Pitutary : Infertility Perl's Prussian blue Black liver
5. Heart : Restrictive cardio myopathy Stains iron in tissue
6. Musculoskeletal system : Pseudogout, Hook shaped metacarpals

Liver tumors and Hepato-toxic drugs

Hepatoblastoma
Rare malignant tumor
Age : 6 months - 3 years
High AFP levels (serum marker) Hepato-toxic drugs and findings
Associated with
1. Prematurity Valproate : Micro-Vesicular steatosis
2. Beckwith-Weidemann Syndrome AllOpurinol : Fibrin ring granuloma
3. FAP syndrome Amiodarone : Mallory Dank bodies
Isoniazid : Epitheloid granulomas
Cavernous Hemangioma
Most common benign tumor of liver

Focal Nodular Hyperplasia

Benign tumor of liver
Characteristic central stellate scar on
imaging.

Central stellate scar

CHAPTER 21
INTEGRATED
RHEUMATOLOGY
 SLE
Systemic lupus erythematosus (SLE) is a
Multi-system
Inflammatory
Autoimmune disorder (loss of tolerance to self-antigens)
Lupus Nephritis
Predisposing factors Lupus Nephritis is seen in
1. HLA region on chromosome 6 almost 50% of patients.
2. Premenopausal women are most commonly affected Full house effect seen on
3. SHIPP drugs IHC in lupus nephritis
4. Ebstein Barr virus may be a trigger for SLE Type 4 lupus nephritis
(Diffuse type) is most
common
Risk of recurrence after
Pathophysiology Full house effect
kidney transplant is low
Exposure of the immune system to cellular remnants from
apoptotic cells.
The cellular remnants (self antigens) activate lymhpocytes
and Antibodies are produced against them.
These antibodies attack other normal tissue across the body.

Antibodies
1. Anti nuclear antibody (ANA)
Positive in about 95% of patients with SLE
Most sensitive (entry criterion for SLE diagnosis)
Non-specific (may be seen in other conditions or entirely
normal patients)
2. Anti Smith antibodies Joints
Most Specific for SLE (Musculoskeletal system features)
3. Anti C1q > Anti DS-DNA antibody "Symmetrical" small joint polyarticular arthritis
Corresponds to disease activity (flares) (most common clinical feature of SLE, seen in
4. Anti histone antibodies 90% patients)
Drug induced lupus Jaccoud arthropathy : Deformity present but
SHIPP drugs cause SLE (Sulfasalazine, Hydralazine, Isoniazid, erosions absent (d/d of RA)
Procainamide, and Penicillamine)
5. Anti ribosomal P antibodies
Psychiatric SLE
6. Anti glutamate receptor antibody/ Anti neuronal antibody
CNS SLE
7. Anti phospholipid antibodies
(past h/o miscarriage or thromboembolism)
Lupus anticoagulant
Anti-cardiolipin antibodies Jaccoud Arthropathy
Anti-beta2-glycoptrotein-1
8. C3/C4 level
Low levels are seen in SLE
Get exhausted due to complement activation in SLE
 Dermatological manifestations Heart and Lungs
Photosensitivity is most common skin manifestation in SLE The most common cardiac manifestation of
The butterfly (malar) rash is characteristic of SLE - SLE is pericarditis
Nasolabial fold sparing (butterfly spares) Pleural effusion and pleuritis seen in lungs
Non scarring alopecia is associated with SLE Shrinking lung syndrome (decreased lung
Discoid lupus refers to a benign version of SLE confined to volume)
the skin (Scarring alopecia seen with DLE)

Apthous Ulcer
Also known as canker sore
A small, shallow sore inside the mouth or at
the base of the gums.
D/d is "cold sore" caused by HSV-1

Rheumatoid Arthritis
Rheumatoid arthritis is a
Chronic, systemic inflammatory disorder Antibodies
Characterised by inflammatory polyarthritis 1. Rheumatoid factor (RF)
An IgM autoantibody against Fc portion of IgG
Seen in 60-70% of patients with RA
Predisposing factors
2. Anti-cyclic citrullinated peptide (CCP)
1. Genetics : HLA DR⁴ (Room has 4 walls)
Autoantibodies that react to citrullinated proteins
2. Females (Symptoms more severe in females) Low sensitivity but high specificity
3. Smoking : strongest lifestyle factor for Positivity predicts erosive disease and worse prognosis
development of RA
Presence of RF and CCP : Seropositive RA

Pathophysiology
Following a suspected triggering event, there is
development of self-citrullination (alteration of a
positively charged arginine amino acid into
neutral citrulline)
Immune system then reacts to these citrullinated
proteins
Development of anti-cyclic citrullinated peptide
(anti-CCP) antibodies
At the joint level, the pro-inflammatory response
leads to synovial membrane hyperplasia, which
subsequently damages cartilage.
This destructive synovial hyperplasia is referred to
as a ‘pannus’
 Joints
(Musculoskeletal system features)
Symmetrical polyarthritis of small joints of
hands and feet.
‘Boggy’ joint swelling due to active synovitis,
often difficult to palpate joint line
Joint pain worse at rest or inactivity (decreases
with exercise/movement)
Early morning stiffness lasting > 1 hour
Erosive arthritis (erosions present)

Joints affected
Metacarpophalangeal (MCP) joints and
joints of wrist affected
Classical signs in Chronic RA
DIP spared (affected in psoriasis)
1. Boutonniere deformity:
"DIP near the nails : affected in Psoriasis" Flexion at PIP
Hyperextension at DIP

2. Swan-neck deformity:
Hyperextension at PIP
Flexion at DIP

3. Ulnar deviation at MCPs

4. Z-deformity at wrist
Ulnar deviation along with
Z deformation at wrist

Extra-Articular manifestations of RA
Ocular
Keratoconjunctivitis sicca
Atlanto-axial dislocation
Scleritis
Cervical myelopathy
Scleromalacia perforans
Hematologic
Neutropenia Pleural effusion
Felty's (low glucose in effusion)
Syndrome

Pericarditis
Non infective endocarditis

Membranous
Vasculitis
nephropathy

Hypoandrogenism
Osteoporosis

Caplan Syndrome
Skin RA + Pneumoconiosis
Rheumatoid nodules
Pyoderma gangrenosum
 Management of RA

1. Initial therapy: DMARDs

First-line of treatment
Methotrexate, Leflunomide or Sulfasalazine
Methotrexate and Leflunomide are contraindicated in pregnancy (DOC in preg : Hydroxychloroquine)
Add bridging steroid therapy and NSAIDs (2-3 months),
which allows time for the DMARD to take effect.

2. Failure to respond: DMARD "step up"

Add another DMARD (DMARD combination therapy)

3. Biologics
Used as second-line in combination with DMARDs
Initial therapy in patients with severely active and progressive disease
TNF Alpha inhibitors : ACE-I ki GOLI
A Adalimumab
C Certolizumab
Rule out TB before initiating
E Etanercept
treatment with TNF Alpha inhibitors
I Infliximab
Goli Golimumab

Other bioligics
Interleukin 1R antagonist : Anakinra (1-R-kinra)
Interleukin 6 inhibitor : Tocilizumab, Sarilizumab (Toci Sari Sixy)
CD 20 inhibitor : Rituximab (ri-2-X-imab)
CTLA-4 inhibitor : Abatacept (BATA = 4)
JAK inhibitor (small mol inhibitor) : Tofacitinib, Baricitinib (nib = small)

4. Managing flares:
Acute courses of corticosteroids (e.g. prednisolone)
Consider reducing or stopping therapy in patient who have
maintained remission (or low disease activity) for > 1 year without corticosteroids.

Osteo Arthritis
Non-inflammatory arthritis (pain decreases on rest)
Occurs as a result of wear and tear of the joints
(cartilage mainly affected)
Over time, the cartilage breaks down, leading to pain,
stiffness, and reduced joint mobility.
Factors like aging, obesity, repetitive joint stress can
contribute to OA development.
Assymetric joint space reduction Osteo-arthritis
Hip and knee more commonly involved along with
other joints
Named nodules in osteo-arthritis
1. Heberden nodules : DIP
2. Bouchard nodules : PIP
DH and BP

Healthy OA RA
 Gout
1st meta-tarso-phalngeal joint m/c affected (aka Podagra)
Acute red great toe
Elderly/Alcoholic
Deposition of monosodium urate crystals
Erosions present (rat bite erosions)
d/d Pseudogout : calcium pyrophosphate crystals (m/c in knee)
Negatively Positively
birefringent birefringent
MSU crystals Calcium pyrophos.
in gout crystals in pseudogout

Drugs that precipitate Gout

'CANT LEAP'
C Cyclosporine or cancer drugs
A Aspirin (low dose)
N Niacin
T Thiazide

L Lasix (furosemide)
Martel G sign Pseudogout E Ethambutol
seen in Gout aka chondrocalcinosis A Alcohol
Rat bite erosions Calcification in joint cartilage P Pyrazinamide
m/c joint : 1st MTP m/c joint : Knee
(great toe)

Purines
Management of Gout
Xanthine oxidase

1. Acute Gout : NSAIDs and Steroids Uric acid

First-line of treatment (except Aspirin because it causes uric acid Pegloticase /
retention) Rasburicase
Preferred NSAID : Indomethacin (PCM not preferred because it Allantoin
has no anti-inflammatory action) (water soluble)

2. Colchicine (most effective drug for acute gout)

Prevents polymerisation of microtubules
Decreases neutrophil recruitment, hence stops the
inflammatory process
S/e : Bone marrow supression (hence not used as first line) Tubular Tubular
secretion reabsorption
3. Chronic Gout : Drugs that lower Uric acid Levels
DOC : Allopurinol (Xanthine oxidase inhibitor)
Pegloticase (converts uric acid to allantoin)
Probenecid (prevents reabsorption of uric acid in renal tubules)
Blocked by Blocked by
Rasburicase is used to manage uric 1. Diuretics 1. Probenecid
acid levels in Tumor Lysis Syndrome 2. Low dose 2. High dose
salicylates salicylates
Seronegative spondylo-arthropathies
Inflammatory arthritis which is negative for - RF, Anti CCP antibodies or ANA
Includes :
1. Ankylosing spondylitis
2. Psoriatic arthritis
3. IBD associated arthritis (aka enteropathic arthritis)
4. Reactive arthritis (aka Reiter syndrome)
Common features :
Enthesitis of
HLA B27 gene association (>90% for Ankylosing Spondylitis)
Achilles tendon
Inflammatory back pain : early morning stiffness >1hr that
improves on exercise
Assymetric peripheral arthritis (LL > UL)
Thoracolumbar spine is m/c involved (spared in RA)
Sacroilitis
Achilles enthesistis (not seen in enterohepatic arthritis)
Dactylitis (sausage shaped digits)
Most common extra articular manifestation is anterior uveitis.

Ankylosing Spondylitis
Young male, HLA B27 Sacroilitis
Ankylosing : Stiffened Spondylitis : Inflammation of spine
Primary clinical feature in ankylosing
Positive Schöber test (assesses decrease in lumbar spine flexion)
spondylitis
Spinal deformity (seen in advanced disease)
Bilateral sacroilitis seen with
seronegative spondylo-arthropathies

Unilateral sacroilitis is seen with

Tuberculosis

Reactive arthritis
Schober test
h/o - GI or Genital infection
detects reduced flexion
Self resolving
Asso. with HLA B27

Circinate Keratoderma
balanitis blenorrhagicum

BAMBOO SPINE DAGGER SIGN

Vertebral body fusion Ossification of the spinous
ligaments

Diffuse idiopathic skeletal

hyperostosis (DISH)
d/d of ank. spond
Seen in elderly
Following ossification along
ant. longitudinal ligament
Systemic Sclerosis
Characterised by thickened, hardened skin, hence also known as scleroderma.
Immune-mediated damage to vascular structures (e.g. blood vessels) and excessive synthesis and deposition of
extracellular matrix structures (e.g collagen). This leads to chronic fibrosis, scarring and damage to organs
Further divided into 2 subtypes :

For screening of
Limited Cutaneous Diffuse cutaneous systemic sclerosis :
systemic sclerosis systemic sclerosis ANA testing is done (ANA is
anti centromere Ab anti topoisomerase Ab/ anti SCL 70 Ab positive in >95% cases)
Most sensitive for both limited
CREST Syndrome Sudden onset of Raynaud's and diffuse type
Long standing history of Raynaud's Rapidly progressive course
Internal organ involvement is very ILD > PAH For confirmation
late Scleroderma renal crisis
Limited cut. : Anti centromere Ab
PAH > ILD Cardiac involvement Diffuse cut. : Anti Topoisomerase/
Anti SCL 70 Ab

CREST syndrome
C - Calcinosis cutis : calcium deposits in the skin
R - Raynaud phenomenon (white-blue-red)
E - Esophageal dysmotility : swallowing difficulty
S - Sclerodactyly : skin thickening and hardening affecting the fingers and toes
T - Telangiectasia : dilated capillaries.

Raynauds Phenomenon
Raynaud’s phenomenon is a condition
that affects the blood vessels.
There are periods of time called
“attacks” when the body does not send
enough blood to the hands and feet.
Attacks usually happen when patient is
cold or feeling stressed.

Capillaroscope
Shows changes to
Sclerodactyly (Sausage fingers) Salt and pepper appearance
capillaries in nail bed

Nail bed capillaroscopy

Perioral skil tightening - fissures can be seen Calcinosis cutis
 Sarcoidosis
Fever + Cough + hilar lymphadenopathy = TB or Sarcoidosis
Multisystem granulomatous disorder that mostly affects the lungs.

1. Pulmonary Sarcoidosis
The lungs are affected in 90% of patients
Bilateral hilar lymphadenopathy is the hallmark finding on CXR
Both TB and sarcoidosis cause cavitating lung lesions
Pulmonary fibrosis in advanced disease

2. Cutaneous sarcoidosis
Papular sarcoidosis: multiple papules develop, generally on the head
and neck or areas of trauma.
Erythema nodosum: a panniculitis (inflammation of subcutaneous
adipose tissue) characterised by red, painful nodules.
Lupus pernio: a violaceous, nodular rash distributed over the nose and
cheeks (pathognomonic but rare)

Papular Sarcoidosis

Bilateral hilar and mediastinal

lymphadenopathy
Scadding staging based on CXR findings

Lupus Pernio Erythema nodosum

3. Other manifestations
Ocular manifestations in 30-60% of cases, most commonly in the form of uveitis
Hypercalcaemia is seen in around 15% of cases (due to extra-renal synthesis of calcitriol)

Clinical Syndromes in Sarcoidosis

Schaumann body
due to excess vitamin D
Heerfordt Waldenstorms's Lofgren's
syndrome Syndrome
Uveitis, Parotitis Hilar Lymphadenopathy
Erythema Nodosum Erythema Nodosum
7th CN palsy (facial nerve) Migratory polyarthritis
"Heer has a pretty face" Lofgren's - Legs - Arthritis

Diagnosis
1. Bilateral hilar lymphadenopathy on CXR
2. Brochoalveolar lavage : CD4/CD8 ratio > 4
3. Serum ACE raised
4. Panda sign on Gallium 67 scan
5. Calcium elevated
Sjogren Syndrome
Associated with auto-antibodies : Anti Ro/ Anti La antibodies "no ROna or LAal tapkana"

Lymphocytic infiltration of exocrine glands

B/L parotid enlargement (rule out lymphoma)
Dry eyes (Keratoconjunctivitis sicca)
Dry mouth

Extra-glandular manifestations
Arthritis (m/c) Schimmer test
Type - 1 RTA "Sjogr-one" (uses rose bengal dye)
Vasculitis and Raynaud's phenomenon
Lymphoma

Inflammatory Myopathies
Auto-immune disorder
Muscle inflammation leading to progressive muscle weakness and wasting
Raised Creatine Kinase

Inflammatory myopathy

Proximal Proximal as well as

weakness distal weakness

Dermato-myositis Poly-myositis Inclusion body

myositis
Characteristic rashes along with Only muscle weakness and no rash
muscle weakness Associated with other auto-immune
Proximal Esophageal weakness (distal conditions
weakness seen in CREST Syndrome)
Peri-fascicular atrophy

Anti synthetase syndrome

Type of inflammatory myopathy
Anti-Jo 1 antibody
Mechanic's hands (hyperkeratotic lesion)
Heliotrope eyelid rash Gottron's Papules
Associated with :
1. Arthritis
2. ILD
3. Raynaud's phenomenon

Nail-bed telengiectasia Shawl Sign

Other Myopathies

ESR raised ESR normal

Polymyalgia Rheumatica
Elderly > 50 yrs No pain Painful
CK normal
Morning stiffness Steroid induced myopathy Statin induced myopathy
 Vasculitis
Inflammation of blood vessels that interrupts blood flow to vital organs.
Leads to ischaemia, tissue damage and ultimately organ dysfunction
(e.g. gut ischaemia, acute kidney injury)

Clinical features
The clinical features of vasculitis depend on both the size of the vessels
involved (large, medium or small) and the location of the vessels involved
(kidney, skin or gut vessels)
1. Palpable purpura
2. Asymmetrical neuropathies (damage to the small blood vessels that supply
peripheral nerves)
3. Unexplained bleeding
4. Constitutional symptoms such as fever, weight loss, and fatigue Palpable purpura

Vasculitis

Granulomatous ANCA Immune complex

Vasculitis associated associated
Wegner's GPA 1. HSP (IgA Vasculitis)
Eosinophilic GPA C-ANCA P-ANCA 2. SLE
(Churg Strauss Sx) aka MPO ANCA 3. PAN (a/w Hep B)
Giant cell arteritis 4. Cryoglobulinemia (a/w Hep C)
Takayasu arteritis Wegner's GPA Eosinophilic GPA 5. Good Pasteur's
egner's Microscopic poly-angitis
(MPA)

ANCA associated diseases involve Lungs

(pulmonary haemorrhage) and Kidney
(glomerulonephritis)

Vasculitis
(Chapel Hill Classification)

Large Vessel Medium Vessel Small Vessel Variable

1. Takayasu arteritis 1. Kawasaki disease 1. Behcet's Syndrome
2. Giant cell arteritis 2. Poly arteritis 2. Cogan's Syndrome
nodosa (a/w Hep B)

ANCA associated Immune complex

1. Eosinophilic GPA - P ANCA associated
Thrombo-angitis Obliterans 2. Microscopic poly-angitis 1. HSP (IgA Vasculitis)
(Buerger's Disease) (MPA) - P ANCA 2. Cryoglobulinemia (a/w Hep C)
3. Wegner's GPA - C ANCA 3. Good Pasteur's
Affects artery, veins and nerves (spares
lymphatics)
Young adult < 35 years
Smoker
Severe limb pain
M/c artery : Radial/Tibial Most common
Corkscrew collaterals seen on DSA Vasculitis in adults : GCA
T/t : Stop smoking (surgery has no role) Vasculitis in children : HSP (Kawasaki in Asia)
 Giant cell arteritis Takayasu arteritis
Also known as temporal arteritis (Superficial temporal Takayasu arteritis is aka "pulse-less disease" and
artery most commonly affected) "aortic arch syndrome"
Granulomatous - Large vessel - vasculitis (type 4 Granulomatous - Large vessel - vasculitis (type 4
hypersensitivity reaction) hypersensitivity reaction)
Older adults > 50 years of age Affects younger adults < 40yrs
Associated with Polymyalgia Rheumatica Affects woman (>80%) and Asian ethnicity
Characterised by a unilateral headache, scalp pain, and Affects the aorta and its major branches (m/c is
visual loss due to involvement of the ophthalmic artery. Subclavian artery)
Classical feature : "Jaw pain that occurs while chewing" BP difference between upper limbs
Immediate management : Start steroids Diagnosis is usually made on imaging.
It is considered a medical emergency because without
prompt recognition and treatment it can lead to
permanent visual loss.
Gold standard for diagnosis : Artery biopsy (VVG Stain)

Inflamed Difference in BP
temporal artery between ULs

Renal artery
Stenosis

VVG staining
(stains elastic fibres)

Poly-arteritis nodosa Wegner's GPA Eosinophilic GPA

Medium vessel vasculitis (immune ANCA asso. granulomatous aka Churg Strauss Syndrome
complex mediated) necrotising vasculitis (C-ANCA) ANCA asso. granulomatous
Associated with Hepatitis B URTI + LRTI + vasculitis (P-ANCA)
Segmental, transmural "necrotizing" Glomerulonephritis (triad) Asthma and Eosinophilia
inflammation of arteries (fibrinoid Cavitatory lung lesions Mono-neuritis complex is an
necrosis) Crescentric RPGN associated condition with EGPA
It never affects the pulmonary system
(PAN - Pulmonary artery never- Microscopic polyangitis
involved)
ANCA asso. vasculitis (P-ANCA)
Clinical features similar to PAN
Glomerulonephritis with rapid
Saddle nose and
progression to renal failure
Cavitations in lung

HSP (IgA vasculitis) Cryoglobulinemia

Fibrinoid necrosis
Henoch-Schönlein purpura Cryoglobulins are
Commonly presents in childhood. immunoglobulins that
Viral prodrome precipitate in cold (<37º) and
Behcet's Disease dissolve upon rewarming.
Self limiting (can lead to intusucception)
aka Neutrophilic Vasculitis Associated with hepatitis C
Oral and genital ulcers
Erythema Nodosum and anterior
uveitis Good Pasteur Sx
IgA nephritis (50%)
Oral ulcers are painful but heal Refers to clinically evident
Abdominal pain (50%)
without scarring while genital ulcers glomerulonephritis and
Joint pain (75%)
are painless but heal with scarring. pulmonary haemorrhage.
Purpuric rash (100%)
Associated with HLA B-51 Anti-GBM antibodies

Differentials
1. HUS/TTP/ITP will have thrombocytopenia
2. JIA will have erythematous rash + fever
Auto-antibodies compiled
Associated with SLE
1. ANA : most sensitive (entry criterion for diagnosis)
2. Anti Smith : most specific
3. Anti C1q > Anti ds-DNA : Corresponds to disease activity in SLE (Flares)
4. Anti histone : drug induced SLE (SHIP drugs)
5. Anti neuronal / Anti glutamate receptor 2 : CNS SLE
6. Anti ribosomal P : Psychaitric SLE

Associated with other connective tissue disorders

1. Anti-U1 RNP : Multiple connective tissue disorder
2. Anti CCP, Rheumatoid factor : Rheumatoid arthritis
3. Anti-Ro / Anti-La : Sjogren's Syndrome
4. Anti-Jo1 : Anti Synthetase Syndrome (Mechanic hands)
5. Anti-topoisomerase 1/Anti-scl-70 : Diffuse cutaneous systemic sclerosis
6. Anti-centromere : Limited cutaneous systemic sclerosis (CREST Syndrome)

Other auto-antibodies
1. AchR antibodies, Anti MUSK antibodies : Myesthania Gravis
2. Anti TPO : Hashimoto's Thyroiditis
3. LATS (Long acting Thyroid stimulant) : Grave's disease
4. Anti LKM-1 : Autoimmune hepatitis type 2
5. AMA : Primary billiary cirrhosis (AMMA = female, has cirrhosis) [PSC seen in males, asso with IBD]
6. P-ANCA : EGPA, MPA, Ulcerative Colitis
7. C-ANCA : Wegner's GPA
8. ASCA (Anti-Saccharomyces cerevisiae antibodies) : Chron's disease
CHAPTER 22
INTEGRATED
RESP. SYSTEM
 Lung Volumes

Inspiratory
reserve volume Inspiratory
capacity Vital capacity

Tidal volume
Expiratory
reserve volume Functional
residual capacity Residual
Residual volume volume Spirometry

1. Tidal volume (normal brething) : 500 ml

Dead space volume
2. Insp. reserve volume (forced inspiration after normal inspiration) : 2-3 L Air inspired that doesn't participate in
3. Exp. reserve volume (forced expiration after normal expiration) : 1 L gas exchange.

• It's of 2 types :
4. Inspiratory capacity : Forced inspiration after normal expiration 1. Anatomical (in resp. tract)
5. Vital capacity : Forced inspiration after forced expiration 2. Alveolar (negligible in healthy lungs)

6. Functional residual capacity : Volume of air left in lungs after normal expiration • Normal value : 150ml of air
7. Residual volume : Volume of air left in lungs after forced expiration • Measurement of dead space : Single breath
Increased in Obstructive lung disease vowels stick N² method
Decreased in Restrictive lung disease

Important Formulae
1. Minute Ventilation : Resp. Rate x Tidal volume
2. Alveolar Ventilation : Resp. Rate x (Tidal volume - Dead space) Dead space = 150 ml
3. Oxygen carrying capacity : 1.34 x Haemoglobin
Increased in Polycythemia (more Hb)
Decreased in Anaemia (less Hb)
Ventialtion-Perfusion (V/Q)
Min blood, air flow
Minimum perfusion
Minimum ventialtion
Ventilation > Perfusion
High V/Q
V/Q
Aerophilic TB bacili
reside here Peaks at apex
Low at base
Max blood, air flow
Maximum perfusion
Maximum ventialtion
Perfusion > Ventilation
Low V/Q

50

Ideal Alveolus
Shunt
Base
No ventilation pCO² : Perfusion
Mod high ventilation
(pO² is 0)
(pO² moderate high) pO² : Ventilation
V/Q : 0
High perfusion
eg. Pneumonia
(pCO² high) Apex
V/Q : Low High ventilation
(pO² High)
Low perfusion
(pCO² Low)
V/Q : high

Dead Space
V/Q ∞

50

Oxygen Dissociation curve

2-3 DPG
SaO²

When affinity to O² increases

"Leftists love O²" Product by RL shunt
Left shift of O² dissociation curve
Causes easy dissociation
Left shift P50 decreases (PaO² when SaO² is 50%)
of O² from Hb (right shift)
O² delivery to tissues ↓

Left shift Right shift

Right shift
(increased affinity to O²) (decreased affinity to O²)
Lower temp Higher temp
Lower [H+] Higher [H+]
Lower 2-3 DPG High 2-3 DPG
Carbon monoxide High Altitude , Anemia
GH/Thyroid/Androgens
PaO²

Sigmoid curve
(due to positive co-operativity of oxygen)
Chest wall vs Lungs

Chest wall : Negative pressure

Lung recoil : Positive pressure
At FRC
If chest wall removed Lung goes
Combined pressure = 0
into minimum volume Positive pressure = Negative pressure

Compliance

∆V = Compliance
∆P

Increases : Elderly, Emphysema

Decreases : Fibrosis

Hysteresis loop
Difference between trans-pulmonary pressure of
inhalation and exhalation

Compliance Surfactant is responsible for hysteresis

= Specific Compliance
FRC
Increases surface area of alveoli
Reduces surface tension
Produced by type-2 pneumocytes (more in
number compared to type-1 but smaller)
Respiratory Regulation

Voluntary respiration Cerebrum Ondine's curse

aka Central hypoventilation Sx

Pneumotaxic Vagus
Center nerve
Pons
Medullary lesion
Both inhibit
No spontaneous breathing
Can't sleep
Apneustic Center
(Apneusis = Inspiratory spasm)

Level of transection and effects

DRG Above pons (APC intact)
(Controls rhythm) Vagus intact : Only voluntary control lost
Vagus also cut : Increased depth (PTC still inhibiting)
VRG Mid pons (APC cut)
(Forceful expiration)
VRG : Vigorous Vagus intact : Increased depth (vagus still inhibiting)
Medulla Vagus also cut : Apneusis (no inhibition to APC)

Pre-Botzinger Pons-Medulla junction

complex Irregular-respiration
(Pacemaker for Below Medulla
inspiration) No breathing at all

Sleep Apnea
Sleep apnea is a condition in which breathing stops and restarts many times while sleeping.
Could be either

Obstructive sleep Central sleep

apnea apnea
H/o snoring No respiratory drive from
Thoraco-abdominal brain
muscles show movement Less common to OSA
on polysomnography

Polysomnography
Pickwickian Syndrome
aka Obesity hypoventilation syndrome
D/d of sleep apnea
Obese patient (BMI > 30)
Can't breathe leading to hypoventilation
PaCO² high even during day
Picking up some breath
 Respiratory Patterns

Biot's breathing : CNS insult

(Break in between, due to Brain insult))

Kussmaul's : Met. acidosis

(High amplitude)

Cheyne stokes : CVS issue

(Crescendo, Cardiac insult)

Respiratory Failure

Type 1 Type 2 Type 3 Type 4

(Hypoxemic) (Hyper-capnic) (Peri-operative) (Shock)
PaO² low (PaCO² normal) PaO² low & PaCO² high Lung atelectasis Hypo-perfusion
secondary to shock
↓ ↓ To prevent
O² can't be perfused Respiratory drive 1. Chest physiotherapy
Alveoli not filling with air : ARDS / absent 2. Incentive spirometer
Pneumonia Obstructive disorder
Alveolar wall thickened : ILD Chest wall issue
Blood not reaching alveoi : PE Diaphragm issue
 Approach to Lung Disorders
Spirometry

FEV¹ : amount of air

expired in first second
of forced expiration
Low Normal or high
FEV¹/FVC FEV¹/FVC
FEV¹ is low, denotes can't breath air out FVC is low, denotes air can't go in.
Known as OBSTRUCTIVE disorder FEV¹ can also be low here
"obstructs exit" Known as RESTRICTIVE disorder
"restricts entry"

Bronchodilator Challenge Diffusion capacity in lungs for CO (DLCO)

FEV¹ increased FEV¹ unchanged Normal DLCO Low DLCO

by > 12%
Chest wall problem 1. P. Fibrosis
Asthma 1. COPD 1. Kyphoscoliosis 2. ILD
2. Brochiectasis 2. Obesity 3. P. Edema
3. M. Gravis 4. ARDS

Scooping
←

Obstructive disorder on Restrictive disorder on

flow volume curve flow volume curve

Inspiratory + Expiratory flattening Expiratory flattening Inspiratory flattening

Fixed airway obstruction (Intra-thoracic obstruction) (Extra-thoracic obstruction)
1. Laryngospasm 1. Foreign body 1. VC palsy
2. Tracheal stenosis

Inspiratory is extrathoracic and expiratory is intrathoracic

"I with E"
 COPD (Chronic Obstructive Pulm. Disorder)

COPD

Diffusion capacity in lungs for CO (DLCO)

Low DLCO Normal DLCO

Emphysema Chronic Bronchitis

Alveoli are affeceted, hence DLCO low Long term irritation of the lungs
Doesn't cause scarring Mucus layer thickened
Classfied as (anatomical classification) Reid's index : > 0.4 "REID has 4 letters"

Centri-Acinar Pan-Acinar Para-Septal

Most common type Due to α-1-antitrypsin Alveoli near septum Flattening of diaphragm
Asso. with cigarette deficiency affected Surest sign of hyperinflation
smoking Lower lobes affected Peripheral small bullae
Upper lobes affected seen
Tall/thin/male
Asso. with Spontaneous
pneumothorax (managed
conservatively)

COPD GOLD criteria (for assessment of severity) Treatment for COPD

Severity FEV¹ If 1 or no exacerbations (not leading to
hospitalisation) : SABA or SAMA
Very severe <30 30 + 50 = 80 ≥ 2 exacerbations or even one leading to
Severe 30-50
FEV¹/FVC < 0.7 for all hospital admission : LABA + LAMA
Moderate 50-80
Mild >80

Bronchiectasis
Irreversible dilatation of the bronchi (signet ring and
tram tracking appearance)
Due to destruction of smooth muscles and elastic tissue
in chronic inflammation.
C/f : Productive cough + foul smelling sputum
Various etiology are
1. B/L upper lobes : Cystic fibrosis
2. U/L upper lobe : TB
3. Middle lobe : Kartagner syndrome Tram tracking Signet ring app.
4. Lower lobe : Aspiration Dilated bronchi Dilated bronchi wrt
vessels
 Asthma

Prophylaxis Treatment

Late response: Bronchial

inflammation hyperreactivity
Anti - IL 5
Exposure to Mediators Anti - IL 4
Antigen and IgE (leukotrienes,
antigen Steroids
on mast cells
histamine, etc.)
Omalizumab Anti-
Avoid antigen
(Monoclonal Ab against IgE) leukotrienes Early response:
Symptoms
1. Zafirlukast
bronchoconstriction
2. Montelukast Beta-agonists
3. Zilueton Muscarinic "BAG MAN"
(anti - LOX) antagonists
PDE inh.

Membrane phospholipids

Phospholipase A2 -----Blocked by steroids → Fluticasone, Budesonide

DOC for prophylaxis
Arachidonic acid Also used in acute attack along with
bronchodilators
(increases the sensitivity of B2 agonists)
LOX pathway COX pathway
Preferred by inhalational route
M/c side effect is oropharyngeal
candidiasis
Leucotrienes A4 PGH2
(Topical Nystatin or Clotrimazole is
used to treat candidiasis)
Prostacyclins Thromboxanes

Leucotriene B4 Cysteinyl leucotrienes Prostaglandins

Allergy, inflammation, gastric damage Inflammation, pain, but also

gastroprotective PGs
LOX pathway blocked by Zilueton

Bronchodilators

B² agonists M³ antagonists Phospho-diesterase inhibitors

Inhalational drugs Inhalational drugs Theophylline and aminophylline
Short acting : Salbutamol, terbutaline Ipratroipum, tiotropium Oral or IV route
Long acting: Salmeterol (slow, hence Metabolised by CYP (avoid
used for prophylaxis), Formeterol (fast) erythromycin with these drugs)
2 mechanisms of action

"BAG MAN" Adenosine A1 Increase cAMP by

receptor antagonist inhibition of PDE
Adverse effects Adverse effects
Arrythmia Arrythmia
Diuresis N and V
Interstitial Lung Disease (ILD)
Interstitial lung disease

Elderly Middle aged female Occupational lung diseases

Usual interstitial pneumonia (UIP) Nonspecific interstitial

aka Idiopathic pulmonary fibrosis (IPF) pneumonia (NSIP)
Poor responce to steroids Middle aged females is a very
Poor prognosis non specific category
Rx : TGF-β inhibitors
Good responce to steroids
1. Nintendanib Good prognosis
2. Pirfenidone Associated with scleroderma
Grandpa wears honey-perfume and chemotherapy
and plays on his nintendo

Honeycombing pattern Ground-glass pattern

Ship repair/ Mining/ Coal

Electrical insulation Construction worker

Asbestosis Silicosis Anthracosis

As-base-tosis Egg shell calcifications aka Coal worker Pneumoconiosis
(b/l hilar LN with calcification) 1. Caplan Sx : RA + CWP
Only occupational lung
d/d : Sarcoidosis 2. Erasmus Sx : Scleroderma + CWP
disease where lower
Associated with TB
lobes are affected.
Complication : Progressive
Pleural plaques seen
Pleural Plaques massive fibrosis (mass like
(holly leaf sign)
opacity in b/l lungs)
Dumbbell bodies on h/p
Complications

Dumbbell bodies
Anthracosis
Adeno-carcinoma Mesothelioma
Most common Most specific Egg shell
complication complication calcifications
Markers : Markers :
1. Napsin A Cytokeratin
2. TTF 1

Progressive massive
fibrosis
Short, stubby Long slender
microvilli microvilli
 Pulmonary Edema
Pulmonary edema is a condition characterized by fluid accumulation in
the lungs
Caused by extravasation of fluid from pulmonary vasculature into the
interstitium and alveoli of the lungs
Can be classified into 2 broad categories

Cardiogenic Non cardiogenic

pulm. edema pulm. edema
Lungs flooded with blood Leaky pulmonary vessels
1. Hypetension 1. ARDS
2. CHF 2. TRALI (transfusion related) ARDS
3. Cardiomyopathy 3. HAPE (high altitiude pulm Acute respiratory distress syndrome
4. Valvular diseases edema)
New global definition 2023
Onset within a week of known risk factor
Pulm. edema (non cardiogenic)
B/L lung infiltrates on X-ray / CT / USG
Hypoxemia : SPO²/FiO² < 315 with SPO² < 97

Severity grading (based on PaO²/FiO²)

1. Mild : 200-300
Batwing appearance Patchy alveolar opacities 2. Moderate : 100-200
Central (Perihilar) Seen with ARDS 3. Severe : <100
opacities
Cardiomegaly Characteristics of Management of ARDS
Pleural effusion pulmonary edema in ARDS Prone positioning
Kerley B lines 1. PCWP < 18 mm Hg Low tidal volume (to avoid barotrauma)
2. Normal left atrial pressure High PEEP (to prevent alveolar collapse)
3. Raised pulm. artery pressure Manage underlying condition
4. Hypoxemia Glucocorticoids not useful

Pleural effusion
Collection of fluid in pleural space
Can be classified as transudative or exudative based on Light's criteria

Light's Criteria Compressed Normal

1. Pleural fluid protein/serum protein > 0.5 lung lung
2. Pleural fluid LDH/serum LDH > 0.6
3. Pleural fluid LDH > 2/3rd of normal LDH upper limit
Pleura

Fluid in
pleural spcae
If any of the conditions satisfy None of the conditions satisfy

Exudative Transudative
Cells expired Transfer of fluid from cells
Due to cell damage Due to low protein (low oncotic pressure)
1. Infections or high hydrostatic pressure in capillaries
2. Malignancy 1. Liver cirrhosis
3. Pulmonary embolism 2. Nephrotic syndrome
3. CHF
Split pleura sign
Drainage of Pleural effusion

Indications for drainage

Chylothorax
1. Empyema (pus) > 100 mg/dl triglycerides
2. Loculated effusion
3. Positive culture Pseudo-chylothorax
4. Low glucose
Seen in RA
(RA/Empyema/Malignancy)
Effusion is milky but
REM
TGs are low
5. pH < 7.2 Pigtail catheter used to drain

Pulmonary Embolism

1. Acute dyspnoea
2. U/l swollen limb
3. Risk factor for DVT (Virchow's triad)

Suspicion of Pulmonary Embolism

Well's Score

<4 >4
(PE unlikely) (PE likely)

D-Dimer CTPA
To rule out PE IOC for PE
If positive : CTPA Shows filling defects in PA
CTPA showing PE

Positive Negative

Start treatment V/Q scan

Stable Unstable
IVC filter
Anticoagulation Anticoagulation +
If anticoagulation Thrombolysis
is contraindicated, If thrombolysis is contraindicated, On ECG : S¹-Q³-T³ pattern
then IVC filter is then surgical embolectomy
used (endovascular) is done.
 Pulmonary Artery Hypertension
Etiology
1. Secondary to left heart disease
2. Secondary to lungs disorder
3. Hereditary : BMPR2 gene mutation

Associated with
1. CREST syndrome (connective tissue disorders)
2. HIV
3. Schistosomiasis
4. Congenital heart diseases

Treatment algorithm
Diagnosis of PAH

(1st line)
Normal PAH
D Diuretics
O Oxygen
A Anticoagulation
D Digoxin

Acute Vasoreactivity test

(Short acting vasodilators used and checked if Dilated
PA pressure reduces by 10mm Hg) pulm.
artery

Responds Doesn't
well respond

CCB
Low risk High risk

1. Endothelin receptor Lung transplant Jug Handle Sign in PAH

antagonists (ERA)
Bosentan
Macitentan
Ambrisentan
2. PDE-5 inhibitors
Guanylate PDE-5
Sildenafil GTP cGMP 5' GMP
cyclase (breaks down)
Tadafil
3. Guanylate cyclase (+) Arterial
Riociguat relaxation

Endothelin is a peptide that constricts vessels

Guanylate cyclase is produced by Nitrates
Nitrates + Sildenafil (PDE - 5) = Excess relaxation of
arteries (hence avoided)
Chest Infections

Consolidation Pneumatocele Air bronchogram Silhouette sign

MCC : Strep pneumonia MCC : Staph aureus If merging with heart border
then in middle lobe

CURB 65 score for pneumonia management

1. Confusion
2. Urea (BUN) > 20 mg/dl
0-1 : 0u1patient Amoxicillin
3. Resp rate > 30
2 : In-patient (FQs/Beta lactams) + (Azithral/Doxy)
4. BP (SBP < 60 or DBP < 90)
≥3 : ICU (3 letters) Beta lactams + FQs
5. Age > 65

Score of 1 for each

"20-30-60-90"

Chest conditions related to Aspergillus

Finger in glove sign Calcified fungal ball Halo sign

ABPA Aspergilloma Invasive aspergillosis

(Allergic broncho pulmonary (Fungal ball) Immunocopromised patient
aspergillosis) Already calcified, Febrile neutropenia
Allergic reaction to Aspergillus no treatment needed DOC : Voriconazole V for A
Hence, positive culture of
aspergillus is not a criteria for
diagnosis
Associated with Asthma and
Cystic fibrosis
Central bronchiectasis seen
Rx : Steroids
Carcinoma of Lung
Carcinoma of Lung

Asso. with SMOKING, Not asso. with smoking,

more in Males more in females
(affects central lung tissues) (affects peripheral lung tissues)

Squamous cell Small cell Adenocarcinoma

carcinoma of lung carcinoma of lung of lung
p53 mutation L-myc mutation Most common ca. lung overall
PNS : PTH releasing peptide PNS : KRAS, EGFR, ALK mutation
(Hypercalcemia) 1. Cushing's Sx, Lepidic spread (spread along
Keratin pearls on h/p 2. SIADH, alveolar septa) on h/p
IHC marker : p40/p63 3. Lambert Eaton Myesthenic Sx IHC marker : TTF-1, Napsin-A
Azopardi effect (basophilic Associated with :
1. Trosseu Sx
nuclear material in blood vessels)
(migratory thrombophlebitis)
and basophilic stippling on h/p
2. Clubbing of digits (hypertrophic
IHC marker : Neuro-endocrine pulmonary osteoarthropathy)
markers (Synaptophysin,
Chromogranin, NSE)
Hematogenous spread
"small cells move via blood
vessels"

Keratin pearls

Lepidic Spread
(spread along alveolar septa)

Pan-coast tumor
Azopardi phenomenon
Tumor at the apices of lungs
M/c type is squamous cell carcinoma
Compresses nearby structures (RLN, C myc : Burkitt's
Sympathetic chain, brachial plexus, SVC) N myc : Neuroblastoma Trosseu Syndrome
IOC : MRI > CT (nervous involvement)
L myc : Small cell carcinoma of Lung (Migratory thrombophlebitis)
Complications :

Large cells
carcinoma of lung
Horner syndrome
Has the same features as small
cell carcinoma of lung (other
than peripheral origin)
Faster growth but presents
with symptoms later due to Clubbing of digits
SVC syndrome
peripheral origin.
Dilated veins
Flushing
Pumberton sign (+)
CHAPTER 23
INTEGRATED
ENDOCRINE
 Hypothalamus-Pitutary Axis
Hypothalamus Somatostatin
inhibits GH and TSH
Anterior pitutary

Basophils Acidophils

inhibits GnRH
ACTH TSH FSH, LH GH Prolactin
(causes pigmentation)

Adrenal glands Thyroid glands Gonads Liver Mammary

IGF -1 glands

Types of receptors

Ionotropic GPCR Enzymatic receptors Intracellular

receptors Water soluble Lipid soluble
Fastest acting receptors Faster Slower
GABA
NMDA
Nicotinic
Tyrosine Kinase JAK Stat Intra Intra
cAMP (MAP K pathway) (Cytokine receptor, Cytoplasmic Nuclear
aka non tyrosine kinase)
Insulin C Corticoids S Sex horm.
P PDGF P Prolactin, GH
Gq Gs D Vit D A Vit A
Gi I IGF I IL 2
Stimulates Inhibits
T T3/T4
Phospholipase C F FGF G GM CSF
IP3 DAG pathway Includes M² E EGF L Leptin
Ca² increases (smooth everything α² E EPO
muscle contraction) else D² T TPO
H¹ A¹ V¹
All 2s are MAD
M¹ n M³
G Gastrin, GnRH cGMP
O Oxytocin
1. NO (from Arginine)
T TRH 2. ANP
3. BNP
Prolactinoma

M/c pitutary adenoma

Conditions that increase prolactin
2nd m/c are "non-functional adenomas"
Sleep
Sex
"S"
In Hypothyroidism, TRH Suckling
TRH
increases : Prolactinemia Promotes Strenous exercise
Stress
inhibits Prolactin
Dopamine inhibits GnRH
Prolactin levels
Drugs that can cause prolactinemia : Prolactinemia presents as
Normal : < 20
Anti-psychotics Amenorrhea
Non functional pitutary
D2 blockers (Domperidone and Infertility
metclopromide) Hot flashes adenoma : 20-100
Prolactinoma : > 200
Drugs that can treat prolactinemia :
Cabergoline
Bromocriptine (in pregnancy)

Prolactinoma work-up
Serum prolactin level

> 20 > 200

Rule out Pitutary MRI

1. Hypothyroidism
2. Pregnancy
3. D2 blockers
4. Renal failure < 10 mm > 10 mm
Micro-adenoma Macro-adenoma
If asymptomatic no t/t needed If mass effect (BTHA) present
If symptomatic then medical then surgery
management with D2 agonists TNTS pituitary resection
1. Cabergoline (Trans nasal trans sphenoidal sx)
2. Bromocriptine (in pregnancy)
 Acromegaly

inhibits Promotes Conditions that increase GH

Somatostatin GH Ghrelin
Increased during Hypoglycemia (counter-regulatory hormone)
Fasting NREM Sleep
Liver
Laron Dwarfism Fasting (ghrelin)
IGF 1
GH receptors defect aka Somatomedin C Strenous exercise
No IGF-1 produced
T/t : IGF-1 injections

Acromegaly work-up
Clinical features
Clinical Suspicion Hyperglycemia
Galactorrhea
Vitamin D ⬆️ (hyperphosphatemia)
IGF 1 levels Screening test
↑ GH after skeletal maturity

Normal Elevated
Rules out acromegaly
Adequate supression Glucose tolerance
Confirmatory test
test
Spade phallanx ⬆️ heelpad thickness Prognathism

Inadequate supression

Pitutary MRI

Normal imaging Pitutary mass

Ectopic GH/ GHRH secreting tumor

Resectable Not resectable

TNTS pituitary resection 1. Radiotherapy
(Trans nasal trans sphenoidal sx) 2. Octreotide (sOmatostatin analogue)
3. PegVisomant (GH receptor antagonist)
S/E : VFD
Diabetes Mellitus

1. HbA1c : 6.5 (5.7 for IGT) IGT : Impaired glucose tolerance

2. FBS : 125 (100 for IGT) on 2 occasions
3. RBS/ 2hr OGTT : 200 (140 for IGT) on 2 occasions

Young Adults

Type 1 DM MODY Type 2 DM LADA

Thin habitus Maturity onset diabetes Obsese habitus Latent auto-immune
Low insulin levels in young (<25 years) Associated with metabolic diabetes in adults.
Low β cell mass >2 generations must be syndrome (insulin resistance) Its like type 1 DM but
Insulin dependent affected for diagnosis Initially insulin levels are presents late
Auto antibodies include : HNF 1 α gene high, gradually become low. Auto antibodies include
Mild diabetes, managed Treated with OHAs 1. Anti GAD Abs
1. Abs against Zn transporter
with OHAs 2. Anti islet cell Abs
2. Anti GAD Abs
3. Anti islet cell Abs Mild diabetes, managed
with OHAs
Associated with other auto-
immune conditions

Insulin Sensitivity NCEP ATP-3 Guidleines

for metabolic syndrome
Fat Cells
National Cholesterol Education Program
Adult Treatment Panel III

1. Central obesity:
90cm in men
80cm in women
2. Elevated triglycerides: >150 mg/dL
3. HDL
Adiponectin < 40 mg/dL in men
Increases insulin sensitivity < 50 mg/dL in women.
Levels are decreased in obesity 4. Blood pressure: >130/85 mm Hg
Cortisol inhibits it (causes insulin 5. Fasting glucose: >100 mg/dL
resistance)
Fat cells also produce Leptin (satiety) (High LDL is not a criteria)
Complications of Diabetes Mellitus

Impaired glucose uptake by cells Good glycemic control

Reduces microvascular
High intra-vascular glucose and low intra-cellular glucose
complications
Reactive oxygen species increase (oxidative stress) Doesn't reduce mortality
Endothelial dysfunction

Increased vascular permeability

Glove and stocking
Tissue damage
neuropathy
Ascending, symmetrical
Macrovascular Microvascular Sensory-motor type
complications complications neuropathy
1. Cardiomyopathy and MI 1. Retinopathy Seen with Diabetes
2. CNS Strokes (TIA) and 2. Nephropathy (KW nodules)
cognitive impairment 3. Peripheral neuropathy (m/c)
3. Peripheral artery disease and gangrene

Necrobiosis Lipodica
Diabeticorum

"end organs"
Insulin

Ultra short acting ( 1hr)

1. LiSpro
2. ASpart "having S in name"
3. GluliSine
Sub-cutaneous administration

Short acting (3 hrs)

Regular insulin
Can be only administered IV
Hence, aka IV insulin

Intermediate acting (5 hrs)

NPH insulin
Neutral Protamine Hagedron
Dosed between meals

Long acting (no peaks)

1. Detemir Intracellular
2. Glargine (acidic, hence can't be mixed) pottasium shift
1. Insulin
Longest acting (42 hrs) 2. ß agonists
Degludec
K+

Side effects of insulin

1. Hypoglycemia
2. Anabolic hormone : Weight gain Pottasium enters cells when
3. Lipo-atrophy around injection site these drugs are administered.
4. Hypokalemia K+ conc. in serum decreases

Dawn effect
Insulin sensitivity reduced in morning
Leads to higher blood glucose levels in morning
Rx : Continuous glucose monitoring

Somogyi effect "so - gyi"

Low blood sugar at night
High blood sugar in morning due to counter
regulatory hormones
High blood sugar levels in morning Rx : Reduce bedtime insulin
 OHAs
Oral anti-diabetic drugs

Enhance insulin secretion Overcome insulin resistance Miscellaneous

drugs

Biguanides Thiazolidinediones
"Metformin" "Glitazones"
Stimulates AMP kinase Activates PPAR-γ
Cause weight loss Cause weight gain
Max reduction of HbA1c 1. Pioglitazone
S/e : Lactic acidosis and (s/e : Bladder cancer)
B12 deficiency 2. Rosiglitazone
(s/e : MI)

K+ channel Glucose dependent

blockers insulin secretion
ide drugs, can cause Increases satiety and
Hypoglycemia, weight gain causes weight loss

Sulfonyl-ureas Meglitinides GLP analogues DPP 4 inhibitors

Teratogenic, hence avoid Increases glucose-dependent Metabolises GLP-1
1. Ripaglutide
in pregnancy insulin secretion S/e : Naso-pharyngitis
2. Nateglinide
Decreases glucagon secretion 1. Sitagliptin
1. Chlorpropamide
Delays gastric emptying 2. Saxagliptin
2. Glipizide
Metabolised by DPP-4 3. Linagliptin
3. Glyburide
S/e : Pancreatitis (Linagliptin is metabolised by
4. Tolbutamide
1. Exenatide Liver, safe in renal failure)
Chlorpropamide has s/e of 2. Liraglutide
C Cholestatic Jaundice 3. Semaglutide - Oral
D Disulfiram like reaction
S SIADH

SGLT 2 inhibitors α glucosidase inhibitors Amylin analogue

"Gliflozins" Reduces intestinal Pramlinitide
Increases renal glucose excretion disaccharide absorption Decreases glucagon
Causes weight loss S/e : Diarrhea, Flatulence secretion
Side effects include : Contraindicated in IBD Delays gastric emptying
1. UTIs, Polyuria (osmotic diuresis) 1. Acarbose Increases satiety
2. Can cause Fournier's gangrene 2. Miglitol
3. Euglycemic DKA Glucagon release is
1. Canagliflozin stimulated by protein
2. Dapagliflozin rich meal
DKA vs HHS

Diabetic Keto Acidosis Hyperglycemic Hyperosmolar State

Presents with severe abdominal pain Presents with altered sensorium
Blood glucose : 250-300 Blood glucose : 500-600
HAGMA (due to keto acids) Normal acid base balance
Type 1 DM (usually first presentation) Type 2 DM (neglected elderly pt.)
Due to fever/stress Due to dehydration
Kussmaul's breathing High mortality (due to cerebral edema)

Management for both

FLIP : Fluids → Insulin → Potassium

Fluids
Start with 0.9% saline
Switch to dextrose when blood glucose <200

Insulin
Administred IV (no role of bolus)
Switch to s/c insulin when any one
is achieved
1. Able to eat
2. <200 glucose
3. Anion gap < 12
4. HCO³ > 15

Potassium
Start if serum potassium < 5.2
Stop insulin if serum potassium < 3.3

In DKA also find and treat the trigger

HCO³ considered if refractory acidosis
 Polydipsia - Polyuria
Urine osmolality
(Normal : 400-800)

< 400 > 800

Plasma osmolality
(Normal : 280) Diabetes Mellitus SIADH
Osmotic diuresis Water loading test :
T/t : Glycemic control ADH stays high

<< 280 >> 280 T/t: Water restriction

↓
Primary polydipsia Diabetes insipidus
Vaptans (V² antagonists)
Water deprivation test : Water deprivation test :
Urine Osmolality ⬆️ Urine Osmolality stays low
SIADH causes
T/t: Fluid restriction
Oxcarbamazepine >
Low Uric acid High Uric acid Carbamazepine
Chlorpropamide
Cyclophosphamide
Nephrogenic DI Central DI Vincristine
Nephrons can't Nephrons are normal SSRIs
reabsorb uric acid T/t: Nasal desmopressin Small cell lung Ca
T/t : Thiazide Pneumonia
Encephalitis
 Cushing's Syndrome
Raised Cortisol
MCC is exogenous steroid intake (anti-inflammatory action of steroids occurs only at high doses)

Hypothalamus
CRH

Ant pitutary
ACTH

Zona fasiculata
Cortisol

Cushing's work-up
Clinical features
Clinical Suspicion Osteopenia
Myopathy
Hypertension
Late night salivary cortisol Diabetes mellitus
or Screening test Moon face
24 hr urinary free cortisol
Buffalo hump

Muscle wasting
Normal Elevated
Rules out Cushing's Stretch marks
Supressed Low dose DST (1 mg) Confirmatory test
Obesity

Easy bruising
Not supressed
Osteopenia
ACTH levels

Low High
Adrenal cause
High dose DST (2 mg) Increased neutrophils
(because decreased
chemotaxis)
Decreased eosinophils and
Supressed Not supressed lymphocytes
Pitutary Adenoma Ectopic ACTH
(Cushing's disease) producing carcinoid

Pseudo Cushing's Metyrapone

Clinical features and cortisol 1. Obesity Inhibits glucocorticoid synthesis
levels are similar to Cushing's 2. Chronic alcoholism Treatment of Cushing's in pregnancy
Due to conditions that cause 3. Depression Ketoconazole
chronic activation of HPA axis 4. ESRD Antifungal used in the treatment of
Differentiator : High CRH Cushing's
Adrenal Insufficiency (Addison's disease)
Clinical Suspicion

Co-Syntropin test
Investigation of choice
(aka ACTH stimulation test)

Cortisol increases Low cortisol

Rules out Addison's

Serum ACTH levels

Low High
Secondary adrenal insufficiency Primary adrenal insufficiency
MCC : Chronic glucocorticoid therapy MCC : TB in India, elsewhere Autoimmune
ACTH low, hence no hyperpigmentation ACTH high, hence hyperpigmentation present
Aldosterone normal (RAAS active) Aldosterone low (hyperkalemia + hypotension)
Less severe symptoms More severe symptoms

Sheehan Syndrome

History of : PPH or severe blood loss

Pitutary ischemia (pan hypo pitutarism)
1. Low PRL : Failure to lactate
2. Low GnRH : Amenorrhea
3. Low ACTH : Fatigue, hypotension
4. Low GH : Hypoglycemia
Growth hormone is first hormone to fall
T/t : High dose glucocorticoids
If Visual disturbance present / altered Empty sella sign
consciousness : Urgent surgical decompression

Hyperaldosteronism - Conn's Syndrome

Hypertension + Hypokalemia

1. Malignant htn 1° hyperaldosteronism 1. ENAC activation: Liddle Sx

2. Renin producing 1. B/l adrenal nodular (Little ENaC)
tumor hyperplasia 2. CAH
2. Conn's syndrome 3. Exogenous mineralocorticoid
 Calcium Metabolism

Vit D ALP
Activated in renal tubules Produced in areas with bone formation
Increases levels of both calcium and phosphate In multiple myeloma no bone formation (ALP normal)
In Paget's there's continuous bone remodelling (ALP high)
PTH
Increases levels of calcium
Decreases levels of phosphate "Phosphate threshing hormone"

Serum Calcium
(Normal : 8-10)

<8 Normal > 10

Low PTH activity Low Vit D Excess Vit D Excess PTH activity
PO⁴ high PO⁴ low

PTH low PTH high PO⁴ low PO⁴ high

Sarcoidosis
Ectopic Vit D PTH high PTH low
1° Hypo Pseudo Rickets CKD production Parathyroid PTH related
Parathroidism hypo PTH (Kidneys can't adenoma peptide
H/o PTH receptors excrete phosphate)
Tc-99 Sestamibi scan Para-neoplastic
thyroid surgery? low/ abnormal XLD rickets is Hypophosphatemic Miami Criteria sx with
aka Vit D resistant rickets Squamous Cell ca.
PHEX gene mutation

Hyper-calcemic crisis
Serum calcium > 14.8
AMS + dehydration
Seen with malignancies
(rapid bone resorption

Pseudo-Pseudo hypo PTH Paget's Disease Osteoporosis

Everything normal Isolated ALP high Everything normal
Defect at CAMP level Low bone mineral density
Osteoporosis treatment

PTH hormone Estrogen

Osteoblast Osteoblast

RANK Ligand Osteoprotegrin Inhibition Steroids, thyroid hormones

Thyroid bone disease

Thyroid hormone causes
Osteoclast precursor Inhibits osteoclast formation
osteoclast activation
Osteopenia with
hyperthyroidism is
known as thyroid bone
Osteoclast disease
Produces acid protease
which cause bone resorption

Prevention of osteoporosis

Inhibition of osteoclasts Stimulate osteoblasts Inhibit osteoclasts

and
1. Bisphosphonates PTH 1-34 Stimulate osteoblasts
Longest acting : Zolendronate Novel anabolic drug 1. Strontium
(once a year tablet) that contains only a
Side effects sequence of 34 amino
2. Romosuzumab
acids in PTH hormone Inhibits sclerostin
1. Esophagitis (advised not to lie
down after taking the medication) Stimulates osteoblasts (Sclerostin inhibits blasts
2. Osteonecrosis of mandible and has no effect on and supports clasts)
3. Atypical femur neck fracture osteoclasts SR in ward has dual action
Available as s/c
2. Raloxifene (SERM)
injection
Selective estrogen receptor Eg. Teriparatide,
modulator Abaloparatide
No risk of malignancy,
dyslipidemia
Only side effect : risk of DVT

3. Denosumab
Monoclonal antibody against
RANK-L

4. Calcitonin
Reduces PTH
Lower bone resorption
 Thyroid Disorders
Suspicion of thyroid disorder
Grave's disease
TSH test LATS (Long acting thyroid stimulator antibodies)
Antibodies against TSH receptor (stimulates the
receptor)
Increased activity of the gland leads to
Hypo-thyroid Hyper-thyroid scalloping of colloids and beefy looking gland
(TSH : High) (TSH : Low)

USG neck RIU scan (I-123)

TIRADS score or
Tc99 Scan
FNAC
for high risk nodules
Bethesda grading

Scalloping of colloids
Normal Cold nodule
Risk of malignancy

Pyramidal lobe Hot nodule

Normal variant aka Toxic nodule
a/w GNAS mutation

Beefy looking gland

Graves disease Reduced uptake Thyroid eye disease (Grave's opthalmopathy)
Overactive thyroid
B/L proptosis
Retro-orbital fat deposits
Muscle belly hypertrophied but
Factitious Struma ovarii Thyroiditis tendons unchanged (coca cola sign)
Taking thyroxine Ovarian tumor Initital presentation Muscles involved in sequence : I M S L O
supplementation producing thyroid is transient M/c eye sign in Grave's : Dalrymple sign
hormones hyperthyroidism

Management of Grave's Disease

Muscle belly hypertrophied
Mainstay is Radio-iodine ablation using Iodine 131 (Recti > Obliques)
(c/i in pregnancy and severe thyroid eye disease)
DOC : Carbimazole / Methimazole Other complications
In pregnancy 1st trimester DOC : PTU
(Carbimazole can cause choanal atresia, cutis aplasia)
Surgery done in severe thyroid eye disease

Thyroid Acropachy Pretibial myxedema

(Periostitis) (GAG deposition)
 Thyroiditis

Auto-immune Infectious Others

De quervain thyroiditis Riedel's thyroiditis

Hashimoto's Sub-acute lymphocytic aka sub-acute granulomatous aka fibrous thyroiditis
thyroiditis thyroiditis thyroiditis Inflammation of the gland
aka "chronic" lymphocytic Painful and enlarged thyroid and normal tissue replaced
thyroiditis Occurs following a viral infection by fibrous tissue
Auto-antibodies against throid
gland
Causes non-reversible damage
to thyroid gland
MCC of hypothyroidism in
developed countries (in poor
countries it's Iodine def.)

Hashimoto thyroiditis

Thyroid eye signs

Stellwag Sign
Staring look

Joeffry sign
Absent forehead creases on upwards gaze

Jellnick sign 🔥 Stella - staring Joeffry - no stress

Hyperpigmentation of the superior eye folds
(no forehead crease)
Hertoge sign
Loss of the lateral third of eyebrows

Dalrymple sign
Retraction of upper eye lid
M/c sign asso. with Grave's opthalmopathy

Von graffe sign

Lid lag of the upper eyelid on down gaze

Mobius sign
Inability to converge
 Pheochromocytoma
Hormone secreting tumor of the adrenal glands
Clinical presentation : Headache (m/c)/ Sweating/ Palpitation
Initial investigation : Urine catecholamines (VMA)
Confirmation : Plasma metanephrines
Best to localise : MRI abdomen (light bulb sign)
Biopsy/FNAC is contraindicated
Best test for mets : MIBG scan (radio-nuclear scan)
Best test for extra-adrenal pheo. : DOPA - PET / DOTANOC PET
M/C site for extra-adrenal pheo. : Organ of Zuckerkandl (para aortic)
Treatment : α blocker ➡️ ß blocker ➡️ Surgery

Other light bulb appearances

Light bulb sign Zellballen appearance

seen on h/p

Rule of 10 for pheochromocytoma

Extra-adrenal : 10%
Not asso. with hypertension : 10%
Bilateral : 10% (50% are b/l in syndromic pheo)
Malignant : 10% Posterior dislocation of
shoulder

Syndromes asso. with pheochromocytoma

1. Von Hippel Lindau
2. NF-1
3. Men 2A, 2B
4. Familial paraganglioma syndrome (SDH gene mutation)

Liver hemangioma

Familial paraganglioma syndrome

CHAPTER 24
GENERAL
PHYSIOLOGY
Body fluid compartments
60% of body weight is water
Markers to measure total body water are 2/3 of TBW
1. D²O Can't be measured
2. T²O
3. Antipyrene

Total body water is further divided into 1/4 of ECF

Can be measured

Intra-cellular Extra-cellular
2/3 of total body water 1/3 of total body water
Inside cells, hence can't be Has more Na+, Cl- & Ca++
3/4 of ECF
measured Major buffer : HCO³- Can't be measured
Has more proteins Can be measured using :
More K+ & Mg++ Mannitol/Sucrose/Inulin
Higher acidity (lower pH) ECF is further divided into
Major buffer : Proteins

Interstitial fluid Plasma (in blood)

Major portion of ECF Minor portion of ECF
Can't be measured Can be measured using
1. RISA (Radio iodine
serum albumin)
2. Evan's blue

Plasma osmolarity
Normal value : 290 mosm/L Insensible loss of water
90% is due to Na+ Water loss from body via
Hence, can be empirically calculated as : 1. Evaporation from skin
2 X [Na+ conc] = 2 X [140] = 280 (≈ 290) (doesn't include sweating)
Serum proteins don't conribute towards 2. From lungs during breathing
osmolarity because of its low
concentration and high weight Quantity
500-600 ml/day
50 ml/hour
Calculation of Sodium deficit

*0.6 X (body weight) X (140 - Na+)

*0.5 for females

Eg. 70 kg person with [Na+] of 120 mosm/L

Na deficit = 0.6 X 70 X (140-120) = 840 mosm/L
Darrow Yannet Diagrams

Approach to D-Y diagrams

Total body water divivded into ICF (intra-cellular fluid)
and ECF (extra cellular fluid)
Any fluid lost or gained is from ECF compartment ICF ECF

Osmolarity
ICF and ECF have to maintain same osmolarity, hence
free water moves from more dilute to less dilute
comaprtment (like osmosis) Volume

Check if ECF volume contracted or expandede

Contracted Expanded

Loss of fluid Gain of fluid

Isotonic loss Hypertonic loss Hypotonic loss

ICF ECF ICF ECF ICF ECF

Overall osm. same Overall osm. reduced Overall osm. increased

Isotonic loss : No osm Hypertonic loss : ECF Hypotonic loss : ECF

change osmolarity reduced osmolarity increased
ECF gives free water to ICF ICF gives free water to ECF
Conditions :
to reach a common to reach a common
1. Hemorrhage
osmolarity osmolarity
2. Diarrhea
Conditions : Conditions :
1. Addison's dis 1. Sweating (H²O loss is more
2. Loop diuretics than Na+ loss in sweat)

Isotonic gain Hypertonic gain Hypotonic gain

ICF ECF ICF ECF ICF ECF

Overall osm. same Overall osm. increased Overall osm. reduced

Isotonic gain : No osm Hypertonic gain : ECF Hypotonic gain : ECF
change osmolarity increases osmolarity decreases
ICF gives free water to ECF gives free water to
Conditions :
ECF to reach common ICF to reach common
1. Isotonic saline infusion
osmolarity osmolarity
Conditions : Conditions :
1. 3% NaCl infusion 1. Polydypsia
2. SIADH
Equilibrium Potential
Nernst Equation Equilibrium potential of various ions in body
Used to calculate equilibrium 1. Na+ : 60mV
potential 2. Ca++ : 100mV
Formula : 3. Cl- : -70mV
4. K+ : -90mV
Most positive : Calcium
T : Temperature Most negative : Pottasium
Z : Valency
R,F : constants Resting membrane potential is most sensitive
to change in K+ concentration
in
[Conc] Hypokalemia : RMP more negative
+/- 61 log _______ Hyperkalemia : RMP more positive
[Conc] Out

Cell Signalling
Cell Signalling

Endocrine Paracrine Direct Signalling

Released into blood, Acts on nearby cells Acts on immediate cells
effect on distant sites
Juxtacrine

Eg. Somatostatin in stomach

Eg. TGF-α
Autocrine
A special type of paracrine signalling Via Gap Junctions or
where it acts on the same cell Plasmodesmata

Eg. PDGF released by platelets

 Cytoskeleton

Cytoskeleton

Micro-tubules Micro-filaments Intermediate-filaments

Responcible for movement 1. Actin : Muscle contraction Maintain structure of cells
and cell division 2. Microvilli : Cytokinesis Compose imp. IHC markers
"Moves through tube"
Cytokeratin : Epithelial
1. Cilia & Flagella Desmin : Muscle
2. Mitotic spindle Vimentin : Mesenchyme
3. Axoplasmic transport in GFAP : Neuronal
neurons
Keratin filaments present in Mallory Denk
bodies are also intermediate filaments

Cilia structure Drugs affecting Axoplasmic

mitotic spindle transport

Microtubules get
contracted very tightly
Retrograde Anterograde
Microtubules Mebendazole Dynein Kinesin
Get Griseofulvin
9 + 2 arrangement HSV HSV
Contracted Colchicine
Polio reactivation
Very Vinca alkaloids
C Tetanus
Tightly Taxane
Rabies
"Retro dine"
Basal body : Triplets

Ciliary dyskinesia
(Kartagener Syndrome)
Dynein arm of Cilia defect
Situs inversus
Bronchiectasis
Sinusitis
Infertility

Fundal bubble on right side

Regulatory Mechanisms

Regulatory mechanisms

Feed-back Feed-forward
(Anticipatory)
Cephalic phase of gastric acid secretion
Negative Positive
Anticipatory Tachycardia : an increase
feedback feedback
in heart rate that occurs in anticipation
Most common feedback 1. Parturition of an activity or event
1. Baro receptors 2. Coagulation cascade
2. Chemo receptors
3. Renshaw cells : Present
in spinal interneurons
and release Glycine

Organelles and Enzyme Markers

1. Mitochondria 5. Lysosome
Cytochrome - C oxidase Acid phosphatase
Succinate dehydrogenase Cathepsin
ATP synthase

6. Endoplasmic Reticulum
2. Cytoplasm Glucose-6-phosphatase
LDH

7. Plasma membrane
3. Golgi apparatus Na-K ATPase
Galactosyl Transferase Adenylyl cyclase
5' Nucleotidase

4. Peroxisome
Uric acid oxidase 8. Nucleus
Catalase RNA polymerase
"Pero, U-R a Cat" Histone deacetylase
 Sarcomere structure
Z - line M - line Myosin Actin Z - line M - line

I - Band A - Band H - Zone I - Band A - Band

Contains Contains
1. Z line 1. Actin (thin filament)
2. Myosin (thick filament)
3. M line
4. H zone (zone with only
Myosin)

Individual G-actin
(globular)
During contraction
1. I band shortens "I contract"
2. H zone disappears "H hides"
3. A band stays constant, M line becomes
more prominent.

Troponin absent in smooth muscles

Cardiac muscles have both α and β myosin

Excitation-Contraction coupling
Excitation-Contraction Coupling (ECC) links muscle fiber excitation to contraction.
Occurs in both skeletal and cardiac muscle function

Steps of ECC Action potential

1. Depolarisation of plasma membrane of muscle fiber

2. The action potential travels along the sarcolemma and down Na+
Sarcoplasmic
the T-tubules (transverse tubules) Ry-R
DHPR Reticulum
3. The action potential activates dihydropyridine receptors Ca² Ca² Ca²Ca²

(DHPR) on the T-tubules SERCA

pump
4. DHPR receptors are coupled with Ryanodine receptors in T tubule uses ATP
Ca²
sarcoplasmic reticulum and cause opening of Ca²+ channels
of sarcoplasmic reticulum
5. Concentration of Ca²+ in cytosol increases
6. Calcium binds to trop-C and exposes binding site of Actin
"Cytosolic Calcium is crucial for contraction"
7. Actin-Myosin cross bridge formed and myosin pulls actin.
8. Attachment of ATP to myosin causes release of actin filament Calcium : Contraction
"ATP is crucial for relaxation" ATP : Relaxation
(Absence of ATP : No relaxation)
Skeletal muscles : electro-mechanical coupling, RyR1 receptors Eg. Rigor mortis
Cardiac muscles : electro-chemical coupling, RyR2 receptors
Muscle contraction

Muscle twitch
Muscle twitch occurs following a single
action potential and consists of 3 phases
1. Latent phase
2. Contraction period (from latent period
to point of maximum contraction)
3. Relaxation

Tetanising frequency = ___

1
Contraction
period

Summation Treppe
When a muscle fibre is stimulated before it aka Staircase phenomenon
has relaxed completely. When a muscle fibre is stimulated exactly at
(Results in a stronger contraction) the end of relaxation phase,
(Results in increased tension and better
Another action efficiency of the muscle)
potential
Action potential
"Basis of warm-up exercises"
Increased force generated
by the second twitch
(summation)
Force (N)

Time

Tetanus
Tetanus, tetany or tetanisation is the term
given to when new action potential arrives
before relaxation period.

Frequency of stimulus required for teatnus

is known as tetanising frequency

Tetanising freq =
___
1
Contraction
period

Types of Muscle fibres

Type-1 (Slow) Type-2 (Fast) Slow

Red muscles S Slow White muscles
↑ Blood vessels I Type 1 ↓ Blood vessels
R Red Fast Intermediate
↑ Myoglobin ↓ Myoglobin
↑ Mitochondria ↓ Mitochondria
Oxidative metabolism Glycolytic metabolism
Muscle reflexes
Stretch reflex Inverse - Stretch reflex
Type of a spinal reflex (doesn't involve brain) Also a spinal reflex
Causes muscle contraction in responce to stretch A reflex causing muscle relaxation in response to
(responsible for normal muscle tone) excessive tension (protective mechanism during
Sensory receptor : Muscle spindle heavy lifting)
Stimulus : Stretch "Duh!" Sensory receptor : Golgi tendon
Stimulus : Tension "Tendon - Tension"

Monosynaptic Bi-synaptic reflex

reflex
Type : 1b
Type : 1a

Agonists (+)
Agonists (-)
Antagonists (-)

Withdrawal reflex
Also a spinal reflex
A protective response that pulls a body part away from
harmful stimuli, like touching something hot or sharp.
Stimulus : Pain receptors
Flexors activated and Extensors inhibited
It's a polysynaptic reflex
CHAPTER 25
GENERAL
PATHOLOGY
Vacutainers
Vacutainer Additive Inversion Uses

Sodium citrate - 3.2 % 3 Coagulation Studies

Sodium citrate - 3.8 % 3 ESR estimation

Silica gel 5
Serum
Silica gel 5 Analysis
Lithium heparin
(Lithium -Light) 8
Plasma assays
Sodium heparin 8
(ABG, Osm fragility test)

EDTA 8 CBC, HbA1c

EDTA 8 Blood bank

EDTA 8 Rare elements analysis (As, Cu)

NaF (inhibits enolase)

8 Blood sugar tests
Pottasium Oxalaate

Ageing
Telomere shortening is responsible for ageing
Hayflick limit : Telomere can replicate 50-60 times before shortening

Free radical mediated damage is also responsible for ageing

Sirtuins prevent free radical damage
Sirtuins level increase with fasting and red wine
Gram Staining / ZN staining

Gram Staining
Come in and Stain

ZN Staining
CAMe

Carbol fuscin Heat Acid-alcohol Meth. blue

Primary stain (fixing) Decolouriser Counter stain

If H²SO⁴ is used instead

for fixing
↓
Kinyoun's Method
aka modified ZN, Cold ZN
Used to stain filamentous bacteria
(Actinomyces, Nocardia)
Stains

Fat staining

Oil-Red-O stain Sudan Black Sudan IV

Metal staining

Calcium Copper Iron

On routine H/E staining, (Hemosiderin)
calcium is basophilic
Alizarin Red used for
minimal calcifications

RhodaNine stain
Perl's stain
(Prussian blue)

Von Kossa

Rubeonic acid

RhodaMine :
used to stain acid fast bacilli
Alizarin Red

Amyloid staining

Congo red stain Bielchowsky Stain

Stains amyloid : Salmon pink Stains amyloid ß plaques in
Under polarised light shows apple green birefringence Alzheimer's disease
Special Stains

Masson trichome Masson fontana

Collagen : Blue Stains melanin
Nuclei : Black Melanin also stained by :
Muscles : Red Schmel's stain, DOPA oxidase

Movat's pentachrome stain Sweet's reticulin stain

Stains various layers of vessels Stains reticulin (Type 3 collagen)
Used to detect vascular pathologies in liver

Toluidine blue Acridine orange

Detection of mast cells Stains DNA and RNA
Also stains pre-cancerous lesions DNA also stained by : Feulgen stain

Lipofuscin stain PAS - Diastase stain

Yellow brown pigment from lipid peroxidation Only glycogen is PAS (+) and diastase sensitive
Peri-nuclear staining Everything else which is PAS positive is diastase
Represents wear and tear, common in aging cells resistant
 Calcification

Calcification

Dystrophic Metastatic
calcification calcification
Associated with destruction of tissue Associated with hypercalcemia
Psammoma bodies present Usually diffuse Calcification
Serum calcium is normal Psammoma bodies are absent
eg - 1. TB lymph nodes Involves : Lungs > Kidney, Stomach mucosa
2. Atherosclerosis Seen in all conditions that cause hypercalcemia
3. Monckeberg sclerosis of vessels such as : 1. PTH adenoma (sestamibi scan)
(doesn't cause lumen narrowing) 2. PTHrp (small cell ca of lung)
4. Rhuematic heart disease 3. Sarcoidosis (excess vitamin D)
5. Tumors 4. Paget's disease
5. Milk alkali Syndrome

Psammoma bodies

" (PSM)² "

P Papillary carcinoma (orphan annie eye nucleus)

P Prolactinoma (most commom functional pitutary tumor)

S Somatostatinoma
S Serous ovarian tumors

M Mesothelioma (asbestosis)
M Meningioma (m/c benign CNS tumor in adults)

Amyloidosis
IOC in systemic amyloidosis: Abdominal fat staining

Primary amyloidosis AL chain (Light chain) Multiple myeloma

Amyloidosis in spleen
Secondary amyloidosis AA chain Chronic inflammation (TB, IBD, Bronchiectasis)
Dialysis-related amyloidosis A-ß² chain Hemodylaser unable to filter ß² microglobulin
Alzheimer disease A-ß chain 1 brain 2 kidneys Deposition in Deposition in
Type 2 diabetes mellitus IAPP-Islet associated polypeptide red pulp white pulp
Medullary thyroid cancer A-calcitonin
Lardaceous Sago
Isolated atrial amyloidosis A-ANP
spleen spleen
Systemic senile amyloidosis A- TTR (transthretin)
 Cell Injury
Most common cause of cell injury is ischemia

Ischemia...

1st step : Hydropic change (reversible)

In ischemia, ATP pumps stop functioning due to low ATP
causing cellular swelling (cytotoxic edema)

2nd step : Ribosomal detachment (reversible)

reduced protein production.

3rd step : Myelin figures (reversible)

aggregation of phospholipids from membranes

4th step : Plasma membrane damage (irreversible)

5th step : Mitochondrial permeability increased (irreversible)

Amorphous densities on EM

6th step : Nuclear degradation (irreversible)

Chromatin condensation : Pyknosis
Nuclear fragmentation : Karyorrhexis
Nuclear lysis : Karyolysis

...Cell death

Cell Adaptation

Muscle cells undergo Hypertrophy

α-isoform of myosin heavy chain
replaced by ß-isoform in hypertrophy

Muscle|Size|Trophy
 Apoptosis (Programmed cell death)

Extrinsic Pathway Intrinsic Pathway

Receptor mediated Mitochondria mediated
8-10sic i92rinCic
receptor mitochondria
Caspase 2
TNF/ FAS

Induce executioner Reduced permeability of

caspase mitochondrial membrane

↑ expression : BAD/BIM, BAX/BAK, P⁵³

Caspase 8/10 Cytochrome C ↓ expression : BCL²

Caspase 9

Caspase 3/6/7 Over expression of BCL- 2 : B cell lymphomas

Under expression of P-53 : Li Fraumani Sx
Glucocorticoids : Pro - apoptotic
Apoptosis Sex Corticoids : Anti - apoptotic
(Cell size decreases, Inflammation absent)

Protein present in caspase : Cysteine

Hallmark feature of apoptosis : Chromatin condensation

Physiological apoptosis :Embryogenesis, Breast/endometrium involution

Apoptosis
(sex corticoids are anti-apoptotic)

Control

Necrosis
Pathological apoptosis : DNA damage, Viral hepatitis (councilman bodies)

Gel electrophoresis : Step ladder pattern (Necrosis has a smear pattern)

Stain : Annexin V, DAP-i

Apoptosis with inflammation Apoptosis has many

1. Necroptosis : RIPK-1 and MLKL (programmed necrosis) "steps"
2. Pyroptosis : Caspase 1,4,5,11 (bacterial infection)
3. Ferroptosis : Iron involved

Necrosis

Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat necrosis Fibrinoid necrosis
Most common type Brain abscess TB (mycolic acid in cell wall) Saponification of fat Vasculitis (PAN, HSP)
MI / Renal infarct Histoplasma, Nocardia Calcium deposits Malignant hypertension
Pancreas, breast

Dry gangrene : Coagulative necrosis

Wet gangrene : Liquefactive necrosis
Inheritance patterns
All neuro-cutaneous syndromes
(except Sturge Weber syndrome)

Marfan Sx
Achondroplasia

Ehler Danlos
Osteogenesis imperfecta
No gender preference : Autosomal
MEN syndromes
No skip generations : Dominant
Myotonic dystrophy
Autosomal dominant
Hereditary Spherocytosis
Huntingtons's chorea

Leber syndrome
LHON
MELAS
Kearns Syre Syndrome
Pearson Syndrome
DIDMOAD (aka Wolfram Syndrome)
Only maternal transmission : Mitochondrial
Mitochondrial

Gender preference to females : X linked Gender preference to males : X linked

No skip generations : Dominant Skip generations present : Recessive
X linked Dominant X linked Recessive

Dominant father gives Recessive father saves for his

everything to daughters grandson only

Rett's Syndrome (MECP 2 gene) Duchene muscular dystrophy G6PD deficiency

Alport Syndrome Lesch Nyhan (HGPRT) Fabry's, Hunter's
Vit D dependent rickets Menke's kinky hair
Incontinentia pigmenti Wiscott Aldrich
Hemophilia (A and B)
Color blindness
 Trinucleotide repeat disorders

Huntington's chorea Fragile X syndrome Myotonic Dystrophy Friedrich ataxia

Cerebral ventricles enlarged Mitral regurgitation Hatchet facies Pes cavus
(box shaped ventricles) Mental retardation Frontal baldness Halus valgus
Caudate lobe affected Increased size of Testicular atrophy Scoliosis
Manifests primarily as Gonads and ear Christmas tree cataract HOCM : mcc of death
movement disorders

CAG repeat CGG repeat CTG repeat GAA repeat

Hunter in a CAGe Congenital Giant Can't Terminate Fredie Mercury
Gonads Grip GAAta tha
Chromosome 4
Huntington gene FMR (familial mental Chromosome 19 Chromosome 9
AD inheritance pattern retardation) gene DMPK gene FRATAXIN gene
X linked inheritance AD inheritance pattern AR inheritance pattern
It's the most common genetic
cause of mental retardation

Complement Pathway
1. Classical pathway : Antibody mediated C3b (opsonin) is common for all pathways
2. Alternate pathway : Microbe antigens C5a and C3a cause inflammatory responce (a : inflammation)
3. BTR by Dr.: Mannose
Lectin pathway Zainabbinding
Voralectin MAC causes lysis of microbe General Pathology

Alternative C5a, C3a: Inflammation

Microbe
pathway
Destruction of microbes
by leukocytes

C3b C3b causes

Phagocytosis
Classical
C3b
pathway

C3b is deposited
on microbe
Antibody

Lectin MAC causes

Formation of Lysis of microbe
pathway Mannose
membrane attack
binding lectin
complex (MAC)

MAC deficiency : Neisseria infection ↑

C1 INH deficiency : Hereditary angioedema
 Immunology
Lymphocytes T- regulatory cell
Suppress immune response.
Prevents auto-immunity
Secrete IL-10, TGF-ß and
B Cells T Cells express CD 25 and FOX P3.
Mature in lymphoid organs Mature in thymus FOX P³ mutation : IPEX syndrome
One of the antigen presenting cells
Produce antibodies (plasma cells)
Memory CD 8 T cells CD 4 T cells
Cyto-toxic Helper
(Perforin -granzyme)

Important CD Markers
Blast : CD-34 and HLA-DR Th 1 Th 2
34 yr old Dr at blast site Cell mediated immunity, granuloma Humoral immunity, eosinophils
T cells : CD (1-8, 28)
Produces IL 2,12 and IFN γ IL 4, 5, 13 : Recruit Eosinophils
1 to 8 and 28 2 X 4 + 5 = 13
forms Granuloma
B cells : CD - 10, 20(19-23), 40, 80(79a,79b) Do - baara - Granuloma IgE and IgA class switching in B cels
10 20 40 80 Recruits macrophages Involved in Parasite killing
NK cells : CD 16, 56, 94 IgG class switching in B cells Produces anti inflammatory
16 ka dola, 56 ka chest, weight 94 Inhibits Th2 IL - 10 and IL - 4
Myeloid cells : CD 13, 33
3 rotated forms M
Monocytic cells : CD 11, 14, 64 Interleukins
Single (1 and 1) on Feb 14 till age 64
Th1 : IL 2, IL 12, IFN γ Do baara granuloma
Megakaryocyte : CD 41 and 61
Th2 : IL 4, IL 5, IL 13 2 X 4 + 5 = 13
M416
Pyrogens : IL 1, IL 6, TNFα 16 yr hot alpha
Anti inflammatory : IL 4, IL 10, TGFβ Chaar das bas

Chemokines : IL 8, C5a Clean up on isle 8

MHC
Opsonins : C3b, IgG C3b sauce
MHC class 1 MHC class 2

Immunoglobulins
IgM
B cell receptor (along with IgD)
Pentamer (max weight)

IgD
Presents in all Presents in all APCs
B cell receptor
nucleated cells (Dendritic cells,
(except platelet, sperm) Macrophages, B cells) IgG
Cleft made only of α Cleft made of both alpha
Maximum concentration
chains 1-α and beta
Most crucial for secondary immune response
Presents to CD 8 Presents to CD 4
Can cross the placenta
1X8=8 1X8=8 Opsonisation
2X4=8 2X4=8
IgA
Present in secretions
MHC class 3 Dimer in secretions while monomer in serum
Encode for secreted proteins that have immune
functions. Ex. Complement proteins, cytokines, HSP IgE
Do not play role in presentation of antigenic peptides Type 1 hypsñ rxn
Anti helminthic
Hypersensitivity reactions

Type 1 Type 2 Type 3 Type 4

IgE mediated Ab mediated Ag-Ab complex T cell mediated
mediated

IgE causes mast 1. Myesthania Gravis 1. Arthus reaction 1. Contact dermatitis

cells degranulation 2. Grave's disease 2. SLE 2. GVHD
3. Pemphigus 3. IgA Vasculitis 3. Chronic transplant
1. Allergy, Atopy, 4. Hyper-acute 4. PAN rejection
Asthma, ABPA transplant 5. PSGN 4. All skin tests
2. PK allergy test rejection
3. Casoni test 5. Good Pasteur Sx
(Hydatid cyst) 6. AIHA

Transplant Immunology

Transplant rejection

Hyper-acute Acute Chronic

On operation table Weeks to months After years
Preformed Abs Can be either cell mediated Due to cell mediated
(Type 2 hypersensitivity) or humoral (Type 4 or 2) immunity (Type 4)
Intra op thrombosis Intimal thickening
(Blue kidney) Fibrosis of graft vessel
H/o multiple blood Atherosclerosis
transfusions/ multi-parity

Types of donor grafts

1. Auto-graft : Self
2. Iso-graft : Identical twin Most important HLA to match : HLA DR
3. Allo-graft : Same species (not needed in Cornea, heart, lungs)
4. Xeno-graft : Different species

Graft VS Host disease

Graft attacks immunocopromised host
Stem cells in graft form new blood cells
m/c organ affected: Skin > Liver, BM
Billingham criteria
 Immuno-deficiency disorders

Hyper IgM sx Immunodef. + Hyper IgE

Problem with class switching
Defective B cells and Th cell interaction (CD40-CD40L)
CD - 40 absent
Wiscott Aldrich Sx Jobb Sx

Combined immuno deficiency

both B and T cells absent
Absent germinal centres / thymus
Recurrent infections since birth

WASP gene Cold abscess

XLR disorder Retention of primary teeth
SCID Di-George Sx T Thrombocytopenia Eczema (High IgE)
Adenosine deaminase Abnormal facies I Immunodeficiency
(ADA) def Hypocalcemia E Eczema (High IgE)
CATCH 22

Phagocyte Dysfunction

Chediak Higashi Syndrome Leucocyte Adhesion defect Chronic Granulomatous

disease
Catalase (+) organisms
NADPH oxidase deficiency
LAD 1 LAD 2
No respiratory burst
Adhesion defect Rolling defect

Integrins Selectins
ICAM-1 Sialyl Lewis
Failure of fusion of phagosome with CD 18
lysosome (microtubule defect) LFA 1 Bombay blood group
Lyst gene mutation Short stature
Asso. with albinism, neurodegeneration Delayed separation of
Neutrophil dense granules umbilical cord
Neutrophilia
No pus formation

B Cell maturation defect

Bruton's a-gamma Selective IgA

globulinemia deficiency
BTK gene defect Most common
Boys affected (XLR) immunodeficiency disease
Absent germinal centres Giardiasis
(no tonsils) Anaphylaxis with BT
Neoplasia

Tumor Markers
AFP : HEMAN H Hepatoblastoma/HCC
HCG : Chorio-carcinoma E Endidermal sinus tumor/yolk sac tumor
Calcitonin : Medullary thyroid cancer M Mixed GCT
NSE/Chromogranin : Neuroendocrine tumors A Acute tubular necrosis
CEA : Ca colon / Ca Pancreas N Neural tube defect
Ca 125 : Ovarian (epithelial) cancer
Ca 15-3, Ca 27-9 : Breast cancer (breast easily divisible)
Ca 19-9 : Pancreatic cancer (9 looks like P)
Ca 72-4 : Stomach cancer
NMP 22 : Bladder cancer

Carcinogens
Aflatoxin : HCC
Arsenic : Lungs, Skin
Vinyl chloride : Hepatic Angiosarcoma
Benzidine : Urinary bladder
Benzene : ALL

B : Burns, Skin cancer

Features of malignant transformation A : Ageing
1. Anaplasia (lack of differentiation)
2. Pleomorphism
3. Increased N/C ratio
4. Hyperchromasia
5. Increased mitosis
6. Loss of polarity

Metaplasia
Reversible cell change

Squamous metaplasia Coloumnar metaplasia Connective tissue metaplasia

Myositis ossificans
(bone formation inside
muscle tissue after trauma)

1. Airways : Chronic smoking

2. Urinary bladder : Bladder stones 1. Barrett's esophagus
3. Cervix : Low pH (Chronic GERD)
CHAPTER 26
GENERAL
PHARMACOLOGY
Important Graphs

Effective at
lower dose Effective but
at higher dose

HELP
Height - Efficacy
Left - Potency
Least effective

Plasma conc. VS time graph

"Area under curve" denotes bioavailability
Dose-response curve
IV route : 100% bioavailability
Potency and efficacy of drugs can
SC/IM route : 75% bioavailability
be compared with this.
Oral route : >5 but <100 bioavailability
Potency (left) : X > Y > Z
Efficacy (height) : X = Y > Z
Pure agonist
DRC can also be used to determine
competitive vs non competetive anatagonists

Partial agonist

Antagonist

Inverse agonist
Competitive Non - competitive
antagonist antagonist
(reduced potency) (reduced efficacy)
Dose-response curve
"Compotency"
To compare effect of various drugs on a receptor

Therapeutic Index (TI)

TI in animals = LD⁵⁰ (Median lethal dose)

ED⁵⁰ (Median effective dose)

TI in humans = TD⁵⁰ (Median toxic dose)

ED⁵⁰ (Median effective dose)
"Toxic people on top"

Drugs with narrow therapeutic index :

Logarithmic Dose-response curve
Lithium
Used to determine Therapeutic index MgSO⁴
Theophylline
 Apparent volume of distribution
Indicates the extent to which a drug distributes into tissues versus remaining in the plasma.

Vd = Amount of drug in body

Plasma drug conc.

Drugs with high Vd distribute extensively into tissues (e.g., lipophilic drugs).
Drugs with low Vd are largely confined to the plasma (e.g., hydrophilic drugs or highly protein-bound drugs).

blood = B"low"d
tissue = T"high"ssue

Application of Vd
1. Loading dose = Target conc X Vd Maintenance dose = Target conc X Clearance
2. Clearance = Vd X Elimination const.
3. Half life = (0.7 X Vd) / Clearance

Drug Metabolism

Drug can be either

P Glycoprotein pump
Hydrophobic Hydrophilic Other names of P-glycoprotein pump
1. ATP binding casette (ABC) as it uses
ATP to remove drugs from cells.
Highly Slightly 2. Multi drug resistance protein (MDR1)
Hydrophobic Hydrophobic because it causes resistance to
chemotherapy.
3. CD-243
Phase 1 metabolism
Oxidation/reduction
Hydrolysis Increased PGP expression reduces
drug absorption
Slightly Decreased PGP expression causes
Hydrophobic increased absorption

eg. Digoxin excreted by PGP, inhibition

Phase 2 metabolism
causes toxicity
conjugation
Glucoronidation
Acetylation
Methylation
Sulfation
"GAMS"

Conjugated

excreted through excreted through

bile or urine kidney
CYP enzyme
Cytochrome P450 enzymes aka CYP enzymes
Catalyze Phase I reactions, particularly oxidation reaction, in metabolism of hydrophobic drugs.
Major CYP enzymes include
1. CYP3A4 : Metabolizes > 50% of clinically used drugs.
2. CYP2D6 : Antidepressants (SSRI), opioids, Beta blockers
3. CYP2C9 : Warfarin, phenytoin
4. CYP2C19: NSAIDs, Clopidogrel, PPIs

CYP enzyme inducers vs inhibitors

Inducers Inhibitors
"GPRS" Compare to GPRS
G Griseofulvin Ketoconazole
P Phenobarb., Phenytoin Valproate
R Rifampicin Isoniazid
S Smoking Cimetidine, Omeprazole

Kinetics

Zero order 1st order

Amount of drug eliminated Fraction of drug
is constant eliminated is constant
T½ decreases as T½ is constant
concentration decreases Most drugs follow this
Only Ethan0l shows true
"First - Fraction
zero order elimination
constant"
Other drugs that show zero
order elimination are known
Steady state of a first order drug
as Pseudo zero order
When the rate of drug
availability in the body and
First order but behaves like zero order at
elimination from the body are
high concentration
equal
W Warfarin Achieved after 4-5 T½
A Aspirin
T Theophylline
T Tolbutamide
Power Phenytoin
 ANS Pharmacology

Sympathetic Parasympathetic
Nervous System Nervous System
Pre-ganglionic is always acetylcholine
Preganglionic Preganglionic (acts on nicotinic Ach receptor)
Neuron Neuron Post-ganglionic

Acetylcholine
Sympathetic
Neurotransmitter : Noradrenaline
Postganglionic Nicotinic Receptor : Adrenergic receptors
Postganglionic
Neuron Acetylcholine (except sweat glands that use Ach)
Neuron
Receptor

Parasympathetic
Neurotransmitter : Acetylcholine
Receptor : Muscarinic Ach receptors
Norepinephrine
Adrenergic Muscarinic
Acetylcholine
receptor Acetylcholine
Target tissue Receptor

Adrenergic Receptors Muscarinic Receptors

Post-ganglionic sympathetic receptors Post ganglionic parasympathetic
Divided broadly as α and ß receptors receptors
Functions Classified as M1-M5
Functions
α receptor ß receptor
Excitatory Inhibitory
α1 α2
Vasoconstriction Negative M1, M3, M5 M2, M4
Mydriasis feedback to
IP³ DAG pathway & uses cAMP pathway & uses
Urinary retention sympathetic
phosphotidyl inositol adenylyl cyclase
Ejaculation system
M1 : CNS M2 : Heart
M3 : Smooth
muscles & glands
ß1 ß2 ß3
(M4, M5 function is not known)
Stimulate Heart Bronchial relaxation Bladder
Renin secretion Vasodilation relaxation
Reduce secretions
1 heart 3 makes
Hyperglycemia
bladder
Tocolytic
free
2 lungs

Vasoconstriction : α-1 2s are always different

Vasodilation : ß-2 α-2 : Anti-adrenergic
Prevents hypoglycemia : ß-2 ß-2 : Vasodilation
Warning symptoms of hypoglycemia M-2 : Inhibitory
Tachycardia & palpitations : ß-1
Tremors : ß-2
Sweating : M-3

Hence, sweating is the only warning sign for

hypoglycemia in a patient on ß-blockers.
 Drugs acting on sympathetic system

Agonists (ß blockers)

ẞ² > ẞ¹ 1. Timolol
For asthma t/t : Albuterol, salmeterol, terbutaline Used in Glaucoma
As tocolytic : Ritodrine, Isosuxprine
2. Propranolol
ẞ¹ > ẞ² : Dobutamine DOC for
DOC for cardiogenic shock Performance anxiety
Essential tremors
ẞ > α : Epinephrine Migraine proph
Anaphylactic shock - 1: 1k (SC or IM) Thyrotoxicosis
ACLS protocol - 1: 10k (IV) Akathisia
Local anesthesia - 1: 100k Portal htn

α¹ > α² > ẞ¹ (no ẞ²) : Norepinephrine

Potent vasoconstriction Contraindications for ẞ blockers
DOC for Septic Shock 1. Bradycardia, AV block : will further slow down
heart conduction
α¹ > α² : Phenylephrine
2. Asthma : ß² responsible for bronchodilation
For mydriasis (eye drops)
(blocking it will cause further bronchoconstriction)
ẞ¹ = ẞ² : Isoproterenol 3. PVD : ß² responsible for vasodilation
ß¹ : increases SBP (blocking it will cause further vaso-constriction)
ß² : decreases DBP 4. DM : Masks signs of hypoglycemia
Wide pulse pressure 5. Prinzmetal angina : ß² responsible for vasodilation
(blocking it will cause further vaso-constriction)
ẞ³ : Mirabegron 6. Acute CHF : it's used for chronic CHF
Bladder relaxation

D¹ : Vasodilation (max in renal vessels) 2nd generation ẞ blockers

D > ẞ > α : Dopamine "DBA" Blocks only ẞ¹
DOC for cardiogenic shock + oliguria Relatively safer in asthma, PVD
Drugs include :
D¹ : Fenoldopam 1. Bisoprolol
Used in Hypertensive crisis 2. Carvedilol
3. Metoprolol

(α² agonists) : Have anti-adrenergic action ẞ blocker toxicity

Symptoms include
α²: Clonidine Bradycardia, Hypotension
Used in Hypertensive emergency Arrhythmias
Psychiatric conditions : ADHD, Tourette Sx Hypothermia, Hypoglycemia
Seizures
α²: α-Methyldopa
DOC for toxicity : Glucagon
Used for hypertension in pregnancy

( α blockers)

Non selective α blockers Selective α blockers

1. Phenoxybenzamine used for pheochromocytoma
(A before B) "Vasomotor reversal of Dale" Selective α1-blockers Selective α2-blocker
2. Phentolamine : DOC for Cheese reaction & clonidine 1. Prazosin : DOC for scorpion bite Mirtazapine : antidepressant
withdrawal htn 2. Tamsulosin : DOC for BPH with minimum sexual s/e
 Drugs acting on parasympathetic system

Cholinergic drugs Anti-cholinergics

Directly acting Indirectly acting cholinergics Drugs causing

cholinergics (Block Ach Esterase) mydriasis
1. Atropine (Strong mydriatic,
Pilocarpine hence used in kids)
Causes miosis Drugs used to Other drugs 2. Hom-atropine
Used in aungle treat Alzheimer's 1. Neostigmine : Reversal of 3. Tropicamide (short acting and
closure 1. Donepezil neuromuscular block less potent, used in adults)
glaucoma 2. Rivastigmine (also used for post-op ileus &
3. Galantamine snake bite) Other drugs
2. Pyridostigmine : t/t of
"Dr.G" 1. Benzatropine (aka Trihexyphenidyl) : EPS
myesthania gravis
associated with antipsychotics
Rivastigmine comes as 3. Physostigmine : t/t for
2. Glycopyrrolate : Reduce post op secretions
transdermal patch Datura poisoning (crosses BBB)
3. Hyoscine (Scopolamine) : Motion sickness
Aducanumab is a new 4. Edrophonium : Short acting,
4. Dicyclomine : Morning sickness
monoclonal antibody hence used for diagnosis of
5. Ipratropium & tiotropium : COPD/Asthma
approved for myesthania gravis.
Alzheimer's 5. Varenicline : Anti smoking drug
6. Organophosphates and
carbamates : irreversible AchE
blockers

Drugs acting on bladder

Receptors on bladder

Adrenergic Muscarinic

ẞ³ receptor α¹ receptor M³ receptor

Relaxes bladder (can't pee) Present on prostatic Contracts bladder (too much pee)
Agonist : Mirabegron urethra and causes
(used for urge incontinence contraction of urethral
Agonist Antagonist
/ overactive bladder) sphincter (can't pee)
α¹ blocker : Tamsulosin
Bethanechol (used for urge incontinence /
relaxes the urethral
(used for flaccid bladder) overactive bladder)
sphincter (reduces dynamic
"SOFT-D"
component of BPH) "Bethany called for a
flaccid bladder" S Solifenacin
Finasteride reduces the static O Oxybutynin
component of BPH F Flavoxate
T Tolterodine
D Darfenacine
Atropine poisoning (Anti-chol. poisoning)
Atropine is active ingredient in datura plant
Competitive inhibition of Ach (anti-cholinergic)
poisoning
Presenting features
1. Dry mouth/eyes
2. Hyperthermia
3. Tachycardia (M² blocked)
4. Delirium
Datura flowers Datura fruit
Treatment : Physostigmine (indirectly acting
cholinergic drug)

Organophosphate poisoning (Chol. poisoning)

Organophosphates are present in various
pesticides and insecticides
Indirect cholinergic action (cause irreversible
blockade of Acetylcholine esterase)
Presenting features
1. Excess secretions (Lacrimation, salivation,
sweating, urination, diarrhea)
2. Pin point pupil (characteristic feature)
3. Bradycardia (M² action) OP poisoning patient
Treatment : Atropine (anti cholinergic drug) "drowns in their own secretions"

Cocaine
Only indirect adrenergic (Inhibits reuptake of NE)
Only Local anaesthetic that causes vaso-constriction.
Overdose causes sympathetic symptoms (tachy, mydriasis, htn, MI)
Cocaine bugs (tactile hallucinations → Ekbom syndrome)
May cause palatine perforation (due to vasoconstriction)
 Opioids
Opioid receptors
Full agonists
1. Morphine
2. Pethidine
Mu ( ) Kappa Delta 3. Heroin
Physical dependence Miosis Antidepressant 4. Meperedine
Euphoria Dysphoria effects 5. Methadone
Resp & Cardiac depression (dissatisfied 6. Codeine
Constipation feeling) 7. Fentanyl
Sedation Sedation

Analgesia shown by all opioid receptors Partial agonists

1. Buprenorphine
(DOC for Morphine
dependence)

Conditions where opoioids are contraindicated

Antagonists
1. Billiary colic 1. Nalaxone (IV)
Causes sphinter of Oddi spasm 2. Naltrexone (oral,
Can lead to bile duct rupture longer acting)
Pethidine can be used
2. Head injury
Can cause resp. depression
CO² retention Methadone
3. Asthma DOC for long term withdrawal
Histamine released can exaggerate broncho-constriction Long acting , rapid action
Also an SSRI and NMDA antag.
4. MAO inhibitors
(used for neuropathic pain)
Pethidine is avoided when patient is on MAO-I
(Pethidine is metabolised by MAO)
Can lead to seizures Tramadol
Has dual mechanism for analgesia
1. Opioid action
2. SNRI action
S/e : Serotonin Sx
Side effects of opioids
Pruritus due to histamine release
S/e that persist even in tolerance : Miosis and Constipation
Specific side effects
1. Mydriasis : Meperidine
2. Serotonin syndrome : Tramadol
3. Wooden chest syndrome : Fentanyl
 Anti-Cancer drugs
Anti-cancer drugs

Inhibits cell cycle Cytotoxic drugs

(G¹ - S - G² - M) (Independent of cell cycle)

Platinum Compounds Alkylating agents Anthracyclines

1. Cisplatin Form covalent bonds within DNA that interferes 1. Doxorubicin
Most emetogenic with transcription and replication (aka Adriamycin)
Nephrotoxic 2. Daunorubicin
1. Cyclophosphamide (N² mustards)
Ototoxic
S/e : Hemorrhagic cystitis & S/e : Cardiotoxicity
2. Carboplatin Pulm. fibrosis "Cycle"
2. Busulfan (alkyl sulfonate)
Amifostine S/e : Pulm. fibrosis "Bus" Dexrazoxane
Reduces nephrotoxic effects of Reduces cardiotoxic effects of
3. Carmustine (nitrosourea)
anti-cancer drugs anti-cancer drugs
S/e : Pulm. fibrosis "Car"
4. Dacarbazine (nitrosourea)

Acting on only Acting on S and Acting on G2 Acting on

S phase G2 phase and M phase M phase
Inhibits DNA synthesis, Topo-isomerase Microtubule
aka antimetabolites inhibitors inhibitors

1. Methotrexate Topoisomerase - 1 inhibitors Bleomycin 1. Taxanes

DHF reductase blocker 1. Irinotecan "1 can" S/e : Flagellate dermatitis & Hyperstabilize the
Folinic acid supplementation 2. Topotecan Pulm. fibrosis "blow horn" tubules (don't divide)
needed Spares bone marrow "Taxes stabilize
S/e : Pulm fibrosis Topoisomerase - 2 inhibitors economy"
"metho-Truck-sate" 1. Etoposide "2 sides"
2. Teniposide 2. Vincristine
2. Hydroxyurea
(Vinca alkaloids)
Increases HbF (useful in SCA)
Breakdown the
3. Fludaribine (DOC : CLL) Affects non-specific microtubules
4. Pentostatin phase of cell cycle S/e : Peripheral
neuropathy & SIADH
5. 5-fluorouracil
6. 6-Mercaptopurine
Cladribine
Flagellate Dermatitis
(used for Hairy Cell Leukemia)
Allopurinol is added to anti- "Cladded hair"
cancer drugs to prevent Anti-cancer drugs that
Hyper-uricemia spare bone marrow
Allopurinol reduces efficacy 1. Vincristine
of 6-mercaptopurine, hence 2. Bleomycin
not added along with it. 3. L-asparaginase
 Side effects of anti-cancer drugs

Chemotherapy induced emeseis

Most emetic drug : Cisplatin
Cisplatin
Oto-toxic DOC (overall/early) : Ondansetron (5HT³ blocker )
DOC (delayed) : Aprepitant (Substance P inhibitor)

Drugs causing pulmonary fibrosis

Busulfan
Pulm-fibrosis 1. Doxyrubicin 1. Cyclophosphamide "cycle"
Cardio-
2. Daunorubicin toxic 2. Busulfan "bus"
Cisplatin 3. Trastuzumab 3. Bleomycin "blow horn"
Nephro-toxic 4. Carmustine "car"
5. Methotrexate "truck"
Cyclophosphamide 6. Amiodarone "drone"
Hemorrhagic cystitis
Hemorrhagic Cystitis
Caused by a compound "Acrolein" in
Vincristine cyclophosphamide
Peripheral neuropathy Ifosfamide (cyclophosphamide analog)
has higher risk of hemor. cystitis
Prevention : Mesna
Treatment : Steroids
Evomoz
Have fun studying