‫اھﺪاء‪.....

‬‬
‫ﺷﻜﺮ ﺧﺎص ﻟﻠﺪﻛﺘﻮر اﻟﻤﺘﻤ ‪ 4 13 2‬ﻋﻤﺮو ﺣﺎﻣﺪ‪.‬‬
‫ﺣ‪:‬ﺚ اﻧﻪ ﻗﺎم @ﺎﻹﻋﺪاد واﻹ‪CD‬اف واﻟﻤﺮاﺟﻌﺔ ﻟﻠﻤﺎدة‬
‫اﻟﻌﻠﻤ‪:‬ﺔ ﻟ‪J‬ﺘﺐ‪:‬‬
‫‪Internal Medicine‬‬
‫وﻧﺘﻤ‪ M3‬ﻟﻪ اﻟﺘﻮﻓﻴﻖ واﻟﻨﺠﺎح واﻟﺘﻤ ‪.13 2‬‬

‫ﻣﻊ ﺗﺤ‪:‬ﺎت‪:‬‬
‫ﻓ‪YX‬ﻖ وﻣﺆﺳﺴﻪ‪Doctor X‬‬
d
Content
LECTURE Page number
History taking 3

General Examination 6

General Look 9

Vital Signs 25

Upper Limb Examination 38

Lower Limb Examination 46

Head & Neck Examination 50

Neck Vein Examination 56

Lymph node Examination 59

Cardiac Examination 61

Chest Examination 70

Cardio-Respiratory 77
Symptoms

Multiple notes 85

2
d 1 History taking
v The art of History Taking:
Ø History taking in medicine is the most important aspect of the medical examina6on.
Ø Good and effec*ve history taking can:
a) Focus the a:en6on to the system or systems affected.
b) Give a be:er judgment of the severity and progress of the case.
c) Largely diagnose some diseases (e.g., epilepsy, migraine, and renal colic).
Ø History taking is a special form of the art of communica*on, this is the beginning of the
good doctor pa6ent rela6onship:
a) The pa6ent should be put at ease and encouraged to talk freely.
b) Make it clear that the pa6ent has your whole a:en6on.
c) Common things towards good communica6on are to greet the pa6ent, by name if
possible.
d) Don't be angered or shocked by anything he or she says.
e) Pa6ents must be allowed to tell their story in their own
words and in their own way.
f) When the pa6ent telling his story always watches his body
language (e.g., face expression, eyes, clenched fist, etc.).
g) Be a good listener.
Medical History Taking
v

1- Personal Data 7- Family history

2- Chief Complaint 6- Social history

3- History of Present Illness 5- Drug history and allergies

History of Present
4- Past Medical History
1- Personal Data:

a) Name.
b) Age:
ü Certain diseases are more common in special age groups (e.g., infec6ous fever
and congenital anomalies in childhood).
c) Sex:
ü Certain diseases are related to sex (e.g., hemophilia in males).
ü Certain diseases are more common in special sex (e.g., rheumatoid arthri6s and
systemic lupus are more common in females).
d) Occupa*on:
ü Certain works may expose the individual to certain hazards (e.g., infec6on in
medical staff, physical factors like radia6on, and some occupa6onal lung
diseases).
3
History Taking

e) Residence:
ü E.g., Schistosomiasis in countryside.
f) Habits:
ü e.g., smoking and alcohol intake.
g) Marital state and number of children.
h) date of admission.

2-Chief Complaint:

Ø (recent or con6nuos event).

Ø In pa*ent's own words:
• These are the symptoms that make the pa6ent come to the doctor.
• Try to define the main complaint and its dura6on.
• Most pa6ents with long history tend to date them by events rather than by
years.
• Mul6ple symptoms should be arranged chronologically (old to most recent)

3-History of Present Illness:

Ø Ask the pa6ent to tell you the story from the beginning, ideally without interrup6on.
Ø Your goal is:
• To find out how exactly symptoms begin.
• In what seTng they arise.
• How symptoms have evolved since ini6al onset.
Ø So, the history of the present condi*on should include:
a) Mode of onset. e) relieving factor.
b) Course. f) medical consult.
c) Dura6on. g) Nega6ve data.
d) aggrava6ng factor. h) Review of other systems.
a) Types of onsets:
• Sudden onset: seconds to minutes (e.g., vascular disease).
• Acute onset: hours to days (e.g., infec6ons).
• Sub-acute onset: 1-2 weeks (e.g., chronic infec6ons)
• Gradual and insidious onset months to years (e.g., malignant diseases)
b) Types of courses:
• Progressive: malignant and degenera6ve diseases.
• Regressive: self-limited (common cold), or response to treatment (acute infec6on
and vascular accidents).
• Fluctua*ng (remissions and relapses): some chronic inflamma6on.
• Sta*onary: hereditary diseases.
• Paroxysmal aNacks: bronchial asthma.
c) Nega*ve data:
Ø Nega6ve informa6on is some6mes more important than posi6ve informa6on.

4
History Taking

d) Review of other systems:

Ø Other systems should be evaluated for evidence of any disturbances related to the present
illness

4-Past Medical History:

a) History of
History ofprevious
Present illnesses:
• History of rheuma6c fever in heart disease.
Illness.
• History of parasi6c diseases like Schistosomiasis.
• History of high blood pressure, DM.
b) Trauma and surgical opera6ons.
c) Hospitaliza6ons.
d) Blood transfusion.
e) Pregnancies, abor6on.
f) History of travel abroad.
g) similar condi6on in the past.
h) previous inves6ga6on.

5-Drug history and allergies:

a)History
Details ofof
drugs taken name, dosage, frequency, and length of usage.
Present
b) Certain drug families known to cause problems (e.g. Aspirin for ulcers, steroids, etc.).
c)Illness.
Adverse effects to any drug.
d) Allergic reac6ons to any drugs: e.g., to penicillin or sulpha.
e) recent change in medica6on.
f) OCP, HRT.
g) Compliance.
h) Herbs and Herbal Medicines these can interact with many drugs.
i) Tradi6onal Medicines.
6-Social history:
Ø The social environment may affect the pa6ent's health or may be affected by it.
a) The exact nature of occupa6on.
b) The domes6c and marital rela6onships.
c) His home surroundings.
d) Use of alcohol or tobacco.
e) Economic condi6on.
7-Family history:
Ø Certain diseases run in families (secondary to hereditary or environmental factors):
a) History of similar condi6ons or diseases in the other family members.
b) History of consanguinity. e) dura6on of cycle. f) amount.
c) menstrual history. f) Time.
d) age of menarche. g) Period.
5
2 General Examination
Introduction:

Ø The purpose of the physical examina*on:

ü Look for the presence, or absence, of physical signs that confirm or disprove the
differen6al diagnoses you have obtained from the history.

Ø The extent of the examina*on will depend on the symptoms and the circumstances:
ü Focused consulta6on (such as a pa6ent presen6ng to a general prac66oner with
headache), a single system (the nervous system in this case) will be examined.
ü In other circumstances, however, a full integrated physical examina6on will be
required.
ü There is no single correct way to perform a physical examina6on but standardized
systema6c approaches help to ensure that nothing is omi:ed.
ü With experience, you will develop your own style and sequence of physical
examina6on.

Ø Any systema*c examina*on involves:

a) Inspec*on: looking at the pa6ent (for skin changes, scars, abnormal pa:erns of
breathing or pulsa6on, for example).
b) Palpa*on: laying hands on the pa6ent to palpate (feel).
c) Percussion: tapping on the body.
d) Ausculta*on: using a stethoscope, where appropriate, to listen to the relevant
system.

General Examination:
Ø A general inspec6on of the pa6ent as a whole is most valuable to obtain a general
impression.
Ø General examina6on begins as soon as the pa6ent enters the room or is lying in his bed.
Ø It is con6nued during obtaining the history, so that many important observa6ons
(Preliminary observa*ons) can be made such as the way he is dressed, how he lies in bed,
the way he talks and reacts to ques6ons, his emo6onal and mental state, etc.
Ø Occasionally, a spot diagnosis is possible in certain diseases e.g., thyrotoxicosis,
myxedema, Parkinsonism.

Ø The pa6ent should next be par6ally or completely undressed and examined in a good
light.

6
 Before beginning do 3 steps:
1) The hands shake:
Ø Introduce yourself and shake hands.
Ø This may provide diagnos9c clues.
Ø Greet your pa9ent in a friendly but professional manner.
Ø Note if his right-hand work or not for (a right hemiparesis).
Ø Avoid too firm a grip, par9cularly in pa9ents with arthri9s.
v Information from a handshake:
Features Diagnosis
Cold, sweaty hands Anxiety
Cold, dry hands Raynaud's phenomenon
Hot, sweaty hands Hyperthyroidism
Large, fleshy, sweaty hands Acromegaly
Dry, coarse skin Regular water exposure
Manual occupa9on
Hypothyroidism
Delayed relaxa9on of grip Myotonic dystrophy
Deformed hands/fingers Trauma
Rheumatoid arthri9s
Dupuytren's contracture
2) The patient's clothes:
Ø Is he dressed appropriately?
• Clothing gives clues about personality, state of mind and social circumstances,
as well as a pa6ent's physical state.
• Inappropriate clothing a pa6ent with thyrotoxicosis may come to you dressed for
summer in the depths of winter due to heat intolerance.
• Pa6ents with recent weight loss may be wearing clothes that look very baggy and
loose.
• Are there signs of self-neglect (which may be underpinned by other factors such as
cogni6ve impairment, immobility or drug or alcohol dependence).
3) Some clues to the diagnosis:
Ø Clues from the person (SC insulin pump).
Ø Clues from the bedside (hearing aid, inhaler device, and note any walking aid, commode
and wheelchair).
Ø Pa6ents may be wearing a medical iden6ty bracelet.
Ø Note any ta:oos or piercings, (infec6on risks, background informa6on).

Ø Venipuncture marks of intravenous drug use.

Ø Linear (usually transverse) scars from recent or previous deliberate self-harm.

Venipuncture marks
SC insulin pump Hearing aid medical iden2fy bracelet medical alert tatoo Linear Scars

7
 Items of general examination

General Look Vital Signs Skin & mucous Head & Neck
membrane cardiac
&chest&
v
1- General Look: v v Extremities
abdomen
v v
a) general state of health (well-ill).
v b) mental State (Conscious or not).
c) Built & nutri6on (average or not).
d) Face, decubitus, gait.
e) Pallor, Jaundice, Cyanosis.
2-Vital Signs:
a) Pulse.
b) Blood Pressure.
v c) Temperature.
d) Respiratory Rate.
3-Skin & mucous membrane:
a) Pallor, Jaundice, Cyanosis.
b) Pigmenta6on.
c) purpura.
d) Ulcer.
e) Scar.
f) Scratch marking.
g) Elas6city.
h) Swea6ng.
4-Head & Neck:
a-Head:
v
a) Hair. Scratch marking Purpura
v b) eye.
c) mouth.
d) around eye.
e) Paro6d gland
b- Neck:
a) thyroid gland.
v b) Lymph Nodes.
c) Caro6d arteries.
5-Extremities: d) Jugular Veins.
v b-Lower Limb:
a-Upper Limb: a) Clubbing. a) Edema.
b) palmar erythema.
v
8
 1 General Look

1- General Look

v General Look: v

Ø normal:
a) pa$ent Look well Conscious.
b) pa$ent oriented.
c) average built & nutri$on.

d) No Specific:
1) face.
2) decubitus.
3) gait.
4) No Pallor, jaundice and cyanosis.

so, you need to examine:

6-Vital color

5-Gait
4-Decubites
v
3-Posture
v
2-bodybuilt &Nutrition a-flushing
v b-erythema
1-Face v c-pallor
d-jaundice
v e-cyanosis
v

9
 1-Face (3x3)

a-Skin b-muscles c-Bone

A- Colors:
v Ø Redness Plethoric in vpolycythemia. v

Ø Bu2erfly rash SLE Spare Nasolabial.

MS.
dermatomyosi$ts.
pregrancy.
pellagra

Ø Red spot fade on pressure telangectasia

Wheal ‘’allergy’’

Ø Red spot not fade on pressure telangectasia

Wheal ‘’allergy’’

Ø Hyperpigmenta?on ‘’brown’’ leprosy

ACTH dependant Cushing
Addison
O.M
Ø Bronze haemochromatosis.
Ø Pale anemia.
Ø Cyanosis.
Ø Jaundice.
Ø Hypopigmenta?on albinism, Vi$ligo.

B- Scratch: RF, Cholestasis.

C- Scar.

10
 Face (3x3)

d-Eye e-Mouth f-Specific face

v v v

1-Eye lid 2-Eye brow 3-Inside eye

A-Eye:
v v v
1-Eye lid:
Ø Pre esrbital edema ‘’puffy eye’’ nephro6c
Myxedema
angio edema
part of any general edema
S.V.C. obst
Pericardial eff
const Pericaditn
Ø Xanthlasma dyslipedemia.
Ø Stye, chalazion ptosis Diabe$es Mellituis.
horner syndrome.
2-Eye brow:

Ø loss of outer 1/3 myxedema leprosy.

3- Inside Eye:

Ø Sclera scleri$n Episcleri$n (red)

Scler malacia (blue)
Jaundice (yellowish)

Ø ons conjuc$vily
chymosis
hge severe HTN.
Pallor anemia
Ø Exophthalmun Thyrotoxicosis .

11
e-Mouth:
1-Lips:

v Ø crackled.
Ø Angular stoma66s (IDA).
Ø Pigment > pegler syndrome.
Ø Macrochelia > acromegaly.
Ø Pallor > anemia.

Crackled lips Angular stomatitis Pigmented lips Macrochelia pale lips

2-Oduor:
Ø Fecal musty > feature hepa6cus.
Ø Fishy > uremia.
Ø Acetone > DKA.
Ø Foul > anaerobic infec6on.

3-Inside:

a) Inner lips: cyanosis.

b) Gum: hypertrophy (AML-Vit deficiency).
c) Tongue:
1) glazed > IDA
2) cyanosis under surface
3) macroglossia > acromegaly
4) strawberry > scarlet fever
5) atrophy >megaloblasEc anemia
d) Palate: cleF.

cyanosis of the lips Hypertrophic of gum

Atrophic glossitis Strawberry tongue.
cleft palate.

12
 specific face in general appearance
1) Liver failure:
Ø darkish complexion-yellowish 6nge -mild puffiness.
v

2) Scleroderma:
Ø bird like -pinched nose -puckered lips - mouth half opened exposing teeth.

3) Toxic look:
Ø 6red-flushed-sweaty.

4) Hyperthyroidism:
Ø anxious-staring look – exophthalmos.

5) Myxedema:
Ø dull apathe6c look, puffed pale face, malar flush.

6) Acromegaly: 7) Cushing:
Ø protruded forehead. - Moon face.
Ø Enlarged frontal sinus. -dark reddish (plethoric complexion)
Ø enlarged nose, lips.

13
Ø Some picture on Face Examination:
• Vital colors (pallor, jaundice, cyanosis).
• Facies.
• Eyes, lids, brows.
• Nose.
• Mouth, lips, tongue.
• Skin (complexion, rash...).
• Muscle bulk.
• Salivary glands.
v Facies:

Acromegaly Uremia
Cushing
v Eye Examination:
a) Thyroid diseases:

Thyrotoxicosis Myxedema
b) Cardiovascular disease:

Xanthelasma Ocular hypertension

14
 c) Periorbital edema:

d) Eyebrows:
• Loss of outer third.
• Leprosy Myxedema.

Loss of outer third Leprosy myxedema

e) Fundus examina?on:
• Diabe6c re6nopathy.
• Hypertensive re6nopathy.
• Re6nal pulsa6on (in AR).
• Re6nal artery embolism (in infec6ve endocardi6s). Diabetic retinopathy
v Mouth:
• Vital colors.
• Ulcers.
• Dental hygiene
• Gum (bleeding, hypertrophy).

Oral ulceration Gum bleeding Gum hypertrophy

Ø Signs of vitamin deficiency:
• Angular stoma66s.
• Cheilosis.
• Atrophic glossi6s.

Angular stomatitis Cheilosis Atrophic glossitis

15
 Ø Tongue:
• Candidiasis.
• Geographic tongue.
• Strawberry tongue.
Geographic tongue. Strawberry tongue.
Candidiasis

v Skin:
Ø Pigmenta6on (Hypo- or hyperpigmenta6on).
Ø Rash (vesicles, macules, papules).
Ø Acne.
Ø Petechiae, purpura, ecchymosis.
Ø Malar rash pigmentation:
hyperpigmentation hypopigmentation
• Mitral stenosis (malar flush).
• Systemic lupus.
• Dermatomyosi6s.
• Chloasma of pregnancy.
• Pellagra.
• Sun Burn.
Malar rash pigmentation
v Muscles:

Facial muscles atrophy

v Salivary Gland Enlargement:

Paro?d Submandibular
+ Liver failure. Sialadeni$s.
Mumps. Sialolithiasis.
Sarcoidosis.
Sjogren's syndrome.
Chronic nutri$onal Insufficiency.

16
v Swelling (Puffiness):
Ø Soe edema most marked in the eyelids and around the lips: nephri6s, angio6c Edema.
Ø Myxedema.
Ø Very high venous conges6on (e.g., SVC obstruc6on).

Edema due to nephrotic syndrome Myxedema

angiotic Edema

Edema due to SVC obstruction

v Surgical emphysema:
Ø Subcutaneous air leak from the medias6num, palpated like sponge and may give a
crepitus.

Surgical emphysema

v Asymmetry of the face:

Ø One half of the face is abnormal due to:
• Congenital maldevelopment.
• Trauma or Facial palsy.

Asymmetry of the face

due to facial palsy

17
 2-bodybuilt &Nutrition
v Body built and nutrition:
Ø The physical built is influenced by several factors:
v
• Racial and familial characteris6cs.
• Gene6c disorders.
• Endocrine disorders.
• Malnutri6on in young age.
• Chronic diseases in childhood.
Ø It can be assessed by no*ng
• Height.
• Weight.
• Body propor6ons: span, Type of body configura6on:
a) Height.
b) Weight.
Ø For rou6ne measurement, par6cipants should remove shoes, outer clothing such as
jackets and sweaters, heavy jewelry, and contents of pockets, such as loose change,
mobile phones and keys.
Ø Body mass index (BMI):

Ø abnormal built and nutrition:

a) Cachexia:
• Loss of body weight and muscle mass, and weakness that may occur in
pa6ents with cancer, AIDS, or other chronic diseases.
• Con6nuous decline in skeletal muscle mass, with or without fat loss.

b) Emacia*on:
• Extreme weight loss and unnatural thinness due to a loss of subcutaneous
fat (the fa:y, or adipose 6ssue beneath the skin) and muscle throughout
the body.

18
 3-Posture

v Posture:
v
Ø Posi6on or aTtude constantly preferred and assumed
by a pa6ent at rest or in mo6on.
Ø When the pa6ent walks it is called gait.
Ø When the pa6ent stands it is called → Stance.
Ø When the pa6ent lies in bed it is called → Decubitus.
Ø Many diseases give rise to characteris6c postures.

4-Decubites
v Decubitus:
Ø Normally, a pa6ent in bed prefers to be flat on his
back (dorsal recumbent posture).
v that the
Ø This tends to be modified in disease, so
pa6ent may prefer to assume a constant posture.
Ø The decubitus in such cases may be diagnos6c.
Ø Le^ lateral decubitus: The pa6ent had massive lee pleural effusion (Tuberculosis).

Ø Orthopnea (acute asthma): pa6ent characteris6cally holds the bed or chair while
pursuing her lips.

v Gait: 5-Gait
Ø If pa6ents are ambulant, watch how they rise from a chair and walk towards you:
• Are they using a walking aid?
• Is the gait normal or is there evidence of pain,
immobility or weakness? v
• Abnormali6es of gait can be pathognomonic signs of
neurological or musculoskeletal disease:
a) The hemiplegic gait → aeer stroke.
b) The ataxic gait→ cerebellar disease.
c) The marche a pe6ts pas (walk of li:le steps) gait → pa6ent with diffuse
cerebrovascular disease or Parkinsonism.

19
 6-Vital color
v Vital color:
Ø Varia*on of normal color:
• Flushing, Erythema, Pallor, Hypo- or hyperpigmenta6on.
Ø Abnormal colors: v
• Cyanosis, Jaundice.
Ø Sites to examine:
a) Skin (Face, Creases of the palms, Nails).
b) Mucous membrane:
• Inner surface of the lower lip
• Undersurface of the tongue(cyanosis).
• Sclera and inner surface of lower eyelid (jaundice).
1-Flushing and erythema:
• Flushing:
ü Episodic, transient a:acks of redness of the skin together
with a sensa6on of warmth or burning of the face and
neck.
• Erythema:
ü persistent redness of the skinless frequently, the upper
trunk and abdomen.
Ø Pathophysiology:
• Increased amount of saturated hemoglobin.
• Increase in the diameter or actual number of skin capillaries increased blood Flow
through the skin.
• Combina6on of both Warmth and redness.
Ø Causes of flushing:
• Local:
– Physiological(emo6onal).
– Spicy food.
• General:
– Physiological: effort.
– Menopausal flushing.
– Drugs (cholinergic, vasodilators, alcohol).
– Carcinoid syndrome (in neuroendocrine tumors).
Ø Causes of erythema:
• Local:
– Inflamma6on.
– Photosensi6vity.
– Acute contact reac6ons.
– Malar flush (MS: mul6ple sclerosis).
– Palmar erythema (liver failure).
• Generalized:
– Fever.
– Angioneuro6c edema.
– Polycythemia.
20
 2-Pallor:
Ø Defini*on:
• Unusual lightness of skin color when compared with your normal hue/Loss of the
usual color of the skin, more evident on the face, palms and inner aspect of the
lower lip.
Ø Causes:
• Causes inside blood vessels:
– Anemia.
– Hypercholesterolemia.
• Causes in blood vessels (may be local):
– Vasoconstric6on (e.g., vasovagal a:ack, cold).
– Arterial thromboembolism.
– Shock, heart failure.
• Causes outside blood vessels
– Edema.
– Obesity.
– Hypothyroidism (Thick skin).
3- Cyanosis:
Ø Defini*on:
• Bluish discolora6on of the skin and mucous membranes due to increased reduced
hemoglobin in the capillaries above 5 gm/dl. It is less apparent in anemia and
exaggerated in polycythemia.
A-Peripheral Cyanosis:
• Cyanosis of the peripheries only (fingers 6ps and fingernails, toes, 6p of nose, car
lobule).
• Due to:
a) General decrease in blood flow.
b) Stasis of blood in the peripheries:
– shock, Heart failure, Low cardiac output.
c) Local decrease in blood flow due to:
– Peripheral vasoconstric6on (cold exposure,
Raynaud's disease).
– Arterial or venous occlusion.
Ø Raynaud's phenomenon:
• Spasm of the arteries supplying the fingers and/or toes.
• Precipitated by cold and relieved by warmth.
• Three stages:

21
 Ø Cause of peripheral cyanosis:
• Low Cop HF.
• Raynaud's disease.
• Art of Venous obstruc6on
• exposure to Cold.
Note:
ü Cyanosis is less apparent in anemia.
B-Central cyanosis:
Ø Cyanosis all over the body (peripheral + in mucous membranes as lips, tongue)
Ø pathogenesis:
a) Due to increased deoxyhemoglobin in systemic circula6on.
b) Right to lee shunt (congenital cyano6c heart disease).
c) Defec6ve oxygena6on of blood (any severe lung disease).
d) Abnormal hemoglobin (methemoglobin).
Ø Mechanism of central cyanosis:
a) Decrease atmospheric pressure (high al6tude).
b) Ven6la6on defect (Bronchial asthma, Emphysema).
c) Diffusion defect (inters66al pulmonary fibrosis).
d) Perfusion defect (pulmonary arteriovenous fistula, congenital cyano6c heart
disease).
Ø Causes of central cyanosis:
a) ↓ O2 in the lung:
• COPD.
• High aTtude.
• ILF.
• Asphyxia.
b) Congenital Cyano*c Heart disease:
• "Rt to Lt shunt so mixing systemic & pulm blood".
• Fallot tetralogy: pulm stenosis→ Rt vent enlargement→ VSD→ overriding A.
• Eisen monger syndrome→ Reversed shunt (RT-LT) VSD.
c) abnormal HB"false Cyanosis":
• Met Hb, Sulf Hb.
Central cyanosis peripheral cyconsis
1- Site all the body central: inner surface of lips back of Peripheral only eg Finger nails. (nail
tongue peipheral + finger nails. beds).
=p of nose, lobule of ear.
2- Extermi7es usually warm Cyanosis not disappear. usually cold Cyanosis disappear.
3- Exercise not improved improved (d.T periphral
vasodilata=on)
4- O2 inhala7on improved except Cong cyano=c Heart disease. NOT improved.
5- clubbing Common Abscent
6- polycythemia Common Abscent
7- Art. O2 sat < 85%. Normal (95%)

22
 C-Mixed cyanosis:
Ø cyanosis due to peripheral & central causes i.e.: defec6ve oxygena6on in lung
&stagna6on of blood in periphery.
Ø Causes → Shock/HF
Ø Clubbing: Hyper Trophy of 6ssues at nail bed.
4-Jaundice:
Ø Yellowish colora6on of the skin and mucous membrane due to
increase in the serum bilirubin (2.5 to 3 mg/dl).
Ø Subclinical jaundice: the serum bilirubin up to mg/dl.
Ø Normal serum bilirubin: 0.2 to 1 mg/dl.
Ø It is detected in the skin and mucous membrane of the sclera.
Ø Types:
a) Hemoly*c (pre hepa*c):
• Hemoly6c anemia.
• Pulmonary infarc6on (due to hemolysis of the RBCs).
• Ar6ficial valves.
• There is excess produc6on of unconjugated bilirubin→ Unconjugated
hyperbilirubinemia.
• There is excess produc6on of stercobilinogen and urobilinogen.
b) Hepato-cellular (hepa*c):
• Hepa66s.
• Hepatotoxic drugs.
• Liver cirrhosis.
• Liver malignancy.
• Failure of the liver to conjugate all unconjugated bilirubin→ Unconjugated
hyperbilirubinemia.
• Failure of the liver to excrete all conjugated bilirubin→ Conjugated
hyperbilirubinemia.
c) Obstruc*ve (post hepa*c):
• Extrahepa6c biliary obstruc6on: Stone in the common bile duct and carcinoma of head
of the pancreas.
• Intrahepa6c biliary obstruc6on: primary biliary cirrhosis and drugs(sulfonylurea).
• The cholebilirubin cannot be excreted in the intes6ne which retained in the blood →
Conjugated hyperbilirubinemia.
• Excess excre6on of cholebilirubin
in urine.
• Excess excre6on of bile salts in
urine (frothy urine) and its
reten6on in the blood (itching,
bradycardia).
• No sterchobilinogen in the stool
and no urobilinogen in the urine.

23
 Comparison between types of jaundice
Haemoly6c jaundice Hepato-cellular jaundice Obstruc6ve jaundice
Unconjugated Mixed hyperbilirubinemia Conjugated
hyperbilirubinemia v hyperbilirubinemia
Dark stool Light brown stool Clay color stool
Normal color urine Dark frothy urine Dark frothy urine
(no cholebilirubin) (milder than obstruc6ve type)
No iching.no bradycardia Mild iching, bradycardia Iching, bradycardia
↑stercobilinogen ↓stercobilinogen no stercobilinogen
↑urobilinogen ↓ urobilinogen no urobilinogen
Indirect Van den berg test Biphasic Van den berg test Direct Van den berg test
v Unconjugated Hyperbilirubinemia:
Ø Mild jaundice (usually <4mg/dl).
Ø Lemon yellow.
Ø Excess urobilinogen in urine.
Ø Normal color of urine but darkens when lee stand (urobilinogen is oxidized to urobilin).
Ø Dark stools due to excess stercobilinogen and stercobilin.
Ø Normal liver func6on tests.
v Obstructive jaundice:
Ø Mild to severe.
Ø Greenish yellow.
Ø Dark urine due to conjugated bilirubin.
Ø Pale stools due to absence of stercobilinogen.
Ø -/+ itching, bradycardia and frothy urine due to bile salts.
Ø Increased alkaline phosphatase.
v Hepatocellular jaundice:
Ø Mixed direct and indirect bilirubin.
Ø Variable features depending on prominent type of bilirubin.
Ø Increased AST and ALT.
some pictures on vital colors:
v Cyanosis:
Ø Inside of lips-tongue (central cyanosis).

v Jaundice:
Ø Note degree of jaundice: yellowish-yellowish green or olive green.
Ø Light jaundice due to infec6ve hepa66s // Deep olive-green jaundice (obstruc6ve)

v Malar flush:
Ø Reddish discolora6on of the bu:erfly area similar to that seen in
young girls. Mitral stenosis, myxedema, pernicious anemia.

24
2 Vital Signs

Vital Signs
v

Pulse Respiratory Rate Blood Pressure Temperature

v
v v v
1-Pulse:
v Defini(on:
v
Ø Propaga6on of ventricular contrac6on along the blood
vessels.
Ø Felt by applying soe pressure on an artery against a hard
surface causing par6al occlusion.
Ø Start with the radial artery.
v Steps:
Ø Greet the pa6ent, stand on his right side, introduce yourself and explain what you will do.
Ø Assist the pa6ent to pronate and slightly fix the forearm of the pa6ent on his chest.
Ø Right hand to palpate lee radial pulse and vice versa.
Ø Place 6ps of the middle three fingers on the radial artery.
Ø Press gently 6ll you feel the pulse.
v Comment on pulse:
a) Rate.
b) Rhythm.

c) Force.
d) Volume.
Radial Artery

e) Equality on both sides.

f) Vessel wall.

g) Special Character.
h) Other/peripheral pulsa(ons.

25
a-Heart Rate:
Ø Regular rhythm → count in 1 minute.
v
Ø Irregular rhythm→ count in 3 minutes.
Ø Report counts in beats per minute.
Ø Normal rate=60-90 bpm.
Ø Increase rate > 90 bpm → (Tachycardia).
Ø Decrease rate<60 bpm → (Bradycardia).
Tachycardia:
a) Physiological tachycardia:
v 1) Exercise.
2) Emo6ons.
b) Pathological tachycardia:
1) Fever.
2) Heart failure.
3) Rheuma6c fever, Bacterial endocardi6s.
4) Thyrotoxicosis Drugs e.g., sympathomime6cs, atropine
5) Arrhythmias (Paroxysmal tachycardia, AF).
Bradycardia:
a) Physiological bradycardia:
v 1) Athletes.
2) Old age.
b) Pathological bradycardia:
1) Myxedema.
2) Drugs: e.g., digitalis overdose, beta-blockers.
3) Arrhythmias (heart block).
4) Obstruc6ve jaundice.

b- Rhythm:

v Ø Definition:
• Interval between beats (normally
equal).
Ø Types:
1) Regular rhythm.
2) Irregular rhythm:
a) Regular irregularity.
b) Irregular irregularity.

26
1) Regular Rhythm:
Ø Misnomer.
v
Ø Actually, sinus arrhythmia (more in children).
Ø Increase HR during inspira6on (due to
increased venous return).
2) Irregular Rhythm:

v Irregular Rhythm:
a) Regular
Ø Irregularity repeated in a steady pa:ern.
v
Ø For example:
1) Pulse bigeminies:

2) Pulse Trigeminus:

b) Irregular Irregular Rhythm:

v a definite pa:ern.
Ø Irregularity without
Ø most commonly:
1) Atrial fibrilla*on.
2) Extrasystoles/premature beat.
1) Atrial fibrilla?on:
Ø Mul6ple ectopic foci in the atria firing chao6cally at a rate of 400-600 bpm.
Ø AV node blocks most → ventricular rate 100-150, irregular.
Ø Each beat has a different force and volume.

27
 2) Extrasystoles/premature beat:
Ø Extra beats arising from an ectopic focus (atrial or ventricular).
Ø Occasional irregularity followed by a long pause.
Ø May be mul6ple (e.g., in HF, MI).
Ø Felt as an extra beat, a strong beat or a dropped beat.

Atrial Extrasystole Ventricular Extrasystole

v Differential diagnosis of Atrial fibrillation and Extrasystole:

Ø Try to count 4-6 successive regular beats.
Ø Exercise:
• Extrasystoles disappear, while AF becomes worse.
Ø Vagal maneuvers:
• No effect on extrasystoles, reduce rate or reverse AF.
Ø Pulse deficit: difference between pulse rate and apical heart rate):
• In extrasystoles <10, In AF >10.
c- Force:
Ø Defini*on: External pressure needed to occlude the blood flow.
v
Ø Pressure applied by:
• Proximal finger to occlude the artery.
• Distal finger to occlude collaterals.
• Feel the pulse disappearing as force is increased by
middle finger.
• Correlates with the systolic blood pressure.
• Average force, weak, forceful, variable.

d- Volume:
Ø Amount of eleva6on or the upstroke of the finger with each pulsa6on.
v
Ø Reflects the pulse pressure (directly related to stroke volume and inversely related to
peripheral resistance).
Ø May be:
ü Average.
ü Increased (hyperkine6c, bounding).
ü Decreased (hypokine6c).
ü Variable.

28
Ø causes of abnormal volume:
HYPOKINETIC HYPERKINETIC:
Low cardiac output: Decreased distensibility of
- Heart failure. arteries (atherosclerosis).
- MI. Increased stroke volume:
- Shock. - Anxiety, exercise.
- Cardiomyopathy. - Aor6c regurgita6on.
- Cardiac tamponade. - Complete heart block.
Peripheral vasoconstric*on: Hyperkine*c states (VD & Inc
- Hypovolemia. COP):
- Fever, anemia.
- Thyrotoxicosis.

e- character or type:

Ø Moderate,vgradual ascent, descent with a smooth dome-shaped

summit with a less dominant dicro*c notch.
Ø Can only be recorded by tracer.

Hypokine*c, thready pulse (pulsus Hyperkine*c, bounding pulse:

parvus)
- Weak rapid pulse. - Large volume.
- E.g., Shock.

1-Water Hammer (collapsing Pulse):

Ø Rapid ascent to a high,

v brief summit and descends rapidly
Exaggerated type of bounding pulse.
Ø Due to ↑ SBP and ↓DBP→ ↑ pulse pressure.
Ø Present in:
• Aor6c regurge.
• AV fistula.

29
Ø How to detect water hammer pulse?
• Raise the arm of the pa6ent above the level of the heart
to augment the pulse pressure.
• Gentle pressure (or you will feel muscular pulsa6on).

2- Anacrotic (plateau pulse):

Ø Low amplitude rises slowly to a late summit and descends slowly.
Ø Summit is flat and of long dura6on.
v
Ø In aor6c stenosis.

3- Pulsus bisferiens:

Ø Palpable double pulse with 2 peaks during systole.

Ø Seen in:
v • Double aor6c lesion.
• Idiopathic hypertrophic cardiomyopathy.

4- Dicrotic Pulsus:
Ø Palpable double pulse with a prominent dicro6c notch (one peak during systole and
another in diastole).
Ø Seen in:
v • Fever (some types).

5- Pulsus Alternans:
Ø Alternate beats that are strong and weak Regular rhythm to differen6ate it from pulsus
pegamines.
Ø In:
•v Massive MI.
• Myocardi6s.

30
 6- Pulsus Paradoxus:
Ø Exaggera6on of a normal phenomenon.
Ø Blood pressure normally falls during inspira6on (but
less than 1 0 mmHg).
v
Ø Measured by Sphygmomanometer.
v Mechanism of the normal phenomenon:

v Causes of pulses paradoxus:

Ø Cardiac tamponade (↓↓ RV filling).
Ø Constric6ve pericardi6s.
Ø Obstruc6ve airway disease.

f-Arterial wall condition:

Ø Aeer milking the artery and occluding it, roll its wall.
v
Ø Normally arterial wall not felt (because of elas6c 6ssue).
Ø Wall felt in atherosclerosis.

g-Equality on both sides:

Ø As regards force and volume.
Ø Causes ofvunequal pulse:
1) Aberrant radial artery. 4) Coarcta6on of aorta.
2) Arterial compression. 5) Aor6c aneurysm.
3) Arterial thromboembolism. 6) Aor6c dissec6on.
h-Other Pulsations:
v Comment:
v
Ø Whether felt or not.
Ø Equal bilateral or not.
Ø If not:
• causes Same causes of unequal pulse.
v Sites:
a) Brachial artery. d) Popliteal artery.
b) Caro6d artery. e) Posterior 6bial artery.
c) Femoral artery. f) Dorsalis pedis.

31
a) Brachial artery:

b) Caro?d artery:
Ø Best site for comment on force, volume and character.
Ø Palpate while seated or lying down.

c) Lower limb pulsa?ons:

32
2-Respiratory Rate:
v Normal Rates:
v
Ø Unit → Breaths per minute.

Acceptable Range of Respiratory Rates for Age

Age Rate (Breaths per Minute)
Newborn 30-40
Infant (6 months) 20-40
Toddler (2 years) 25-32
Child 20-30
Adolescent 16-19
Adult 12-20
v Tachypnea (>20):
Ø Physiological:
• Exercise.
Ø Pathological:
• Pulmonary: Acute respiratory distress (e.g., bronchial asthma, pneumonia
pulmonary edema).
• Cardiac: Heart failure.
• General: fever, anemia,
thyrotoxicosis.
Ø Psychogenic:
• Hyperven6la6on.
v Bradypnea (<12):
Ø Chest deformity.
Ø Myosi6s.
Ø Pleurisy.
Ø CNS depression (Increase intracranial pressure,
drugs).
Ø Drugs e.g., opioids, hypno6cs.
Ø Hypothyroidism.
3-Blood Pressure:
Ø Blood pressure is the measurement of force applied
v
to artery walls.

33
v Hypotension:
Ø SBP less than 90 mm Hg.
Ø And/or DBP less than 60 mm Hg.
Ø In prac6ce, blood pressure lower than the pa6ent's usual BP causing symptoms.
v Hypertension:
Ø Defined as:
• SBP of 140 mm Hg or more OR DBP of 90 mm Hg
or more OR taking an6hypertensive medica6on.
Ø Isolated systolic hypertension:
• Elevated SBP with normal DBP.
• in elderly with lost aor6c elas6city.
• Treat if SBP > 160.
v Rules:
Ø The pa6ent is in siTng posi6on aeer 5 minutes rest.
Ø 3 parts should be supported: back, feet and the arm.
Ø The cuff should be at the level of mid sternum ((it should be applied closely to the upper
arm, with the lower border not less than 2 cm from the cubital fossa)).
Ø It should not be wrapped very 6ght or very loose.
Ø The 2 rubber tubes should be adjusted
during wrapping the cuff to be in the
middle of the cubital fossa.
Ø The manometer is placed so as to be at
the same level as the observer's eye and
the cardiac level.
Ø The diaphragm of the stethoscope is
posi6oned at the lower margin of the cuff
over the brachial artery (medial wall of the cubital fossa).
Ø Strat palpatory then the auscultatory method.

34
v What can go wrong in a 'casual' office measurement?

BP (mm Hg) if not done

Rest ≥ 5 min, quiet ↑12/6
Seated, back supported ↑ 6/8
Cuff at midsternal level ↑↓ 2/inch
Correct cuff size ↑6-18/4-13
Bladder center over artery ↑3-5/2-3
Deflate 2mmHg/sec ↑SBP/ ↓DBP
If initial BP > goal BP: 1st reading higher
3 readings, 1 min apart •"Alerting response"
Discard 1st, average last 2
v Method of Blood pressure Measurement:
a) Palpatory method:
Ø Avoid causing pain → 1 BP
Ø Avoid auscultatory gap
Ø Palpatory SBP usually 5-10 mmHg lower than
auscultatory.
b) Auscultatory method:
Ø Raise pressure 20 mmHg above the palpatory SBP.
Ø First sound → SBP.
Ø Disappearance of sound → DBP.
Ø In aor6c regurge → use muffling of sound for DBP.

Ø Next Step:
• Measure BP:
ü In another arm.
ü In lower limbs.
ü Aeer standing up for 1 min.

35
Ø BP in another arm:
• If: difference > 10/5 mmHg →
ü Peripheral artery disease (atherosclerosis, thrombus, embolus).
ü External pressure (cervical rib, hematoma, tumor).
ü If lower in lee arm → coarcta6on of aorta before lee subclavian artery.
Ø BP in lower limbs:
• Over popliteal or posterior 6bial artery
• Up to 20/10 mmHg higher (if using same cuff) is acceptable.
• Higher LL BP → aor6c regurge (Hill's sign)
• Lower LL BP → Peripheral Cause:
ü Coarcta6on of the aorta.
ü Local cause (PVD, external pressure).
Ø BP on standing:
• Normally → proper autonomic response maintains BP.
• Postural hypotension → fall of >=20/10 mmHg Neural cause such as:
ü Autonomic neuropathy (e.g., diabe6c neuropathy).
ü Hypovolemia.
ü Old age.
ü Drug induced (direct vasodilators, diure6cs).

4-Temperature:
v Methods of measuring:
1) v (standard).
Oral
2) Rectal (-0.5° C).
3) Axillary (+0.5° C).
4) Tympanic (ear).
5) Digital.
v Definitions:
Ø Normal oral temperature: 36.5-37.2° C.
Ø Pyrexia >37.2 ° C.
Ø Hyperpyrexia >41.1 ° C.
Ø Subnormal temperature <36.5 ° C.
Ø Hypothermia < 35 ° C.
v Measurement of body temperature:
1) Gree6ng the pa6ent, stand on his right side, introduce yourself and explain to the pa6ent
what you are going to do.
2) Prepare the thermometer tray; mercury thermometer, alcohol, and co:on balls.
3) Wash the hands.
4) Hold the thermometer at the end of the stem, with the finger6ps of the right hand at eye
level.

36
 5) Rotate slowly the thermometer back and forth un6l the mercury in the shae is clearly
visible.
6) Wipe the thermometer by co:on balls and alcohol.
7) Shake the thermometer down to 35° C using quick, sharp, downward wrist mo6ons.
v oral method:
Ø Ask the pa6ent to open his mouth and raise his tongue.
Ø Place the bulb of the thermometer on a heat pocket located on the floor of the mouth at
the base of the tongue.
Ø Tell the pa6ent to relax his tongue (thus covering the bulb of
the thermometer) and to close his lips firmly over the
thermometer.
Ø Wait at least 3 minutes before removing the thermometer
from the pa6ent's mouth.
Ø Remove any secre6ons from the thermometer by wiping by
co:on balls from the stem to the bulb.
Ø Read the thermometer by holding it at eye level and rota6ng
the stem un6l the mercury is seen clearly.
v Axillary method:
Ø Ask the pa6ent to lie in a supine or semi-siTng posi6on.
Ø Place the bulb of the thermometer in the pa6ent's clean, dry axilla.
Ø Hold the arm of the pa6ent firmly to the side with the
elbow flexed and the hand in contact with the chest.
Ø Wait at least 3 minutes before removing the
thermometer.
Ø Remove the thermometer from the axilla and dry it by
wiping by co:on balls from the stem to the bulb.
Ø Read the thermometer by holding it at eye-level and
rota6ng the stem un6l the mercury is clearly seen.
Ø Record the results by adding 0.5°C to the measured
temperature.
v Causes of fever:
Ø Most common → infec6ous disease (bacterial, viral...)
Ø Inflammatory (e.g., lupus, rheumatoid arthri6s)
Ø Malignancy (e.g., lymphoma, leukemia, ...)
Ø Hematological diseases
Ø Allergic reac6ons
Ø Ischemic disease (myocardial infarc6on, pulmonary embolism)
v Causes of hypothermia:

Ø Most commonly → cold exposure.

Ø Hypothyroidism.

37
 Upper Limb Examination
Hand Examination
v

What to look at?

v

5- Muscles
v
4- Nails & Nail beds 6- Joints
v v
3- Temperature & Sweat 7- Abnormal movement
v v
2- Skin (palm& dorsum) 8- Rest of Hand
v
1- Vital Colors
v
1- Vital Colors:
v Especially pallor and cyanosis.
Ø

Pallor cyanosis
Palmar Erythema:
v
Ø Erythema of the bases of fingers, thenar, and hypothenar eminences with central
pallor.
Ø In:
• Liver cirrhosis.
• Pregnancy.
• Thyrotoxicosis.
• Polycythemia.

Palmar erythema

38
2-Skin:
v
Ø Pigmenta6on (hypo- or hyperpigmenta6on).
Ø Rash (vesicles, macules, papules).
Ø Petechiae, purpura, ecchymosis.

Hyperpigmentation Hypopigmentation

Vesicles Macules Papules

v Comparison between Janeway lesion and Osler node:

Variable Janeway Lesion Osler Node

Loca*on Soles, palms, thenar and Finger and toe 6ps, thenar
hypothenar eminences, plantar and hypothenar eminences
surfaces of the toe
Size and shape Macules of variable size and Nodules of 1 mm to > 1 cm
irregular shape
Tender No Yes

3- Temperature & Sweat:

a- Temperature:

Warm hands Cold Hands

Hot weather. Cold weather.
Exercise. Anxiety.
Fever. Peripheral vascular disease.
Hyperdynamic circulation: Low cardiac output (e.g. HF).
Anemia.
Thyrotoxicosis.

39
 b- Sweat:
Ø Excessive sweating:
• Normal in some individuals.
• Cold clammy swea6ng (sympathe6c s6mula6on):
ü Hypoglycemia.
ü Anxiety.
ü Angina or infarc6on.
ü Heart failure.
• With warm hands:
ü Thyrotoxicosis.
ü Fever and toxemia.

4-Nails & Nail beds:

v
What to look at Nails?
v

c- Shape

b- Lusters d- Capillary Refill

a- Color of the nail beds. e- Nail Diseases

a- Color of the nail beds.

a) Muehrcke's lines:
• In hypoalbuminemia.
b) DD Beau's lines:
• with indenta6on.
• Occur with aging, HF, shock, chemotherapy.

Muehrcke's lines Beau's lines

40
c) Half and half nail:
• (Distal brown transverse band) in chronic renal failure.

d) White nail:
• in liver failure.

e) Splinter hemorrhages:
• in infec6ve endocardi6s

f) Dark lines:
Ø may be:
ü Trauma (ecchymosis).
ü Melanoma.

41
b- Lusters of nails:

• Normal: clear, glistening.

• in peripheral ischemia: Dull, opaque.

Normal Nail diseased nail in peripheral

ischemia

c- Shape of the nail:

1) Nail pitting and rippling:

Ø Psoriasis.
Ø Inflammatory arthri6s.

2) Koilonychia / Spooning of the nails:

Ø In iron deficiency anemia.

3) Clubbing:
Ø Angle between nail plate and proximal nail fold greater than 180 degrees.

42
 v Window test:

v Clubbing stages:
• 1st : Oblitera6on of the angle and filling of the nail bed.
• 2nd: increase convexity of the nail (parrot peak appearance).
• 3rd: Drum s6ck appearance (increase bulk of the soe 6ssue).
• 4th : Pulmonary osteo- arthropathy (perios6eits of long bone→
swelling of distal end of radius & ulna).

Drum stick appearance Pulmonary osteo- arthropathy

v Pathophysiology of clubbing:
Ø Mechanism largely unknown (chronic hypoxia, chronic
toxemia).
Ø Hypervasculariza6on.
Ø Fibrosis.
Ø Edema.
v Causes of clubbing:
1) Unilateral clubbing:
Ø Occupa6onal.
Ø Thoracic outlet syndrome.
Ø Aor6c aneurysm.
Ø AVF.
Ø Spasm or thrombosis of an artery.
2) Idiopathic / Familial. Unilateral clubbing

43
 3) Pulmonary causes:
Ø Chronic suppura6ve lung.
Ø Hypoxic corpulmonale.
Ø Bronchogenic syndrome.
Ø Inters66al lung fibrosis.
Ø Mesothelioma
Ø Miliary TB.
4) Cardiac causes:
Ø Subacute infec6ve endocardi6s.
Ø Congenital cyano6c heart disease.
Ø Atrial myxoma.
5) Other causes:
Ø Inflammatory bowel disease (Crohn's disease and ulcera6ve coli6s).
Ø Primary biliary cirrhosis.
Ø Familial polyposis.
Ø Chronic diarrhea.
Ø Hyperthyroidism.
d- Capillary
Ø Press the nail beds to detect:
1)Capillary refill ?me:
• Normal < 2 sec.
• Prolonged in shock and decreased peripheral
perfusion.
2)Capillary pulsa?on: Capillary refill time test

• Par6al blanching of nail bed and observe pulsa6on of the line with systole.
• In AR.

5-Muscles:
v
Ø Was*ng of the small muscles of the hand:
• Rheumatoid arthri6s.
• Neurological lesion at the spinal cord, root or brachial plexus.
• Ulnar or median nerve palsy.
6-Joints:
v
1) Monoarthri?s (e.g. gout).
2) Polyarthri?s:
a) Rheumatoid arthri6s.
b) Systemic lupus.

44
v Joint deformity:

v Nodules:
Ø Bouchard nodes (found at the PIP) and Heberden's nodes (found at DIP) are bony
outgrowths seen in osteoarthri6s (DJD) of the hand.

7-Abnormal Movement:

Ø Fine tremors of the hand of outstretched hands (e.g. in thyrotoxicosis).

Ø Asterixis / flapping tremors (in hepa6c and uremic encephalopathy).

45
 Lower Limb Examination
Lower Limb Examination
v

Inspection Palpation
v v

4-Muscles

3-Nails

2-Skin 5-Joints

5-Neurological
3-Temperature Examination
1-Edema 6- the sole & Between
& Swelling the toes

2-Pulsations 4-Joint
Examination
1-Elicit Edema
Lower limb edema:
v
Edema:
v
Ø Accumula6on of fluid in the inters66al space.
Ø May be accompanied by accumula6on of fluid in serous cavi6es (pleural effusion, ascites,
pericardial effusion).
Ø Best seen in:
• Lower limbs.
• Sacrum (in bed-ridden pa6ents).
• Face (in some causes).

Edema in lower limb Edema in face

Edema in sacrum

46
v Physiology of interstitial space:
• The force promo6ng fluid outshie from capillary to inters66al compartment includes
blood pressure and nega6ve inters66al pressure.
• The force a:rac6ng fluid from inters66al
compartment to capillary is blood colloid
osmo6c pressure.
• At the arterial end, the sum of the forces
causes fluid to move from the capillary into
the 6ssue.
• At the venous end, the sum of the forces causes fluid to move into the capillary.
• About nine-tenths of the fluid that leaves the capillary at its arterial end reenters the
capillary at its venous end. About one-tenth of fluid passes into the lympha6cs.
v In Edema:

v Causes of Edema:
a) Increase Hydrosta*c pressure:
• Volume overload, heart failure, deep vein thrombosis.
b) Decrease plasma onco*c pressure:
• Hypoalbuminemia (Nephro6c syndrome, starva6on, liver disease).
c) Increase capillary permeability:
• Inflamma6on, angineuro6c edema/allergic.
d) Lympha*c drainage obstruc*on:
• Lymphedema.
v Comment on lower limb edema:
1) Present.
2) Unilateral or bilateral.

3) Symmetrical (equal bilateral) or not.

4) Pipng or not.

5) Consistency.
6) Severity.

7) Upper level.
8) Skin overlying.

47
-Present or not:
Ø Inspec*on→ observe swelling.
Ø Palpa*on →Elicit edema by firm pressure over a bony
prominence for 15 sec→ maintained pit.
Ø Dorsum of foot, over ankle, over 6bia, sacrum.

-Unilateral Edema:

Ø Deep vein thrombosis.

Ø Inflamma6on.
Ø Lymphedema.
Ø Allergic.

-Bilateral symmetrical Edema:

Ø Cardiac → Conges6ve heart failure.
Ø Renal → Nephro6c syndrome, renal failure.
Ø Hepa6c → Liver cirrhosis.
Ø Nutri6onal → protein- energy malnutri6on.
Ø Allergic.
Ø Lymphedema.
Ø Myxedema.

-Bilateral unequal Edema:

Ø Complica6on on top of bilateral edema.
Ø Inflamma6on (Celluli6s).
Ø DVT.

-Pitting or not:

Ø Most piTng.
Ø Non-piTng (with inflamma6on and exuda6on):
• Inflamma6on.
• Allergic.
• Lymphedema.
• Myxedema.
-Consistency:
hgbn
Ø So^ pipng (pits and persists due to low protein content in edema fluid):
• Hypoalbuminemia (Nephro6c, cirrhosis, nutri6ona).
Ø Hard:
• Lymphedema.
• Rest → firm.

48
-Severity of edema:
hgbn
Ø Rela6ve by degree of piTng
Ø +, ++, +++, ++++.

-Upper level Edema:

Ø Another measure of severity.

Ø Ankle → 6bia (lower, middle, upper 1/3) → anterior
superior iliac spine → sacral abdominal wall edema
→ sternum clavicle → face edema.
-Face Edema:
Ankle Edema
Ø Mostly in renal pa6ents (nephro6c syndrome) due to low 6ssue factor and sleeps flat.
Ø In myxedema.
Ø In angioneuro6c edema.

Angioneurotic edema
Renal patient edema Myxedema

-Skin Overlying:

Ø Signs of inflamma6on.
Ø Discolora6on.
Ø Ulcera6on.

Ulceration.
Signs of inflammation Discoloration.

49
 Head & Neck Examination

Head & Neck Examination

What to examine in?

v

Head Neck
v v

8-Salivary gland
v
7-Mouth
6-Ears v
v
5-Nose
v
4-Eye 2-Lymph nodes
v v
3-Vital colors of face 1-Neck Veins
v v
2-Scalp
v
1-Cranium
v
1-Cranium:
1) Size:v
• Large head: Hydrocephalus - Acromegaly - thalassemia.
• Small head: Microcephaly.
2) Shape: Large head

• Acromegalic facies: large head, Lengthening of the face, Prominent Supraorbital ridge,
Prominent zygoma, Protruded maxilla, Prognathism, Diastema, Wide angle between
ramus and body of the mandible.
• Thalassemic facies: large head, Frontal bossing, Protruded maxilla, depressed nasal
bridge.

50
 Thalassemic facies
Acromegalic facies

2-Scalp:
v
1) Hair distribu*on:
Ø Alopecia: diffuse hair falls e.g., SLE.
Ø Coarse bri:le hair e.g., hypothyroidism.
2) Swelling:
Ø Metastasis.
Ø Hematoma.
Alopecia Coarse brittle hair
3) Tenderness:
Ø E.g., over the Temporal artery in temporal Arteri6s.

3-Vital colors of face:

v
a- Pallor: b- Jaundice: c- Cyanosis:

4-Eye:
v
1) Eyebrows:
Ø Loss of the outer third of the eyebrow: Myxedema, Leprosy.
2) Eye lids:
Ø Ptosis:
• Due to Congenital or III cranial nerve (oculomotor) palsy unilateral ptosis.
• Horner syndrome, problem in sympathe6c, or myasthenia bilateral ptosis.
Ø Edema (puffiness): due to Nephro6c syndrome or Myxedema or Angioedema or Surgical
emphysema.
Ø Xanthelasma: due to Dyslipidemia.

Ptosis Edema (puffiness) Xanthelasma

51
3) Conjunc?va:
Ø Palpebral conjunc*va.
Ø Conjunc*val injec*on (hyperemia) e.g., conjunc6vi6s.
Ø Conjunc*val hemorrhage e.g., Severe HTN, blood disease, Valsalva's maneuver or
coughing.
Ø Vit. A deficiency: xerosis with bitot's spots.

conjunctivitis conjunctival hemorrhage bitot's spots

4) Sclera:
Ø Yellowish discolora6on → Jaundice.
Ø Bluish discolora6on Collagen diseases e.g., osteogenesis imperfects, Marfan syndrome,
Ehlers Danlos syndrome.
Ø High myopia, congenital glaucoma.
Ø Scleri*s and episcleri*s in RA, IBD.

Jaundice. Bluish discoloration congenital glaucoma Scleritis Episcleritis

5) Pupil:
Ø Reac6ve to light or fixed.
Ø Dilated or constricted.

6) Cornea:
Ø Corneal opacity due to corneal ulcer or kera66s.
Corneal opacity
Ø Arcus lipoids due to Dyslipidemia.
Ø Kayser Fleisher ring due to copper deposi6on in Wilson's disease.

7) Fundus examina?on:
Ø Diabe6c re6nopathy.
Ø Hypertensive re6nopathy.
Ø Re6nal pulsa6on (in AR).
Ø Re6nal artery embolism (in infec6ve endocardi6s). Diabetic retinopathy

52
5-Nose:
v
1) Shape Enlarged due to Acromegaly.
2) Depressed nasal bridge (Saddle Shaped nose) due to Congenital deformity,
Congenital Syphilis, Repeated trauma due to boxing, leprosy.
3) Pinched (beaked nose) due to scleroderma.
4) Ac6ng ala nasi: pneumonia.
5) Smell of breath: Acetone e.g., DKA. Saddle Shaped nose

6-Ear:
1) vDischarge:
Ø Pus due to o66s media due to rupture tympanic membrane.
Ø CSF otorrhea in fracture base of the skull.
2) Shape:
Ø E.g., Cauliflower ear in relapsing polychondri6s.
3) Nodules:
Ø Tophi in gout.

otorrhea Cauliflower ear Gouty Tophi

7-Mouth:
v
1) Lips:
Ø Pallor and cyanosis in the Inner surface of the lower lip.
Ø Angular stoma66s due to Iron deficiency and Vitamin B2 (riboflavin) deficiency.
Ø Vesicles.
Ø HSN-1
Ø Ulcers e.g., aphthous ulcers or carcinoma or Chancre (upper lip).
Ø Causes of oral ulcers:
• Aphthous ulcers (Idiopathic).
• SLE (painless), Bechet's (painful).
• Crohn's disease, Celiac disease.
• Infec6ons e.g., Viral (HSV), Fungal (candida),
Bacterial (syphilis or TB).
• Neoplasia (SCC). Oral ulceration
• Skin disease e.g., pemphigus, lichen planus.
• Drugs e.g., chemotherapy.

53
2) teeth& gum:
1) Discolora6on e.g., Tobacco, poor mouth hygiene.
2) Loosening of the teeth e.g., DM, hyperparathyroidism.
3) Wide spacing (Diastema) in acromegaly.
4) Gum bleeding in Gingivi6s, Scurvy, purpura.
5) Gum hypertrophy in phenytoin, acute leukemia.
3) tongue: Discoloration of gum
a) Color:
• Cyanosis.
• White coated tongue due to Thrush (Candida) or Leukoplakia (precancerous Lesion).
• Hairy brownish black due to Excessive smoking.
• Magenta red tongue due to riboflavin (vit b2) deficiency.
• Fiery red tongue due to Niacin B3 deficiency (pellagra).
b) Surface:
• Glazed togue (atrophic glossi6s) due to:
ü Iron deficiency anemia, Pernicious anemia (B12 deficiency),
Vitamin B2 deficiency and Pellagra (B3).
• Geographic tongue: benign asymptoma6c map like lesion.
• Strawberry tongue: scarlet fever.
• Leukoplakia precancerous in immunocompromised pa6ents).
• Dry tongue sign of dehydra6on e.g., DKA. atrophic glossitis

c) Size:
• Macroglossia: Cre6nism, myxedema, Acromegaly and Amyloidosis.
• Local inflamma6on e.g., glossi6s.
d) Tongue movement:
• Deviated toward paralyzed side in XII palsy.
• Tremors in the 6p e.g., liver failure.
4) Buccal mucosa:
a) Causes of buccal pigmenta*on:
• Blue line along the edge of the gum in lead poisoning.
• Brown pigmenta6ons in Addison's disease.
• Brown buccal and circumoral pigmenta6on + Intes6nal
polyposis in Peutz Jegher Syndrome.
b) Palate:
Buccal pigmentation
• Clee palate, High arched palate (congenital)
5) Saliva:
Ø Dry mouth (Xerostomia)
• Dehydra6on e.g., DKA.
• Psychogenic e.g., Anxiety.
• Sjogren's Syndrome.
• Drugs e.g., An6cholinergics, an6histaminic.

Dry mouth (Xerostomia)

54
6) ODOUR (V.I.P):
Ø Foe6d odor (Halitosis): Suppura6ve lung disease.
Ø Pyorrhea alveolaris "pus between teeth and gums "and in
Tonsilli6s.
Ø Fetor hepa6cus (mousy odor) in liver failure Fruity odor
(acetone) in DKA.
Ø Fishy odor (Ammonia) in Renal failure.
Ø Signs of vitamin deficiency:
• Angular stoma66s.
• Cheilosis.
• Atrophic glossi6s.

8-Salivary gland:
v
1) Paro?d enlargement:
Ø Mumps, Ancylostomiases, Liver insufficiency, Sarcoidosis, Sjogren's syndrome and
Tumors.
2) Submandibular gland enlargement:
Ø Tumors, Duct obstruc6on, Sialadeni6s, Sialolithiasis.

Submandibular gland enlargement

Parotid gland enlargement

Skin:

Ø Pigmenta6on (hypo- or hyperpigmenta6on).

Ø Rash (vesicles, macules, papules).
Ø Acne.
Ø Petechiae, purpura, ecchymosis.

Malar area pigmentation:

Ø Mitral stenosis (malar flush).
Ø Systemic lupus.
Ø Dermatomyosi6s.
Ø Chloasma of pregnancy.
Ø Pellagra & Sun Burn.

55
 Neck Vein Examination

Neck
v
1-Neck veins:
v
Ø Jugular Venous Pulse (JVP) reflects changes in the right atrium throughout the cardiac cycle.
Ø Iden*fica*on: there are 2 jugular veins on each side of the neck:
Ø External jugular vein: Easy to see but gives false impression of
raised pressure.
Ø Internal jugular vein: More difficult to see, but is accurate for
measurement of pressure & pulsa6ons. Its examina6on depends
on detec6on of its pulsa6ons. It runs deeply from the sterno-
clavicular joint upwards & laterally to the angle of the jaw the
ver6cal line of the neck).
Ø Both can be iden6fied by asking the pa6ent to perform a Valsalva maneuver.
Ø Comment:
• Neck veins should be examined for:
1) The degree of venous conges*on:
ü Usually, the head of the bed needs slight eleva6on (45°
from the horizontal). However, when the pa6ent's
venous pressure is increased, the head of the bed may
need more eleva6on up to 60° or even 90°
ü all these posi6ons, the sternal angle remains about 5 cm
above the right atrium.
Ø Measuring:
• The pa6ent is posi6oned at about 45° to the horizontal (between 30° and 60°),
wherever the top of the venous pulsa6on can be seen in a good light.
• The jugular venous pressure is measured as the ver6cal
distance between the manubriosternal angle and the
top of the venous column.
• The normal jugular venous pressure is usually less than
3 cm, which is equivalent to a right atrial pressure of 8
cm when measured with reference to a point midway
between the anterior and posterior surfaces of the
chest.
• The venous pulsa6ons are not usually palpable (except for the forceful venous
distension associated with tricuspid regurgita6on).
• Venous pressure greater than 3 cm above the sternal angle is considered elevated
with the pa6ent in any posi6on).

56
 2) Pulsa*ons: (pulsa*ng or not?? )
• Normally, the JV pulsa6ons are wavy & consist of 3 posi6ve waves:
ü a wave: right atrial contrac6on while the tricuspid valve is opened. It is a
presystolic wave.
ü c wave: Upward bulge of tricuspid valve into right atrium
due to its sudden closure.
ü v wave: right atrial filling during ventricular systole while
the tricuspid valve is closed it is a systolic wave. and 2
nega6ve waves x and y.

v Clinical significance of neck veins:

1) Abnormal pressure: Congested neck veins
• Congested pulsa*ng:
ü Right sided heart failure.
ü Tricuspid incompetence and tricuspid stenosis.
ü Increased intra-pericardial pressure (cardiac tamponade & constric6ve pericardi6s)
ü Increased intra-thoracic pressure (COPD, Asthma, Pleural effusion, tension
pneumothorax).
ü Hyperdynamic circula6on (high COP state),
ü Increased intra-abdominal pressure (tense ascites, pregnancy, huge abdominal
swelling).
• Congested non-pulsa*ng:
ü Superior vena cava obstruc6on (Thrombosis or Medias6nal syndrome).
2) Abnormal Pulsa*ons: Abnormal waves.
• a-wave:
ü Prominent: it is due to pulmonary hypertension, Pulmonary Stenosis, Tricuspid
Stenosis.
ü Cannon: due to right atrial contrac6on against closed tricuspid valve. it is seen
with Complete A-V dissocia6on (complete heart block) and nodal rhythm.
ü Absent: Atrial fibrilla6on (AF) (due to loss of atrial contrac6lity)
• V- wave:
ü Large prominent V wave systolic venous pulsa6on): Tricuspid regurge (TR).
• Kussmaul's sign:
ü inspiratory filling of the neck veins: cardiac tamponade, constric6ve pericardi6s
and restric6ve cardiomyopathy.

57
 v Difference between venous and arterial pulsations:

Venous pulsations Arterial pulsations

wavy single
Better seen than felt Better felt than seen
Effect of inspiration Empty with inspiration No effect
Effect of compression of More congested No effect
the root of neck
Effect of change of posture Significant No effect

v Jugular Venous Pulse curve:

Abnormality

a-wave v-wave y-wave

Prominent in
giant Canon Tricuspid regurge
double
absent Slow in Rap in
Tricuspid stenosis constr. pericardi?s
cardiac tamponade
TS complete Friedreich sign
Flu.er PS Heart
AF
PHTN block

58
 Lymph node Examination
v Region's lymph node:
a) Cervical LNs.
b) Supraclavicular LNs
c) Axillary LNS.
d) (Abdominal Examina6on) spleen.
e) Inguinal and Femoral LNs
f) Other LNs
v Examine for:
Ø Symmetry.
Ø Lymphadenopathy:
• Disease of the lymph nodes Usually refers to enlarged
lymph nodes.
Ø If lymphadenopathy present comment on:
• Site.
• Size (in cm).
• Consistency.
• Discrete or amalgamated.
• Tenderness.
• Skin overlying.
• Adherence to underlying structure or overlying skin.

Lymphadenopathy

Lymphadenopathy:

Ø Consistency → soe (insignificant), rubbery (Classically

lymphoma), hard (classically malignancy & granulomatous
infec6on).
Ø Tender → (classically infec6on), non-tender → (classically
malignancy).
Ø Pa*ent 2-12 years old→ commonly present with insignificant
lymph nodes in neck secondary to frequent viral infec6on.

v Suggestive of malignant LNS:

Ø Large
Ø Hard.

Ø Non-tender.
Ø Amalgamated.

Ø Fixed to underlying 6ssue.

Ø Fixed to overlying skin.

59
 v Causes of Lymphadenopathy:
1) Localized:
a) Reac*ve:
• Infec6ous: bacterial, viral, fungal or mycobacterial.
• Non-infec6ous: sarcoidosis, Irrita6on, trauma.
b) Infiltra*ve:
• Metastasis from drained area.
2) Generalized:
a) Reac*ve:
• Infec6ous viral (infec6ous mononucleosis).
• Non-infec6ous: sarcoidosis, connec6ve 6ssue disease, serum.
b) Infiltra*ve:
• Malignant leukemia, lymphoma.
• Benign: lipidosis, his6ocytosis.
Cervical Lymph node:

Ø Insignificant if <2cm.
Ø Scalp, ENT, head and neck infec6on or malignant
Lymphoma.

Supraclavicular Lymph node:

Ø Significant if> 1 cm.
Ø Thoracic or GI malignancy.
Ø Enlarged lee supraclavicular→ Virchow's node (Abdominal malignancy).
Ø Enlarged right supraclavicular → Sen6nel lymph node (intrathoracic
malignancy).
Ø Axillary LNS:
• Insignificant if <3 cm.
• Unilateral Axillary L.N enlargement:
ü Infec6ons in upper limb (Most common).
ü Breast cancer.
ü Lymphoma.
Inguinal and Femoral Lymph node: Others Lymph node:
Ø If Insignificant <3 cm.
Ø Causes of enlargement:
ü Infec6ons of LL and genitalia including STD
(Sexually transmi:ed diseases).
ü Lymphoma.

60
 Cardiac Examination
Cardiac Introduction:
Ø Heart is 4 chambers:
• 4 values which have one way.
• 4 vessels.
Ø Systole mean ventricular contrac6on.
Ø Diastole mean ventricular relaxa6on.
Ø 1st HT Sound is closure of MV &TV during systole.
Ø 2nd HT Sound is closure of AV, PV during distole.
Ø Cop amount of blood come out from LT vent/m.6L.
Ø S.V amount of blood come out from LT vent/beat.
Ø 2 Types of HTN in HT:
1) pulmonary HTN.
2) systemic HTN.
Ø Systemic BP = Systole / diastole.
• Systole depend on:
1) stroke volume.
2) elas6city of aorta.
• Diastole depend on:
Ø Murmur > Turbulence of blood flow.
Ø Thrill → low pitched vibra6on "palpable murmur".
Ø Bs of HT → Coronary CT.
Ø Ventricular dilata?on versus hyper Trophy.
Ø pressure overload "volume overload".

Valve disease:
Ø stenosis:
1) mitral Tricusped.
2) Aor6c Pulm.
Ø Regurge:
1) Mitral tricuspid.
2) Aor6c Pulm.

1) mitral stenosis:
• so, in mitral stenosis there are:
1) Pulm Conges6on.
2) Pulm HTN.
3) Rt vent dilata6on & failure.
4) Systemic venous Conges6on.

61
 • Ausculta*on:

2) mitral regurge:
• So, in mitral regurge:
ü Lee Ventricle failure due to vol:
o Pulm cong.
o Pulm HTN.
o RT vent failure.
o SVC.
• Ausculta?on:

3) Aortic regurge:
Ø So, in AR L.T ventricle failure due to volume
overload.
Ø But 1st these in HC d.t ↑ Cop.
Ø Ausculta?on:

62
 4) Aortic stenosis:
Ø So, in ASLT vent hypertrophy & failure.
Ø Ausculta*on:

Apex of the heart :

• Defini*on:
Ø lower most & outer most part of Heart.
• normal:
Ø Lt Vent apex at Lt 5th ICS MCL.
• Туреs:
1) Lt vent apex Localized:
a) Hyperdynamic:
Ø Strong & not sustained in Vol overload.
Ø shieed downward outward dt It vent dilata6on.
Ø in MR, AR.
b) Heaving apex:
Ø strong & sustained in pressure overload.
Ø not shieed d.t Lee ventricular Hypertrophy.
Ø in As.
2) Rt vent apex Diffuse:
Ø shieed outward only in R.T Vent dilata6on as PR TR.
Mitral stenosis Mitral regurge Aor<c regurge Aor<c stenosis
S1 Accentuated Weak, muffled, masked Heard Heard
S2 Heard Heard Normal ‘’ringing in Weak or absent
aneurysm’’ Aor;c component
S3 - Present Present -
S4 - - - Present
Added sound Opening snap Func;onal MS Ejec;on systolic click
Murmur Mid diastolic Pansystolic Early diastolic Ejec;on systolic
Mitral area MA apex A2 A1
Localized Selec;ve propagate to axilla AI. LT sternal border, apex Caro;d
Rumbling & presys accent Harsh SoP blowing Harsh
LT lateral posi;on & exercise SiRng leaning forward at SiRng leaning
& cone end of expira;on forward at end of
expira;on
- Rare except if severe If severe -

63
 1-Heart Failure:

• Defini*on:
Ø inability of Heart to pump adequate
amount of blood to meet O2 requirement
or metabolic requirement of 6ssue
although normal filling pressure.
• Classifica*on:
1) Lt Side HF Rt Side HF.
2) Systolic HF diastolic HF.
3) a Cute HF Chronic HF.
4) ↑ Cop HF ↓COP HF.

Ø ↑ Cop HF: in hyperdynamic circula6on.

Left side heart failure:

• clinical picture:
a) pulmonary Congesion "backward" hallmark.
Ø Symptoms:
• Cough.
• dyspnea.
• orthopnea.
• PND.
• hemoptysis.
Ø Sign:
• Bilateral.
• Fine.
• Basal.
• Crepita6on.
b) ↓COP “forward":
Ø Symptoms:
• efforts →ASD+ dizziness.
Ø Sign:
• pallor.
• Cyanosis.
• cold extreme.
• Ischemia (liver, bowel, kidney).
• Hypotension.
• Rapid&weak pulse

64
 Right side heart failure:

• clinical picture:
1) systemic venous Conges*on: SVC. "back word", hallmark:
Ø Symptoms:
• abdominal distension.
• Jaundice.
• L.L swelling.
Ø Sign:
• Ascites.
• Tander hepatomegaly.
• L.L edema.
• Congested neck vein.
2) ↓Cop:
Ø "Forward manifesta6on".

cardiac examination:

cardiovascular system examination

Inspection Palpation Auscultation

- Shape of precordium.
-apex beat. i. Apex beat localization. i. Heart sounds:
- Pulsation in other areas: ii. Pulsation in following areas: -Mitral area M.
A) Pulmonary. - Pulmonary. - Pulmonary area P.
B) Parasternal. - Parasternal. - Aortic area A.
C) Artic. - Aortic. - Tricuspid area T.
D) Neck. iii.Thrills: - Opening snap.
E) Epigastric. - Mitral. ii. Murmurs:
F) JVP. - Aortic. - Mitral area.
- Carotid artery. - Aortic area.
- Pulmonary. - Bruit over carotids.
- Parasternal. - Pulmonary area.
iv. Palpates liver for hepatojugular - Tricuspid area.
reflux. - Parasternal area.
v. Feels for pulsatile liver. iii. Pericardial rub.
vi. Palpates for oedema. iv. Listening to the base of lungs.

65
Ø Epigastric Pulsa*on: Right Ventricle, Aorta Or Lee lobe of
the liver (Differen6ated By Palpa6on).
Ø Lt Parasternal Pulsa*on: Right Ventricle Enlargement.
Ø Aor*c Area Pulsa*on (2nd Right ICS): Aor6c Aneurysm,
Systemic Hypertension.
Ø Pulmonary Area Pulsa*on (2nd Le^ ICS): Pulmonary
Hypertension.
Ø Suprasternal/Caro*d Pulsa*on: Aor6c Regurgita6on
(Corrigan's Sign).

palpate apex:
Ø Defini*on:
• lower most & outer most part of Heart normal.
Ø Normal:
• Lt vent apex Located in.
• Lt 5th IC MCL Localized.
types of abnormal apex:
1- LT vent apex:
a) Heaving:
Ø Localized.
Ø At Lt 5th IC MCL.
Ø Occur d.t pressure overload LT vent
hypertrophy as AS sys HTN.
b) Hyperdynamic:
Ø Localized.
Ø Shieed outward & downward.
Ø Occur d.t vol overload ‘’l.t vent dil’’ as MR,AR.
2- RT vent apex:
Ø Diffuse.
Ø Shieed outward only.
Ø Due to Right ventricle dilata6on as in PR,TR.

Comments:
• Site: as L.T 4th IC MCL.
• Size: as localized.
• Force: strong.
• Dura6on: sustained or not.
• Characters: heaving or hyperdynamic.
• Rate.
• Rhythm.
• Thrill.

66
Auscultate Heart failure:

1st supine to auscultate HT 1st PT supine to auscultate

sound. HT sound.
2nd siTng & leaning forward at 2nd LT lateral posi6on to
end of exp to auscultate auscultate murmur.
murmur. IF:
IF: MS:
AS: - mid diastolic rumbling
- Ejec6ng sys harsh murmur. murmur & presys accent.
- prop to caro6d. - localized.
- auscultate on A1. - by conc.
AR: - accent S1.
- early diast soe blowing. MR:
- prop percordial. - pansystolic harsh murmur.
- auscultate on A2. - Prop to axilla.
- By diaph.
- masked S1.

Ø Mitral Area.

67
Ø Tricuspid Area.

Ø Pulmonary Area.

Ø Aor*c Area.

Ø Best Posi*on for Aor*c valve Ausculta*on.

Ø Le^ Lateral Pos. for Mitral stenosis.

68
Ø Radia*on:
• Murmur of Aor6c Stenosis Will Radiate To The Caro6ds.
• Murmur Of Mitral Regurgita6on radiates to The Lee Axilla.

Ø Grade:
• Grading The Murmurs According to Loudness Into Six Grades
(Levine's Grading System):

Grade Descrip*on
1 Barely audible
2 Soe but easily heard
3 Loud without a thrill
4 Loud with a thrill
5 Loud with minimal contact between stethoscope and chest
6 Loud with no contact between stethoscope and chest

Notes:

Ø S3: is addi6onal HT sound auscut on mitral or tricuspid area only in cases of

hyperdynamic S vol overload as: MR – AR -TR – PR.
Ø S4: is addi6onal HT sound auscut in case of pressure overload as: AS-SYS HTN.
Ø Sign of pulmonary Hypertension:
• Accent S2.
• Pulse on PA.
• Diast shock.
• Early diast murmur graham PR
• Or eject syst P5.

69
 Chest Examination
Local Examination of chest:

1) inspec?on:
a) Shape:
Ø Look tangen6ally from the feet of the pa6ent, check the back while the pa6ent is
siTng.
• Normal:
ü Ellip6cal.
ü AP (anterior axillary to posterior axillary fold) to transverse (from ant. axillary to ant.
axillary fold) = 5/7.
ü Symmetrical.
ü Oblique ribs.
ü Subcostal angle = 70-110°.
ü Moves freely with inspira6on.
• Barrel-shaped:
ü ↑ AP diameter.
ü Wide subcostal angle.
ü Kyphosis.
ü Transverse ribs.
ü IN: COPD, old age.
• Pectus excavatum:
ü Dt short central tendon of the diaphragm which may displace the heart →
arrhythmia.
ü May be acquired in shoemakers
• Pigeon-shaped:
ü Forward prominence of the sternum with the adjacent costal margin & triangular
cross sec6on.
• Rachi*c rosary:
ü Swelling of the costochondral junc6on of the ribs.
• Harrison's sulcus:
ü Horizontal groove running from the sternum outwards at the origin of diaphragm
from the ribs dt trac6on of the diaphragm on the lower ribs.
• Scoliosis of the spine:
ü Rt or It according to the site of convexity.
ü It leads to crowding of the ribs & thoracic bulge on the opposite side.
b) Symmetry:
ü Normal: symmetrical.
ü Flat: in fibrosis, coilapse.
ü Bulge: in pleural effusion, pneumothorax, large tumor, empyema necessitans.
c) Chest Wall:
1) Retrac*on of intercostals, suprasternal, supraclavicular spaces:

70
 Ø Normal: slight suprasternal or lower intercostals retrac6on in thin persons.
Ø ↑ retrac6on in obstruc6ve airway diseases.
Ø N.B.: Accessory muscles of respira6on are:
• Neck muscles which fix the clavicle.
• Upper limb muscles (la6ssimus dorsi) which approximate the ribs.
• Intercostal & abdominal muscles.
2) LiNen's sign:
Ø Normal shadow of the diaphragm during inspira6on in the last 6 intercostal spaces,
wavy movement.
Ø Absent in diaphragma6c paralysis
Ø Not apparent in: COPD, effusion, pneumothorax & obesity.
3) Hoover's sign:
Ø Inspiratory indrawing of the costal margin
a) Dt unopposed ac6on of the diaphragm on the
costal margin (which indraws), and loss of
ac6on of the intercostals (which outdraws).
b) Also in emphysema the diaphragm is flat &
moves towards the central tendon → was
considered a sure sign of emphysema in the
past.
4) Scar.
5) Abscess.
6) Collaterals.
7) Sinuses.
Hoover's sign
8) Pigmenta*on.
9) Nipple lines.
10) trauma.
2) Palpa?on:
1) Posi*on of the medias*num:
a) Upper medias*num by no*ng the posi*on of the trachea:
Ø Pa6ent's head should be central, siTng or lying down. The index finger is thrust
gently into the suprasternal notch in the midline, then inserted between the
trachea & the sternomastoid muscle on each side.
Ø If the trachea is deviated, the finger will encounter less resistance on the opposite
side of devia6on.
b) Lower medias*nal shi^ detected by the apex of the heart:
Ø The mechanism of shi^ is related to the-ve IPP i.e.
always pull.
Ø Shi^ to the same side: in fibrosis or collapse.
Ø Shi^ to the opposite side: in pleural effusion or
pneumothorax.

71
 2) Chest Movements:
Ø Examined for synchrony & range.
a) For upper chest:
Ø Put your hand flat over the apices with the thumbs mee6ng in the midline while the
pa6ent is supine. OR stand behind the siTng pa6ent & place the hands over the
shoulders onto the ant, chest below the clavicle.
b) For lower chest:
Ø Bimanually grasp the sides of the chest firmly to approximate the 6ps of the
outstretched thumbs with a skin fold over the chest.
c) The lower back:
Ø Examine the lower back in the same manner while the pa6ent is siTng.
3) Tac*le Vocal Fremitus (TVF):
Ø Feeling of vibra6on produced by a voice transmi:ed through the lungs & chest wall.
Ø Compare by flat or ulnar side of the hand on iden6cal areas of the chest wall ant., post.
& laterally. Ask the pa6ent to repeat 4 or 54 or 99 in English.
Ø Normal TVF:
• Equal, symmetrical.
• Except in the rt upper lobe where it is
↑ dt the rt main bronchus is near to
the chest wall (no barrier as in the lee
side), also the rt bronchus is wider.
• Normally ↓ in females, child (high
frequency), in old, ↑ in males (low
frequency)
Ø Abnormal ↑↑ in:
• Consolida6on.
• Large cavity near to the surface.
• Lung collapse with patent bronchus
• ↓↓in: fibrosis, collapse, effusion, COPD, pneumothorax.
4) Rhonchus Fremitus:
Ø In obstruc6on (with rhonchi).
5) Fric*on Fremitus:
Ø With pleural rub.
6) Others:
Ø Pulsa6on of the pulmonary artery.
Ø Crepitus (surgical emphysema).
3) Percussion:
Ø How?
• The middle finger is placed firmly in the intercostal space. The middle phalanx of
the middle finger is struck sharply. Light percussion from the front, heavy
percussion from the back. Move the wrist not the elbow. You must compare
between equal ant areas. Normal percussion note is resonance.

72
 • Abnormali6es:
a) Hyperresonance → COPD, pneumothorax.
b) Impaired.

c) Dull → collapse, fibrosis, consolida6on.

d) Tympani6c → normal on Traube's arca, pathological in large superficial
air cyst.
Ø Where? Percussion lines.
a) Anterior chest: the pt is semi-recumbent, arms slightly abducted in the mid- clavicular
lines with comparison.
• Normally: resonant 6ll the 5th space on the rt (→ liver dullness); & 6ll
the 3rd space on the lee (→ cardiac dullness)

b) Lateral chest: the pt is siTng raising the arm above the head in the mid- axillary lines.
• Normally: resonant 6ll the 7th space on the rt (→ liver dullness); & 6ll
the 9th space on the It (→ spleen).

c) Posterior chest wall: pt is siTng, folding the arms across the chest, heavy percussion
at the paravertebral line (midway between the scapular & the mid lines), scapular line
(at the inferior angle of the scapula).
• Normally: resonant 6ll the 10th ICS.
• NB: the angle of the scapula is at the level of the 7th rib, while its spine is at the 4th
ICS.

d) The clavicle: is percussed directly → medial 1/3 resonant, middle 1/3 impaired, lateral
1/3 dull as it is a:ached to thick muscles.

e) Traube's arca: a semilunar tympanic area over the lower lee hemithorax which
overlies the fundic air bubble. It is bounded by: the spleen from the lee, the liver from
the right, lower lee margin of the lung from above and lee costal margin from below.
ü If hyper resonant → COPD.
ü It is dull in → effusion, Splenomegaly, hepatomegaly, cancer stomach &
achalasia.
f) Krönig's isthmus: a band of resonance overlying the apex of the lung, it lies in the
supraclavicular fossa, 5-7 cm in width.
o Boundaries:
ü Imaginary line between sternoclavicular joint & C7.
ü Another imaginary line joining 2 points, one at the junc6on between the
medial 2/3 & the lateral 1/3 of the clavicle, & the other at the junc6on of
the medial 1/3 & lateral 2/3 of the spine of the scapula.

Ø Dull in → apical TB, Pancoast tumor, fibrosis, consolida6on & massive effusion.

73
Special percussion

a) Tidal percussion:
Ø It is important to detect the degree of lung expansion & the range of
diaphragma6c movements (by lung resonance between full insp & full exp on the
back)
Ø Also is important to differen6ate between supradiaphragma6c dullness (e.g.
basal consolida6on, fibrosis, pleural effusion) & infra- diaphragma6c dullness
(e.g. subphrenic & amebic abscess).
Ø Lastly it is important to detect diaphragma6c paralysis.

b) Shi^ing dullness:
Ø In hydropneumothorax.
+ve when you percuss the siTng pa6ent from above down 6ll the dull space, then fix
the percussing finger in this space. Ask the pa6ent to lic supine. The note will become
resonant, because the air is now towards the ant chest wall.
4) Ausculta?on:
a) Breath Sounds:
Normal → vesicular (alveolar): soe, with no pause, insp/exp=3:1, like‫ﺣﻔﻒ اﻻﺷﺠﺎر‬
best heard in the axilla & the inferior scapular area, it is louder (puerile) in children thin
persons.
Comment on:
I. Intensity: normal or ↓in any chest disease
II. Character:
1) Normally vesicular.
2) Vesicular with prolonged expira6on (harsh vesicular) in COPD & bronchial
asthma.
3) Bronchial:
Ø equal insp & cxp, gap is present, hollow character.
Ø Mechanism: loss of alveolar component which normally filters the high frequency
sounds > 200 Hertz, & allows transmission of low frequency sounds.
Ø Normally heard over the trachea, upper rt lung, above T1 & over the manubrium
sterni.
Ø Types of bronchial breathing:
a) Tubular (‫ )ح‬which is high pitched in consolida6on, Garland triangle of
effusion & D'espine's sign.
b) Cavernous (‫)خ‬: low pitched, over a cavity with relaxed wall.
ê
c) Amphoric (‫ زﺟﺎﺟﺔ‬èë ‫ﻨﻔﺦ‬å‫ )واﺣﺪ ﺑ‬over a cavity with tense wall & tension
pneumothorax.
4) Bronchovesicular: inspiratory vesicular & expiratory bronchial.
5) Vesicular bronchial: the reverse Both 4. & 5. in cases of localized fibrosis &
resolving consolida6on.

74
b) Adven??ous sounds:
I. Rhonci:
Ø Musical, con6nuous, mainly expiratory because expira6on is a passive process. - It
occurs dt obstruc6on.
Ø Types:
a) Sibilant (high-pitched, wheezes) if size of obstruc6on is marked.
b) Sonorrus (low-pitched) if size of obstruc6on is ↓↓↓.
II. Crepita*ons (crackles, rales):
Ø Interrupted, inspiratory
Ø Intensity may be:
a) Fine: (‫ )ﺻﻮت اﻟﺸﻌﺮ‬in pulmonary conges6on or early pneumonia.
b) Medium-sized: fluid in medium-sized bronchi, in cavity, collapse, bronchi6s,
bronchiectasis or consolida6on.

c) Coarse: fluid in large bronchi, in cases of pulmonary edema.

Ø Pitch may be:
a) Consona6ng: if consolida6on around the diseased bronchi (‫)ﻃﺮﻗﻌﺔ ﻓﺸﺎر‬.
b) Non-consona6ng: if no consolida6on around the diseased bronchi, it is
applied to medium-sized, ± coarse
Ø The old mechanism: passage of air into fluid
Ø Recent mechanism of crackles: sudden explosive opening of the collapsed alveoli .
Ø It may be:
a) Early in inspira6on: in COPD.
b) Late in inspira6on: in restric6ve lung disease.
Ø Leathery Crepita6ons (Velcro) in inters66al lung fibrosis dt unequal opening of the
alveoli.
III. Pleural rub:
Ø In pleurisy.
Ø Scratchy
Ø At the end of insp & early in expira6on.
Ø Disappears when the pa6ent stops his breath.
c) Vocal resonance:
Ø It corresponds to TVF.
1) Intensity:
Ø ↑↑ in consolida6on.
Ø ↓↓ in fibrosis, collapse, effusion.
2) Character:
ü Normally: unclear syllables.
ü Bronchophony: clear syllables, in consolida6on.
ü Whispering pectoriloquy: in consolida6on (‫ﺴﻤﻌﻬﺎ ﻋﺎﻟﺔ‬ß ‫ﺎﻟﻬﻤﺲ‬£ 44 ‫)اﻟﻌﺎن †ﻘﻮل‬.
ü Agophony: nasal tone above the level of effusion.
ü E → A sign.
Ø Compressed lung be:er transmits sound & fluid absorb low-pitched sound.

75
 d) Special signs:
1) Succussion splash: in hydropneumothorax.
2) Coin test: in tension pneumothorax, you hear ringing bell on the posterior wall
when you percuss two coins on the ant chest.
3) D'Espine's sign: bronchial breathing below T4 in adults & T2 in children in
tracheobronchial lymph node enlargement.

Remember:

1) The lung apices extend 3-5 cm above each clavicle and back to the level of C7. The ant borders
meet in the midline at the sternal angle.
Ø On the rt side: it descends 6ll it reaches the 6th costosternal junc6on, 8th in mid-axillary
line, 10th in the scapular line.

Ø On the lee side: it descends 6ll it reaches the 4th costochondral junc6on, 6th in mid-
clavicular, 8th in the mid-axillary, 10th scapular.
Ø Pleura is 2 spaces below.
2) The oblique fissure from T2 → 6 costal car6lage MCL, horizontal line from the 4th costal margin to
meet with the oblique at the MAL (only in the rt lung).
3) Bifurca*on of the trachea is at the Lewis angle & T4.
Ø The most prominent spine: C7.
Ø The spine of the scapula is at T3.
Ø The angle of the scapula is at T7, 7th rib.
4) The bare area of the heart:
Ø The rt border is the midline, the lee border is a
line running from the midline opposite to the 4th
costal car6lage to the 6th rib in the parasternal
line. The inferior border con6nues with the liver
dullness.

76
 Cardio-Respiratory Symptoms

Dyspnea
v Dyspnea:
Ø It is a subjec6ve feeling of difficulty breathing.
v Grades of dyspnea:
Ø Grade I: Dyspnea on doing more than the usual daily effort.
Ø Grade II: Dyspnea on doing the usual daily effort.
Ø Grade III: Dyspnea on doing less than the usual daily effort.
Ø Grade IV: Dyspnea at rest.
v Other forms of dyspnea:
Ø Paroxysmal nocturnal dyspnea (PND) :
• It is a paroxysmal a:ack of dyspnea that usually occurs at night, awake the pa6ent 2-3
hours aeer sleep with marked inspiratory dyspnea, cough with frothy expectora6on,
figh6ng for air.
• It occurs in pa6ents with conges6ve heart failure.
• The main mechanism is aggrava6on of pulmonary venous conges6on due to absorp6on
of edema fluid from ECS to the circula6on increasing the venous return to the heart.
• When it is associated with wheezes due to bronchospasm it is known as "Cardiac
Asthma".

v Differentiation between cardiac and bronchial asthma:

cardiac Bronchial
Age Any age Usually, young age
History Cardiac symptoms Chest symptoms
Dura*on Usually, short Usually long
Time of aNack 2-3 hours aFer sleep Early morning
Dyspnea Mainly inspiratory Mainly expiratory
Sputum Frothy ± blood Enged Thick pellets
Chest examina*on Basal crepitaEons Generalized wheezes
Heart examina*on Gallop and murmurs Normal
ECG Abnormal Normal
Adrenaline Contraindicated Improve the condiEon
Morphine Drug of choice Contraindicated
Aminophylline Improve the condiEon Improve the condiEon

77
 Orthopnea
v Orthopnea:
Ø It is dyspnea that occurs or increases on lying flat and is relieved par6ally or
completely by siTng.

Ø Cardiac: Increased venous return on lying flat.

Ø Pulmonary: Disturbed V/Q ra6o on lying down.

Ø Abdominal: Eleva6on of diaphragm.

Ø Platypnea: It is a type of dyspnea that occurs on siTng and relieved on lying down. It
is usually due to a disturbed V/Q ra6o on siTng.

Ø Trepopnea: It is a type of dyspnea that occurs on lying on one side. It is usually due to
a disturbed V/Q ra6o on lying to that side.

Ø Pathogenesis of dyspnea: it is either due to:

a) Increased ven*la*on:
• This is due to s6mula6on of the respiratory center either by:
a) Chemical factors: Hypoxia, hypercapnia or acidosis.
b) Reflex s*mula*on from pulmonary vessels, lung *ssues, pulmonary veins or
right atrium.
1) Ac6va6on of Hering-Breuer reflex due to inters66al pulmonary
oedema result into tachypnea and dyspnea.
2) Ac6va6on of Churchill-Cope reflex; due to pulmonary venous
conges6on.
b) Decreased vital capacity of the lung:
• This is due to:
1) Mechanical factors:
a) Pulmonary conges6on.
b) Low cardiac output leads to fa6gue and weakness of respiratory muscles.
c) Hydrothorax leads to mechanical compression of the lungs.
d) Ascites and enlarged tender liver which may elevate the diaphragm and
decreases its mobility.
e) Massive pericardial effusion and huge cardiomegaly occasionally compress
the lungs and bronchi.

2) Disturbed V/Q ra*o:

Ø The well-ven6lated areas of the lung should be well perfused with blood and
vice versa. This keeps the V/Q ra6o within the normal range. If this is disturbed
dyspnea occurs.

78
• Causes of dyspnea:
Ø Non-cardiorespiratory: anemia, metabolic acidosis, Psychogenic.

Ø Cardiac: Lee ventricular failure, mitral valve disease, massive

pericardial effusion.

Ø Respiratory:
o Chronic Obstruc6ve Pulmonary Diseases (emphysema, asthma).
o Parenchymal lung diseases (Inters66al pulmonary fibrosis,
TB,Pneumonia).
o Pleural diseases (effusion, pneumothorax, fibrosis) Pulmonary
embolism.
o Bronchogenic carcinoma.
o Diseases of the chest wall (Kyphoscoliosis).
o Neuromuscular diseases (Myasthenia Gravis).

79
 Chest Pain
v Chest Pain:
• Causes of chest pain:
Ø Cardiac:
ü Ischemic: angina, myocardial infarc6on, aor6c
stenosis.
ü non-ischemic: aor6c dissec6on, Pericardi6s.

Ø Non cardiac:
a) Gastro-esophageal: Reflux esophagi6s.
b) Radia*ng pain from upper abdominal organs: Perforated pep6c ulcer, biliary colic,
acute cholecys66s, acute pancrea66s.

c) Pulmonary:
• Pulmonary vasculature: Acute pulmonary thromboembolism.
• Pulmonary parenchymal: Pneumonia, Bronchi6s, Cancer.
• Pleural: Pneumothorax, Pleurisy
• Medias6nal diseases.
d) Musculoskeletal: Rib fracture, Costochondri6s, osteomyeli6s, metastases.

e) Neuro*c (Herpes zoster)

f) Psychiatric.

Ø Life threatening causes: All of these could lead to sudden death.

• Acute Coronary Syndrome/Myocardial infarc6on.
• Pulmonary embolus.
• Aor6c dissec6on.
• Tension Pneumothorax.

Ø Chest pain due to myocardial infarc*on

1) > 30 min.
2) Retrosternal.

3) Radiate to lower jaw, medial aspect of Lt arm, medial 2 fingers (never affect upper
jaw).
4) Character: burning, constric6ng, heaviness, stabbing. (never s*tching).

5) Aggravated by: effort, emo6on, cold, intercourse.

6) Relieved by: rest or sublingual nitroglycerine.

7) Associated with (N, V, dyspnea, swea6ng, and palpita6on).

80
 Palpitation
v Palpitation:
Ø Palpita6on is awareness of the heartbeat.
Ø It results from:
• Change in rhythm, e.g. arrhythmias.
• Change in rate, e.g. tachycardia or
bradycardia.
• Change in force of cardiac contrac6on
(volume overload).
Ø Ask about: Rela6on to exer6on, Onset, dura6on, offset, Regularity.

Syncope
v Syncope:
Ø It is sudden transient loss of consciousness with a fairly quick recovery, due to acute
cerebral hypoxia and ischemia.
Ø The most common cause is simple fain6ng due to vagal
over ac6vity.
Ø Differen*al diagnosis: Epilepsy, hysteria, hypoglycemia.
Ø Causes of Syncope:
1) Cardiac syncope (due to low COP):
a) Cardiac arrhythmias
b) Acute heart failure e.g. in myocardial infarc6on.
c) Acute reduc6on of venous return e.g. in severe hemorrhage, severe
hypovolemia, and excessive peripheral vasodilata6on.
d) Obstruc6on of blood flow: Aor6c stenosis, Defec6ve prosthe6c valve,
Massive pulmonary embolism, Ball and valve thrombus in the lee atrium.
2) Vasomotor syncope:
ü Vasovagal aNack: due to severe vagal s6mula6on leading to marked
bradycardia and vasodilata6on. This may occur due to severe emo6onal
stress - severe pain - trauma (e.g. to tes6cles). There will be hypotension,
pallor, swea6ng and bradycardia.
3) Postural syncope (orthosta*c syncope)
a) Autonomic neuropathy (Diabe6c).
b) Hypovolemia.
c) Prolonged recumbency.
d) Pregnancy.
4) Cerebral syncope:
ü due to brain or brain stem ischemia.
5) Miscellaneous:
a) Hypoxic syncope: Fallot's tetralogy-high al6tude- severe anemia.
b) Tussive syncope.
c) Micturi6on syncope.

81
 Cough
v Cough:
Ø It is a characteris6c sound caused by a forced expulsion against an ini6ally closed
gloTs.
Ø Acute cough is one las6ng less than 3 weeks. The most common cause of acute cough
is acute upper respiratory tract viral infec*on. Acute cough is usually self-limi6ng and
benign but may occur in more serious condi6ons.
Ø Chronic cough lasts more than 8 weeks. Chronic cough in a
non-smoker with a normal chest X-ray is usually caused by
gastro-esophageal reflux disease, chronic sinus disease with
postnasal drip or angiotensin-conver6ng enzyme inhibitors.
Ø Dry cough Trachei6s and pneumonia cause dry, centrally
painful and nonproduc6ve cough. Chronic dry cough occurs in
inters66al lung disease, e.g. idiopathic pulmonary fibrosis.
Ø Produc*ve cough It is mucus produced from the respiratory tract. The normal lung
produces about 100 ml of clear sputum each day, which is transported to the
oropharynx and swallowed. There are four main types of sputum:
• Clear or 'mucoid' sputum is produced in chronic bronchi6s and COPD with
no ac6ve infec6on.
• Yellow sputum occurs in acute lower respiratory tract infec6on (live
neutrophils) and in asthma (eosinophils).
• Green purulent sputum (dead neutrophils) indicates chronic infec6on,
e.g.in COPD or bronchiectasis.
• Rusty red sputum can occur in early pneumococcal pneumonia, as
pneumonic inflamma6on causes lysis of red cells.

Ø Amount:
ü Bronchiectasis causes large volumes of purulent sputum, which varies
with posture.
ü Suddenly coughing up large amounts of purulent sputum on a single
occasion suggests rupture of a lung abscess or empyema into the
bronchial tree.
ü Large volumes of watery sputum with a pink 6nge in an acutely breathless
pa6ent suggest pulmonary edema. If occurring over weeks
(bronchorrhea), suggests alveolar cell cancer.

Ø Taste or smell:
ü Foul-tas6ng or smelling sputum suggests anaerobic bacterial infec6on,
and occurs in bronchiectasis, lung abscess and empyema. In
bronchiectasis a change of sputum taste may indicate an infec6ve
exacerba6on.

82
 Hemoptysis
v Hemoptysis:
Ø It is coughing of blood.

Ø Common causes: chronic bronchi6s, bronchogenic carcinoma,

bronchiectasis.
, tuberculosis, aspergilloma, lung abscess, pulmonary embolism,
mitral stenosis.

Ø It should be differen6ated from hematemesis.

Hemoptysis Hematemesis
Cough of blood Vomi6ng of blood
alkaline Acidic
Bright red Coffee ground
frothy Contain food par6cles
Associated with thoracic Associated with
symptoms gastrointes6nal or hepa6c
symptoms
No melena Associated with melena

83
 Hoarseness of voice

v Hoarseness of voice:
Ø It is most commonly caused by laryngi6s. Damage to the lee
recurrent laryngeal nerve by lung cancer at the lee hilum causes
hoarseness with a prolonged, low-pitched, 'bovine' cough as the
lee vocal cord cannot adduct to the midline.

Wheezy chest

v Wheezy chest:
Ø It is a high-pitched whistling sound produced by air
passing through narrowed small airways. It occurs with
expira6on. Wheeze on exercise is common in asthma
and COPD. Night wakening with wheeze suggests
asthma or paroxysmal nocturnal dyspnea, but wheeze
aeer wakening in the morning suggests COPD.

84
 Multiple notes
1) Defini?on of chronic bronchi?s:
Ø Cough & sputum for 3m of 2 successive years.
2) Defini?on of emphysema:
Ø irreversible distension of air space distal to terminal bronchiole & destruc6on
of will ↑ dead space→ hypoxia→ Corpulmonale.
3) Risk factor of COPD:
1) Smoking main.
2) air pollu6on.
3) Occupa6onal.
4) gene6c & FH.
4) sign of COPD.
5) Sign of HF.
6) NYHA class of Hf:
1) Class 1: no limit physical ac6vity.
2) Class 2: mild physical ac6vity.
3) Class 3: marked physical ac6vity.
4) Class 4: sym at rest.

7) ACC/AHA staging of HF:

a) high risk
b)structure HF & no sym.
c) Sym.
d)Refractor HF.

8) Cardiac Cachexia in long stand Hf especially Rt:

Ø d.t Svc (liver-intes*ne).

9) early Careline sign in decompensated if in most pathologic S3 gallop proto

diastolic.

10) edema is cardinal sym of Hf but not correlate & level of SVC.
11) Head & neck exam:
• cranium: Salivary gland, Eye, Ear.
• scalp: Eye, Mouth, Nose.
12) Large head:
ü Hydrocephalus.
ü Acromegaly.
ü Thalassemia.

85
13) Small head → microcephaly.

14) acromegelic face:

ü large head & prolonged.
ü prominent Supraorbital ridge.
ü Prominent zygoma.
ü Protruded maxilla.
ü Proganithm.
ü Diastema.
ü Side angle between ramus & body of mandible.
15) Thalassemic face:
ü Large head.
ü Frontal bossing.
ü Protruded maxilla.
ü Depressed nasal bridge.
16) alopecia: SLE.
17) Course bri2le hairs: hypothyroid.
18) Tender over temporal art: Temporal artri6s.
19) Loss of outer third of eyebrow:
• myxedema.
• leprosy.
20) ptosis III Cranial N palsy: horner syndrome, myasthenes, cong.
21) pully eye: Nephro6c, Myxedema, Angioedema, surgical emphysema.
22) xanthelasma: hyperlipidemia.
23) Sub Conjunc?ve Hemorrhage → HTN or severe Cough.
24) Vit A deficiency: Xerosis é biotot spot.
25) bluish sclera scleromalacia→ RA, Marfan, Ehlers Danlos.
26) Arcus lipider in cornea in dyslipidemia.
27) Kayser flesher in cornea in dyslipidemia.
28) Corneal obacity: Inflamma6on or ulcer.
29) Nose:
• enlarge acromegaly.
• depressed nasal bridge, Sadelle shape:
ü syph, cong.
ü leprosy, trauma.
• Pinched → systemic sclerosis.
• Ac6ng ala nasain → pheum.
30) Oduor:
• Acetone DM.
• fetor hepa6c -liver Failure.
• Fish → uremia.

86
31) Nodule in ear → tophi of good.
32) Angular stoma??s → Iron deficiency anemia.
33) Causes of oral ulcer:
• Aphthous.
• Infec6on.
• Chemotherapy.
• Becht painful.
• SLE painless.
34) Diastema: separa6ng teeth acromegaly.
35) Loss teeth → Diabetes mellitus , hyperparathyroidism
36) Gum bleeding → Scurvy.
37) Gum hypertrophy → vit c ↓ phenytoin, AML.
38) white Coated tongue → Candida, leukoplakia.
39) brown → smoking.
40) Magenta red → riboflavin deficiency.
41) fiery red → vitamin B3 deficiency ‘Pellagra’.
42) glazed tongue at DA ↓B12, 2,3 "atrophic glossi6s.
43) Geographic tongue→ benign asym map like.
44) Strawberry tongue → Scarlet fever.
45) leukoplakia →precancerous in immunodeficiency.
46) Dry tongue → dehydra6on in DKA.
47) Macroglossia:
ü Acromegaly.
ü Amyloid.
ü Myxedema.
ü Inflamma6on.
48) deviated toward paralyzed > facial nerve palsy.
49) Tremor → liver failure.
50) Buccal:
ü Blue →lead.
ü Brown → Addison.
ü brown around mouth + polyps.
51) Xerostomia: dehydra6on Sjogren, an6histamine, an6cholinergic.
52) Paro?d gland enlargement:
ü Mumps.
ü sjorgens syndrome.
ü ancylostoma.
ü sarcoidosis.

87
53) Flushing: episode, transient a:ack of redness of skin & warmth or burning of face, neck:
• Physical
• Effort
• Menapam.
• Spicy.
• Carcinoid.
• V D alcohol choline.
54) Erythema: persistent redness of skin.
ü Palmar erythema → liver failure.
ü Malar (MS-SLE).
ü Polycythemia

88