200 POINTS TO RMEMBER IN GENERAL PATHOLOGY - DR EJAZ WARIS

200 Important Points with Definitions to
Remember in General Pathology
By
Dr. Ejaz Waris, Associate Professor Histopathology AMDC
1. Hyperplasia is an increase in the number of cells in an organ or tissue,
usually resulting in increased volume of the organ or tissue.
2. Hypertrophy refers to an increase in the size of cells, resulting in an
increase in the size of the organ.
3. Atrophy is the shrinkage in the size of the cell by loss of cell
substance.
4. Metaplasia is defined as a reversible change in which one adult cell
type (epithelial or mesenchymal) is replaced by another adult cell
type.
5. Cell swelling is the earliest sign of a reversible cell injury.
6. Free radical is a chemical species that have a single unpaired electron
in an outer orbit.
7. Necrosis is a spectrum of morphological changes that follow cell death
in a living tissue largely resulting from the progressive degradative
action of enzymes on the lethally injured cell.
8. Necrosis has six major type; coagulative, Caseous, Liquefactive,
fibrinoid,gangrenous and Fat.
9. Apoptosis (Greek falling off) is defined as a pathway of programmed
cell death that is aimed at a highly regulated intracellular programme
in which cells destined to death by activated enzyme that degrade the
cell’s DNA and nuclear and cytoplasmic proteins.
10. Morphologically an apoptotic cell shows: a) cell shrinkage, b)
chromatin condensation c) formation of cytoplasmic blebs and
apoptotic bodies, d) phagocytosis by macrophages.
11. Apoptosis has two phases a) Initiation phase extrinsic and intrinsic
pathways b)Execution phase c)phagocytosis of dead cell

12. Genes promoting apoptosis are: bax,bak,bim
13. Genes inhibiting apoptosis are bcl 2 family.
14. Initiator caspase are 8 & 9, while executioner caspases are mainly 3 &
6.
15. Dystrophic calcification is always seen in damaged tissues while
metastatic calcification may occur in normal tissues whenever there is
hyperplasia.
16. Inflammation is a complex reaction to injurious agents such as
microbes and damaged, usually necrotic cells that consists of vascular
responses, migration and activation of leukocytes, and systemic
reactions.
17. Inflammatory response consist of TWO main components: vascular &
cellular, and divided into TWO main patterns: Acute and Chronic.
18. Vasodilatation is one of the earliest manifestation of acute
inflammation, if follows a transient vasoconstriction of arterioles
lasting few seconds.
19. Increased vascular permeability leading to the escape of a protein-rich
fluid (exudate) into the extravascular tissue in the HALL MARK of acute
inflammation.
20. Formation of endothelial gaps in venules is the most common cause of
vascular leakage.
21. Leukocytes Adhesion molecular families have a major classes: a)
Selectins (E,L & P types), b) Integrins, c) Immunoglobulin family of
adhesion molecules and d) Mucin like glycoproteins.
22. Selectins mainly involved in rolling of leukocytes, PECAM in
transmigration and immunoglobulin family in adhesions.
23. Chemotaxis is defined as uni directional migration of leukocytes
towards the site of injury under chemical gradient action.
24. Most important chemotactic agents are C5a,LTB4 and bacterial
products.
25. Major opsonins are: C3b & Fc fragment of IgG proteins

26. H202-MPO-Halide systein is the most efficient bactericidal system in
neutrophils.
27. Chediak-Higashi Syndrome is an autosomal recessive condition
characterized by failure of fusion of phagosome with lysosome.
28. Chronic granulomatous disease of childhood results from inherited
defects in the components of NAPDH oxidase which generates
superoxide, leading to body infections.
29. Vasoactive amines are histamine and serotonin which are the main
players of early inflammation.
30. Plasma Proteins are: Complement system proteins, clotting system
and fibrinolytic system.
31. Prostaglandins are vasodilators.
32. MAC (C5B6789) is the membrane attack complex, which finally kills
the bacteria.
33. Activated Hageman factor initiates FOUR systems involved in
inflammatory responses Kinin, Clotting, fibrinolytic and complement
system
34. SRS-A (slow releasing substance of anaphylaxis) constitutes LTC4,
LTD4 & LTE4 promote vasoconstriction, bronchospasm & increased
vascular permeability.
35. Lipoxins are bioactive products generated from transcellular
biosynthetic mechanisms involving neutrophils and platelets.
36. IL-1 & TNF are two of the MAJOR cytokines that mediate inflammation.
37. Major chemokines include: IL-8, MCP-1, eotaxin, MIP-1, Lymphotactin
and RANTES.
38. Nitric oxide plays major role in production of vasodilation by relaxing
vascular smooth muscle in ischemic conditions.
39. The major mediators of pain are Bradykinin & Prostaglandins
40. Potent vasodilators are : Vasoactive Amines, Prostaglandins & NO.

41. Acute inflammation is defined as a rapid response to an injurious agent
that serves to deliver mediators of host defense – leukocytes and
plasma proteins to the site of injury.
42. Chronic inflammation is defined as an inflammation of prolonged
duration, in which active inflammation, tissue destruction and attempts
at repair are proceeding simultaneously.
43. Neutrophils are the main cells of acute inflammation (exudates) while
Mononuclear cells (with one nucleus are the main cells of chronic
inflammation .Mononuclear cells include Lymphocytes, Monocytes,
Macrophages and Plasma cells.
44. Macrophages are the prima donna (main working cell) of chronic
inflammation, while lymphocytes are present in increased number.
45. Granuloma is a focus of chronic inflammation, consisting of
microscopic aggregation of macrophages that are transformed into
epithelium like cells surrounded by a collar of mononuclear leukocytes.
Don’t confuse it with Granulation tissue which has capillaries,
fibroblasts, and a variable amount of inflammatory cells.
46. Classical tuberculous granulomas is composed of epithelioid cells,
Langhan’s multinucleated giant cells, caseation necrosis and collar of
lymphocytes. There are two types of Granulomas: Immune & foreign
body.
47. There are 3 types of cells in the body: Continously dividing labile cells,
Quiscent or stable cells and Permanent Non-dividing cells.
48. Stem cells are cells characterized by their prolonged self renewal
capacity and by the asymmetric replication. They are of two types:
embryonic & adult stem cells.
49. VEGF & fibroblast Growth factor are mainly involved in angiogenesis.
50. TGF-B is a growth inhibitor for most epithelial cells and leukocytes,
potent fibrogenic agent and a strong anti-inflammatory effect.
51. Extracellualr matrix is formed of these groups of molecules : a)
fibronectin b) adhesive glycoproteins and c) proteoglycans &
hyaluronic acid.

52. Collagens is the most common protein in the animal world, with 27
types discovered so far. Types I, II, III, V & X) are fibrillar and most
common while type IV is non fibrillar.
53. Healing by 2nd
intention differs from 1st
intention in three ways; a)
inflammatory reaction is more intense, b) Much more granulation
tissue forms and c) wound contraction phenomenon.
54. Accumulation of excessive amounts of collagen may give rise to a
hypertrophic scar while if scar tissue grows beyond the boundaries of
the original wound and does not regress, it is called keloid.
55. Edema is defined as accumulation of fluid in the interstitial tissue
spaces and body cavities.
56. Local increased volume of blood in a particular tissue leads to
Hyperemia and congestion. Hyperemia is an active process, resulting
from augmented tissue inflow because of arteriolar dilation while
Congestion is a passive process resulting from impaired outflow from
tissue.
57. Heart failure cells are hemosiderin laden macrophages seen in chronic
pulmonary congestion.
58. Petechiae are minute 1 to 2 mm hemorrhages into skin, mucous
membranes or serosa surfaces, while >3 mm hemorrhages are called
Purpura and more larger > 1 to 2 cm subcutaneous hematomas are
called Ecchymoses.
59. Virchow’s triad include: a) Endothelial injury b) Stasis or turbulent
blood flow & c) blood hypercoagulability.
60. Of the inherited causes of hypercoagulability, mutation in the factor V
gene and prothrombin gene are the most common.
61. Lines of Zahn are laminated lines produced by alternating pale layers
of platelets admixed with some fibrin and darker layers containing
more red cells.
62. Fate of thrombus include: propagation embolization, dissolution,
organization and recanalization.

63. Embolus is a detached intravascular solid, liquid or gaseous mass that
is carried by the blood to a site distant from its point of origin. The
phenomenon is called embolism.
64. Infarct is an area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage in a particular tissue.
65. The most dominant histologic characteristic of infarction is ischemic
coagulative necrosis.
66. Shock is the systemic hypoperfusion caused by reduction either in
cardiac output or in the effective circulating blood volume, and
resulting in hypotension followed by impaired tissue perfusion and
cellular hypoxia.
67. Major types of shock include: cardiogenic, hypovolemic, septic,
neurogenic and anaphylactic.
68. Mutation is defined as a permanent change in the DNA.
69. Marfan’s syndrome is a disorder of the connective tissue of the body,
characterized by changes in the skeleton, eyes and cvs. Mainly cause
by defects in an extracellular glycoprotein Firbillin-1.
70. Ehlers-Danlos Syndrome comprise a clinically and genetically
heterogenous groups of disorders that result from some defect in the
syntesis or structure of fibrillar collagen.
71. Amyloid is a pathologic proteinaceous substance deposited between
cells in various tissues and organs of the body in a wide variety of
clinical settings.
72. Neoplasm is an abnormal mass, the growth of which exceeds and in
uncoordinated with that of the normal tissue and persists in the same
excessive manner after cessation of the stimuli which evoked the
change.
73. Tumor has two basic components: Parenchyma & stroma, while
tumors are of two types: Benign and Malignant.
74. Benign tumors are well differentiated, grow slowly and don’t show
invasion and metastases, while Malignant tumors range from well to
undifferentiated, grow fast and show invasion and metastasis.

75. Single most important feature to differentiate benign from malignant
tumor is METASTASIS.
76. Carcinomas mostly use lymphatic routes and sarcomas mostly use
hematogenous routes of spread.
77. Four types of genes are normally working in human body: a) proto-
oncogens b) antioncogenes, c) apoptotic genes and d)DNA repair
genes
78. Proto-oncogenes are changed to oncogenes by three processes:
mutation, translocation and amplification.
79. Major oncogenes are; RAS, ERB-B1, RET, KIT, ABL, C-MYC & N-MYC.
80. Major antioncogenes are: RB, TP53, W.-1, NF-1, BRCA-1, APC.
81. Oncogenic viruses include; Human Papilloma virus, Hepatitis B virus,
Epstein Barr virus ,Kaposi Sarcoma Herpes viruses & Human T-Cell
leukemia virus (The only oncogenic RNA virus).
82. Chemical carcinogenesis is a multistep process, divided into initiation
and promotion phases.
83. Major chemical carcinogens associated as include: Asbestos with
Mesothelioma, Aniline dyes with TCC, Nitrates-Gastric carcinoma,
Aflatoxin with HCC, Vinyl chloride with Angiosarcoma Liver.
84. Radiation induced malignancies include leukemias and papillary
carcinoma thyroid.
85. Major paraneoplastic synbdromes include, Cushing syndrome, ADH
secretion by small cell carcinoma lung, Hypercalcemia by Squamous
cell carcinoma lung, hypoglycemia by Fibrosarcoma and HCC,
Polycythemia by RCC and hypertrophia osteoarthropathy by CA lung.
86. Major tumor markers included : HCG for Choriocarcinoma, calcitonin
for medullary carcinoma thyroid, alpha fetoprotein-HCC and Non-
seminomatous germ cell tumor testis, CEA-CA colon, PAP For CA
prostate, CA-125 for Ovarian CA , Ca 19-9 for CA Colon and
pancreas ,CA 15-3 for CA breast.
87. Major immunomarkers for epithelial tumors are cytokeratin, for
mesenchymal tumor – vimentin, for leukocyte origin tumor – leukocyte

common antigen, S100 for neural origin tumors and for skeletal
muscle tumors – desmin.
88. Type I hypersensitivity (“anaphylactic”) or “immediate
hypersensitivity”) is the result of antigen binding to IgE on the surface
of mast cells and basophils. These instantly degranulate and release
active substances into the surrounding tissue.
89. Type II cytotoxic hypersensitivity, antibodies attach to antigens on the
surfaces of a cell and then something injures or destroys the cell.
90. In type III immune-complex hypersensitivity reaction, “Soluble
antigens” precipitate with antibodies, usually this happens 2-4 hours
after exposure. This sort of tissue injury is mediated by antigen-
antibody complexes (“immune complexes”).
91. Type IV Hypersensitivity reaction is called “delayed hypersensitivity”.
It is mediated by sensitized CD4+T lymphocytes which process
antigens in association with class II HLA molecules and release
lymphokines.
92. Immune reactions are divided into two broad categories: A) Humoral
immunity-B-cell lymphocyte mediated via production of antibody and
Often develops as a response to soluble antigens, and B) Cellular
immunity-T-Cell lymphocyte mediated. CD4+helper lymphocytes: help
B cells make antibody and also help to generate cytotoxic T cells.
93. Major histocompatibility complex is present on all nucleated cells.
94. The HLA system is a key factor in most Transplant rejection reactions.
Reactions are mediated by either T lymphocytes or by antibody.
95. Toll like receptors are membrane proteins that recognize a variety of
microbe derived molecules and stimulate innate immune responses
against the microbes.
96. CD4 molecule is a high affinity receptor for HIV
97. Major autoimmune disease include Hashimoto’s thyroiditis,
Rheumatoid Arthritis, Sjogren’s syndrome, ankylosing spondylitis.

98. Gamma interferon is one of the cytokine to activate macrophages and
also play major Role in Granuloma formation.
99. Cytokines are mediators released from one cell and modulate the
actions of another cell.
100. Squamous cell carcinoma is characterized by sheets, groups and
clusters of pleomorphic malignant epithelial cells with high N/C
ratio,hyperchromatic nuclei and pale cytoplasm.Keratin epithelial
pearls,intercellular bridges and individual cell keratinization are seen.
101. Adenocarcinoma is characterized by back to back closely packed
glands lined by pleomorphic malignant epithelial cells with high N/C
ratio,hyperchromatic nuclei and eosinophilic cytoplasm.Wall sharing is
often noted.
102. Two types of vaccines include: Live vaccines; Measles, Mumps,
Rubella, Varicella, Polio etc and Killed vaccines: Rabies, Polio, Hepatitis
A.
103. Protooncogenes are converted into oncogenes.
104. p53 works by DNA repair and promoting apoptosis.
105. RB gene activates and Works in hypophosphorylated form.
106. RAS gene protooncogene protein is GTP bound and Works with GAP in
cooridination with GTPase.
107. Gliomas and BCC are highly malignant but dont usually metastasize.
108. AFB is acid fase bacillus ( Mycobacterium tuberculosis ) and called so
because it resists decolourization by Concentrated Acids.
109. Tigered lipid effect is seen in Herat.
110. Major complement proteins include :
Opsonization by C3b
Chemotaxis by C5a
Anaphylatoxin C3a, C4a, C5a
Membrane breakdown and killing C5b,6,7,8,9 MAC complex
Enhancement of antibody production C3b

111. FNAC and biopsy are key investigations to early diagnose a tumor.
112. Active Immunity is the resistance induced after contact with foreign
antigens eg microorganisms, immunization with live or killed infectious
agents, exposure to microbial products (toxins, toxoids)
Passive immunity is resistance based on antibodies preformed in
another host eg administration of antibody against tetanus, botulism,
diphtheria, rabies etc.
113. Sudden death is majorly linked with embolism.
114. 24 to 48 hours post acute inflammation ,monocytes start
accumulating.
115. ubiquitin proteosome pathway & autophagic vacuoles are mainly
involved in atrophy.
116. Reserve stem cells are main players in metaplasia.
117. Mechanical and trophic factors are involved in hypertophy.
118. Eosinophils are players in allergic infections.
119. Sequence of events in acute inflammation is :
Transient asoconstriction,vasodilation stasis, margination, rolling,
adhesion, diapedesis, chemotaxis and phagocytosis.
120. Macrophages seen as a part of reticuloendothelial system include:
Osteoclasts – bone,microglia – brain,kupffer cells – liver,alveolar
macrophages – lung.Sinus histiocytes – lymph nodes.
120. Tuberculosis is the leading cause of granuloma in Pakistan.
121. Major granulomatous causes include: sarcoidosis, leprosy, cat scratch
disease, fungal infections.
122. Grading of a tumor is based on differentiation,atypia and mitoses.
123. Staging of a tumor is based on TNM – tumor,nodes,metastasis.
124. Major autosomal dominant disorders include: Skeletal – Marfan;
syndrome
Nervous – Huntington disease,neurofibromatosis
Gastrointestinal – familial polyposis coli

Urinary – polycystic kidney disease
Haematopoietic – hereditary spherocytosis
125. Major intracellular accumulations are :
Melanin – melanoma,bile – cholestasis,carbon – anthracosis,copper –
Wilson disease
lipofuscin – aging
126. Fatty change is also known as steatosis.
127. Point mutations are often caused by chemicals or malfunction of DNA
replication, exchange a single nucleotide for another e.g RAS.
128. Giant cells are cells containing more than one nucleus.
129. Major giant cells are : Langhan giant cells – Tuberculosis,Tuton giant
cells – xanthoma Warthin finkeldey giant cells – measles,Reed
Sternberg cells – Hodgkin Lymphoma
Foreign body giant cells – foreign body
130. IgG fixes complement and crosses placenta.
131. IgM is the most heavy antibody.
132. IgE is the allergic reaction player antibody.
133. Ig A is found in secretions.
134. ABL gene is seen translocated in CML.
135. Lines of Zahn confirms a thrombus.They are alternate layers of
platelets with fibrin and RBCs’
136. Psamomma bodies are lamellated bodies of dystrophic calcification
seen in meningioma,papillary carcinoma thyroid and serous ovarian
malignant tumors.
137. Nuclear changes in a necrotic cell include: pyknosis, karyolysis,
karryorrhexis and loss of nucleus.
138. Macrophages get accumulated in chronic inflammation by continuous
recruitment,proliferation and immobilization.
139. Ischemic injury leads to coagulative necrosis.

140. Major sensitive cell components: maintenance of integrity of cell
membrane, aerobic respiration, protein synthesis, genetic integrity
141. Liquefactive necrosis: Usually caused by focal bacterial infections,
because they can attract polymorphonuclear leukocytes.
142. Coagulative necrosis is characterised by the preservation of cellular
and tissue architecture
143. Fat Necrosis: A term for necrosis in fat, caused either by release of
pancreatic enzymes from pancreas or gut (enzymic fat necrosis) or by
trauma to fat, either by a physical blow or by surgery (traumatic fat
necrosis).
144. Caseous necrosis – cheese like : A distinct form of coagulative necrosis
seen in mycobacterial infections (e.g., tuberculosis), or in tumor
necrosis, in which the coagulated tissue no longer resembles the cells,
but is in chunks of unrecognizable debris
145. Gangrene ("gangrenous necrosis") is not a separate kind of necrosis at
all, but a term for necrosis that is advanced and visible grossly with
super added putrefaction.
146. Fibrinoid necrosis occurs in the wall of blood vessels when endothelium
and smooth muscle cells are injured and dying.
147. Unlike necrosis, where the cell dies by swelling and bursting its content
in the area, which causes an inflammatory response, apoptosis is a
very clean and controlled process where the content of the cell is kept
strictly within the cell membrane as it is degraded.
148. The extrinsic pathway of apoptosis is initiated through the stimulation
of the transmembrane death receptors, such as the Fas receptors,
located on the cell membrane.
149. In contrast, the intrinsic pathway of apoptosis is initiated through the
release of signal factors by mitochondria within the cell
150. In males bronchogenic carcinoma and in females breast carcinoma are
at the top.
151. Preneoplastic conditions include: Cirrhosis of liver, Atypical hyperplasia
of endometrium, Leukoplakia, Inflammatory bowel disease,
Adenomatous colonic polyps

152. Initiator chemicals - Cause irreversible damage to DNA, but at
maximum they can cause severe dysplasia.
153. Promoter chemicals itself cannot induce cancer,they propagate or
enhance the effects of initiators
154. Known chemical carcinogens include :A- Asbestos - Lung,
mesothelioma. GI tract (esophagus, stomach, large intestine)
b- Arsenic - Lung, skin, hemangiosarcoma
c- Beryllium - Lung
d- Cadmium - prostate
e. Benzene - Leukemia
155. Ionizing radiation leads to dysjunction à random fusion à mutation.
156. Exposure long term of radiations lead to leukemia and thyroid cancers.
157. Initiation, Latent stage, Promotion and Malignant transformation are
recognizable stages in carcinogenesis.
158. Mast cells are the main source of histamine and platelets the main
source of serotonin.
159. Thromboxane A2 (TXA2), from platelets, aggregates platelets,
constricts blood vessels. Great for hemostasis.
160. Prostacyclin (PGI2), from the vessel wall, prevents platelet
aggregation, dilates vessels. Great for whenever hemostasis is
unnecessary.
161. Suppurative or purulent inflammation is characterized by the
production of large amounts of pus or purulent exudate consisting of
neutrophils, necrotic cells, and edema fluid.
162. An ulcer is a local defect, or excavation, of the surface of an organ or
tissue that is produced by the sloughing (shedding) of inflammatory
necrotic tissue
163. Teratoma is a tumor derived from more than one germ cell layer.
164. Seminomas,Melanomas,Hepatomas are malignant tumors.
165. Extent to which the tumor cell resemble its parent cell is
differentiation.

166. Ranges of differentiation include: well, moderately, poorly,
undifferentiated (anaplasia).
167. A malignant cells shows: high N/C ratio,hyperchromatic nuclei,
prominent nucleoli, scanty cytoplasm and pleomorphism.
168. Carcinoma in situ is : Full-thickness dysplasia extending from the
basement membrane to the surface of the epithelium.
169. Dysplasia :Atypical proliferation of cells characterized by nuclear
enlargement and failure of differentiation which falls short of
malignancy
170. The change that occurs in the stroma as tumor invades is called
desmoplasia
171. Benign tumors never locally invade and Malignant tumors always
invade the surrounding tissues.
172. Carcinoma of the ovary spreads through seeding of body cavities.
173. Commonest places for mets deposits are liver and lungs.
174. Perineural spread is seen by carcinoma of prostate and pancreas (2 P’s
).
175. Nuclear damage is the hall mark of irreversible cell injury.
176. Scientific study of structural changes and functional consequences of
injurious stimuli on cells, tissues and organs is Pathology.
177. Metaplasia is a two edges sword because it can lead to dysplasia and
the original function of cells is lost.
178. Metaplasia can lead to dysplasia.
179. ALTHOUGH ATROPHIC CELLS MAY HAVE DIMINISHED FUNCTION,THEY
R NOT DEAD.
180. Pathologic hyperplasia constitutes a fertile soil in which cancerous
proliferation may eventually arise like bph and endometrial
hyperplasia.
181. Dysplasia can regress and does not always lead to cancer.

182. Transudates are fluid accumulations that are essentially salt-water,
accumulated because of pressure problems. Exudates are protein-rich
fluid accumulations, due to leaky vessels.
183. In disseminated intravascular coagulation, the clotting cascades are
activated throughout the body. This is bad, since it tends to shut down
organs due to microthrombi, and also causes bleeding due to
consumption of clotting factors and activation of plasmin.
184. Some people reserve the word "thrombus" for the ante-mortem kind,
and call post-mortem thrombi "clots".
185. Arterial thrombi usually occur over ruptured atherosclerotic plaques,
less often at sites of other vascular disease or old surgery.
186. Vegetations are thrombi that occur on cardiac valves. They may be
loaded with bacteria ("bacterial endocarditis"), or sterile ("marantic",
"verrucous", "bland"; also the thrombi of acute rheumatic fever).
187. Embolus" comes from the Greek for "bottle stopper".
188. Pulmonary embolization is one of the great killers of hospitalized
patients, and that ante-mortem diagnosis is notoriously unsatisfactory
even today.
189. A paradoxical embolus (* crossed embolus) is one from the systemic
veins that passes through a right-to-left intracardiac shunt (i.e., a
birth defect), to occlude a systemic artery.
190. Long bone fractures are the main cause of fat embolism.
191. Tumor emboli are bits of cancer that invaded a vein and then broke
off. Renal cell carcinoma is famous for this.
192. White infarcts ("anemic infarcts", from "an-", not, and "-eme", blood)
are usual when arteries are occluded in solid organs
193. Red infarcts ("hemorrhagic infarcts", sounds like an oxymoron but
isn't) result when veins are occluded, or when arteries are occluded in
loose tissues (bowel) or with a dual blood supply, or when the organ
was already very congested.

194. Monocytes are the largest cells in blood stream.
195. Histiocytes are mature tissue macrophages.
196. Cell membrane damage is the first sign of irreversible cell injury.
197. Lysosomal leakage confirms irreversible cell injury.
198. Choristomas and hemartomas are not neoplasms.
199. FGF,TGF,VEGF,EGF are main growth factors.
200. Endothelium gets leaky in acute inflammation due to: 1) formation of
endothelial gaps in venules 2) cytoskeletal reorganization 3) increased
transcytosis 4) direct endothelial injury 5) leukocyte dependent injury
6) delayed prolonged leakage 7) leakage from new blood vessels

200 POINTS TO RMEMBER IN GENERAL PATHOLOGY - DR EJAZ WARIS

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200 POINTS TO RMEMBER IN GENERAL PATHOLOGY - DR EJAZ WARIS