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Contents
Cell Injury, Cell Death and Adaptations
Inflammation and Repair
Hemodynamic Disorders, Thromboembolism and Shock
Diseases of the Immune System
Neoplasia
Genetics
By: Abu hurayrah saber
SMDC Lahore
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Pathology Scientific study of structural changes and functional consequences of
injurious stimuli on cells, tissues and organs is Pathology.
Cell Injury, Cell Death and Adaptations:
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. Mechanical and trophic factors are involved in hypertrophy.
4. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation
may eventually arise like BPH and endometrial hyperplasia.
5. Atrophy is the shrinkage in the size of the cell by loss of cell substance.
6. Mechanism of atrophy:
 Decreased protein synthesis (b/c of low metabolic activity)
 Degradation by Ubiquitin-proteosome pathway
 Autophagic vacuoles (Self Eating)
7. Although atrophic cells may have diminished function, they are not dead.
8. Metaplasia is defined as a reversible change in which one adult cell type
(epithelial or mesenchymal) is replaced by another adult cell type.
9. Metaplasia is a two edges sword because it can lead to dysplasia and the original
function of cells is lost.
10. Reserve stem cells are main players in metaplasia.
11. Causes of cell injury are:
 Oxygen deprivation-hypoxia
 Chemical agents
 Infections
 Immune reactions
 Genetic factors- HbS, Damaged DNA, Misfolded Protiens
 Nutritional imbalance
 Physical agents- Trauma, Radiation, Temp.
 Aging
12. Mechanism of cell injury are:
 Depletion of ATP
 Mitochondrial damage & dysfunction
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Influx of calcium
Oxidative stress-ROS
Defects in membrane permeability
Damage to DNA & protiens
13. Cell swelling is the earliest sign of a reversible cell injury.
14. Major sensitive cell components: maintenance of integrity of cell membrane,
aerobic respiration, protein synthesis, genetic integrity.
15. Cell membrane damage is the first sign of irreversible cell injury.
16. Lysosomal leakage confirms irreversible cell injury.
17. Nuclear damage is the hall mark of irreversible cell injury.
18. Free radical is a chemical species that have a single unpaired electron in an outer
orbit.
19. 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.
20. Nuclear changes in a necrotic cell include: pyknosis, karyolysis, karryorrhexis and
loss of nucleus.
21. Necrosis has six major types:
Coagulative
Liquefactive
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Caseous
Fibrinoid
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Gangrenous
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Fat
22. Types of necrosis (summarized in table):
Type
Coagulative
Liquefactive
Patterns of tissue necrosis
Mechanism
Appearance
In ischemic tissue, cells are
dead, Tissue architecture
preserved
Enzymatic digestion of tissue
“liquefy” it. Seen in focal
bacterial & fungal infections.
Gangrenous Coagulative necrosis involving
Caseous
Fat
Fibrinoid
multiple layers (dry gangrene)
Super added bacterial/ fungal
infection can turn into
liquefactive type (wet
gangrene)
A distinct form of coagulative
necrosis seen in mycobacterial
infections or in tumor necrosis,
in which the coagulated tissue
no longer resembles the cells,
but is in chunks of
unrecognizable debris
Necrosis 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)
Usually associated with immune
reactions
Example
Homogenous glassy
appearance, Inc
Eosinophilia
Nuclear changes visible
Dead cells are
completely digested and
transfoermed into a
liquid viscous mass
Multiple layers of
Coagulative or
liquefactive necrosis
Characteristic of
Infarcts (in
Solid organs
except Brain)
Involves CNS,
Abcesses
Collection of lysed cells,
granular appearance
(pink), cell outline is
altered
Seen in foci of
Tuberculosus
infection
Areas of fat destruction.
(enzymatic)
Pancreatitis,
Trauma to the
breast
Chalky white
appearance of cells
(sponification)
Ag-Ab complexes
deposits in walls of
vessels
Affects limbs
(ischemic limb
injury)
Affects blood
vessls
23. 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.
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24. Morphologically an apoptotic cell shows: a) cell shrinkage, b) chromatin
condensation c) formation of cytoplasmic blebs and apoptotic bodies, d)
phagocytosis by macrophages.
25. Apoptosis has two phases a) Initiation phase extrinsic and intrinsic pathways
b)Execution phase c) phagocytosis of dead cell
26. 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.
27. 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.
28. In contrast, the intrinsic pathway of apoptosis is initiated through the release of
signal factors by mitochondria within the cell
29. Genes promoting apoptosis (Pro-apoptotic): bax,bak,bim
30. Genes inhibiting apoptosis (Anti-apoptotic): bcl 2 family.
31. Initiator Caspases are -8 & -9, while executioner caspases are mainly 3 & 6.
32. Major intracellular accumulations are :
 Melanin – melanoma
 bile – cholestasis
 carbon – anthracosis
 copper – Wilson’s disease
 lipofuscin – aging
33. Fatty change is also known as Steatosis.
34. Dystrophic calcification is always seen in damaged tissues, while Metastatic
calcification may occur in normal tissues whenever there is hyperplasia.
35. Psammoma bodies are lamellated, Concentric, Calcific spherules of dystrophic
calcification seen in meningioma, papillary carcinoma thyroid and serous ovarian
malignant tumors.
36. (Mnemonic for sites of Psammoma Bodies) PSaMMoma:
 Papillary carcinoma thyroid
 Serous papillary cystadenoma of ovary
 Meningioma
 Malignant mesothelioma
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Inflammation and Repair:
1. Inflammation is a complex reaction to injurious agents such as microbes and
damaged, usually necrotic cells that consist of vascular responses, migration and
activation of leukocytes, and systemic reactions.
2. Steps
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of inflammatory response are: 5 R(s)
Recognition of injurious agent
Recruitment of leukocytes
Removal of the agent
Regulation (control) of the response
Resolution (repair)
3. Inflammatory response consists of TWO main components: vascular & cellular,
and divided into TWO main patterns: Acute and Chronic.
4. Vasodilatation is one of the earliest manifestation of acute inflammation, it follows
a transient vasoconstriction of arterioles lasting few seconds.
5. Increased vascular permeability leading to the escape of a protein-rich fluid
(exudate) into the extravascular tissue in the HALL-MARK of acute inflammation.
6. Mast cells are the main source of histamine and platelets the main source of
serotonin.
7. Thromboxane A2 (TXA2), from platelets, aggregates platelets, constricts blood
vessels. Great for hemostasis.
8. Prostacyclin (PGI2), from the vessel wall, prevents platelet aggregation, dilates
vessels. Great for whenever hemostasis is unnecessary.
9. Transudates are fluid accumulations that are essentially salt-water, accumulated
because of pressure problems. Exudates are protein-rich fluid accumulations, due
to leaky vessels.
10. Formation of endothelial gaps in venules is the most common cause of vascular
leakage.
11. Endothelium gets leaky in acute inflammation due to:
 formation of endothelial gaps in venules
 cytoskeletal reorganization
 increased transcytosis
 direct endothelial injury
 leukocyte dependent injury
 delayed prolonged leakage
 leakage from new blood vessels
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12. Leukocytes Adhesion molecular families have a major classes:
 Selectins (E,L & P types),
 Integrins,
 Immunoglobulin family of adhesion molecules and
 Mucin like glycoproteins.
13. Selectins mainly involved in rolling of leukocytes, PECAM in transmigration and
immunoglobulin family in adhesions.
14. Chemotaxis is defined as uni-directional migration of leukocytes towards the site
of injury under chemical gradient action.
15. Most important chemotactic agents are C5a, LTB4 and bacterial products.
16. Major opsonins are: C3b & Fc fragment of IgG proteins.
17. H202-MPO-Halide systein is the most efficient bactericidal system in neutrophils.
18. Chediak-Higashi Syndrome is an autosomal recessive condition characterized by
failure of fusion of phagosome with lysosome.
19. Chronic granulomatous disease of childhood results from inherited defects in the
components of NAPDH oxidase which generates superoxide, leading to body
infections.
20. Vasoactive amines are histamine and serotonin which are the main players of
early inflammation.
21. Plasma Proteins are: Complement system proteins, clotting system and fibrinolytic
system.
22. Prostaglandins are vasodilators.
23. MAC (C5b, 6789) is the membrane attack complex, which finally kills the
bacteria.
24. Activated Hageman factor initiates FOUR systems involved in inflammatory
responses:
 Kinin
 Clotting
 Fibrinolytic
 Complement system
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25. SRS-A (slow releasing substance of anaphylaxis) constitutes LTC4, LTD4 & LTE4
promote vasoconstriction, bronchospasm & increased vascular permeability.
26. Lipoxins are bioactive products generated from transcellular biosynthetic
mechanisms involving neutrophils and platelets.
27. IL-1 & TNF are two of the MAJOR cytokines that mediate inflammation.
28. Major chemokines include: IL-8, MCP-1, Eotaxin, MIP-1, Lymphotactin and
RANTES.
29. Nitric oxide plays major role in production of vasodilation by relaxing vascular
smooth muscle in ischemic conditions.
30. The major mediators of pain are Bradykinin & Prostaglandins
31. Potent vasodilators are: Vasoactive Amines, Prostaglandins & NO.
32. 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.
33. 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.
34. 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.
35. Sequence of events in acute inflammation is :
 Transient vasoconstriction
 Vasodilation
 Stasis
 Margination
 Rolling
 Adhesion
 Diapedesis
 Chemotaxis
 Phagocytosis
36. Chronic inflammation is defined as an inflammation of prolonged duration, in
which active inflammation, tissue destruction and attempts at repair are
proceeding simultaneously.
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37. Neutrophils are the main cells of acute inflammation (exudates) while
Mononuclear cells (with one nucleus are the main cells of chronic inflammation.
Mononuclear cells are (Lymphocytes, Monocytes, Macrophages and Plasma cells).
38. Macrophages get accumulated in chronic inflammation by continuous recruitment,
proliferation and immobilization.
39. Macrophages are the prima donna (main working cell) of chronic inflammation,
while lymphocytes are present in increased number.
40. 24 to 48 hours post-acute inflammation, monocytes start accumulating.
41. 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.
42. Classical Tuberculous Granuloma is composed
of:
 Epithelioid cells
 Langhan’s multinucleated giant cells
 Caseation necrosis
 Collar of lymphocytes.
43. There are two types of Granulomas: Immune &
foreign body.
44. Tuberculosis is the leading cause of granuloma
in Pakistan.
45. Major granulomatous causes include: sarcoidosis, leprosy, cat scratch disease,
fungal infections.
46. Giant cells are cells containing more than one nucleus.
47. 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
48. There are 3 types of cells in the body: Continously dividing labile cells, Quiscent or
stable cells and Permanent Non-dividing cells.
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49. 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.
50. VEGF & fibroblast Growth factor are mainly involved in angiogenesis.
51. TGF-B is a growth inhibitor for most epithelial cells and leukocytes, potent
fibrogenic agent and a strong anti-inflammatory effector.
52. Extracellualr matrix is formed of these groups of molecules :
 Fibronectin
 Adhesive glycoproteins
 Proteoglycans
 Hyaluronic acid
53. Collagen is the most common protein in the animal world, with 30 types
discovered so far. Types I, II, III, V & X are fibrillar and most common while type
IV is non fibrillar.
54. 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.
55. 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.
56. Monocytes are the largest cells in blood stream.
57. Histiocytes are mature tissue macrophages.
58. FGF, TGF, VEGF, EGF are main growth factors.
59. 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
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Hemodynamic Disorders, Thromboembolism and Shock:
1. Edema is defined as accumulation of fluid in the interstitial tissue spaces and
body cavities.
2. 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.
3. Heart failure cells are hemosiderin laden macrophages seen in chronic
pulmonary congestion.
4. 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.
5. Virchow’s triad include: a) Endothelial injury b) Stasis or turbulent blood flow &
c) blood hypercoagulability.
6. Of the inherited causes of hypercoagulability, mutation in the factor V gene and
prothrombin gene are the most common.
7. Lines of Zahn are laminated lines produced by alternating pale layers of platelets
admixed with some fibrin and darker layers containing more red cells.
8. Lines of Zahn confirms a thrombus.
9. Fate of thrombus include: propagation, embolization, dissolution, organization and
recanalization.
10. 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.
11. Sudden death is majorly linked with embolism.
12. Embolus" comes from the Greek for "bottle stopper".
13. Pulmonary embolization is one of the great killers of hospitalized patients, and
that ante-mortem diagnosis is notoriously unsatisfactory even today.
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14. 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.
15. Long bone fractures are the main cause of fat embolism.
16. Tumor emboli are bits of cancer that invaded a vein and then broke off. Renal
cell carcinoma is famous for this.
17. Infarct is an area of ischemic necrosis caused by occlusion of either the arterial
supply or the venous drainage in a particular tissue.
18. Ischemic injury leads to coagulative necrosis.
19. The most dominant histologic characteristic of infarction is ischemic coagulative
necrosis.
20. 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.
21. Major types of shock include: cardiogenic, hypovolemic, septic, neurogenic and
anaphylactic.
22. In disseminated intravascular coagulation DIC, 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.
23. Some people reserve the word "thrombus" for the ante-mortem kind, and call
post-mortem thrombi "clots".
24. Arterial thrombi usually occur over ruptured atherosclerotic plaques, less often at
sites of other vascular disease or old surgery.
25. 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).
26. White infarcts ("anemic infarcts", from "an-", not, and "-eme", blood) are usual
when arteries are occluded in solid organs
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27. 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.
Diseases of the Immune System:
1. Active Immunity is the resistance induced after contact with foreign antigens
e.g: microorganisms, immunization with live or killed infectious agents, exposure
to microbial products (toxins, toxoids).
2. Passive immunity is resistance based on antibodies preformed in another host
e.g: administration of antibody against tetanus, botulism, diphtheria, rabies etc.
3. Amyloid is a pathologic proteinaceous substance deposited between cells in
various tissues and organs of the body in a wide variety of clinical settings.
4. 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.
5. Type II cytotoxic hypersensitivity, antibodies attach to antigens on the
surfaces of a cell and then something injures or destroys the cell.
6. 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”).
7. 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.
8. Immune responses are divided into two broad categories:

Humoral immunity-B-cell lymphocyte mediated via production of antibody and
Often develops as a response to soluble antigens, and

Cellular immunity-T-Cell lymphocyte mediated. CD4+helper lymphocytes: help
B cells make antibody and also help to generate cytotoxic T cells.
9. Major histocompatibility complex is present on all nucleated cells.
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10. The HLA system is a key factor in most Transplant rejection reactions. Reactions
are mediated by either T lymphocytes or by antibody.
11. Toll like receptors are membrane proteins that recognize a variety of microbe
derived molecules and stimulate innate immune responses against the microbes.
12. CD4 molecule is a high affinity receptor for HIV
13. Major autoimmune disease include Hashimoto’s thyroiditis, Rheumatoid Arthritis,
Sjogren’s syndrome, ankylosing spondylitis.
14. Gamma interferon is one of the cytokine to activate macrophages and also play
major Role in Granuloma formation.
15. Cytokines are mediators released from one cell and modulate the actions of
another cell.
16. NK cells (Natural Killer cells):
 Have no immunological memory
 Active participants against cancer cells & viral infected cells (can kill cancer
cells within 24 hours when they appear in circulation)
 Kills any cell that lacks or have insufficient MHC-1
17. Eosinophils are players in allergic infections.
18. Macrophages seen as a part of reticuloendothelial system include:
 Osteoclasts – bone
 Microglia – brain
 Kupffer cells – liver
 Alveolar macrophages – lung
 Sinus histiocytes – lymph nodes.
19. IgG fixes complement and crosses placenta.
20. IgM is the most heavy antibody.
21. IgE is the allergic reaction player antibody.
22. IgA is found in secretions.
23. Two types of vaccines include: Live vaccines; Measles, Mumps, Rubella,
Varicella, Polio etc and Killed vaccines: Rabies, Polio, Hepatitis A.
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Neoplasia:
1. 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.
2. Tumor has two basic components: Parenchyma & stroma, while tumors are of two
types: Benign and Malignant.
3. 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.
4. Seminomas, Melanomas, Hepatomas are malignant tumors.
5. Benign tumors never locally invade and Malignant tumors always invade the
surrounding tissues.
6. Single most important feature to differentiate benign from malignant tumor is
METASTASIS.
7. The change that occurs in the stroma as tumor invades is called desmoplasia
8. Carcinoma of the ovary spreads through seeding of body cavities.
9. Commonest places for metastasis deposits are liver and lungs.
10. Perineural spread is seen by carcinoma of prostate and pancreas (2 P’s).
11. Choristomas and hemartomas are not neoplasms.
12. Carcinomas mostly use lymphatic routes and sarcomas mostly use hematogenous
routes of spread.
13. A malignant cells shows: high N/C ratio, hyperchromatic nuclei, prominent
nucleoli, scanty cytoplasm and pleomorphism.
14. 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.
15. 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.
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16. Carcinoma in situ is: Full-thickness dysplasia extending from the basement
membrane to the surface of the epithelium.
17. Dysplasia: Atypical proliferation of cells characterized by nuclear enlargement
and failure of differentiation which falls short of malignancy.
18. Dysplasia can regress and does not always lead to cancer.
19. Teratoma is a tumor derived from more than one germ cell layer.
20. Four types of genes are normally working in human body:
 Proto-Oncogenes
 Anti-Oncogenes
 Apoptotic genes
 DNA repair genes
21. Proto-oncogenes are changed to oncogenes by three processes: mutation,
translocation and amplification.
22. Protooncogenes are converted into oncogenes.
23. p53 works by DNA repair and promoting apoptosis.
24. RB gene activates and Works in hypophosphorylated form.
25. RAS gene protooncogene protein is GTP bound and Works with GAP in
cooridination with GTPase.
26. Major Oncogenes are; RAS, ERB-B1, RET, KIT, ABL, C-MYC & N-MYC.
27. Major Antioncogenes are: RB, TP53, W.-1, NF-1, BRCA-1, APC.
28. Gliomas and BCC are highly malignant but dont usually metastasize.
29. ABL gene is seen translocated in CML.
30. In males bronchogenic carcinoma and in females breast carcinoma are at the top.
31. Preneoplastic conditions include: Cirrhosis of liver, Atypical hyperplasia of
endometrium, Leukoplakia, Inflammatory bowel disease, Adenomatous colonic
polyps.
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32. 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).
33. Chemical carcinogenesis is a multistep process, divided into initiation and
promotion phases.
34. Initiator chemicals - Cause irreversible damage to DNA, but at maximum they can
cause severe dysplasia.
35. Promoter chemicals itself cannot induce cancer, they propagate or enhance the
effects of initiators.
36. Major chemical carcinogens associated as include:
 Asbestos with Mesothelioma
 Aniline dyes with TCC
 Nitrates-Gastric carcinoma
 Aflatoxin with HCC
 Vinyl chloride with Angiosarcoma Liver
 Arsenic - Lung, skin, hemangiosarcoma
 Beryllium - Lung
 Cadmium - prostate
 Benzene - Leukemia
37. Radiation induced malignancies include leukemias and papillary carcinoma thyroid.
38. Ionizing radiation leads to dysjunction  random fusion  mutation.
39. Exposure long term of radiations lead to leukemia and thyroid cancers.
40. Initiation, Latent stage, Promotion and Malignant transformation are recognizable
stages in carcinogenesis.
41. Some viruses associated with neoplasms are:
 HTLV-1
Adult T-cell leukemia/ Lymphoma
 HPV
Squamous cell carcinoma of cervix
 EBV
Burkitt lymphoma, B-cell lymphoma in AIDS pt.
Hodgkins’ lymphoma



HBV
H. pylori
HHV-8
Hepatocellular carcinoma
MALTomas
Kaposi sarcoma
42. Major para-neoplastic syndromes 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.
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43. 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.
44. 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.
45. FNAC and biopsy are key investigations to early diagnose a tumor.
46. Tumor diagnosis is made upon:
 History & Clinical examination
 Imaging: X-rays, USG, CT, MRI
 Tumor markers- lab analysis
 Cytology- histopathology markers
 Molecular techniques- gene detection
47. Extent to which the tumor cell resembles its parent cell is differentiation.
48. Ranges of differentiation include: well, moderately, poorly, undifferentiated
(anaplasia).
49. Grading of a tumor is based on: differentiation, atypia and mitoses.
50. Staging tells the extent of a tumor nad based on: TNM – tumor, nodes,
metastasis.
51. Usually




cancers are
Grade I
Grade II
Grade III
Grade IV
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classified as Grade I to IV with increasing anaplastic changes:
Low grade
Well differentiated
Intermediate grade
Moderately differentiated
High grade
Poorly differentiated
Anaplastic
Anaplastic
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Genetics:
1. Mutation is defined as a permanent change in the DNA.
2. Major autosomal dominant disorders include:





Skeletal – Marfan syndrome
Nervous – Huntington disease, neurofibromatosis
Gastrointestinal – familial polyposis coli
Urinary – polycystic kidney disease
Haematopoietic – hereditary spherocytosis
3. Point mutations are often caused by chemicals or malfunction of DNA replication,
exchange a single nucleotide for another e.g RAS.
4. 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.
5. Ehlers-Danlos Syndrome comprises clinically and genetically heterogeneous
groups of disorders that result from some defect in the synthesis or structure of
fibrillar collagen.
By: Abu hurayrah saber
SMDC Lahore
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