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INI CET Pathology Syllabus

The Pathology syllabus for INI CET in full: 4 chapters, 23 topics and 95 sub-topics, every one listed below, plus 52 Pathology flashcards with answers.

4Chapters
23Topics
95Sub-topics
52Flashcards

Pathology syllabus: all 4 chapters

Expand any chapter to see its topics and sub-topics.

  1. General Pathology

     6 topics
    • Cellular adaptations
      • Hypertrophy
      • Hyperplasia
      • Atrophy
      • Metaplasia
      • Dysplasia
    • Cell injury and cell death
      • Necrosis
      • Apoptosis
      • Causes of cell injury
    • Inflammation
      • Acute vs. chronic inflammation
      • Cellular and chemical mediators
      • Outcomes
    • Healing and repair
      • Regeneration
      • Fibrosis
      • Wound healing
      • Factors affecting wound healing
    • Hemodynamic disorders
      • Edema
      • Congestion
      • Hemorrhage
      • Thrombosis
      • Embolism
    • Neoplasia
      • Classification
      • Benign vs. malignant tumors
      • Tumor nomenclature
      • Cancer metastasis

  2. Systemic Pathology

     8 topics
    • Cardiovascular System Pathology
      • Ischemic heart disease
      • Hypertensive heart disease
      • Cardiomyopathies
      • Valvular heart diseases
      • Vascular diseases
    • Respiratory System Pathology
      • Acute respiratory infections
      • Chronic respiratory infections
      • Obstructive lung diseases
      • Restrictive lung diseases
      • Lung tumors
      • Pulmonary embolism
    • Gastrointestinal System Pathology
      • Peptic ulcer disease
      • Inflammatory bowel disease
      • Liver diseases (e.g., hepatitis, cirrhosis)
      • Gastrointestinal tumors
    • Renal Pathology
      • Acute kidney diseases
      • Chronic kidney diseases
      • Glomerulonephritis
      • Nephrotic syndrome
      • Renal tumors
    • Hematopoietic System Pathology
      • Anemia
      • Leukemia
      • Lymphoma
      • Myeloproliferative disorders
      • Coagulation disorders
    • Endocrine System Pathology
      • Thyroid diseases
      • Adrenal diseases
      • Diabetes mellitus
      • Pituitary disorders
    • Nervous System Pathology
      • Stroke
      • Neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease)
      • CNS tumors
      • Demyelinating diseases
    • Musculoskeletal System Pathology
      • Osteoarthritis
      • Rheumatoid arthritis
      • Osteoporosis
      • Bone tumors
      • Connective tissue disorders

  3. Special Pathology

     5 topics
    • Infectious diseases
      • Bacterial
      • Viral
      • Fungal
      • Parasitic infections
    • Immunopathology
      • Autoimmune diseases
      • Hypersensitivity reactions
      • Immunodeficiency disorders
      • Transplantation immunology
    • Environmental and nutritional diseases
      • Nutritional deficiencies (e.g., vitamin deficiencies)
      • Chemical toxins
      • Environmental pollutants
    • Genetic and developmental diseases
      • Inherited disorders
      • Chromosomal abnormalities
      • Congenital malformations
    • Neoplastic diseases
      • Pathogenesis
      • Histological classification
      • Grading
      • Staging
      • Molecular diagnostics of tumors

  4. Laboratory Investigations in Pathology

     4 topics
    • Hematological investigations
      • Complete blood count (CBC)
      • Peripheral blood smear
      • Bone marrow examination
      • Coagulation tests
    • Microbiological investigations
      • Microscopic examination
      • Culture
      • Sensitivity testing
    • Histopathological techniques
      • Gross examination
      • Tissue processing
      • Staining (H&E, special stains)
      • Interpretation of histopathology slides
    • Immunohistochemistry and molecular pathology
      • Applications in diagnosis
      • Applications in prognosis
      • Applications in targeted therapy of tumors

INI CET Pathology flashcards — 52 questions with answers

  1. Differentiate the four cellular adaptations: hypertrophy, hyperplasia, atrophy, and metaplasia.

    Hypertrophy = increased cell size (e.g., cardiac muscle in hypertension). Hyperplasia = increased cell number (e.g., endometrial hyperplasia). Atrophy = decreased cell size/number (e.g., disuse atrophy). Metaplasia = reversible replacement of one differentiated cell type by another (e.g., squamous metaplasia of bronchial epithelium in smokers; Barrett esophagus = squamous to columnar).

  2. What is the key biochemical/morphologic distinction between reversible and irreversible cell injury?

    Reversible injury: ATP depletion, cellular and mitochondrial swelling, membrane blebbing, ribosomal detachment — all recoverable. Irreversibility hallmarks are severe mitochondrial dysfunction (cannot restore oxidative phosphorylation) and profound plasma membrane damage causing massive Ca2+ influx and enzyme leakage (e.g., elevated cardiac troponins).

  3. Name and locate the five classic patterns of necrosis.

    Coagulative (ischemic infarcts of solid organs except brain; architecture preserved), liquefactive (brain infarcts, bacterial abscesses), caseous (TB; cheese-like granuloma center), fat necrosis (acute pancreatitis, breast trauma; saponification), and fibrinoid (immune vascular damage, malignant hypertension; pink amorphous wall deposits).

  4. Compare apoptosis and necrosis (energy, membrane, inflammation, DNA).

    Apoptosis: ATP-dependent, single cells, intact membrane, no inflammation, internucleosomal DNA laddering, apoptotic bodies. Necrosis: ATP-independent, cell groups, membrane rupture with enzyme leakage, marked inflammation, random DNA breakdown. Apoptosis = programmed/regulated; necrosis = accidental.

  5. Outline the intrinsic (mitochondrial) pathway of apoptosis.

    Cell injury/loss of survival signals shifts the BCL-2 family balance: pro-apoptotic BAX/BAK form pores releasing cytochrome c. Cytochrome c + APAF-1 + caspase-9 form the apoptosome, activating executioner caspases 3 and 6. Regulated by anti-apoptotic BCL-2/BCL-XL. p53 promotes this pathway after DNA damage.

  6. List the five cardinal signs of acute inflammation and their Latin terms.

    Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). The first four were described by Celsus; functio laesa was added by Virchow.

  7. What are the sequential steps of leukocyte extravasation in acute inflammation?

    Margination and rolling (selectins: E-, P-, L-selectin binding sialyl-Lewis X), firm adhesion (integrins binding ICAM-1/VCAM-1, upregulated by TNF/IL-1), transmigration/diapedesis (PECAM-1/CD31), and chemotaxis toward agents like C5a, LTB4, IL-8, and bacterial N-formyl peptides.

  8. Distinguish transudate from exudate.

    Transudate: low protein (<3 g/dL), low specific gravity (<1.012), few cells; due to altered hydrostatic/oncotic pressure (e.g., CHF, nephrotic syndrome). Exudate: high protein (>3 g/dL), high specific gravity (>1.020), many cells; due to increased vascular permeability from inflammation/infection. Light's criteria distinguish pleural effusions.

  9. What characterizes granulomatous inflammation and name caseating vs non-caseating causes.

    Chronic inflammation with epithelioid macrophages, often Langhans/foreign-body giant cells, surrounded by lymphocytes. Caseating: tuberculosis, some fungi. Non-caseating: sarcoidosis, Crohn disease, leprosy, foreign body, berylliosis, cat-scratch disease. Driven by Th1 cells and IFN-gamma/TNF.

  10. Contrast healing by primary vs secondary intention.

    Primary intention: clean, approximated wound edges (surgical incision), minimal tissue loss, little granulation tissue, small scar. Secondary intention: large tissue defect, abundant granulation tissue, significant wound contraction (via myofibroblasts), larger scar, slower healing.

  11. Outline the phases and timeline of cutaneous wound healing.

    Hemostasis/inflammation (0–3 days: clot, neutrophils then macrophages), proliferation (3–10 days: granulation tissue, angiogenesis, re-epithelialization, type III collagen), and maturation/remodeling (weeks–months: type III collagen replaced by type I, increasing tensile strength to ~70–80% by ~3 months).

  12. What is the difference between a labile, stable, and permanent cell with regard to regeneration?

    Labile cells continuously divide (surface epithelia, hematopoietic, GI mucosa) — excellent regeneration. Stable cells are quiescent (G0) but can re-enter cycle when stimulated (hepatocytes, renal tubules, fibroblasts). Permanent cells cannot divide (neurons, cardiac/skeletal muscle) — heal by scarring.

  13. Define the components of Virchow's triad in thrombosis.

    Endothelial injury (most important, e.g., atherosclerosis, vasculitis), abnormal blood flow (stasis or turbulence, e.g., atrial fibrillation, aneurysm), and hypercoagulability (e.g., Factor V Leiden, antiphospholipid syndrome, malignancy). Any combination promotes pathologic thrombus formation.

  14. Distinguish lines of Zahn, red (venous) thrombi, and postmortem clots.

    Lines of Zahn = alternating pale platelet/fibrin and dark RBC layers, indicating a thrombus formed in flowing blood antemortem. Red thrombi form in veins with stasis (more RBCs). Postmortem clots are gelatinous 'chicken-fat' yellow over dark 'currant-jelly' red, lack lines of Zahn, and are not attached to the wall.

  15. What are the four types of emboli besides thromboemboli, and a classic feature of each?

    Fat embolism (long-bone fractures; dyspnea, petechiae, neurologic changes). Air/gas embolism (decompression sickness — 'the bends', caisson disease). Amniotic fluid embolism (labor; DIC, sudden dyspnea). Septic/tumor emboli. Most pulmonary emboli arise from deep leg veins; saddle embolus lodges at the bifurcation.

  16. Define the steps of the metastatic cascade.

    Invasion (loss of E-cadherin, matrix metalloproteinase degradation of basement membrane), intravasation into vessels, survival in circulation, arrest and extravasation at distant site, then colonization/growth of micrometastases. Requires epithelial-mesenchymal transition and angiogenesis.

  17. Differentiate benign from malignant neoplasms across key features.

    Benign: well-differentiated, slow growth, no invasion (encapsulated), no metastasis, few/normal mitoses, '-oma' suffix. Malignant: variable differentiation/anaplasia, rapid growth, local invasion, metastasis, atypical mitoses, '-carcinoma/-sarcoma' suffix. Metastasis is the single most reliable sign of malignancy.

  18. What features define anaplasia (markers of malignancy)?

    Pleomorphism (variation in size/shape), hyperchromatic nuclei with high nuclear-to-cytoplasmic ratio (~1:1), prominent nucleoli, abundant and atypical (tripolar) mitoses, loss of polarity, and tumor giant cells. Anaplasia means lack of differentiation.

  19. Compare oncogenes and tumor suppressor genes with examples.

    Oncogenes: gain-of-function, dominant (one mutated allele suffices), promote growth — RAS, MYC, HER2/ERBB2, ABL. Tumor suppressors: loss-of-function, recessive (Knudson two-hit, both alleles inactivated), normally restrain growth — RB, TP53, APC, BRCA1/2, NF1. TP53 is the 'guardian of the genome.'

  20. List important tumor markers and their associated tumors.

    AFP — hepatocellular carcinoma, yolk sac/nonseminomatous germ cell tumors. CEA — colorectal/pancreatic. CA-125 — ovarian. CA 19-9 — pancreatic. PSA — prostate. beta-hCG — choriocarcinoma, germ cell. Calcitonin — medullary thyroid carcinoma. Chromogranin — neuroendocrine tumors.

Show the other 32 Pathology flashcards

  1. Define the stages of atherosclerosis development.

    Endothelial injury -> LDL accumulation and oxidation in intima -> monocyte adhesion and migration becoming foam cells (fatty streak) -> smooth muscle cell migration/proliferation and collagen deposition forming a fibrous cap over a lipid/necrotic core (atheroma). Plaque rupture triggers thrombosis -> acute events.

  2. What is the temporal evolution of microscopic changes in myocardial infarction?

    0–4 h: none (or wavy fibers). 4–12 h: early coagulation necrosis, edema. 12–24 h: contraction bands, neutrophils. 1–3 days: dense neutrophils, loss of nuclei. 3–7 days: macrophages remove dead myocytes (softest, rupture risk). 1–2 wk: granulation tissue. >2 mo: dense collagenous scar.

  3. Differentiate the major cardiomyopathies.

    Dilated (most common): systolic failure, dilated chambers — alcohol, viral myocarditis, peripartum, doxorubicin. Hypertrophic: diastolic dysfunction, asymmetric septal hypertrophy, myofiber disarray — beta-myosin heavy chain mutation, sudden death in athletes. Restrictive: decreased compliance — amyloidosis, sarcoidosis, endomyocardial fibrosis.

  4. Contrast emphysema and chronic bronchitis (COPD subtypes).

    Emphysema ('pink puffer'): permanent airspace enlargement distal to terminal bronchiole with alveolar wall destruction; centriacinar (smoking, upper lobes), panacinar (alpha-1 antitrypsin deficiency, lower lobes). Chronic bronchitis ('blue bloater'): productive cough >=3 months/year for >=2 years, mucous gland hyperplasia (increased Reid index).

  5. Distinguish lobar pneumonia, bronchopneumonia, and interstitial pneumonia.

    Lobar: consolidation of an entire lobe (Strep pneumoniae); stages = congestion, red hepatization, gray hepatization, resolution. Bronchopneumonia: patchy consolidation around bronchi (Staph, Klebsiella). Interstitial/atypical: inflammation of alveolar walls/interstitium, no alveolar exudate (Mycoplasma, viruses).

  6. What are the histologic hallmarks distinguishing small cell from non-small cell lung carcinoma?

    Small cell (neuroendocrine, central, smoking, paraneoplastic ADH/ACTH, treated with chemo): small cells, scant cytoplasm, nuclear molding, Azzopardi effect, chromogranin/synaptophysin+. NSCLC: adenocarcinoma (peripheral, glands/mucin, TTF-1+, EGFR/ALK), squamous (central, keratin pearls/intercellular bridges), large cell (undifferentiated).

  7. Compare the inflammatory bowel diseases Crohn disease and ulcerative colitis.

    Crohn: any site mouth-to-anus (terminal ileum), skip lesions, transmural inflammation, non-caseating granulomas, cobblestoning, fistulae/strictures, Th1/Th17. UC: colon only, continuous from rectum, mucosa/submucosa only, crypt abscesses, pseudopolyps, toxic megacolon, higher cancer risk, p-ANCA+, Th2.

  8. Describe the histologic basis and consequences of celiac disease.

    Immune reaction to gliadin (gluten) with anti-tissue transglutaminase and anti-endomysial antibodies, HLA-DQ2/DQ8. Duodenal biopsy: villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis -> malabsorption. Associated with dermatitis herpetiformis and increased risk of enteropathy-associated T-cell lymphoma.

  9. Outline the morphologic stages of nephrotic vs nephritic syndrome.

    Nephrotic: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia/lipiduria (minimal change, FSGS, membranous, diabetic nephropathy). Nephritic: hematuria with RBC casts, hypertension, oliguria, mild-moderate proteinuria, azotemia (post-streptococcal GN, IgA nephropathy, RPGN, lupus nephritis).

  10. What are the key features of post-streptococcal glomerulonephritis on microscopy and EM?

    Follows group A strep infection (1–4 weeks). LM: hypercellular, enlarged glomeruli with neutrophil infiltration. IF: granular ('lumpy-bumpy') IgG/C3 deposits along GBM and mesangium. EM: subepithelial 'humps.' Presents as nephritic syndrome with low complement; usually self-limited in children.

  11. Differentiate acute tubular necrosis ischemic vs nephrotoxic types.

    ATN is the commonest cause of acute kidney injury. Ischemic ATN: patchy tubular necrosis, especially straight proximal tubule and thick ascending limb; granular/muddy-brown casts. Nephrotoxic ATN: proximal tubule injury from drugs (aminoglycosides), contrast, heavy metals, myoglobin. Recovery possible since tubular cells regenerate.

  12. Classify anemias by morphology (MCV) with examples.

    Microcytic (MCV<80): iron deficiency, thalassemia, anemia of chronic disease, sideroblastic, lead poisoning. Normocytic (80–100): acute blood loss, hemolysis, aplastic, chronic disease. Macrocytic (MCV>100): megaloblastic (B12/folate deficiency — hypersegmented neutrophils) and non-megaloblastic (alcohol, liver disease, hypothyroidism).

  13. What peripheral smear findings characterize key anemias?

    Iron deficiency: microcytic hypochromic, target cells. B12/folate deficiency: macro-ovalocytes, hypersegmented neutrophils. Hereditary spherocytosis: spherocytes, increased osmotic fragility. Sickle cell: sickled cells, Howell-Jolly bodies (autosplenectomy). Thalassemia: target cells, basophilic stippling. G6PD: bite cells, Heinz bodies.

  14. Differentiate the acute leukemias AML and ALL.

    ALL: children, lymphoblasts, TdT+, CD10/CD19 (B) or CD3 (T), responds well, CNS/testes involvement, t(12;21) good prognosis. AML: adults, myeloblasts with Auer rods (peroxidase+), t(15;17) = APL (treat with ATRA, risk of DIC). Both show >20% blasts in marrow, pancytopenia of normal lines.

  15. Contrast Hodgkin and non-Hodgkin lymphoma.

    Hodgkin: Reed-Sternberg cells (CD15+/CD30+, 'owl-eye'), contiguous nodal spread, localized, bimodal age, B symptoms common, better prognosis. Non-Hodgkin: heterogeneous B/T cell, non-contiguous spread, more often extranodal and disseminated at presentation, includes Burkitt (t(8;14), 'starry sky'), follicular (t(14;18), BCL2).

  16. Describe the diagnostic findings of multiple myeloma.

    Clonal plasma cell malignancy: CRAB — hyperCalcemia, Renal insufficiency, Anemia, Bone lytic 'punched-out' lesions. Serum/urine M-spike (IgG most common), Bence-Jones proteinuria (free light chains), rouleaux on smear, marrow >10% plasma cells, increased risk of AL amyloidosis and infections.

  17. What are the morphologic and lab features of Graves disease vs Hashimoto thyroiditis?

    Graves: hyperthyroidism, diffuse hyperplastic goiter, 'scalloped' colloid, TSH-receptor stimulating antibodies, exophthalmos, pretibial myxedema. Hashimoto: hypothyroidism, lymphocytic infiltrate with germinal centers, Hurthle cells, anti-TPO/anti-thyroglobulin antibodies, increased risk of B-cell (MALT) lymphoma.

  18. Differentiate the major thyroid carcinomas.

    Papillary (most common, best prognosis): Orphan-Annie eye nuclei, psammoma bodies, lymphatic spread, RET/BRAF. Follicular: capsular/vascular invasion, hematogenous spread, RAS. Medullary: parafollicular C cells, calcitonin, amyloid stroma, MEN2/RET. Anaplastic: elderly, undifferentiated, very poor prognosis.

  19. What is the morphologic basis of diabetic complications in tissues?

    Chronic hyperglycemia causes nonenzymatic glycation (AGEs), polyol pathway, and protein kinase C activation. Microvascular: hyaline arteriolosclerosis, thickened basement membranes, Kimmelstiel-Wilson nodules (nodular glomerulosclerosis), retinopathy, neuropathy. Macrovascular: accelerated atherosclerosis.

  20. Distinguish the morphology and causes of the major CNS hemorrhages.

    Epidural: middle meningeal artery (skull fracture), biconvex/lens-shaped, lucid interval. Subdural: bridging veins (trauma, elderly/alcoholics), crescent-shaped, crosses sutures. Subarachnoid: ruptured berry aneurysm (Circle of Willis), 'worst headache of life.' Intraparenchymal: hypertension (basal ganglia), Charcot-Bouchard aneurysms.

  21. What histologic features characterize Alzheimer disease?

    Extracellular neuritic (senile) plaques of beta-amyloid (from APP cleavage) and intracellular neurofibrillary tangles of hyperphosphorylated tau. Cerebral atrophy (widened sulci, narrowed gyri, hydrocephalus ex vacuo), amyloid angiopathy. Risk: ApoE4; APP/presenilin mutations in familial early-onset.

  22. Differentiate osteoarthritis from rheumatoid arthritis.

    Osteoarthritis: degenerative, wear-and-tear, weight-bearing joints, Heberden (DIP)/Bouchard (PIP) nodes, osteophytes, eburnation, no systemic inflammation. Rheumatoid: autoimmune (anti-CCP, RF), symmetric small joints (MCP/PIP), pannus, morning stiffness, ulnar deviation, systemic, HLA-DR4.

  23. What are the characteristic bone tumors and their key features?

    Osteosarcoma: metaphysis of long bones, adolescents, Codman triangle/sunburst, RB/p53. Ewing sarcoma: diaphysis, children, t(11;22), onion-skin periosteum, 'small round blue cells.' Osteochondroma: most common benign. Giant cell tumor: epiphysis, 'soap-bubble', multinucleated giant cells. Chondrosarcoma: malignant cartilage, older adults.

  24. Describe the pathology of tuberculosis (primary vs secondary).

    Mycobacterium tuberculosis causes type IV hypersensitivity granulomas with caseous necrosis and acid-fast bacilli. Primary: Ghon focus (subpleural) + hilar nodes = Ghon/Ranke complex. Secondary (reactivation): apical cavitary lesions. Miliary TB = hematogenous dissemination. Langhans giant cells present.

  25. What organisms cause the classic granulomatous and special-stain-identified infections?

    Acid-fast (Ziehl-Neelsen): Mycobacteria, Nocardia (partial). PAS/GMS (silver): fungi (Aspergillus septate acute-angle, Mucor broad nonseptate wide-angle, Cryptococcus mucicarmine capsule). Warthin-Starry: spirochetes/Bartonella/H. pylori. India ink: Cryptococcus. Giemsa: Leishmania, malaria, H. pylori.

  26. Compare the four (Gell and Coombs) hypersensitivity reactions.

    Type I (immediate/anaphylactic): IgE, mast cells/histamine (asthma, anaphylaxis). Type II (antibody-mediated cytotoxic): IgG/IgM vs cell antigens (autoimmune hemolytic anemia, Goodpasture). Type III (immune complex): complexes deposit, complement (SLE, serum sickness, PSGN). Type IV (delayed/T-cell): T cells/macrophages (TB test, contact dermatitis, transplant).

  27. What are the diagnostic autoantibodies in common autoimmune diseases?

    SLE: ANA (sensitive), anti-dsDNA and anti-Smith (specific). Drug-induced lupus: anti-histone. Systemic sclerosis: anti-Scl-70 (diffuse), anti-centromere (CREST). Sjogren: anti-Ro(SSA)/La(SSB). Polymyositis: anti-Jo-1. Granulomatosis with polyangiitis: c-ANCA (PR3). Microscopic polyangiitis: p-ANCA (MPO).

  28. Differentiate the classic vitamin deficiency syndromes (A, D, C, B1, B3, B12).

    Vit A: night blindness, xerophthalmia, Bitot spots. Vit D: rickets/osteomalacia. Vit C: scurvy (defective collagen, bleeding gums, poor wound healing). B1 (thiamine): Wernicke-Korsakoff, beriberi. B3 (niacin): pellagra (dermatitis, diarrhea, dementia). B12: megaloblastic anemia + subacute combined degeneration.

  29. Explain the pathology and inheritance of the major genetic/developmental diseases (Down, CF, sickle cell, fragile X).

    Down (trisomy 21): flat facies, AV septal defect, duodenal atresia, AML/ALL, early Alzheimer. Cystic fibrosis (autosomal recessive, CFTR del-F508): thick secretions, recurrent lung infections, pancreatic insufficiency. Sickle cell (autosomal recessive, beta-globin Glu->Val): vaso-occlusion. Fragile X (X-linked, CGG repeat): macroorchidism, long face.

  30. What does the ESR (erythrocyte sedimentation rate) and CRP indicate, and what raises/lowers them?

    ESR measures RBC settling rate, an indirect marker of acute-phase proteins (mainly fibrinogen). Raised in inflammation, infection, malignancy, anemia, pregnancy, and especially temporal arteritis/PMR. Lowered by polycythemia, sickle cell, microcytosis. CRP is a more rapid, direct acute-phase reactant produced by the liver.

  31. Describe the steps and tissue handling of routine histopathology processing.

    Fixation (10% neutral buffered formalin prevents autolysis, cross-links proteins) -> grossing -> dehydration (graded alcohols) -> clearing (xylene) -> paraffin embedding -> microtomy (~4–5 micron sections) -> staining (H&E: hematoxylin stains nuclei blue, eosin stains cytoplasm pink) -> mounting. Frozen section gives rapid intraoperative diagnosis.

  32. What is the principle of immunohistochemistry and key diagnostic markers?

    IHC uses labeled antibodies against tissue antigens, visualized by chromogen (e.g., DAB), to identify cell lineage/origin. Cytokeratin = epithelial (carcinoma); vimentin = mesenchymal; S-100/HMB-45/Melan-A = melanoma; LCA(CD45) = lymphoma; chromogranin/synaptophysin = neuroendocrine; ER/PR/HER2 = breast cancer prognostic/predictive.

Same Pathology syllabus in other exams

The Pathology outline above is identical in these 3 exams:

INI CET Pathology FAQ

What is in the INI CET Pathology syllabus?

INI CET Pathology is split into 4 chapters: General Pathology, Systemic Pathology, Special Pathology and Laboratory Investigations in Pathology. Together they contain 23 topics and 95 sub-topics.

How many chapters are in INI CET Pathology?

4 chapters, containing 23 topics and 95 sub-topics. The largest chapter is Systemic Pathology, with 8 topics.

Are there flashcards for INI CET Pathology?

Yes — a 52-card Pathology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.