DNB CET Pathology Syllabus

Pathology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology in DNB CET, not a summary of it.

1. 1

   General Pathology

   6 topics

   • Cell injury, adaptation and cell death
   • Acute and chronic inflammation
   • Tissue repair, healing and granulation
   • Hemodynamic disorders, thrombosis and embolism
   • Neoplasia, carcinogenesis and tumor markers
   • Immunopathology and amyloidosis
2. 2

   Hematology

   4 topics

   • Anemias
     • Iron deficiency and megaloblastic anemia
     • Hemolytic anemias and hemoglobinopathies
     • Aplastic and myelophthisic anemia
   • Leukemias and myeloproliferative disorders
   • Lymphomas - Hodgkin and non-Hodgkin
   • Bleeding disorders and coagulation cascade
3. 3

   Systemic Pathology

   5 topics

   • Cardiovascular - atherosclerosis, MI, cardiomyopathies
   • Respiratory - COPD, pneumonia, lung tumors
   • GIT and hepatobiliary pathology
   • Renal and urinary tract pathology
   • CNS, breast and female genital tract pathology
4. 4

   Clinical Pathology and Lab Medicine

   3 topics

   • Peripheral smear and bone marrow interpretation
   • Urinalysis and body fluid examination
   • Immunohistochemistry and special stains

Pathology flashcards for DNB CET

24 of 72 cards from the Pathology deck — real questions with worked answers.

1. What is the difference between hydropic change (cellular swelling) and fatty change, and which one is reversible?

   Both are reversible injuries. Hydropic change is accumulation of water from failure of the Na+/K+ ATPase pump (cell swelling, clear cytoplasmic vacuoles). Fatty change (steatosis) is abnormal accumulation of triglycerides within parenchymal cells, classically in liver, heart and kidney.

2. List the morphological and biochemical features that distinguish apoptosis from necrosis.

   Apoptosis: single cells, cell shrinkage, chromatin condensation (pyknosis), apoptotic bodies, intact membrane, no inflammation, ATP-dependent, caspase-mediated. Necrosis: groups of cells, cell swelling, membrane rupture, enzymatic digestion, leakage of contents causing inflammation, ATP-independent.

3. Name the types of necrosis and give a classic example of each.

   Coagulative (MI/ischemia in solid organs), Liquefactive (brain infarct, abscess), Caseous (TB), Fat (acute pancreatitis), Fibrinoid (vasculitis, malignant hypertension), Gangrenous (limb ischemia).

4. What are the intracellular and extracellular reversible cellular adaptations to stress?

   Hypertrophy (increased cell size), Hyperplasia (increased cell number), Atrophy (decreased size/number), Metaplasia (reversible change from one differentiated cell type to another), and Dysplasia (disordered growth, considered preneoplastic).

5. Which two key events mark the irreversible (point of no return) transition in cell injury?

   Severe mitochondrial dysfunction (inability to generate ATP, mitochondrial permeability transition) and profound plasma membrane damage. Calcium influx and loss of membrane integrity are hallmarks.

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

   Rubor (redness), Tumor (swelling), Calor (heat), Dolor (pain), and Functio laesa (loss of function).

7. What are the vascular changes in acute inflammation and what causes increased vascular permeability?

   Transient vasoconstriction then vasodilation (increased blood flow), and increased vascular permeability. Permeability is due mainly to endothelial contraction (immediate transient, histamine/bradykinin mediated), plus endothelial injury and transcytosis (VEGF).

8. Name the chemical mediators of inflammation derived from arachidonic acid and their pathways.

   Cyclooxygenase pathway produces prostaglandins and thromboxane A2. Lipoxygenase pathway produces leukotrienes (LTB4 chemotactic; LTC4/D4/E4 cause vasoconstriction/bronchospasm/permeability) and lipoxins (anti-inflammatory).

9. Give the morphological patterns of chronic inflammation and name the predominant cell type.

   Chronic inflammation features mononuclear cells—macrophages (predominant), lymphocytes and plasma cells—with tissue destruction and attempts at repair (angiogenesis, fibrosis). Granulomatous inflammation is a distinct pattern with epithelioid cells.

10. What is a granuloma and what are the two types with examples?

    A granuloma is a focal collection of activated epithelioid macrophages, often with multinucleate giant cells. Foreign-body type (around inert material) and Immune type (T-cell mediated, e.g., TB, sarcoidosis, leprosy, fungi).

11. Distinguish healing by first intention versus second intention.

    First (primary) intention: clean, approximated wound edges (surgical incision), minimal granulation tissue, small scar. Second intention: large open wound with extensive tissue loss, abundant granulation tissue, wound contraction by myofibroblasts, larger scar.

12. What is granulation tissue composed of, and when does it appear in wound healing?

    Granulation tissue = new capillaries (angiogenesis), proliferating fibroblasts, and loose ECM with inflammatory cells. It appears around day 3-5 and gives a soft, pink, granular appearance.

13. Which growth factor is most important for angiogenesis and which for fibroblast proliferation/collagen in wound healing?

    VEGF is the key angiogenic factor. TGF-beta is the most important fibrogenic agent, stimulating fibroblast migration/proliferation and collagen deposition while suppressing degradation.

14. What is the difference in collagen type during early wound healing versus a mature scar?

    Early granulation tissue/wound has predominantly Type III collagen, which is later replaced and remodeled (by matrix metalloproteinases) into stronger Type I collagen in the mature scar.

15. Define the three lines of Virchow's triad for thrombosis.

    Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability of blood.

16. What are the lines of Zahn and what do they indicate?

    Lines of Zahn are alternating pale (platelet/fibrin) and dark (RBC) laminations seen in a thrombus. Their presence indicates the thrombus formed in flowing blood antemortem (in life), distinguishing it from a postmortem clot.

17. Differentiate transudate from exudate (specific gravity, protein, cause).

    Transudate: specific gravity <1.012, low protein (<2.5-3 g/dL), few cells, due to altered hydrostatic/oncotic pressure (e.g., CHF). Exudate: specific gravity >1.020, high protein, many cells, due to increased vascular permeability/inflammation.

18. What is the most common source of pulmonary emboli and what is a saddle embolus?

    Most pulmonary emboli arise from deep veins of the lower legs (DVT, popliteal/femoral/iliac). A saddle embolus is a large embolus lodged at the bifurcation of the main pulmonary artery, often causing sudden death.

19. What is a fat embolism syndrome and its classic triad?

    Fat embolism follows long-bone fractures/soft tissue trauma. Classic triad: pulmonary insufficiency (dyspnea), neurologic symptoms, and petechial skin rash, typically appearing 1-3 days after injury.

20. Differentiate a benign from a malignant tumor (4 key features).

    Benign: well-differentiated, slow growth, encapsulated/non-invasive, no metastasis. Malignant: poorly to well-differentiated (anaplasia), rapid growth, invasive/infiltrative, capable of metastasis.

21. Define anaplasia and list its cytologic hallmarks.

    Anaplasia is lack of differentiation, the hallmark of malignancy. Features: pleomorphism, hyperchromatic nuclei, high nuclear-to-cytoplasmic ratio, prominent nucleoli, abnormal/atypical mitoses, and loss of polarity.

22. Name the major routes of metastatic spread and which is typical of carcinomas versus sarcomas.

    Lymphatic spread (typical of carcinomas), hematogenous spread (typical of sarcomas), and seeding of body cavities (transcoelomic, e.g., ovarian carcinoma to peritoneum).

23. List important tumor markers and their associated tumors: AFP, CEA, PSA, CA-125, CA-19-9, beta-hCG.

    AFP: hepatocellular carcinoma, yolk sac/germ cell tumors. CEA: colorectal, pancreatic, gastric, lung carcinomas. PSA: prostate carcinoma. CA-125: ovarian (epithelial) carcinoma. CA-19-9: pancreatic carcinoma. beta-hCG: choriocarcinoma, germ cell tumors.

24. Name two classic tumor suppressor genes and their associated cancers, and the 'two-hit' hypothesis.

    RB (retinoblastoma, osteosarcoma) and TP53 (Li-Fraumeni, most human cancers). Knudson's two-hit hypothesis: both alleles of a tumor suppressor gene must be inactivated for tumor development.

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