PGIMER Entrance 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 PGIMER Entrance, not a summary of it.

1. 1

   General Pathology

   5 topics

   • Cell injury, adaptation and cell death
   • Acute and chronic inflammation
   • Tissue repair and wound healing
   • Hemodynamic disorders
     • Edema, thrombosis and embolism
     • Shock and infarction
   • Neoplasia and carcinogenesis
     • Tumor markers and grading vs staging
     • Oncogenes and tumor suppressor genes
2. 2

   Hematology

   4 topics

   • Anemia classification and morphology
   • Hemolytic anemias and hemoglobinopathies
   • Leukemias and lymphomas
   • Bleeding and coagulation disorders
3. 3

   Systemic Pathology

   5 topics

   • Cardiovascular pathology
     • Atherosclerosis and ischemic heart disease
     • Rheumatic heart disease and endocarditis
   • Respiratory and renal pathology
   • Gastrointestinal and hepatobiliary pathology
   • Endocrine and breast pathology
   • CNS and bone tumor pathology
4. 4

   Immunology and Lab Medicine

   3 topics

   • Hypersensitivity reactions and autoimmunity
   • Immunodeficiency disorders
   • Amyloidosis and transplantation immunology

Pathology flashcards for PGIMER Entrance

24 of 50 cards from the Pathology deck — real questions with worked answers.

1. What is the difference between hypertrophy and hyperplasia as cellular adaptations?

   Hypertrophy is an increase in cell size (and thus organ size) due to increased synthesis of structural components, occurring in permanent (non-dividing) cells like cardiac and skeletal muscle. Hyperplasia is an increase in cell number from proliferation, occurring only in cells capable of dividing (e.g. endometrium, liver). Both increase organ size and often coexist.

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

   Reversible injury shows ATP depletion, cellular and mitochondrial swelling, and plasma membrane blebbing without membrane rupture. The hallmark of irreversibility is severe mitochondrial dysfunction with inability to recover oxidative phosphorylation plus profound plasma membrane damage, allowing massive calcium influx and leakage of enzymes.

3. Differentiate coagulative, liquefactive, caseous, and fat necrosis with their typical locations.

   Coagulative necrosis preserves tissue architecture (firm), typical of ischemic infarcts in solid organs except brain. Liquefactive necrosis digests tissue into liquid/pus, seen in brain infarcts and bacterial abscesses. Caseous necrosis is 'cheese-like' amorphous debris, classic of tuberculosis. Fat necrosis (chalky deposits) occurs in pancreatitis and trauma to fat (breast).

4. What are the morphologic features and key molecular regulators that distinguish apoptosis from necrosis?

   Apoptosis is programmed, energy-dependent, single-cell death with cell shrinkage, chromatin condensation, apoptotic bodies, and NO inflammation; regulated by caspases (intrinsic mitochondrial/BCL-2 family and extrinsic Fas/TNF death-receptor pathways). Necrosis is passive, affects cell groups, causes cell swelling, membrane rupture, enzyme leakage, and elicits inflammation.

5. What are the cardinal signs of acute inflammation and the vascular events producing them?

   The cardinal signs are rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). They arise from transient vasoconstriction then vasodilation (redness, heat), increased vascular permeability causing exudation (swelling), and mediators such as bradykinin and prostaglandins causing pain.

6. Name the chemotactic agents for neutrophils and the steps of leukocyte extravasation.

   Major chemoattractants: C5a, LTB4, IL-8 (CXCL8), and bacterial N-formyl-methionyl peptides. Steps of extravasation: margination and rolling (selectins), firm adhesion (integrins binding ICAM-1/VCAM-1), transmigration/diapedesis (PECAM-1/CD31), then chemotaxis through the interstitium.

7. What is a granuloma, what are its cellular components, and what is the difference between caseating and non-caseating types?

   A granuloma is a focal collection of activated (epithelioid) macrophages, often with multinucleated giant cells, surrounded by lymphocytes, characteristic of chronic inflammation. Caseating granulomas have central caseous necrosis (classically tuberculosis, fungal infections). Non-caseating granulomas lack central necrosis (sarcoidosis, Crohn disease, foreign body reactions, leprosy).

8. Differentiate labile, stable, and permanent cells in tissue regeneration.

   Labile cells continuously divide and regenerate readily (surface epithelia, bone marrow, GI/skin). Stable cells are quiescent (G0) but can divide when stimulated (hepatocytes, renal tubular cells, endothelium, fibroblasts). Permanent cells cannot regenerate and heal only by scarring (neurons, cardiac and skeletal muscle).

9. What is the difference between healing by primary intention and secondary intention?

   Primary intention healing occurs in clean, closely-apposed wounds (e.g. surgical incision) with minimal tissue loss, little granulation tissue, and a small scar. Secondary intention healing occurs in large wounds with extensive tissue loss, requiring abundant granulation tissue, wound contraction (myofibroblasts), and producing a larger scar.

10. What is granulation tissue, what growth factor drives its angiogenesis, and what is the role of metalloproteinases and the difference between a keloid and a hypertrophic scar?

    Granulation tissue is the hallmark of healing: proliferating fibroblasts and new thin-walled capillaries (angiogenesis, driven mainly by VEGF) in a loose matrix with macrophages. Matrix metalloproteinases (MMPs), which are zinc-dependent collagenases, degrade collagen during ECM remodeling. A hypertrophic scar has excess collagen confined within the original wound boundaries; a keloid has excess collagen extending beyond the original wound margins and tends to recur after excision (more common in darker skin).

11. Define edema and list the four main mechanisms causing it.

    Edema is increased fluid in interstitial tissue spaces. Mechanisms: (1) increased hydrostatic pressure (venous obstruction, heart failure), (2) reduced plasma oncotic pressure/hypoproteinemia (nephrotic syndrome, liver failure), (3) lymphatic obstruction (lymphedema), and (4) sodium/water retention and increased vascular permeability (inflammation).

12. Differentiate hyperemia from congestion.

    Hyperemia is an active process from arteriolar dilation causing increased inflow of oxygenated blood, making tissue red (erythema), e.g. exercise or inflammation. Congestion is a passive process from impaired venous outflow, causing accumulation of deoxygenated blood, making tissue blue-red (cyanosis), e.g. heart failure (nutmeg liver).

13. What are the components of Virchow triad for thrombosis?

    Virchow triad: (1) endothelial injury, (2) abnormal blood flow (stasis or turbulence), and (3) hypercoagulability. Endothelial injury is dominant for arterial/cardiac thrombi; stasis and hypercoagulability dominate venous thrombi.

14. Differentiate red (hemorrhagic) infarct from white (anemic) infarct and where each occurs.

    Red infarcts occur in loose tissues with dual blood supply or collateral circulation, or in venous occlusion and reperfusion (e.g. lung, intestine, testis); blood seeps into the necrotic zone. White infarcts occur in solid organs with end-arterial supply (heart, spleen, kidney) where dense tissue limits hemorrhage.

15. What is the difference between an embolus and a thrombus, and what is a paradoxical embolus?

    A thrombus is a solid mass formed in situ within the circulation; an embolus is any detached intravascular mass (solid, liquid, or gas) carried by blood to a distant site. A paradoxical embolus is a venous embolus that crosses into arterial circulation through a cardiac defect (e.g. patent foramen ovale).

16. What is the difference between disseminated intravascular coagulation (DIC) and a localized thrombus?

    DIC is a widespread thrombohemorrhagic disorder: systemic activation of coagulation forms microthrombi throughout the microvasculature, consuming platelets and clotting factors (consumption coagulopathy) and causing simultaneous thrombosis and bleeding. A localized thrombus is a single confined clot without systemic factor consumption.

17. Differentiate the terms hyperplasia, metaplasia, dysplasia, and anaplasia.

    Hyperplasia: increased number of normal cells. Metaplasia: reversible replacement of one differentiated cell type by another (e.g. squamous metaplasia in bronchus). Dysplasia: disordered, atypical (pre-neoplastic) growth, often reversible. Anaplasia: lack of differentiation with marked pleomorphism, a hallmark of malignancy.

18. What features distinguish benign from malignant tumors?

    Benign: well differentiated, slow growth, encapsulated/non-invasive, no metastasis, few mitoses, uniform cells. Malignant: poorly differentiated (anaplastic), rapid/erratic growth, invasive with no capsule, capable of metastasis, many and atypical mitoses, pleomorphism and hyperchromatic nuclei.

19. Give the nomenclature rules for naming benign vs malignant tumors of epithelial and mesenchymal origin.

    Benign tumors generally add suffix '-oma' (e.g. adenoma, lipoma, fibroma). Malignant epithelial tumors are 'carcinomas' (adenocarcinoma, squamous cell carcinoma). Malignant mesenchymal (connective tissue) tumors are 'sarcomas' (osteosarcoma, liposarcoma).

20. What are the differences between oncogenes, tumor suppressor genes, and the function of p53 and RB?

    Oncogenes are mutated/over-active proto-oncogenes that promote growth (gain of function, dominant; e.g. RAS, MYC). Tumor suppressor genes normally inhibit growth and are lost in cancer (loss of function, usually need both alleles). p53 (the 'guardian of the genome') arrests the cycle/triggers apoptosis on DNA damage; RB controls the G1-to-S checkpoint.

21. List the hallmarks of cancer (Hanahan and Weinberg).

    Self-sufficiency in growth signals, insensitivity to growth inhibitors, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, ability to invade and metastasize, reprogrammed metabolism (Warburg effect), evasion of immune destruction, with enabling characteristics of genomic instability and tumor-promoting inflammation.

22. What are the routes of metastatic spread and which routes typify carcinomas vs sarcomas?

    Routes: (1) lymphatic spread, (2) hematogenous (blood) spread, and (3) seeding of body cavities (transcoelomic). Carcinomas typically spread first via lymphatics; sarcomas typically spread hematogenously (though there is overlap).

23. What is the morphologic classification of anemia based on MCV and MCHC, with an example of each?

    Microcytic hypochromic (low MCV, low MCHC): iron deficiency, thalassemia. Normocytic normochromic (normal MCV/MCHC): acute blood loss, anemia of chronic disease, hemolysis. Macrocytic (high MCV): megaloblastic anemia from B12/folate deficiency.

24. Differentiate the lab findings of iron-deficiency anemia from anemia of chronic disease.

    Iron deficiency: low serum iron, low ferritin, HIGH TIBC, low transferrin saturation, absent marrow iron. Anemia of chronic disease: low serum iron, NORMAL or HIGH ferritin, LOW TIBC, normal/increased marrow iron stores (sequestered, mediated by hepcidin).

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