NEET PG 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 NEET PG, not a summary of it.

1. 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. 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. 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. 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

Pathology flashcards for NEET PG

24 of 67 cards from the Pathology deck — real questions with worked answers.

1. What are the morphologic hallmarks of reversible cell injury seen by light microscopy?

   Cellular swelling (hydropic change) and fatty change (steatosis). Ultrastructurally: plasma membrane blebbing, mitochondrial swelling, ER dilation, ribosomal detachment.

2. Name the two key irreversible events that mark the transition to cell death in injury.

   Inability to restore mitochondrial function (no ATP even after reperfusion) and profound disturbance of membrane function (lysosomal/plasma membrane damage).

3. Contrast the morphology and mechanism of necrosis versus apoptosis.

   Necrosis: cell swelling, membrane rupture, enzymatic digestion, inflammation, pathologic, ATP-independent. Apoptosis: cell shrinkage, intact membrane, apoptotic bodies, no inflammation, physiologic/pathologic, ATP-dependent, regulated.

4. Match each necrosis type to its classic setting: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous.

   Coagulative = ischemic infarct (except brain); Liquefactive = brain infarct/abscess; Caseous = TB; Fat = acute pancreatitis; Fibrinoid = immune vasculitis/malignant HTN; Gangrenous = limb ischemia.

5. List the intrinsic (mitochondrial) apoptosis pathway: trigger, key proteins, executioner.

   Trigger: cell injury/growth factor loss. Pro-apoptotic BAX/BAK form pores (inhibited by BCL-2/BCL-XL) -> cytochrome c release -> APAF-1 apoptosome -> caspase-9 -> executioner caspases 3/6/7.

6. Define hypertrophy, hyperplasia, atrophy and metaplasia with one example each.

   Hypertrophy = increased cell size (cardiac muscle in HTN); Hyperplasia = increased cell number (endometrium in estrogen excess); Atrophy = decreased size/number (disuse muscle); Metaplasia = one mature type replaced by another (Barrett esophagus: squamous->columnar).

7. Which free radical injury describes ischemia-reperfusion, and what enzymes defend against ROS?

   Reperfusion generates ROS (superoxide, H2O2, hydroxyl radical) damaging restored tissue. Defenses: superoxide dismutase, catalase, glutathione peroxidase, plus antioxidants (vitamins A, C, E).

8. What are the five cardinal signs of acute inflammation and their Latin terms?

   Redness (rubor), heat (calor), swelling (tumor), pain (dolor), loss of function (functio laesa).

9. List the sequential steps of leukocyte extravasation in acute inflammation.

   Margination -> rolling (selectins) -> firm adhesion (integrins/ICAM-1) -> transmigration/diapedesis (PECAM-1) -> chemotaxis to tissue.

10. Name the chemotactic agents that recruit neutrophils in acute inflammation.

    C5a, LTB4 (leukotriene B4), bacterial products (N-formyl-methionine peptides), and chemokines (e.g., IL-8/CXCL8).

11. Distinguish exudate from transudate by protein and specific gravity.

    Exudate: protein-rich, specific gravity >1.020, due to increased vascular permeability (inflammation). Transudate: protein-poor, specific gravity <1.012, due to hydrostatic/oncotic imbalance (non-inflammatory).

12. What is a granuloma, and which cells compose it?

    A focus of chronic inflammation: aggregate of activated epithelioid macrophages, often with multinucleated giant cells, surrounded by a rim of lymphocytes. Seen in TB, sarcoidosis, fungal infections, foreign bodies.

13. Compare healing by primary versus secondary intention.

    Primary: clean, approximated wound edges, minimal tissue loss, little granulation tissue, small scar. Secondary: large tissue defect, edges not approximated, abundant granulation tissue, wound contraction, larger scar.

14. Which collagen predominates early in granulation tissue versus the mature scar?

    Type III collagen predominates early in granulation tissue; it is gradually replaced by stronger Type I collagen during maturation/remodeling.

15. What is the time course of tensile strength recovery in a sutured wound?

    ~10% at 1 week (suture-dependent), ~70-80% of original strength by 3 months, and it plateaus there (never reaches 100%).

16. Define edema, and give Starling's forces that govern fluid movement across capillaries.

    Edema = excess interstitial fluid. Governed by capillary hydrostatic pressure (pushes out), plasma oncotic pressure (pulls in), interstitial pressures, and lymphatic drainage. Net imbalance causes edema.

17. Distinguish a thrombus from a postmortem clot.

    Thrombus: attached to wall, firm, has lines of Zahn (alternating platelet/fibrin and RBC layers). Postmortem clot: not attached, gelatinous, 'chicken fat' (yellow) over 'currant jelly' (red), no lines of Zahn.

18. State Virchow's triad of thrombosis.

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

19. Differentiate a red (hemorrhagic) infarct from a white (pale) infarct.

    Red infarct: loose tissue with dual blood supply or venous occlusion (lung, intestine, testis). White infarct: solid organ with end-arterial supply (heart, kidney, spleen).

20. What is the most common source of pulmonary thromboembolism and a fatal consequence?

    Deep veins of the lower extremities (popliteal/femoral/iliac). A large saddle embolus at the pulmonary bifurcation can cause sudden death.

21. Define neoplasia and contrast benign versus malignant tumors on key features.

    Neoplasia = abnormal autonomous tissue growth. Benign: well-differentiated, slow, encapsulated, non-invasive, no metastasis. Malignant: poorly differentiated/anaplastic, rapid, infiltrative, metastasizes.

22. What is the classic naming rule for benign and malignant tumors of epithelial vs mesenchymal origin?

    Benign: tissue + '-oma' (e.g., adenoma, lipoma). Malignant epithelial = carcinoma (adenocarcinoma); malignant mesenchymal = sarcoma (osteosarcoma, leiomyosarcoma).

23. List the hallmarks of malignancy (Hanahan & Weinberg).

    Sustained proliferative signaling, evading growth suppressors, resisting apoptosis, replicative immortality, inducing angiogenesis, activating invasion/metastasis, deregulated metabolism, evading immune destruction; enabled by genome instability and tumor-promoting inflammation.

24. Differentiate tumor grading from staging.

    Grading = degree of differentiation/anaplasia (histologic; low to high grade). Staging = extent of spread (TNM: Tumor size, Node involvement, Metastasis). Staging has greater prognostic value.

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