MBBS 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 MBBS, 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 MBBS

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

1. Define hypertrophy and atrophy as cellular adaptations, and give a physiological example of each.

   Hypertrophy is an increase in cell size (and thus organ size) due to increased synthesis of structural proteins/organelles, occurring in non-dividing cells (e.g., uterine smooth muscle in pregnancy, cardiac muscle in hypertension). Atrophy is a decrease in cell size due to loss of cell substance (e.g., skeletal muscle after disuse or denervation).

2. What is metaplasia, and what is its clinical significance using Barrett esophagus as an example?

   Metaplasia is a reversible change in which one differentiated (adult) cell type is replaced by another better suited to a stress. In Barrett esophagus, stratified squamous epithelium is replaced by columnar (gastric/intestinal) epithelium due to chronic acid reflux. It is significant because persistent stress in metaplastic epithelium predisposes to dysplasia and malignancy (adenocarcinoma).

3. List the four main mechanisms (key targets) of cell injury.

   (1) ATP depletion (mitochondrial damage), (2) Influx of calcium and loss of calcium homeostasis, (3) Accumulation of oxygen-derived free radicals (oxidative stress), and (4) Defects in membrane permeability. Damage to DNA and misfolded proteins are also key contributors.

4. Contrast reversible and irreversible cell injury in terms of the key ultrastructural and biochemical markers.

   Reversible injury: cellular swelling, mitochondrial swelling, ATP depletion, ribosomal detachment, membrane blebbing — but intact membranes and no nuclear changes. Irreversible injury: severe mitochondrial damage (with amorphous densities), profound membrane damage (lysosomal enzyme leakage), and nuclear changes (pyknosis, karyorrhexis, karyolysis).

5. List the morphologic patterns of necrosis and give a classic example of each.

   Coagulative (ischemic infarcts of solid organs, e.g., heart), Liquefactive (brain infarcts, abscesses), Caseous (tuberculosis), Fat necrosis (acute pancreatitis), Fibrinoid (immune vasculitis/malignant hypertension), and Gangrenous (lower limb ischemia — clinical term).

6. Compare apoptosis and necrosis with respect to cell size, membrane integrity, and inflammation.

   Apoptosis: cell shrinks, membrane intact (forms apoptotic bodies), energy-dependent, regulated, no inflammation. Necrosis: cell swells, membrane disrupted (enzymatic leakage), passive/uncontrolled, and elicits an inflammatory response.

7. Name the intrinsic (mitochondrial) apoptosis pathway's key regulators and the initiator/executioner caspases involved.

   The intrinsic pathway is regulated by the BCL-2 family: anti-apoptotic (BCL-2, BCL-XL) vs pro-apoptotic (BAX, BAK, and BH3-only proteins like BIM, BID). Mitochondrial outer membrane permeabilization releases cytochrome c, which with APAF-1 activates initiator caspase-9, which then activates executioner caspases-3 and -6.

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

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

9. Describe the vascular changes in acute inflammation and the formula relating to fluid movement.

   Transient vasoconstriction followed by vasodilation (increased blood flow → heat/redness) and increased vascular permeability leading to exudate formation. Fluid movement follows Starling forces; net filtration $J_{v} = K_{f}\left[(P_{c}-P_{i}) - \sigma(\pi_{c}-\pi_{i})\right]$, where increased $P_{c}$ and reduced $\pi_{c}$ (protein leak) drive exudation.

10. Outline the sequence of leukocyte extravasation (recruitment) in acute inflammation.

    (1) Margination and rolling (selectins — E-selectin, P-selectin, L-selectin binding sialyl-Lewis X), (2) Firm adhesion (integrins binding ICAM-1/VCAM-1), (3) Transmigration/diapedesis (PECAM-1/CD31), and (4) Chemotaxis toward the site (e.g., C5a, LTB4, IL-8, bacterial N-formyl peptides).

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

    Exudate: protein-rich, cloudy, specific gravity $> 1.020$, high protein (often $> 3\,\text{g/dL}$), due to increased vascular permeability (inflammation). Transudate: protein-poor, clear, specific gravity $< 1.012$, low protein, due to hydrostatic/oncotic imbalance (e.g., heart failure).

12. What cells and features characterize chronic inflammation, and what is a granuloma?

    Chronic inflammation features macrophages, lymphocytes, and plasma cells, with tissue destruction and simultaneous repair (angiogenesis, fibrosis). A granuloma is a focal collection of activated (epithelioid) macrophages, often with multinucleated giant cells, surrounded by lymphocytes — seen in TB (caseating) and sarcoidosis (non-caseating).

13. Compare healing by first intention vs second intention.

    First (primary) intention: clean, approximated wound edges (e.g., surgical incision) — minimal tissue loss, little granulation tissue, small scar. Second intention: large wound with significant tissue loss — heals by abundant granulation tissue, extensive ECM, wound contraction (myofibroblasts), and a larger scar.

14. Name the major growth factors in tissue repair and their primary roles.

    VEGF (angiogenesis), PDGF (recruits fibroblasts/smooth muscle, fibroblast proliferation), FGF (angiogenesis, wound repair), TGF-β (fibrosis — stimulates collagen, inhibits inflammation/MMPs), and EGF (epithelial/fibroblast proliferation).

15. Describe the role of collagen types and remodeling in wound healing, including the enzyme involved.

    Type III collagen is laid down early in granulation tissue (weak), then replaced by stronger Type I collagen during remodeling. Remodeling is mediated by matrix metalloproteinases (MMPs, zinc-dependent), balanced by tissue inhibitors of metalloproteinases (TIMPs). Wound strength reaches ~70–80% of normal by ~3 months.

16. Differentiate a hypertrophic scar from a keloid.

    A hypertrophic scar is raised but remains within the boundaries of the original wound and may regress over time. A keloid extends beyond the original wound margins, does not regress, results from excess type III then type I collagen, and is more common in darker-skinned individuals.

17. Define thrombosis and state Virchow's triad.

    Thrombosis is the pathologic formation of a blood clot (thrombus) within an intact vessel. Virchow's triad describes its predisposing factors: (1) Endothelial injury, (2) Abnormal blood flow (stasis or turbulence), and (3) Hypercoagulability.

18. Differentiate an embolus from a thrombus and list common types of emboli.

    A thrombus is a clot formed in situ; an embolus is a detached intravascular mass carried by blood to a distant site. Types: thromboembolus (most common, e.g., pulmonary embolism from DVT), fat embolism (long bone fractures), air/gas embolism (decompression sickness), amniotic fluid embolism, and atheroembolism.

19. Distinguish a red (hemorrhagic) infarct from a white (pale/anemic) infarct.

    Red infarcts occur in loose tissues with dual blood supply or collateral circulation, or after reperfusion, allowing blood to seep in (e.g., lung, intestine, testis). White infarcts occur in solid organs with end-arterial circulation where blood cannot re-enter (e.g., heart, spleen, kidney).

20. Define shock and list its three major categories with mechanisms.

    Shock is systemic hypoperfusion due to reduced cardiac output or reduced effective circulating blood volume, causing cellular hypoxia. Categories: (1) Cardiogenic (pump failure, e.g., MI), (2) Hypovolemic (loss of blood/fluid volume), and (3) Distributive — septic, anaphylactic, neurogenic (peripheral vasodilation).

21. Define neoplasia and distinguish the key features of benign vs malignant tumors.

    Neoplasia is an abnormal, autonomous, uncoordinated proliferation of cells persisting after the stimulus stops. Benign: well-differentiated, slow growth, encapsulated, non-invasive, no metastasis. Malignant: poorly differentiated (anaplasia), rapid/erratic growth, invasive, and capable of metastasis.

22. Explain the nomenclature: -oma, carcinoma, sarcoma, and give examples of mixed/misleading names.

    -oma generally denotes a benign tumor (e.g., adenoma, lipoma). Carcinoma = malignant epithelial tumor; Sarcoma = malignant mesenchymal tumor. Misleading: lymphoma, melanoma, seminoma, and mesothelioma are malignant despite the -oma suffix. Teratoma arises from germ cells (≥2 germ layers); hamartoma is disorganized native tissue.

23. 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, tissue invasion and metastasis — plus enabling/emerging hallmarks: genomic instability, tumor-promoting inflammation, deregulated metabolism (Warburg effect), and evasion of immune destruction.

24. Differentiate proto-oncogenes from tumor suppressor genes, giving an example of each and the relevant 'hit' requirement.

    Proto-oncogenes promote growth; a gain-of-function mutation in one allele (dominant) creates an oncogene (e.g., RAS, MYC, HER2). Tumor suppressor genes restrain growth; both alleles must be inactivated (Knudson two-hit hypothesis, recessive at cell level) to lose function (e.g., RB, TP53, APC).

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