AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine Syllabus

Pathology, Microbiology and Laboratory Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology, Microbiology and Laboratory Medicine in AIIMS PG (DM/MCh) Entrance, not a summary of it.

1. 1

   General and Systemic Pathology

   4 topics

   • Cell Injury and Inflammation
     • Reversible and irreversible injury
     • Acute and chronic inflammation
   • Neoplasia
     • Carcinogenesis and tumor markers
     • Grading, staging and metastasis
   • Hemodynamic Disorders
     • Thrombosis, embolism and infarction
     • Shock and edema
   • Systemic Pathology
     • Cardiovascular and renal pathology
     • GI and hepatobiliary pathology
2. 2

   Hematology and Transfusion Medicine

   3 topics

   • Anemias and Hemoglobinopathies
     • Iron deficiency and megaloblastic anemia
     • Thalassemia and sickle cell disease
   • Hematological Malignancies
     • Leukemias and lymphomas
     • Myeloproliferative and plasma cell disorders
   • Coagulation and Transfusion
     • Bleeding and clotting disorders
     • Blood components and transfusion reactions
3. 3

   Microbiology and Infectious Disease

   4 topics

   • Bacteriology
     • Gram-positive and gram-negative pathogens
     • Tuberculosis and atypical mycobacteria
   • Virology
     • Hepatitis viruses and HIV
     • Emerging and respiratory viruses
   • Parasitology and Mycology
     • Malaria and tropical parasites
     • Systemic and opportunistic fungal infections
   • Immunology and Hospital Infection
     • Hypersensitivity and immunodeficiency
     • Antimicrobial resistance and infection control
4. 4

   Clinical Pathology and Diagnostics

   3 topics

   • Cytopathology and Histotechniques
     • FNAC and Pap smear interpretation
     • Immunohistochemistry and special stains
   • Molecular Diagnostics
     • PCR and sequencing applications
     • Flow cytometry and FISH
   • Laboratory Quality and Biosafety
     • Internal and external quality control
     • Biosafety levels and specimen handling

Pathology, Microbiology and Laboratory Medicine flashcards for AIIMS PG (DM/MCh) Entrance

23 of 56 cards from the Pathology, Microbiology and Laboratory Medicine deck — real questions with worked answers.

1. What are the four classic morphologic hallmarks of irreversible cell injury seen on electron microscopy?

   Severe mitochondrial swelling with amorphous (flocculent) densities, extensive plasma membrane damage, swelling/rupture of lysosomes, and profound nuclear changes (pyknosis, karyorrhexis, karyolysis).

2. List the five cardinal signs of acute inflammation described by Celsus and Virchow.

   Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function).

3. Which arachidonic acid metabolite is the most potent eosinophil chemoattractant and a key mediator in asthma bronchoconstriction?

   Leukotriene B4 is the potent neutrophil/leukocyte chemoattractant; LTC4, LTD4, and LTE4 (the cysteinyl leukotrienes) cause bronchoconstriction and increased vascular permeability in asthma.

4. Differentiate the four morphologic types of necrosis by their characteristic tissue and appearance.

   Coagulative (ischemia of solid organs, preserved architecture); liquefactive (brain infarcts, abscesses); caseous (TB, cheese-like); fat necrosis (pancreatitis, chalky saponification); fibrinoid (immune vascular injury).

5. What is the role of the transcription factor HIF-1α in cell adaptation to hypoxia?

   HIF-1α (hypoxia-inducible factor) accumulates under low oxygen, driving transcription of VEGF (angiogenesis), erythropoietin, and glycolytic enzymes to promote survival.

6. Define metaplasia and give the classic example seen in Barrett esophagus.

   Metaplasia is reversible replacement of one differentiated cell type by another. In Barrett esophagus, squamous epithelium is replaced by intestinal columnar epithelium with goblet cells due to chronic acid reflux.

7. What are the two broad categories of cell death and their key biochemical distinction?

   Necrosis (passive, ATP-independent, membrane rupture, inflammation) and apoptosis (programmed, ATP-dependent, caspase-mediated, intact membrane, no inflammation).

8. Name the intrinsic (mitochondrial) apoptotic pathway's key pro- and anti-apoptotic regulators.

   Pro-apoptotic: BAX and BAK (effectors), BID/BIM/BAD (sensitizers). Anti-apoptotic: BCL-2, BCL-XL, MCL-1. Cytochrome c release activates caspase-9 via APAF-1 (apoptosome).

9. Distinguish the two main mechanisms of carcinogenesis: the difference between proto-oncogenes and tumor suppressor genes.

   Proto-oncogenes promote growth; gain-of-function (dominant) mutations make them oncogenes. Tumor suppressor genes restrain growth; require loss-of-function of both alleles (Knudson two-hit) to lose protection.

10. What is the Knudson two-hit hypothesis and which tumor exemplifies it?

    Both alleles of a tumor suppressor gene must be inactivated for tumorigenesis. Retinoblastoma (RB1 gene): hereditary cases inherit one mutated allele and need only one somatic hit; sporadic cases need two somatic hits.

11. List the recognized hallmarks of cancer (Hanahan and Weinberg).

    Self-sufficiency in growth signals, insensitivity to anti-growth signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, tissue invasion/metastasis, plus enabling traits: genome instability, tumor-promoting inflammation, deregulated energetics (Warburg), and immune evasion.

12. What is the difference between grading and staging of a malignant tumor?

    Grading assesses degree of differentiation/anaplasia and mitotic activity (cellular features); staging (TNM: Tumor size, Node involvement, Metastasis) assesses anatomic extent of spread. Staging has greater prognostic value.

13. Name three classic tumor markers and their associated malignancies.

    AFP (hepatocellular carcinoma, yolk sac tumor); CEA (colorectal, pancreatic); CA-125 (ovarian); PSA (prostate); CA 19-9 (pancreatic); β-hCG (choriocarcinoma, germ cell).

14. What is the Warburg effect in tumor metabolism?

    Cancer cells preferentially use aerobic glycolysis (glucose to lactate even with adequate oxygen) to rapidly generate biosynthetic intermediates for proliferation; basis of FDG-PET imaging.

15. Define Virchow triad for thrombosis.

    The three contributors to thrombus formation: endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability.

16. Differentiate a transudate from an exudate by protein content and specific gravity.

    Transudate: protein-poor (<3 g/dL), specific gravity <1.012, low cellularity (e.g., CHF, hypoalbuminemia). Exudate: protein-rich (>3 g/dL), specific gravity >1.020, inflammatory cells (e.g., infection, malignancy). Light's criteria distinguish pleural effusions.

17. What are the lines of Zahn and what is their diagnostic significance?

    Alternating pale (platelet/fibrin) and dark (RBC) laminations in a thrombus. They indicate the thrombus formed in flowing blood antemortem, distinguishing true thrombi from postmortem clots.

18. What is the most common source of pulmonary thromboembolism and the consequence of a massive (saddle) embolus?

    Deep veins of the lower extremity (popliteal, femoral, iliac). A massive saddle embolus lodging at the pulmonary artery bifurcation causes acute right heart failure and sudden death.

19. Distinguish red (hemorrhagic) from white (anemic) infarcts and where each occurs.

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

20. What are the laboratory and clinical features distinguishing the stages of disseminated intravascular coagulation (DIC)?

    Prolonged PT/aPTT, low fibrinogen, elevated D-dimer/FDPs, thrombocytopenia, and schistocytes on smear. Caused by widespread activation of coagulation consuming platelets and clotting factors, leading to both thrombosis and hemorrhage.

21. In systemic pathology, what histologic finding defines a granuloma and name two infectious causes.

    A granuloma is an aggregate of epithelioid macrophages, often with multinucleated giant cells and a lymphocyte rim. Infectious causes: Mycobacterium tuberculosis (caseating) and fungal infections; non-infectious: sarcoidosis (non-caseating).

22. What is the characteristic renal lesion of diabetic nephropathy?

    Kimmelstiel-Wilson nodules: nodular glomerulosclerosis with PAS-positive mesangial nodules, plus diffuse glomerular basement membrane thickening and afferent/efferent arteriolar hyalinosis.

23. Name the morphologic types of cirrhosis and the hallmark of Wilson disease in the liver.

    Micronodular and macronodular cirrhosis (regenerative nodules with fibrous septa). Wilson disease shows copper accumulation (rhodanine stain), steatosis, and Mallory-Denk bodies; Kayser-Fleischer rings in eye.

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