🇮🇳 AIIMS PG (DM/MCh) Entrance · subject
AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine Syllabus
The Pathology, Microbiology and Laboratory Medicine syllabus for AIIMS PG (DM/MCh) Entrance in full: 4 chapters, 14 topics and 28 sub-topics, every one listed below, plus 56 Pathology, Microbiology and Laboratory Medicine flashcards with answers.
Pathology, Microbiology and Laboratory Medicine syllabus: all 4 chapters
Expand any chapter to see its topics and sub-topics.
-
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
- Cell Injury and Inflammation
-
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
- Anemias and Hemoglobinopathies
-
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
- Bacteriology
-
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
- Cytopathology and Histotechniques
AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine flashcards — 56 questions with answers
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).
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).
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.
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).
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.
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.
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).
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).
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.
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.
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.
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.
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).
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.
Define Virchow triad for thrombosis.
The three contributors to thrombus formation: endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability.
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.
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.
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.
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).
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.
Show the other 36 Pathology, Microbiology and Laboratory Medicine flashcards
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).
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.
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.
Give the Mentzer index formula and its use in differentiating iron deficiency from beta-thalassemia trait.
Mentzer index = MCV ÷ RBC count. Index >13 suggests iron deficiency anemia; index <13 suggests beta-thalassemia trait (where RBC count is relatively preserved/elevated).
What is the reticulocyte production index (RPI) formula and what does it distinguish?
RPI = reticulocyte % × (patient Hct ÷ normal Hct) ÷ maturation factor. RPI >2-3 indicates adequate marrow response (hemolysis/blood loss); RPI <2 indicates hypoproliferative anemia.
Differentiate the peripheral smear and lab findings of iron deficiency anemia from anemia of chronic disease.
Iron deficiency: low ferritin, high TIBC, low transferrin saturation, microcytic hypochromic. Anemia of chronic disease: normal/high ferritin (acute phase), low TIBC, normal/low iron; mediated by hepcidin.
What is the molecular defect in sickle cell anemia and the protective heterozygote advantage?
Point mutation: glutamic acid to valine at position 6 of the beta-globin chain (HbS). Heterozygotes (sickle trait) have resistance to Plasmodium falciparum malaria.
Classify the thalassemias by the number of affected alpha-globin genes and their clinical severity.
1 gene: silent carrier; 2 genes: alpha-thal trait (mild microcytosis); 3 genes: HbH disease (β4 tetramers, moderate-severe); 4 genes: Hb Bart (γ4) hydrops fetalis, incompatible with life.
What deficiency causes hereditary spherocytosis and which lab test confirms it?
Defect in RBC membrane proteins (ankyrin, spectrin, band 3). Confirmed by osmotic fragility test (increased fragility) or the more specific eosin-5-maleimide (EMA) binding flow cytometry; spherocytes on smear with increased MCHC.
Name the peripheral smear findings characteristic of megaloblastic anemia.
Macro-ovalocytes (oval macrocytes), hypersegmented neutrophils (>5 lobes), anisopoikilocytosis; bone marrow shows megaloblasts with nuclear-cytoplasmic asynchrony. Causes: B12 and folate deficiency.
What chromosomal translocation defines chronic myeloid leukemia and its molecular product?
t(9;22)(q34;q11) — the Philadelphia chromosome — producing the BCR-ABL1 fusion gene with constitutive tyrosine kinase activity, targeted by imatinib.
List the French-American-British (FAB) and key WHO distinctions between AML and ALL on lab testing.
AML: myeloperoxidase-positive, Auer rods, ≥20% myeloblasts, CD13/CD33/CD117 positive. ALL: TdT-positive, MPO-negative; B-ALL (CD19/CD10) and T-ALL (CD3/CD7).
What is the diagnostic cell of Hodgkin lymphoma and its immunophenotype?
Reed-Sternberg cell — a large binucleate ('owl-eye') cell, classically CD15-positive and CD30-positive, CD45-negative, CD20-negative (classical HL).
Which translocation and oncogene characterize Burkitt lymphoma, and what is the histologic appearance?
t(8;14) juxtaposing MYC to the IgH locus. 'Starry sky' appearance from tingible-body macrophages amid a sea of monomorphic intermediate B cells; very high proliferation (Ki-67 ~100%).
What defines multiple myeloma diagnostically (CRAB criteria)?
CRAB: hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions. Plus clonal plasma cells ≥10% in marrow, M-protein (monoclonal spike), Bence-Jones proteinuria, and rouleaux on smear.
Describe the coagulation cascade's intrinsic vs extrinsic pathway and the tests that assess each.
Intrinsic pathway (factors XII, XI, IX, VIII) assessed by aPTT. Extrinsic pathway (factor VII + tissue factor) assessed by PT/INR. Common pathway (X, V, II, fibrinogen) affects both.
Differentiate Hemophilia A from von Willebrand disease in terms of deficiency and lab findings.
Hemophilia A: factor VIII deficiency, X-linked, prolonged aPTT, normal bleeding time/platelets. von Willebrand disease: vWF deficiency, autosomal, prolonged aPTT and bleeding time, abnormal ristocetin aggregation; most common inherited bleeding disorder.
What are the major ABO blood group compatibility rules for RBC transfusion?
Type O is universal RBC donor (no A/B antigens); type AB is universal RBC recipient (no anti-A/anti-B antibodies). For plasma, AB is universal donor and O is universal recipient (reverse of RBC).
Distinguish acute hemolytic transfusion reaction from febrile non-hemolytic reaction.
Acute hemolytic: ABO incompatibility, complement-mediated intravascular hemolysis, fever, flank pain, hemoglobinuria, DIC, shock — a medical emergency. Febrile non-hemolytic: most common, from recipient antibodies to donor leukocytes/cytokines, fever and chills without hemolysis.
Give the Gram stain mechanism and classify Staphylococcus vs Streptococcus on catalase.
Gram-positive bacteria retain crystal violet (thick peptidoglycan, stain purple); gram-negative lose it and take safranin (pink). Staphylococcus is catalase-positive; Streptococcus is catalase-negative.
How is Staphylococcus aureus distinguished from coagulase-negative staphylococci, and what test identifies it?
S. aureus is coagulase-positive (and DNase/mannitol-fermenting on MSA, golden colonies). Coagulase-negative staphylococci (S. epidermidis, S. saprophyticus) are coagulase-negative; S. saprophyticus is novobiocin-resistant.
Classify streptococci by hemolysis and Lancefield grouping with key species.
Alpha-hemolytic (green): S. pneumoniae (optochin-sensitive, bile-soluble), viridans (resistant). Beta-hemolytic: Group A S. pyogenes (bacitracin-sensitive), Group B S. agalactiae (CAMP-positive). Gamma (non-hemolytic): Enterococcus.
What is the mechanism of action of the diphtheria and cholera toxins (ADP-ribosylation targets)?
Diphtheria toxin ADP-ribosylates elongation factor 2 (EF-2), halting protein synthesis. Cholera toxin ADP-ribosylates Gs (stimulatory G protein), permanently activating adenylate cyclase, raising cAMP and causing watery diarrhea.
Which acid-fast organism causes tuberculosis and what stain identifies it?
Mycobacterium tuberculosis, identified by the Ziehl-Neelsen (acid-fast) stain due to mycolic acid in its cell wall; auramine-rhodamine fluorescent stain is more sensitive for screening.
Describe the Baltimore classification basis and give an example of a positive-sense ssRNA virus.
The Baltimore system classifies viruses by genome type and mRNA synthesis strategy (I dsDNA, II ssDNA, III dsRNA, IV +ssRNA, V -ssRNA, VI ssRNA-RT, VII dsDNA-RT). Example of +ssRNA: poliovirus, hepatitis C, SARS-CoV-2.
Interpret the hepatitis B serology pattern: HBsAg+, anti-HBc IgM+, HBeAg+.
Acute hepatitis B infection with high infectivity. HBsAg = active infection; anti-HBc IgM = recent/acute; HBeAg = active viral replication and high transmissibility. (Anti-HBs alone = immunity/vaccination.)
Which malaria species causes the most severe disease and relapse, respectively, and why?
P. falciparum causes the most severe disease (cerebral malaria, high parasitemia, no hypnozoites). P. vivax and P. ovale cause relapses due to dormant liver hypnozoites (treated with primaquine).
Name the dimorphic fungi and the diagnostic India ink finding for Cryptococcus.
Dimorphic fungi (mold in cold/environment, yeast at 37°C in body): Histoplasma, Blastomyces, Coccidioides, Paracoccidioides, Sporothrix. Cryptococcus neoformans shows a halo (clear capsule) around yeast on India ink prep of CSF.
Classify the four Gell and Coombs hypersensitivity reactions with one example each.
Type I (IgE/immediate — anaphylaxis, atopy); Type II (antibody-mediated cytotoxic — autoimmune hemolytic anemia, Goodpasture); Type III (immune complex — SLE, serum sickness); Type IV (delayed cell-mediated/T cell — TB skin test, contact dermatitis).
What is the gold-standard surveillance metric for hospital-acquired infection control and a key prevention bundle?
Surgical site infection and device-associated infection rates (CLABSI, CAUTI, VAP) per 1000 device-days. Hand hygiene (WHO 5 moments) is the single most effective measure; central-line bundles prevent CLABSI.
Differentiate the Papanicolaou (Pap) stain components and the Bethesda system's purpose.
Pap stain: hematoxylin (nuclei blue), with OG-6 and EA cytoplasmic counterstains showing transparency for cell overlap. The Bethesda system standardizes cervical cytology reporting (e.g., ASC-US, LSIL, HSIL) including specimen adequacy.
What fixative is standard for histopathology and what is the principle of immunohistochemistry?
10% neutral buffered formalin (cross-links proteins via methylene bridges) is the standard fixative. IHC uses labeled antibodies (with chromogen like DAB) to detect specific tissue antigens, localizing protein expression in situ.
Explain the principle of PCR and the key role of Taq polymerase.
Polymerase chain reaction exponentially amplifies a target DNA sequence through repeated cycles of denaturation (~95°C), primer annealing (~50-65°C), and extension (~72°C). Taq, a thermostable polymerase from Thermus aquaticus, survives denaturation temperatures.
What does the Ct (cycle threshold) value indicate in real-time quantitative PCR?
Ct is the cycle number at which fluorescent signal crosses the detection threshold; it is inversely proportional to the starting target nucleic acid amount (lower Ct = higher initial template/viral load).
Define the components and purpose of a Westgard rule and a Levey-Jennings chart in lab QC.
A Levey-Jennings chart plots control results against mean ± SD over time. Westgard multirules (e.g., 1-3s, 2-2s, R-4s, 1-2s warning) detect random and systematic error to flag out-of-control runs before reporting patient results.
What are the four biosafety levels (BSL) and an example organism handled at BSL-3?
BSL-1 (non-pathogenic, e.g., E. coli K-12), BSL-2 (moderate, e.g., Staph, Salmonella, HBV), BSL-3 (serious airborne, e.g., Mycobacterium tuberculosis, SARS-CoV-2), BSL-4 (lethal, no treatment, e.g., Ebola, Marburg) requiring maximum containment.
AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine FAQ
What is in the AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine syllabus?
AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine is split into 4 chapters: General and Systemic Pathology, Hematology and Transfusion Medicine, Microbiology and Infectious Disease and Clinical Pathology and Diagnostics. Together they contain 14 topics and 28 sub-topics.
How many chapters are in AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine?
4 chapters, containing 14 topics and 28 sub-topics. The largest chapter is General and Systemic Pathology, with 4 topics.
Are there flashcards for AIIMS PG (DM/MCh) Entrance Pathology, Microbiology and Laboratory Medicine?
Yes — a 56-card Pathology, Microbiology and Laboratory Medicine deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.