Free NEET PG & INI-CET Pathology MCQs

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Irreversible injury is marked by severe mitochondrial damage with loss of ATP production, plasma membrane damage and lysosomal rupture. Cellular swelling and fatty change are features of reversible injury.

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Apoptosis is programmed, ATP-dependent cell death with cell shrinkage and no inflammation, since membrane integrity is preserved. Necrosis involves swelling, membrane rupture and inflammation.

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Caseous (cheese-like) necrosis is characteristic of tuberculosis, appearing as amorphous granular debris within granulomas. Coagulative necrosis follows ischaemia in most organs, and liquefactive necrosis occurs in the brain and in abscesses.

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Superoxide dismutase converts superoxide to hydrogen peroxide, which catalase and glutathione peroxidase then detoxify to water. These antioxidant systems limit free-radical-mediated cell injury.

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Dystrophic calcification occurs in injured or necrotic tissue despite normal serum calcium. Metastatic calcification occurs in normal tissue when serum calcium is elevated.

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The liver is the main site of fat metabolism, so fatty change is most common there, classically from alcohol. It is reversible but can progress to steatohepatitis and cirrhosis with continued injury.

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Neutrophils are the first responders in acute inflammation, dominating the first 24 hours. Macrophages take over after 24 to 48 hours. Chronic inflammation is dominated by lymphocytes, plasma cells and macrophages.

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Granulomas are collections of epithelioid cells, activated macrophages with abundant pink cytoplasm, often with multinucleated giant cells. Causes include tuberculosis, sarcoidosis, leprosy and fungal infections.

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Histamine, released mainly from mast cells, causes early vasodilation and increased vascular permeability, the immediate transient response. Other mediators include prostaglandins, leukotrienes and bradykinin.

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Vitamin C is a cofactor for prolyl and lysyl hydroxylase in collagen synthesis. Deficiency, or scurvy, causes poor wound healing, bleeding gums and fragile vessels.

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Labile cells such as surface epithelia, bone marrow and gut mucosa divide continuously and regenerate well. Neurons and cardiac myocytes are permanent cells with little regenerative capacity, healing by scar.

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Exudates are protein-rich fluids with high specific gravity above 1.020 and contain cells, resulting from increased vascular permeability in inflammation. Transudates are protein-poor ultrafiltrates from altered hydrostatic or oncotic pressure.

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AFP is raised in hepatocellular carcinoma and yolk-sac (endodermal sinus) tumours. PSA marks prostate cancer, calcitonin marks medullary thyroid cancer and CA-125 marks ovarian cancer.

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CA 19-9 is used to monitor pancreatic carcinoma and some biliary and gastrointestinal cancers. CA 15-3 relates to breast cancer, PSA to prostate, and beta-hCG and AFP to testicular tumours.

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Psammoma bodies occur in papillary thyroid carcinoma, serous ovarian carcinoma, meningioma and papillary renal cell carcinoma. They are not a feature of hepatocellular carcinoma.

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Signet-ring cells are classic of diffuse-type gastric adenocarcinoma, or linitis plastica, associated with loss of E-cadherin. They may also appear in some breast and colonic cancers.

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Metastasis is the single most reliable indicator of malignancy; benign tumours never metastasise. Malignant tumours also show rapid growth, invasion, poor differentiation and lack of a capsule.

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p53, the guardian of the genome, arrests the cell cycle to allow DNA repair or triggers apoptosis if damage is irreparable. Loss of p53 function permits damaged cells to proliferate; it is the most commonly mutated gene in human cancer.

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Carcinomas, being epithelial cancers, typically spread first via lymphatics to regional nodes. Sarcomas characteristically spread haematogenously. Knowing this pattern guides staging and nodal assessment.

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Low serum ferritin is the most specific indicator of iron deficiency, the commonest cause of microcytic hypochromic anaemia. Ferritin is normal or high in thalassaemia and in anaemia of chronic disease.

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Hypersegmented neutrophils with more than five lobes, together with macro-ovalocytes, are hallmarks of megaloblastic anaemia from B12 or folate deficiency. B12 deficiency additionally causes neurological signs, namely subacute combined degeneration.

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The Reed-Sternberg cell, CD15 and CD30 positive, is pathognomonic of classical Hodgkin lymphoma. Its classic form has two mirror-image nuclei giving an owl-eye appearance.

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Chronic myeloid leukaemia is defined by t(9;22) producing BCR-ABL, a constitutively active tyrosine kinase. This is the target of imatinib, a tyrosine kinase inhibitor.

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Auer rods are crystallised azurophilic granules containing myeloperoxidase, seen in acute myeloid leukaemia and especially in acute promyelocytic leukaemia with t(15;17). They are not seen in lymphoid leukaemias.

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Burkitt lymphoma shows a starry-sky pattern of tingible-body macrophages amid rapidly dividing cells, and t(8;14) juxtaposing c-MYC with the immunoglobulin heavy-chain locus. It is one of the fastest-growing human tumours.

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Hereditary spherocytosis results from red-cell membrane protein defects in spectrin or ankyrin, producing spherocytes with increased osmotic fragility, splenomegaly and jaundice. Splenectomy is curative for the anaemia.

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DIC consumes platelets and clotting factors, giving low fibrinogen, prolonged PT and aPTT and thrombocytopenia, while fibrinolysis raises D-dimer. It is a secondary process driven by sepsis, obstetric complications or malignancy.

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Aschoff bodies, foci of fibrinoid necrosis surrounded by Anitschkow cells, are pathognomonic of rheumatic carditis, a sequel to group A streptococcal infection.

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Fatty streaks, lipid-laden foam cells in the intima, are the earliest lesions and can appear even in childhood. They may progress to fibrous plaques and to complicated plaques with rupture and thrombosis.

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Minimal change disease is the leading cause of nephrotic syndrome in children, showing normal light microscopy but podocyte foot-process effacement on electron microscopy. It responds well to corticosteroids.

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Mallory-Denk bodies are eosinophilic cytoplasmic inclusions of damaged intermediate filaments, classically seen in alcoholic hepatitis though not specific to it. They reflect hepatocyte injury.

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Alpha-1 antitrypsin deficiency causes panacinar emphysema with basal predominance, because unopposed elastase destroys alveolar walls. It also causes liver cirrhosis. Smoking-related emphysema is typically centriacinar and upper-zone.

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Helicobacter pylori, a urease-producing gram-negative organism, causes most chronic gastritis and peptic ulcers and increases the risk of gastric carcinoma and MALT lymphoma.

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Papillary thyroid carcinoma shows optically clear Orphan Annie eye nuclei, nuclear grooves and psammoma bodies. It is the commonest thyroid cancer and spreads via lymphatics with a good prognosis.

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Anaphylaxis is a Type I, IgE-mediated hypersensitivity with mast-cell degranulation. Type II is antibody-mediated cytotoxicity, Type III is immune-complex-mediated and Type IV is T-cell-mediated delayed hypersensitivity.

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Amyloid stains with Congo red and shows apple-green birefringence under polarised light because of its beta-pleated sheet structure. Types include AL from light chains and AA from serum amyloid A in chronic inflammation.

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Anti-double-stranded DNA and anti-Smith antibodies are highly specific for SLE. ANA is sensitive but not specific. Anti-dsDNA titres also correlate with disease activity, especially in lupus nephritis.

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The Mantoux reaction is a Type IV delayed hypersensitivity mediated by sensitised T cells and macrophages, peaking at 48 to 72 hours. Contact dermatitis and granuloma formation share this mechanism.

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HIV infects and depletes CD4 T helper cells. A CD4 count below 200 cells per microlitre defines AIDS and predisposes to opportunistic infections such as Pneumocystis pneumonia and cryptococcal meningitis.

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S-100 and HMB-45 mark melanocytic tumours. CD20 marks B cells, desmin marks muscle and cytokeratin marks epithelial or carcinoma cells. Immunohistochemistry helps classify poorly differentiated tumours.

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Bacterial meningitis gives a neutrophilic pleocytosis with high protein and low glucose, as bacteria consume glucose. Viral meningitis shows lymphocytes with normal glucose, and tuberculous meningitis shows lymphocytes with very low glucose.

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Prussian blue, the Perls stain, colours iron and haemosiderin blue and is useful in haemochromatosis and haemosiderosis. Congo red stains amyloid, Ziehl-Neelsen stains acid-fast bacilli and PAS stains glycogen and fungi.

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ABO-incompatible transfusion causes a Type II hypersensitivity: preformed IgM antibodies bind donor red cells and activate complement, causing intravascular haemolysis. It is a medical emergency.

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In sickle cell disease, glutamate is replaced by valine at position 6 of the beta-globin chain. Deoxygenated HbS polymerises, deforming red cells into sickles that cause vaso-occlusion and haemolysis.

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PT assesses the extrinsic pathway and factor VII, while aPTT assesses the intrinsic pathway. Isolated PT prolongation points to factor VII deficiency or early warfarin effect, as factor VII has the shortest half-life.

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Plasmodium falciparum shows characteristic banana or crescent-shaped gametocytes and causes the most severe disease, including cerebral malaria. It parasitises red cells of all ages, producing high parasitaemia.

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PSA is a glycoprotein produced by prostate epithelium; levels rise in prostate carcinoma and also in benign prostatic hyperplasia and prostatitis. It is used for screening, with known limitations, and to monitor treatment response.

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Virchow's triad comprises endothelial injury, stasis or turbulent flow, and hypercoagulability. These factors underlie venous and arterial thrombosis and guide risk assessment for conditions such as deep vein thrombosis.

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Anaemia of chronic disease shows low serum iron but normal or high ferritin, because hepcidin sequesters iron, together with a low TIBC. This distinguishes it from iron deficiency, where ferritin is low and TIBC is high.

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Acute lymphoblastic leukaemia is the commonest childhood leukaemia. Blasts are TdT positive and B-ALL commonly expresses CD10. With modern therapy the prognosis in children is generally favourable.