INI CET Pathology Flashcards

24 sample cards from the Pathology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Outline the morphologic stages of nephrotic vs nephritic syndrome.

   Nephrotic: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia/lipiduria (minimal change, FSGS, membranous, diabetic nephropathy). Nephritic: hematuria with RBC casts, hypertension, oliguria, mild-moderate proteinuria, azotemia (post-streptococcal GN, IgA nephropathy, RPGN, lupus nephritis).

2. What are the key features of post-streptococcal glomerulonephritis on microscopy and EM?

   Follows group A strep infection (1–4 weeks). LM: hypercellular, enlarged glomeruli with neutrophil infiltration. IF: granular ('lumpy-bumpy') IgG/C3 deposits along GBM and mesangium. EM: subepithelial 'humps.' Presents as nephritic syndrome with low complement; usually self-limited in children.

3. Differentiate acute tubular necrosis ischemic vs nephrotoxic types.

   ATN is the commonest cause of acute kidney injury. Ischemic ATN: patchy tubular necrosis, especially straight proximal tubule and thick ascending limb; granular/muddy-brown casts. Nephrotoxic ATN: proximal tubule injury from drugs (aminoglycosides), contrast, heavy metals, myoglobin. Recovery possible since tubular cells regenerate.

4. Classify anemias by morphology (MCV) with examples.

   Microcytic (MCV<80): iron deficiency, thalassemia, anemia of chronic disease, sideroblastic, lead poisoning. Normocytic (80–100): acute blood loss, hemolysis, aplastic, chronic disease. Macrocytic (MCV>100): megaloblastic (B12/folate deficiency — hypersegmented neutrophils) and non-megaloblastic (alcohol, liver disease, hypothyroidism).

5. What peripheral smear findings characterize key anemias?

   Iron deficiency: microcytic hypochromic, target cells. B12/folate deficiency: macro-ovalocytes, hypersegmented neutrophils. Hereditary spherocytosis: spherocytes, increased osmotic fragility. Sickle cell: sickled cells, Howell-Jolly bodies (autosplenectomy). Thalassemia: target cells, basophilic stippling. G6PD: bite cells, Heinz bodies.

6. Differentiate the acute leukemias AML and ALL.

   ALL: children, lymphoblasts, TdT+, CD10/CD19 (B) or CD3 (T), responds well, CNS/testes involvement, t(12;21) good prognosis. AML: adults, myeloblasts with Auer rods (peroxidase+), t(15;17) = APL (treat with ATRA, risk of DIC). Both show >20% blasts in marrow, pancytopenia of normal lines.

7. Contrast Hodgkin and non-Hodgkin lymphoma.

   Hodgkin: Reed-Sternberg cells (CD15+/CD30+, 'owl-eye'), contiguous nodal spread, localized, bimodal age, B symptoms common, better prognosis. Non-Hodgkin: heterogeneous B/T cell, non-contiguous spread, more often extranodal and disseminated at presentation, includes Burkitt (t(8;14), 'starry sky'), follicular (t(14;18), BCL2).

8. Describe the diagnostic findings of multiple myeloma.

   Clonal plasma cell malignancy: CRAB — hyperCalcemia, Renal insufficiency, Anemia, Bone lytic 'punched-out' lesions. Serum/urine M-spike (IgG most common), Bence-Jones proteinuria (free light chains), rouleaux on smear, marrow >10% plasma cells, increased risk of AL amyloidosis and infections.

9. What are the morphologic and lab features of Graves disease vs Hashimoto thyroiditis?

   Graves: hyperthyroidism, diffuse hyperplastic goiter, 'scalloped' colloid, TSH-receptor stimulating antibodies, exophthalmos, pretibial myxedema. Hashimoto: hypothyroidism, lymphocytic infiltrate with germinal centers, Hurthle cells, anti-TPO/anti-thyroglobulin antibodies, increased risk of B-cell (MALT) lymphoma.

10. Differentiate the major thyroid carcinomas.

    Papillary (most common, best prognosis): Orphan-Annie eye nuclei, psammoma bodies, lymphatic spread, RET/BRAF. Follicular: capsular/vascular invasion, hematogenous spread, RAS. Medullary: parafollicular C cells, calcitonin, amyloid stroma, MEN2/RET. Anaplastic: elderly, undifferentiated, very poor prognosis.

11. What is the morphologic basis of diabetic complications in tissues?

    Chronic hyperglycemia causes nonenzymatic glycation (AGEs), polyol pathway, and protein kinase C activation. Microvascular: hyaline arteriolosclerosis, thickened basement membranes, Kimmelstiel-Wilson nodules (nodular glomerulosclerosis), retinopathy, neuropathy. Macrovascular: accelerated atherosclerosis.

12. Distinguish the morphology and causes of the major CNS hemorrhages.

    Epidural: middle meningeal artery (skull fracture), biconvex/lens-shaped, lucid interval. Subdural: bridging veins (trauma, elderly/alcoholics), crescent-shaped, crosses sutures. Subarachnoid: ruptured berry aneurysm (Circle of Willis), 'worst headache of life.' Intraparenchymal: hypertension (basal ganglia), Charcot-Bouchard aneurysms.

13. What histologic features characterize Alzheimer disease?

    Extracellular neuritic (senile) plaques of beta-amyloid (from APP cleavage) and intracellular neurofibrillary tangles of hyperphosphorylated tau. Cerebral atrophy (widened sulci, narrowed gyri, hydrocephalus ex vacuo), amyloid angiopathy. Risk: ApoE4; APP/presenilin mutations in familial early-onset.

14. Differentiate osteoarthritis from rheumatoid arthritis.

    Osteoarthritis: degenerative, wear-and-tear, weight-bearing joints, Heberden (DIP)/Bouchard (PIP) nodes, osteophytes, eburnation, no systemic inflammation. Rheumatoid: autoimmune (anti-CCP, RF), symmetric small joints (MCP/PIP), pannus, morning stiffness, ulnar deviation, systemic, HLA-DR4.

15. What are the characteristic bone tumors and their key features?

    Osteosarcoma: metaphysis of long bones, adolescents, Codman triangle/sunburst, RB/p53. Ewing sarcoma: diaphysis, children, t(11;22), onion-skin periosteum, 'small round blue cells.' Osteochondroma: most common benign. Giant cell tumor: epiphysis, 'soap-bubble', multinucleated giant cells. Chondrosarcoma: malignant cartilage, older adults.

16. Describe the pathology of tuberculosis (primary vs secondary).

    Mycobacterium tuberculosis causes type IV hypersensitivity granulomas with caseous necrosis and acid-fast bacilli. Primary: Ghon focus (subpleural) + hilar nodes = Ghon/Ranke complex. Secondary (reactivation): apical cavitary lesions. Miliary TB = hematogenous dissemination. Langhans giant cells present.

17. What organisms cause the classic granulomatous and special-stain-identified infections?

    Acid-fast (Ziehl-Neelsen): Mycobacteria, Nocardia (partial). PAS/GMS (silver): fungi (Aspergillus septate acute-angle, Mucor broad nonseptate wide-angle, Cryptococcus mucicarmine capsule). Warthin-Starry: spirochetes/Bartonella/H. pylori. India ink: Cryptococcus. Giemsa: Leishmania, malaria, H. pylori.

18. Compare the four (Gell and Coombs) hypersensitivity reactions.

    Type I (immediate/anaphylactic): IgE, mast cells/histamine (asthma, anaphylaxis). Type II (antibody-mediated cytotoxic): IgG/IgM vs cell antigens (autoimmune hemolytic anemia, Goodpasture). Type III (immune complex): complexes deposit, complement (SLE, serum sickness, PSGN). Type IV (delayed/T-cell): T cells/macrophages (TB test, contact dermatitis, transplant).

19. What are the diagnostic autoantibodies in common autoimmune diseases?

    SLE: ANA (sensitive), anti-dsDNA and anti-Smith (specific). Drug-induced lupus: anti-histone. Systemic sclerosis: anti-Scl-70 (diffuse), anti-centromere (CREST). Sjogren: anti-Ro(SSA)/La(SSB). Polymyositis: anti-Jo-1. Granulomatosis with polyangiitis: c-ANCA (PR3). Microscopic polyangiitis: p-ANCA (MPO).

20. Differentiate the classic vitamin deficiency syndromes (A, D, C, B1, B3, B12).

    Vit A: night blindness, xerophthalmia, Bitot spots. Vit D: rickets/osteomalacia. Vit C: scurvy (defective collagen, bleeding gums, poor wound healing). B1 (thiamine): Wernicke-Korsakoff, beriberi. B3 (niacin): pellagra (dermatitis, diarrhea, dementia). B12: megaloblastic anemia + subacute combined degeneration.

21. Explain the pathology and inheritance of the major genetic/developmental diseases (Down, CF, sickle cell, fragile X).

    Down (trisomy 21): flat facies, AV septal defect, duodenal atresia, AML/ALL, early Alzheimer. Cystic fibrosis (autosomal recessive, CFTR del-F508): thick secretions, recurrent lung infections, pancreatic insufficiency. Sickle cell (autosomal recessive, beta-globin Glu->Val): vaso-occlusion. Fragile X (X-linked, CGG repeat): macroorchidism, long face.

22. What does the ESR (erythrocyte sedimentation rate) and CRP indicate, and what raises/lowers them?

    ESR measures RBC settling rate, an indirect marker of acute-phase proteins (mainly fibrinogen). Raised in inflammation, infection, malignancy, anemia, pregnancy, and especially temporal arteritis/PMR. Lowered by polycythemia, sickle cell, microcytosis. CRP is a more rapid, direct acute-phase reactant produced by the liver.

23. Describe the steps and tissue handling of routine histopathology processing.

    Fixation (10% neutral buffered formalin prevents autolysis, cross-links proteins) -> grossing -> dehydration (graded alcohols) -> clearing (xylene) -> paraffin embedding -> microtomy (~4–5 micron sections) -> staining (H&E: hematoxylin stains nuclei blue, eosin stains cytoplasm pink) -> mounting. Frozen section gives rapid intraoperative diagnosis.

24. What is the principle of immunohistochemistry and key diagnostic markers?

    IHC uses labeled antibodies against tissue antigens, visualized by chromogen (e.g., DAB), to identify cell lineage/origin. Cytokeratin = epithelial (carcinoma); vimentin = mesenchymal; S-100/HMB-45/Melan-A = melanoma; LCA(CD45) = lymphoma; chromogranin/synaptophysin = neuroendocrine; ER/PR/HER2 = breast cancer prognostic/predictive.

What this deck covers

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