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59 cards · 14 topics · by Quizcard team · 0 hearts · Updated 2026-11-03
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What is the earliest ultrastructural/biochemical change in reversible cell injury?
Answer: Decreased ATP production → Na+/K+-ATPase failure → Na+ and water influx → cellular and mitochondrial swelling (hydropic change).
Reversible if the insult is removed before mitochondrial and membrane damage becomes irreversible.
Light microscopic findings of reversible cell injury
Answer: Cellular swelling (hydropic change) and fatty change (steatosis), especially in liver and heart.
Two hallmark features that define irreversible cell injury
Answer: Mitochondrial permeability transition (loss of mitochondrial membrane potential) and plasma membrane damage with massive Ca2+ influx.
Ca2+ influx activates proteases, lipases, and endonucleases that destroy the cell.
Nuclear changes seen in irreversible cell injury (3)
Answer: Pyknosis (shrinkage, basophilic), karyorrhexis (fragmentation), karyolysis (dissolution/fading).
These occur in sequence as the cell dies, classically in necrosis.
Apoptosis vs necrosis: energy requirement and inflammation
Answer: Apoptosis = programmed, ATP-dependent, NO inflammation (apoptotic bodies are phagocytosed). Necrosis = unregulated, cell contents spill → inflammation.
Intrinsic (mitochondrial) apoptosis pathway
Answer: Triggered by DNA damage/lack of survival signals → p53 activation → ↑Bax/Bak, ↓Bcl-2 → cytochrome c release from mitochondria → caspase activation.
Bcl-2 overexpression (e.g., follicular lymphoma t(14;18)) blocks this pathway, promoting cancer.
Extrinsic (death receptor) apoptosis pathway
Answer: Fas (CD95)–FasL interaction or TNF-α binding TNF receptor → activates caspases directly.
Used in immune cell–mediated killing and deletion of autoreactive lymphocytes.
Histologic features of apoptosis
Answer: Cell shrinkage, chromatin condensation, membrane blebbing, formation of apoptotic bodies, no surrounding inflammation.
Coagulative necrosis — where and appearance?
Answer: Ischemic infarcts of any organ EXCEPT brain. Protein denaturation preserves cell outline (ghost cells) for days.
Classic example: myocardial infarction, renal infarction.
Liquefactive necrosis — where and mechanism?
Answer: Brain infarcts, bacterial abscesses, pancreatitis. Enzymatic digestion of tissue → liquefied, viscous mass.
Brain is liquefactive (not coagulative) due to high lipid content and enzyme release from microglia.
Caseous necrosis — classic cause and appearance?
Answer: TB and fungal infections. Soft, friable, 'cheese-like' necrotic debris; combination of coagulative + liquefactive, surrounded by granulomatous inflammation.
Fat necrosis — two settings and key finding
Answer: Enzymatic (acute pancreatitis — lipase-mediated) or traumatic (breast). Causes saponification (Ca2+ soap formation) seen as chalky white areas.
Fibrinoid necrosis — setting?
Answer: Immune-mediated vasculitis and malignant hypertension. Appears as pink, amorphous deposits of immune complexes/fibrin in vessel walls.
Dry vs wet gangrenous necrosis
Answer: Dry = coagulative necrosis from ischemia (e.g., limb). Wet = liquefactive necrosis from superimposed bacterial infection.
Predominant cell type in acute inflammation
Answer: Neutrophils.
Recruited first via chemotaxis; mediate the earliest innate response.
Predominant cell types in chronic inflammation
Answer: Lymphocytes, plasma cells, and macrophages (mononuclear cell infiltrate).
Key mediators of vasodilation in acute inflammation
Answer: Histamine and prostaglandins.
Key mediators of increased vascular permeability
Answer: Histamine, bradykinin, C3a/C5a, leukotrienes C4/D4/E4.
These cause endothelial cell contraction, producing exudate.
Key neutrophil chemotactic agents
Answer: C5a, LTB4, IL-8, bacterial products (e.g., N-formylmethionine peptides).
Arachidonic acid pathway: COX products vs LOX products
Answer: COX pathway → prostaglandins and thromboxane A2. LOX pathway → leukotrienes (LTB4 = chemotaxis; LTC4/D4/E4 = bronchoconstriction, permeability).
NSAIDs/aspirin inhibit COX; zileuton inhibits LOX.
Main endogenous pyrogens
Answer: IL-1, IL-6, and TNF-α act on hypothalamus to increase prostaglandin (PGE2) synthesis, raising the thermoregulatory set point.
Definition of a granuloma
Answer: Nodular collection of epithelioid histiocytes (activated macrophages), often with multinucleated giant cells, rimmed by lymphocytes.
Mechanism of granuloma formation
Answer: Th1 CD4+ T cells secrete IFN-γ, which activates macrophages, causing them to differentiate into epithelioid cells and fuse into giant cells.
Explains why granulomas form in chronic infections (TB) and are impaired in Th1 deficiency states.
Caseating vs noncaseating granuloma — examples
Answer: Caseating: TB (central necrosis). Noncaseating: sarcoidosis, Crohn disease, berylliosis, cat-scratch disease, foreign body reaction (no central necrosis).
Three phases of wound healing
Answer: 1) Inflammatory (neutrophils then macrophages clear debris), 2) Proliferative/granulation (fibroblasts, angiogenesis, type III collagen), 3) Remodeling (type III → type I collagen, scar maturation).
Collagen type in granulation tissue vs mature scar
Answer: Granulation tissue = type III collagen (weaker, more pliable). Mature scar = type I collagen (stronger, cross-linked).
Collagenase (requires zinc) degrades type III while type I is deposited during remodeling.
Cell responsible for wound contraction
Answer: Myofibroblasts (contain actin and myosin).
Vitamin C deficiency and wound healing
Answer: Vitamin C is a cofactor for prolyl and lysyl hydroxylase (collagen cross-linking); deficiency → poor wound healing, scurvy, bleeding gums.
Main sources of free radical generation
Answer: Ionizing radiation, redox reactions (Fenton reaction), inflammation (NADPH oxidase 'respiratory burst'), metabolism of drugs (e.g., CCl4 → CCl3 radical).
CCl4 causes hepatocyte fatty change/necrosis via lipid peroxidation (classic toxicology example).
Mechanisms by which free radicals damage cells
Answer: Lipid peroxidation of membranes, protein cross-linking/fragmentation, and DNA strand breakage.
Enzymatic antioxidant defenses against free radicals
Answer: Superoxide dismutase (O2•− → H2O2), catalase/glutathione peroxidase (H2O2 → H2O).
Also vitamins A, C, E and ceruloplasmin act as free radical scavengers.
Amyloid staining property
Answer: Congo red staining shows apple-green birefringence under polarized light due to beta-pleated sheet structure.
AL vs AA amyloid — source and association
Answer: AL = immunoglobulin Light chains, from plasma cell dyscrasias (e.g., multiple myeloma). AA = serum Amyloid A, associated with chronic inflammatory conditions (RA, IBD, chronic infection).
Amyloid protein types: dialysis, Alzheimer disease, T2DM, medullary thyroid carcinoma
Answer: Dialysis = beta-2 microglobulin. Alzheimer = beta-amyloid (APP). Type 2 diabetes = amylin (IAPP). Medullary thyroid carcinoma = calcitonin-derived amyloid.
Suffix for benign vs malignant epithelial tumor
Answer: Benign = '-oma' (e.g., adenoma). Malignant = 'carcinoma' (e.g., adenocarcinoma).
Suffix for benign vs malignant mesenchymal tumor
Answer: Benign = '-oma' (e.g., lipoma, leiomyoma). Malignant = 'sarcoma' (e.g., liposarcoma, leiomyosarcoma).
Carcinoma in situ
Answer: Preinvasive neoplastic cells that have not crossed the basement membrane; low metastatic potential.
Hamartoma vs choristoma
Answer: Hamartoma = disorganized overgrowth of tissue native to the site (e.g., pulmonary hamartoma). Choristoma = normal tissue found in an abnormal location (e.g., gastric tissue in Meckel diverticulum).
List the core hallmarks of cancer
Answer: Sustained proliferative signaling, evasion of growth suppressors, resistance to apoptosis, replicative immortality, induction of angiogenesis, invasion/metastasis, reprogrammed energy metabolism (Warburg effect), and evasion of immune destruction.
Warburg effect
Answer: Cancer cells preferentially use aerobic glycolysis (fermentation to lactate) even with adequate oxygen, to generate biosynthetic precursors for rapid growth.
Basis for FDG-PET tumor imaging.
p53 — function and associated syndrome/cancers
Answer: Tumor suppressor; 'guardian of the genome,' halts cell cycle (G1/S) for DNA repair or triggers apoptosis. Mutated in Li-Fraumeni syndrome and >50% of human cancers.
RB gene — function and associated cancers
Answer: Tumor suppressor controlling G1/S checkpoint by binding E2F. Loss causes retinoblastoma and osteosarcoma.
'Two-hit hypothesis' first described with RB.
BRCA1/BRCA2 — function and cancers
Answer: DNA repair (double-strand break repair) tumor suppressors; mutations increase risk of breast and ovarian cancer.
APC gene — function and associated condition
Answer: Tumor suppressor (regulates β-catenin/Wnt pathway); mutation causes familial adenomatous polyposis (FAP) and sporadic colorectal cancer.
NF1 and NF2 tumor suppressors
Answer: NF1 (neurofibromin) → neurofibromatosis type 1 (neurofibromas, café-au-lait spots). NF2 (merlin) → neurofibromatosis type 2 (bilateral acoustic schwannomas, meningiomas).
VHL gene — associated cancers
Answer: Tumor suppressor; loss causes von Hippel-Lindau disease → renal cell carcinoma (clear cell) and hemangioblastomas.
Common proto-oncogenes and their associated cancers
Answer: RAS (pancreatic, colon), MYC (Burkitt lymphoma), HER2/neu (breast, gastric), BCR-ABL (CML), BCL-2 (follicular lymphoma).
Oncogenes require only one mutated allele (gain-of-function) unlike tumor suppressors.
Tumor markers: PSA, CA-125, CA 19-9, CEA
Answer: PSA = prostate cancer. CA-125 = ovarian cancer. CA 19-9 = pancreatic cancer. CEA = colorectal cancer (also used to monitor recurrence).
Tumor markers: AFP and beta-hCG
Answer: AFP = hepatocellular carcinoma, yolk sac (endodermal sinus) tumor. β-hCG = choriocarcinoma and other germ cell tumors.
S-100 tumor marker
Answer: Marker for melanoma, neural tumors (schwannoma), and Langerhans cell histiocytosis.
Paraneoplastic SIADH and ACTH (Cushing) — classic cancer
Answer: Both classically caused by small cell lung carcinoma (ectopic ADH or ACTH secretion).
Paraneoplastic hypercalcemia — mechanism and cancers
Answer: PTHrP secretion causing hypercalcemia; classically squamous cell lung carcinoma and renal cell carcinoma.
Differs from bone metastasis-driven hypercalcemia (e.g., breast cancer).
Paraneoplastic polycythemia — mechanism and cancers
Answer: Ectopic erythropoietin secretion; seen with renal cell carcinoma and hepatocellular carcinoma.
Lambert-Eaton myasthenic syndrome — associated cancer
Answer: Small cell lung cancer; autoantibodies against presynaptic voltage-gated calcium channels impair ACh release.
Unlike myasthenia gravis, symptoms improve with repeated muscle use.
Acanthosis nigricans as a paraneoplastic sign
Answer: Velvety hyperpigmented skin plaques (axilla/neck) associated with gastric adenocarcinoma.
Aflatoxin and vinyl chloride carcinogens — associated cancers
Answer: Aflatoxin (Aspergillus) → hepatocellular carcinoma (p53 mutation). Vinyl chloride → hepatic angiosarcoma.
Asbestos exposure — associated cancers
Answer: Mesothelioma and bronchogenic (lung) carcinoma; risk is markedly increased with concurrent smoking.
Aromatic amines (e.g., naphthylamine) and arsenic — associated cancers
Answer: Aromatic amines → transitional cell (bladder) carcinoma. Arsenic → squamous cell carcinoma of skin and lung.
Infectious carcinogens and their cancers: HPV, HBV/HCV, EBV, H. pylori
Answer: HPV → cervical/anal/oropharyngeal cancer. HBV/HCV → hepatocellular carcinoma. EBV → Burkitt lymphoma, nasopharyngeal carcinoma. H. pylori → gastric adenocarcinoma, MALT lymphoma.
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