const pptxgen = require("pptxgenjs");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Pathology Flashcards";
pres.author = "Orris";

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const flashcards = [
  // ── CELL INJURY ──────────────────────────────────────────────────────────────
  {
    q: "What are the 6 morphologic types of tissue necrosis?",
    a: "1. Coagulative — ischemic solid organs (preserved outlines)\n2. Liquefactive — brain infarct / bacterial abscess\n3. Caseous — TB (cheesy, structureless debris)\n4. Fat — enzymatic fat necrosis in pancreatitis\n5. Gangrenous — limb ischemia\n6. Fibrinoid — immune vasculitis (deposits in vessel walls)",
    topic: "Cell Injury",
  },
  {
    q: "What distinguishes reversible from irreversible cell injury?",
    a: "Reversible: cell swelling, fatty change, blebbing, mitochondrial swelling, ER dilation — still salvageable.\nIrreversible (point of no return): membrane disruption → massive Ca²⁺ influx, mitochondrial permeability transition, lysosomal rupture → necrosis.\nKey markers of irreversibility: loss of plasma membrane integrity & inability to maintain mitochondrial function.",
    topic: "Cell Injury",
  },
  {
    q: "Compare apoptosis vs. necrosis",
    a: "Apoptosis: programmed, caspase-mediated, cell shrinkage, apoptotic bodies, NO inflammation, phagocytes clear debris.\nNecrosis: pathologic, membrane rupture, cell swelling, enzymatic digestion, INFLAMMATION triggered, leakage of cellular contents.\nKey: apoptosis is tidy; necrosis is messy.",
    topic: "Cell Injury",
  },
  {
    q: "What are the 2 pathways of apoptosis?",
    a: "1. Intrinsic (mitochondrial): DNA damage / loss of growth factors → BCL-2 family shifts → cytochrome c release → caspase-9 → executioner caspases.\n2. Extrinsic (death receptor): FasL/TNF binds death receptor → FADD → caspase-8 activation.\nBoth converge on effector caspases-3/6/7.",
    topic: "Cell Injury",
  },
  {
    q: "Distinguish dystrophic vs. metastatic calcification",
    a: "Dystrophic: calcium deposits at sites of NECROSIS/injury — normal serum calcium (e.g., atherosclerotic plaques, caseous TB, dead tumors).\nMetastatic: calcium deposits in NORMAL tissues — caused by HYPERCALCEMIA (e.g., hyperparathyroidism, vitamin D toxicity, widespread bone metastases).",
    topic: "Cell Injury",
  },
  // ── CELLULAR ADAPTATIONS ─────────────────────────────────────────────────────
  {
    q: "Define hypertrophy, hyperplasia, atrophy, metaplasia",
    a: "Hypertrophy: ↑ cell SIZE (not number) — e.g., cardiac hypertrophy in hypertension.\nHyperplasia: ↑ cell NUMBER — e.g., endometrial hyperplasia (estrogen).\nAtrophy: ↓ cell size/number — e.g., disuse atrophy, denervation.\nMetaplasia: one differentiated cell type replaced by another — e.g., Barrett's (squamous → columnar), smoker's airways (columnar → squamous).",
    topic: "Adaptations",
  },
  {
    q: "What is Barrett's esophagus and why does it matter?",
    a: "Barrett's esophagus = metaplasia of esophageal squamous epithelium → columnar (intestinal-type) epithelium due to chronic GERD.\nSignificance: precursor to esophageal adenocarcinoma via dysplasia sequence.\nRisk of adenocarcinoma: ~0.5%/year; higher with high-grade dysplasia.",
    topic: "Adaptations",
  },
  // ── INFLAMMATION ──────────────────────────────────────────────────────────────
  {
    q: "What are the cardinal signs of acute inflammation and their mediators?",
    a: "Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function).\nVascular mediators: histamine, prostaglandins, bradykinin, leukotrienes.\nEdema: ↑ vascular permeability → fluid/protein exudate.\nLeukocyte recruitment: selectins (rolling) → integrins (adhesion) → diapedesis.",
    topic: "Inflammation",
  },
  {
    q: "Sequence of leukocyte recruitment in acute inflammation",
    a: "1. Margination & rolling — P/E-selectins bind sialyl-Lewis X on neutrophils.\n2. Adhesion — ICAM-1/VCAM-1 bind integrins (LFA-1, Mac-1) on leukocytes.\n3. Transmigration (diapedesis) — through endothelial junctions, guided by PECAM-1.\n4. Chemotaxis — IL-8, C5a, LTB4, fMLP attract neutrophils to injury site.",
    topic: "Inflammation",
  },
  {
    q: "What is a granuloma? Name 5 diseases that cause it.",
    a: "Granuloma = organized collection of activated macrophages (epithelioid cells) ± Langhans giant cells, surrounded by lymphocytes.\nFormed when an agent resists killing → Th1 → IFN-γ → macrophage activation.\n5 causes:\n1. Tuberculosis (caseating)\n2. Sarcoidosis (non-caseating)\n3. Crohn's disease (non-caseating)\n4. Histoplasmosis / fungal infections\n5. Berylliosis / foreign body reactions",
    topic: "Inflammation",
  },
  {
    q: "Th1 vs. Th2 vs. Th17 — roles in inflammation",
    a: "Th1: IFN-γ → classical macrophage activation → kills intracellular pathogens; drives autoimmunity & granuloma formation.\nTh2: IL-4, IL-5, IL-13 → IgE, eosinophils; defense vs. helminths; drives allergy / asthma.\nTh17: IL-17 → recruits neutrophils; defense vs. extracellular bacteria/fungi; drives psoriasis & some autoimmune disease.",
    topic: "Inflammation",
  },
  {
    q: "Distinguish exudate from transudate",
    a: "Exudate: protein-rich, cells present, cloudy — caused by ↑ vascular permeability (inflammation, malignancy).\nTransudate: protein-poor, cell-sparse, clear — caused by ↑ hydrostatic or ↓ oncotic pressure (HF, cirrhosis, nephrotic syndrome).\nLight's criteria differentiates pleural effusions.",
    topic: "Inflammation",
  },
  // ── REPAIR & WOUND HEALING ───────────────────────────────────────────────────
  {
    q: "Primary vs. secondary intention wound healing",
    a: "Primary intention: clean, apposed wound edges → minimal granulation tissue, thin scar (e.g., surgical incision).\nSecondary intention: large/infected wound → extensive granulation tissue, wound contraction (myofibroblasts), re-epithelialization, larger scar.\nKey difference: secondary involves more contraction and granulation tissue.",
    topic: "Repair",
  },
  {
    q: "What growth factors drive wound healing?",
    a: "TGF-β: fibrosis / scar formation; suppresses inflammation.\nVEGF: angiogenesis (new capillaries).\nEGF & TGF-α: epithelial proliferation.\nPDGF: fibroblast recruitment.\nFGF: fibroblast proliferation & angiogenesis.\nIGF-1: cell survival and matrix synthesis.",
    topic: "Repair",
  },
  // ── HEMODYNAMIC DISORDERS ─────────────────────────────────────────────────────
  {
    q: "Virchow's triad — components and examples",
    a: "1. Endothelial injury — atherosclerosis, hypertension, trauma → triggers thrombosis.\n2. Stasis/turbulence — DVT (immobility), atrial fibrillation → sluggish flow allows thrombus.\n3. Hypercoagulability — Factor V Leiden, malignancy, OCP use → prothrombotic state.\nAll three predispose to thrombosis; at least one is needed.",
    topic: "Hemodynamics",
  },
  {
    q: "Fate of a thrombus — 4 outcomes",
    a: "1. Resolution/lysis — plasmin degrades fibrin (e.g., tPA therapy).\n2. Organization & recanalization — fibroblasts invade → scar with new channels.\n3. Propagation — thrombus extends.\n4. Embolization — thrombus detaches → travels to distant site (e.g., PE from DVT).",
    topic: "Hemodynamics",
  },
  {
    q: "Distinguish red vs. white infarct",
    a: "Red (hemorrhagic) infarct: dual blood supply or reperfusion → e.g., lung, liver, bowel, testes (with torsion then reperfusion).\nWhite (pale) infarct: end-artery supply → e.g., heart (MI), kidney, spleen.\nPattern: red infarcts bleed back into necrotic tissue; white infarcts remain pale due to no collateral flow.",
    topic: "Hemodynamics",
  },
  // ── NEOPLASIA ────────────────────────────────────────────────────────────────
  {
    q: "What is the difference between benign and malignant tumors?",
    a: "Benign: well-differentiated, slow growth, capsulated, no invasion, no metastasis (e.g., lipoma, adenoma).\nMalignant: poorly/undifferentiated, rapid growth, invasive, can metastasize.\nKey features of malignancy: nuclear pleomorphism, ↑ mitoses (esp. atypical), necrosis, invasion of BM, vascular/lymphatic invasion.",
    topic: "Neoplasia",
  },
  {
    q: "Routes of metastasis — 3 main pathways",
    a: "1. Lymphatic — most common for carcinomas; spreads to regional nodes first (sentinel node).\n2. Hematogenous — most common for sarcomas; travels via veins → liver, lungs, bone, brain (common sites).\n3. Seeding of body cavities — e.g., ovarian cancer → peritoneum (transcoelomic); GI tumors → peritoneal spread.\nKrukenberg tumor: gastric carcinoma → bilateral ovarian metastasis.",
    topic: "Neoplasia",
  },
  {
    q: "Key tumor suppressor genes: p53 and RB",
    a: "p53 (TP53): 'guardian of genome' — activated by DNA damage → cell cycle arrest, DNA repair, or apoptosis. Mutated in >50% of human cancers. Li-Fraumeni syndrome (germline TP53 mutation).\nRB: controls G1→S checkpoint — phosphorylated RB releases E2F → cell cycle entry. Lost in retinoblastoma, osteosarcoma. 'Two-hit' Knudson hypothesis.",
    topic: "Neoplasia",
  },
  {
    q: "Hallmarks of cancer (Hanahan & Weinberg)",
    a: "1. Sustained proliferative signaling\n2. Evasion of growth suppressors\n3. Resistance to cell death\n4. Replicative immortality (telomerase)\n5. Induced angiogenesis (VEGF)\n6. Activation of invasion & metastasis\n7. Reprogramming energy metabolism (Warburg effect)\n8. Evasion of immune destruction\n+ Enabling hallmarks: genomic instability, tumor-promoting inflammation.",
    topic: "Neoplasia",
  },
  {
    q: "Proto-oncogene vs. oncogene vs. tumor suppressor",
    a: "Proto-oncogene: normal gene promoting cell growth (e.g., RAS, MYC, HER2).\nOncogene: mutated/overexpressed proto-oncogene — acts as 'accelerator stuck on' — dominant gain-of-function (1 mutant allele enough).\nTumor suppressor: brakes on cell growth (e.g., RB, p53, APC, BRCA1/2) — loss-of-function, recessive (need both alleles lost — 'two-hit').",
    topic: "Neoplasia",
  },
  {
    q: "Paraneoplastic syndromes — 5 classic examples",
    a: "1. SIADH → hyponatremia — small cell lung carcinoma (SCLC)\n2. Cushing syndrome (ectopic ACTH) — SCLC\n3. Hypercalcemia (PTHrP) — squamous cell lung carcinoma, renal cell carcinoma\n4. Lambert-Eaton syndrome (anti-VGCC) — SCLC\n5. Trousseau sign (migratory thrombophlebitis) — pancreatic, GI cancers\nNOTE: These are not caused by direct tumor invasion.",
    topic: "Neoplasia",
  },
  // ── AMYLOIDOSIS ──────────────────────────────────────────────────────────────
  {
    q: "Amyloidosis — types, proteins, and diagnosis",
    a: "AL amyloid: plasma cell dyscrasia (myeloma) → immunoglobulin light chains.\nAA amyloid: chronic inflammation (TB, RA, IBD) → serum amyloid A protein.\nAβ amyloid: Alzheimer's disease → amyloid precursor protein (APP).\nATTR: transthyretin mutations → familial/senile amyloidosis.\nDiagnosis: Congo red stain → apple-green birefringence under polarized light.",
    topic: "Amyloidosis",
  },
  // ── IMMUNOPATHOLOGY ──────────────────────────────────────────────────────────
  {
    q: "Hypersensitivity reactions — Gell & Coombs classification",
    a: "Type I (IgE-mediated): anaphylaxis, asthma, atopy — mast cell degranulation.\nType II (antibody-mediated cytotoxicity): hemolytic anemia, Goodpasture, myasthenia gravis.\nType III (immune complex): SLE, serum sickness, post-strep GN.\nType IV (delayed/T-cell mediated): TB skin test, contact dermatitis, transplant rejection, Type 1 DM.",
    topic: "Immunopathology",
  },
  {
    q: "SLE — key pathology and autoantibodies",
    a: "Systemic autoimmune disease: anti-dsDNA (most specific), anti-Smith (most specific), ANA (most sensitive).\nPathology: immune complex (Type III HSR) deposition in kidneys (wire-loop lesion), skin (butterfly rash), joints, serosal surfaces.\nLupus nephritis: most serious; WHO classes I–VI.\nFemale predominance (9:1), young women.",
    topic: "Immunopathology",
  },
  // ── SPECIAL PATHOLOGY ─────────────────────────────────────────────────────────
  {
    q: "Atherosclerosis — pathogenesis in steps",
    a: "1. Endothelial injury (HTN, smoking, hyperlipidemia) → ↑ permeability.\n2. LDL accumulates in intima → oxidized LDL.\n3. Monocytes migrate → macrophages → engulf oxLDL → foam cells → fatty streak.\n4. PDGF/VEGF → smooth muscle migration from media → fibrous cap.\n5. Complicated plaque: calcification, ulceration, thrombosis → MI, stroke.",
    topic: "Vascular",
  },
  {
    q: "Distinguish type 1 vs. type 2 MI",
    a: "Type 1 MI: atherosclerotic plaque rupture → thrombosis → coronary artery occlusion.\nType 2 MI: supply-demand mismatch (no plaque rupture) — e.g., coronary spasm, severe anemia, hypotension, tachyarrhythmia.\nPathology of Type 1: coagulative necrosis of myocardium; reperfusion → hemorrhage, contraction bands.",
    topic: "Cardiac",
  },
  {
    q: "Morphologic zones of acute MI and timeline",
    a: "0–6 hrs: no gross change; wavy fibers on EM/histo.\n6–12 hrs: early coagulative necrosis, edema, scattered neutrophils.\n1–3 days: pallor with hyperemia; neutrophil infiltration (peak day 3).\n5–10 days: macrophage (mononuclear) infiltration; yellow softening.\n2–8 wks: granulation tissue → fibrosis.\n>2 months: dense white scar.",
    topic: "Cardiac",
  },
  {
    q: "Fatty liver (hepatic steatosis) — causes and mechanism",
    a: "Causes: alcohol (most common), obesity/metabolic syndrome (NAFLD), diabetes, malnutrition, drugs (amiodarone, methotrexate).\nMechanism (alcohol): ↑ NADH from alcohol metabolism → ↓ fatty acid oxidation, ↑ triglyceride synthesis → fat accumulates in hepatocytes.\nMicrovesicular: acute toxicity, Reye syndrome.\nMacrovesicular: alcohol, NAFLD.",
    topic: "Liver",
  },
  {
    q: "Coagulation cascade — intrinsic vs. extrinsic pathway",
    a: "Extrinsic: tissue factor (TF) + factor VII → Xa (tested by PT/INR).\nIntrinsic: XII → XI → IX → VIIIa → Xa (tested by aPTT).\nCommon: Xa + Va → prothrombin → thrombin → fibrinogen → fibrin.\nHemophilia A: factor VIII deficiency (↑aPTT).\nHemophilia B: factor IX deficiency (↑aPTT).\nVit K dependent: II, VII, IX, X, protein C & S.",
    topic: "Hemostasis",
  },
];

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