Orris

Pharmacology and therapeutics: comprehensive notes on autocoids on Pharmacological basis as a pptx in clean visible structured

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Running Command

ls /home/daytona/workspace/ && mkdir -p /home/daytona/workspace/autocoids-pptx

Writing File

~/autocoids-pptx/autocoids.js

const pptxgen = require("pptxgenjs");
const prs = new pptxgen();
prs.layout = "LAYOUT_16x9";
prs.title = "Autocoids – Pharmacological Basis";
prs.author = "Orris Medical";

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// ══════════════════════════════════════════════════════════════════
// SLIDE 1 — COVER
// ══════════════════════════════════════════════════════════════════
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  // Title
  s.addText("AUTOCOIDS", {
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  s.addText("Pharmacological Basis", {
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  s.addText("Pharmacology & Therapeutics — Comprehensive Notes", {
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  // Topics list
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    "Histamine  •  Antihistamines  •  Serotonin",
    "Ergot Alkaloids  •  Prostaglandins / Eicosanoids",
    "Kinins  •  Angiotensin  •  Nitric Oxide",
  ];
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// ══════════════════════════════════════════════════════════════════
// SLIDE 2 — WHAT ARE AUTOCOIDS?
// ══════════════════════════════════════════════════════════════════
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  titleBar(s, "What Are Autocoids?");

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  s.addText('"Autocoids" (from Greek autos = self, akos = remedy) are biologically active substances synthesized locally in tissues that exert their effects at or near their site of production — acting as local hormones.', {
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    { text: "Act via specific receptors (GPCRs or ion channels)", options: { bullet: true, breakLine: true } },
    { text: "Short half-life — rapidly inactivated locally", options: { bullet: true, breakLine: true } },
    { text: "Both physiologic (homeostasis) and pathologic roles (allergy, inflammation, pain)", options: { bullet: true, breakLine: true } },
    { text: "Targets for major drug classes: antihistamines, NSAIDs, triptans, ACE inhibitors", options: { bullet: true } },
  ];
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    { text: " ", options: { breakLine: true } },
    { text: "Lipid Mediators", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  Prostaglandins, Thromboxanes,", options: { color: C.white, breakLine: true } },
    { text: "  Leukotrienes, PAF", options: { color: C.white, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Peptide Mediators", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  Kinins (Bradykinin), Angiotensin,", options: { color: C.white, breakLine: true } },
    { text: "  Natriuretic Peptides", options: { color: C.white, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Other: Nitric Oxide (NO), Endothelins", options: { color: C.muted } },
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  footerNote(s, "Katzung's Basic & Clinical Pharmacology, 16th Ed. | Chapter 16 & 18");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 3 — SECTION DIVIDER: HISTAMINE
// ══════════════════════════════════════════════════════════════════
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  const s = prs.addSlide();
  sectionHeader(s, "HISTAMINE", "Synthesis · Storage · Receptors · Pharmacology", "🧪");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 4 — HISTAMINE: CHEMISTRY & SYNTHESIS
// ══════════════════════════════════════════════════════════════════
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  titleBar(s, "Histamine — Chemistry & Synthesis");

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    { text: "Enzyme: Histidine decarboxylase (L-DOPA decarboxylase)", options: { bullet: true, breakLine: true } },
    { text: "Product: Histamine (β-imidazolylethylamine) — MW 111 Da", options: { bullet: true, breakLine: true } },
    { text: "Metabolism: N-methylhistamine → methylimidazole acetic acid (MAO + diamine oxidase)", options: { bullet: true, breakLine: true } },
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  s.addText("Storage & Release", {
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    { text: "ECL cells of gastric fundus → acid secretion trigger", options: { bullet: true, color: C.white, breakLine: true } },
    { text: "Brain neurons → neurotransmitter/neuromodulator", options: { bullet: true, color: C.white, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Release Mechanisms:", options: { bold: true, color: C.cyan, breakLine: true } },
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    { text: "2. Chemical (drugs: morphine, tubocurarine; radiocontrast)", options: { color: C.offWhite, breakLine: true } },
    { text: "3. Physical (trauma, UV, heat, cold)", options: { color: C.offWhite, breakLine: true } },
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  footerNote(s, "Katzung's Basic & Clinical Pharmacology, 16th Ed. | Chapter 16: Histaminergic Drugs");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 5 — HISTAMINE RECEPTORS
// ══════════════════════════════════════════════════════════════════
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      { text: "Subtype / Coupling", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Location", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Pharmacological Effects", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Therapeutic Target", options: { bold: true, color: C.white, fill: C.navy } },
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      { text: "H1", options: { bold: true, color: C.teal } },
      { text: "Gq/11 → ↑IP3/DAG → ↑Ca²⁺", options: {} },
      { text: "Smooth muscle, endothelium, brain, heart", options: {} },
      { text: "Bronchoconstriction, vasodilation, ↑vascular permeability, pruritus, pain, chemotaxis", options: {} },
      { text: "H1-blockers (antihistamines) — allergy, urticaria, rhinitis", options: {} },
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      { text: "H2", options: { bold: true, color: C.orange } },
      { text: "Gs → ↑cAMP → PKA", options: {} },
      { text: "Gastric parietal cells, heart, uterus, basophils", options: {} },
      { text: "↑Gastric acid secretion, ↑heart rate (atria), uterine relaxation", options: {} },
      { text: "H2-blockers — peptic ulcer, GERD", options: {} },
    ],
    [
      { text: "H3", options: { bold: true, color: C.cyan } },
      { text: "Gi → ↓cAMP (presynaptic autoreceptor)", options: {} },
      { text: "CNS (presynaptic), peripheral nerves", options: {} },
      { text: "Inhibits histamine synthesis & release; modulates NE, ACh, 5-HT release", options: {} },
      { text: "Pitolisant (H3-antagonist) — narcolepsy", options: {} },
    ],
    [
      { text: "H4", options: { bold: true, color: C.red } },
      { text: "Gi → ↓cAMP", options: {} },
      { text: "Hematopoietic cells, mast cells, eosinophils, dendritic cells", options: {} },
      { text: "Chemotaxis, immune cell activation, pruritus", options: {} },
      { text: "Investigational — atopic dermatitis, asthma", options: {} },
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  footerNote(s, "All four receptors are GPCRs with constitutive activity. Some ligands act as inverse agonists. | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 6 — HISTAMINE PHARMACOLOGICAL EFFECTS
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Histamine — Organ-Level Pharmacological Effects");

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    { title: "CVS", color: C.red, items: ["H1: vasodilation of small vessels → ↓BP (Triple Response of Lewis)", "H2: ↑heart rate, ↑contractility (atria)", "H1+H2: overall hypotension with flushing", "Venules: ↑permeability → edema, wheal & flare"] },
    { title: "Respiratory", color: C.teal, items: ["H1: bronchoconstriction (asthma trigger)", "Histamine provocation test: dose-response of airways", "Minor role in anaphylaxis vs. leukotrienes"] },
    { title: "GI Tract", color: C.orange, items: ["H2: potent stimulation of gastric acid (parietal cells)", "Co-stimulator with gastrin & ACh", "↑GI smooth muscle contraction (H1)"] },
    { title: "CNS", color: C.navy, items: ["H1: sedation (histaminergic pathways = arousal)", "H3 autoreceptors: regulate sleep-wake cycle", "Vestibular function: motion sickness (H1)"] },
    { title: "Skin", color: C.cyan, items: ["Triple Response (Lewis): red spot → flare → wheal", "H1: pruritus (direct nerve stimulation)", "Urticaria, dermatographism, angioedema"] },
    { title: "Immunology", color: C.yellow, items: ["Mast cell degranulation (type I HSR)", "Chemotaxis of eosinophils & neutrophils", "Modulates T-cell & dendritic cell function (H4)"] },
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    const y = yStart + row * (bH + gapY);

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    s.addShape(prs.ShapeType.rect, { x, y, w: bW, h: 0.32, fill: { color: sys.color } });
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  footerNote(s, "Triple Response of Lewis: Histamine wheal-and-flare test. H1 = bronchoconstriction. H2 = gastric acid. | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 7 — H1-ANTIHISTAMINES
// ══════════════════════════════════════════════════════════════════
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  s.background = { color: C.offWhite };
  titleBar(s, "H1-Antihistamines — Classification & Pharmacology");

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  s.addText("First-Generation (Classical)", {
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    { text: "Cross BBB → SEDATION (antimuscarinic, antiadrenergic)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Subclasses & Examples:", options: { bold: true, color: C.cyan, breakLine: true } },
    { text: "Ethanolamines: Diphenhydramine (marked sedation, anti-emetic)", options: { color: C.offWhite, breakLine: true } },
    { text: "Ethylenediamines: Mepyramine / Tripelennamine (GI upset)", options: { color: C.offWhite, breakLine: true } },
    { text: "Alkylamines: Chlorpheniramine (mild sedation, OTC 'cold')", options: { color: C.offWhite, breakLine: true } },
    { text: "Piperazines: Hydroxyzine (anxiolytic), Cyclizine (motion sick.)", options: { color: C.offWhite, breakLine: true } },
    { text: "Phenothiazines: Promethazine (strong sedation, antiemetic)", options: { color: C.offWhite, breakLine: true } },
    { text: "Misc: Cyproheptadine (also 5-HT blocker, appetite stimulant)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Uses: Allergy, urticaria, motion sickness, insomnia (off-label)", options: { color: C.muted } },
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    { text: "Do NOT cross BBB freely → minimal CNS effects", options: { bullet: true, breakLine: true } },
    { text: "Lipophobic, P-glycoprotein efflux from brain", options: { bullet: true, breakLine: true } },
    { text: "No/minimal antimuscarinic effects", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Key Drugs:", options: { bold: true, color: C.navy, breakLine: true } },
    { text: "Loratadine — OTC, long-acting (24h), no sedation", options: { bullet: true, breakLine: true } },
    { text: "Desloratadine — active metabolite, potent", options: { bullet: true, breakLine: true } },
    { text: "Cetirizine — mild sedation, also antipruritic", options: { bullet: true, breakLine: true } },
    { text: "Levocetirizine — R-enantiomer of cetirizine, potent", options: { bullet: true, breakLine: true } },
    { text: "Fexofenadine — least sedating, safe in pilots", options: { bullet: true, breakLine: true } },
    { text: "Azelastine — intranasal, topical ocular use", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Caution: Terfenadine/Astemizole WITHDRAWN — QT prolongation with CYP3A4 inhibitors (ketoconazole, erythromycin) → torsades", options: { italic: true, color: C.red } },
  ];
  s.addText(gen2, { x: 5.25, y: 1.68, w: 4.4, h: 3.55, fontSize: 12, color: C.text, fontFace: "Calibri", paraSpaceAfter: 3 });

  footerNote(s, "HERG (IKr) potassium channel blockade by early 2nd-gen agents → repolarization delay → arrhythmia. | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 8 — H2-ANTAGONISTS & H3/H4
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "H2-Receptor Antagonists & H3/H4 Pharmacology");

  // H2 block
  addAccentBar(s, 0.25, 1.22, 5.9, 4.1, C.lightBg);
  s.addText("H2-RECEPTOR ANTAGONISTS", {
    x: 0.35, y: 1.28, w: 5.7, h: 0.35,
    fontSize: 14, bold: true, color: C.navy, fontFace: "Calibri",
  });
  const h2 = [
    { text: "Mechanism: Competitive, reversible H2 blockade → ↓cAMP in parietal cells → ↓gastric acid secretion (basal, nocturnal, food-stimulated)", options: { bullet: true, breakLine: true } },
    { text: "Drugs: Cimetidine, Ranitidine, Famotidine, Nizatidine", options: { bullet: true, breakLine: true } },
    { text: "Indications: Peptic ulcer (PUD), GERD, Zollinger-Ellison syndrome, stress ulcer prophylaxis", options: { bullet: true, breakLine: true } },
    { text: "Cimetidine (first H2 blocker): potent CYP450 inhibitor → many drug interactions; also blocks androgen receptors (gynecomastia, impotence)", options: { bullet: true, breakLine: true } },
    { text: "Famotidine: most potent, long-acting, fewer interactions", options: { bullet: true, breakLine: true } },
    { text: "Ranitidine: WITHDRAWN globally (2020) — NDMA carcinogen contamination", options: { bullet: true, color: C.red, breakLine: true } },
    { text: "Nizatidine: least interactions, renal excretion", options: { bullet: true } },
  ];
  s.addText(h2, { x: 0.35, y: 1.65, w: 5.7, h: 3.55, fontSize: 12.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 5 });

  // H3/H4 block
  addAccentBar(s, 6.35, 1.22, 3.4, 4.1, C.navy);
  s.addText("H3 & H4 RECEPTORS", {
    x: 6.45, y: 1.28, w: 3.2, h: 0.35,
    fontSize: 14, bold: true, color: C.cyan, fontFace: "Calibri",
  });
  const h3h4 = [
    { text: "H3 Receptor:", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Presynaptic autoreceptor & heteroreceptor in CNS", options: { color: C.offWhite, breakLine: true } },
    { text: "Controls sleep/wake, cognition, food intake", options: { color: C.offWhite, breakLine: true } },
    { text: "Pitolisant (H3 inverse agonist): approved for narcolepsy with/without cataplexy", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "H4 Receptor:", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Mainly on hematopoietic & immune cells", options: { color: C.offWhite, breakLine: true } },
    { text: "Role in: pruritus, chemotaxis, allergic inflammation", options: { color: C.offWhite, breakLine: true } },
    { text: "Investigational blockers for asthma, atopic dermatitis", options: { color: C.muted } },
  ];
  s.addText(h3h4, { x: 6.45, y: 1.65, w: 3.2, h: 3.5, fontSize: 12, fontFace: "Calibri", paraSpaceAfter: 4 });

  footerNote(s, "PPI (proton pump inhibitors) are superior to H2 blockers for acid suppression — used first-line for GERD/PUD today. | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 9 — SECTION DIVIDER: SEROTONIN
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  sectionHeader(s, "SEROTONIN (5-HT)", "5-Hydroxytryptamine: Synthesis · Receptors · Agonists · Antagonists", "💊");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 10 — SEROTONIN: SYNTHESIS & PHARMACOLOGY
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Serotonin (5-HT) — Synthesis, Storage & Receptors");

  // Left: synthesis
  addAccentBar(s, 0.25, 1.22, 4.5, 4.1, C.lightBg);
  s.addText("Synthesis & Distribution", {
    x: 0.35, y: 1.28, w: 4.3, h: 0.35,
    fontSize: 14, bold: true, color: C.teal, fontFace: "Calibri",
  });
  const synth = [
    { text: "Precursor: L-Tryptophan", options: { bullet: true, breakLine: true } },
    { text: "Step 1: Tryptophan hydroxylase → 5-Hydroxytryptophan (5-HTP)", options: { bullet: true, breakLine: true } },
    { text: "Step 2: AAAD (aromatic amino acid decarboxylase) → Serotonin (5-HT)", options: { bullet: true, breakLine: true } },
    { text: "Metabolism: MAO-A → 5-HIAA (major urinary metabolite — elevated in carcinoid syndrome)", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Distribution:", options: { bold: true, color: C.navy, breakLine: true } },
    { text: "90% in enterochromaffin cells of GI tract", options: { bullet: true, breakLine: true } },
    { text: "~8% in platelets (taken up, not synthesized)", options: { bullet: true, breakLine: true } },
    { text: "~2% in CNS (raphe nuclei of brainstem)", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Note: Does NOT cross BBB. CNS pool is independent.", options: { italic: true, color: C.red } },
  ];
  s.addText(synth, { x: 0.35, y: 1.65, w: 4.3, h: 3.6, fontSize: 12.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 4 });

  // Right: receptors
  addAccentBar(s, 5.1, 1.22, 4.6, 4.1, C.navy);
  s.addText("5-HT Receptor Subtypes (Key)", {
    x: 5.2, y: 1.28, w: 4.4, h: 0.35,
    fontSize: 14, bold: true, color: C.cyan, fontFace: "Calibri",
  });
  const rec = [
    { text: "5-HT1 (Gi → ↓cAMP):", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  1A: raphe autoreceptors, anxiety; buspirone partial agonist", options: { color: C.offWhite, breakLine: true } },
    { text: "  1B/1D: vasoconstriction; TRIPTAN TARGET (migraine)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "5-HT2 (Gq → ↑IP3/DAG):", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  2A: vasoconstriction, platelet aggregation, hallucinations", options: { color: C.offWhite, breakLine: true } },
    { text: "  2B: cardiac valvulopathy (fenfluramine, ergot) — fibrosis", options: { color: C.offWhite, breakLine: true } },
    { text: "  2C: appetite, mood; clozapine blocks (weight gain)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "5-HT3 (Ion channel — Na+/K+):", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  Vomiting center; ondansetron blocks (antiemetic)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "5-HT4 (Gs → ↑cAMP):", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "  GI prokinesis; cisapride/metoclopramide partial agonism", options: { color: C.muted } },
  ];
  s.addText(rec, { x: 5.2, y: 1.65, w: 4.45, h: 3.55, fontSize: 12, fontFace: "Calibri", paraSpaceAfter: 3 });

  footerNote(s, "5-HT7 also exists — receptors for circadian rhythm, thermoregulation. 14 receptor subtypes in 7 families (5-HT1–7). | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 11 — SEROTONIN AGONISTS & CLINICAL USE
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Serotonergic Drugs — Agonists, Antagonists & Clinical Use");

  const rows = [
    [
      { text: "Drug Class / Agent", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Receptor Action", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Mechanism", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Clinical Use", options: { bold: true, color: C.white, fill: C.navy } },
    ],
    [
      { text: "Triptans (Sumatriptan, Zolmitriptan, etc.)", options: { bold: true, color: C.teal } },
      { text: "5-HT1B/1D agonist", options: {} },
      { text: "Cranial vasoconstriction; inhibit trigeminal pain signalling", options: {} },
      { text: "Acute migraine & cluster headache; DO NOT use in CVD/CAD", options: {} },
    ],
    [
      { text: "Buspirone", options: { bold: true, color: C.teal } },
      { text: "5-HT1A partial agonist; D2 antagonist", options: {} },
      { text: "Reduces serotonergic & dopaminergic firing; no GABA modulation", options: {} },
      { text: "Generalized anxiety disorder (GAD); non-sedating, non-addictive", options: {} },
    ],
    [
      { text: "Ondansetron, Granisetron (setrons)", options: { bold: true, color: C.teal } },
      { text: "5-HT3 antagonist", options: {} },
      { text: "Block vomiting reflex at CTZ and vagal afferents", options: {} },
      { text: "Chemotherapy-induced / post-op nausea & vomiting (CINV/PONV)", options: {} },
    ],
    [
      { text: "Metoclopramide", options: { bold: true, color: C.orange } },
      { text: "5-HT4 agonist + D2 antagonist", options: {} },
      { text: "Prokinetic + antiemetic; also central D2 block", options: {} },
      { text: "GERD, gastroparesis, CINV; risk: tardive dyskinesia (EPS)", options: {} },
    ],
    [
      { text: "SSRIs (Fluoxetine, Sertraline, etc.)", options: { bold: true, color: C.orange } },
      { text: "Inhibit SERT (serotonin transporter)", options: {} },
      { text: "↑Synaptic 5-HT; no direct receptor agonism", options: {} },
      { text: "Depression, OCD, PTSD, panic disorder, anxiety", options: {} },
    ],
    [
      { text: "Cyproheptadine", options: { bold: true, color: C.red } },
      { text: "H1 + 5-HT2 antagonist", options: {} },
      { text: "Blocks H1 and 5-HT2 receptors", options: {} },
      { text: "Serotonin syndrome (antidote), allergic pruritus, appetite stimulant", options: {} },
    ],
    [
      { text: "Ergotamine / Methysergide", options: { bold: true, color: C.red } },
      { text: "5-HT1 agonist + partial 5-HT2 antagonist", options: {} },
      { text: "Complex: vasoconstriction (ergotism risk); also DA/NE effects", options: {} },
      { text: "Methysergide: migraine prophylaxis (retroperitoneal fibrosis risk)", options: {} },
    ],
  ];

  s.addTable(rows, {
    x: 0.2, y: 1.22, w: 9.6,
    colW: [2.1, 1.9, 2.5, 3.1],
    border: { type: "solid", pt: 0.5, color: "C5D8E0" },
    fontSize: 11, fontFace: "Calibri",
    rowH: 0.5,
  });

  footerNote(s, "Serotonin syndrome: hyperthermia + clonus + altered mental state — treat with cyproheptadine + supportive care. | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 12 — SECTION DIVIDER: ERGOT ALKALOIDS
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  sectionHeader(s, "ERGOT ALKALOIDS", "Vasoactive • Uterotonic • Neurological Actions", "🍄");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 13 — ERGOT ALKALOIDS PHARMACOLOGY
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Ergot Alkaloids — Pharmacology & Clinical Applications");

  // Background box
  addAccentBar(s, 0.25, 1.22, 9.5, 0.72, C.teal);
  s.addText("Derived from Claviceps purpurea (rye fungus). Complex partial agonists/antagonists at α-adrenergic, dopamine, and serotonin receptors. Historical: St. Anthony's Fire (ergotism from contaminated grain).", {
    x: 0.35, y: 1.24, w: 9.3, h: 0.7,
    fontSize: 12.5, color: C.white, fontFace: "Calibri", valign: "middle",
  });

  const data = [
    { drug: "Ergotamine", receptor: "5-HT1 agonist, α partial agonist", use: "Acute migraine (oral/sublingual); DO NOT use in CAD, pregnancy", tox: "Ergotism: gangrene, vasospasm, GI upset, contraindicated in pregnancy" },
    { drug: "DHE (Dihydroergotamine)", receptor: "5-HT1B/1D agonist, α-adrenergic antagonist", use: "Acute/refractory migraine (nasal spray or IV); less vasoconstrictive", tox: "Nausea, weakness; safer CVS profile than ergotamine" },
    { drug: "Methysergide", receptor: "5-HT2A/2C antagonist, 5-HT1 partial agonist", use: "Migraine prophylaxis (NOT acute); also carcinoid-related diarrhea", tox: "Retroperitoneal & cardiac valvular fibrosis — drug holiday required every 6 months" },
    { drug: "Bromocriptine", receptor: "D2 agonist (potent), 5-HT partial agonist, α-adrenergic partial agonist", use: "Parkinsonism, prolactin-secreting adenoma (hyperprolactinemia), type 2 DM (Cycloset)", tox: "Nausea, postural hypotension, psychiatric symptoms, erythromelalgia" },
    { drug: "Cabergoline", receptor: "D2 agonist (longer-acting than bromocriptine)", use: "Hyperprolactinemia, prolactinoma (first-line); Parkinson's disease", tox: "Cardiac valvulopathy (5-HT2B) — echocardiographic monitoring" },
    { drug: "Ergometrine (Ergonovine) / Methylergonovine", receptor: "α + 5-HT agonism → uterine smooth muscle contraction", use: "Postpartum hemorrhage (3rd stage of labor), uterine atony", tox: "Hypertension, coronary vasospasm; CONTRAINDICATED with triptans & vasoconstrictors" },
  ];

  const tRows = [
    [
      { text: "Drug", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Key Receptor Actions", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Clinical Use", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Toxicity / Notes", options: { bold: true, color: C.white, fill: C.navy } },
    ],
    ...data.map(d => [
      { text: d.drug, options: { bold: true, color: C.teal } },
      { text: d.receptor, options: {} },
      { text: d.use, options: {} },
      { text: d.tox, options: {} },
    ])
  ];

  s.addTable(tRows, {
    x: 0.2, y: 2.0, w: 9.6,
    colW: [1.85, 2.4, 2.85, 2.5],
    border: { type: "solid", pt: 0.5, color: "C5D8E0" },
    fontSize: 10.5, fontFace: "Calibri",
    rowH: 0.48,
  });

  footerNote(s, "Ergotamine + triptans: both serotonin agonists → DO NOT combine (additive vasospasm). | Katzung Ch 16");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 14 — SECTION DIVIDER: EICOSANOIDS
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  sectionHeader(s, "EICOSANOIDS", "Prostaglandins · Thromboxanes · Leukotrienes · PAF", "🔬");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 15 — EICOSANOID SYNTHESIS PATHWAY
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Eicosanoid Synthesis — Arachidonic Acid Cascade");

  // Main pathway visual (text-based diagram)
  // Top box: stimulus
  s.addShape(prs.ShapeType.rect, { x: 3.7, y: 1.22, w: 2.6, h: 0.45, fill: { color: C.muted } });
  s.addText("Cell Membrane Phospholipids", { x: 3.7, y: 1.22, w: 2.6, h: 0.45, fontSize: 11, bold: true, color: C.white, align: "center", valign: "middle", fontFace: "Calibri" });

  // Arrow down
  s.addShape(prs.ShapeType.rect, { x: 4.9, y: 1.67, w: 0.2, h: 0.35, fill: { color: C.text } });
  s.addText("↓ Phospholipase A2 (inhibited by glucocorticoids → lipocortin/annexin)", { x: 3.3, y: 1.69, w: 3.4, h: 0.35, fontSize: 9.5, color: C.navy, fontFace: "Calibri", italic: true });

  // Arachidonic acid
  s.addShape(prs.ShapeType.rect, { x: 3.5, y: 2.02, w: 3.0, h: 0.45, fill: { color: C.teal } });
  s.addText("ARACHIDONIC ACID (20:4, ω-6)", { x: 3.5, y: 2.02, w: 3.0, h: 0.45, fontSize: 12, bold: true, color: C.white, align: "center", valign: "middle", fontFace: "Calibri" });

  // Three branches
  // COX branch
  s.addShape(prs.ShapeType.rect, { x: 0.2, y: 3.0, w: 2.85, h: 0.42, fill: { color: C.navy } });
  s.addText("COX-1 / COX-2 Pathway", { x: 0.2, y: 3.0, w: 2.85, h: 0.42, fontSize: 11, bold: true, color: C.white, align: "center", valign: "middle", fontFace: "Calibri" });
  s.addText("→ PGG2 → PGH2 →", { x: 0.2, y: 3.45, w: 2.85, h: 0.3, fontSize: 10.5, color: C.navy, fontFace: "Calibri", align: "center" });
  s.addShape(prs.ShapeType.rect, { x: 0.2, y: 3.78, w: 2.85, h: 1.22, fill: { color: C.lightBg } });
  const coxProducts = [
    { text: "PGE2: vasodilator, ↓pain threshold, fever, uterine contraction", options: { bullet: true, breakLine: true } },
    { text: "PGI2 (Prostacyclin): vasodilator, ↓platelet aggregation (endothelium)", options: { bullet: true, breakLine: true } },
    { text: "TXA2 (Thromboxane): vasoconstriction, ↑platelet aggregation (platelets)", options: { bullet: true, breakLine: true } },
    { text: "PGD2: bronchoconstriction, sleep-promoting (brain)", options: { bullet: true } },
  ];
  s.addText(coxProducts, { x: 0.25, y: 3.8, w: 2.75, h: 1.18, fontSize: 9.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 2 });

  // LOX branch
  s.addShape(prs.ShapeType.rect, { x: 3.57, y: 3.0, w: 2.85, h: 0.42, fill: { color: C.orange } });
  s.addText("5-LOX Pathway", { x: 3.57, y: 3.0, w: 2.85, h: 0.42, fontSize: 11, bold: true, color: C.white, align: "center", valign: "middle", fontFace: "Calibri" });
  s.addText("→ 5-HPETE → LTA4 →", { x: 3.57, y: 3.45, w: 2.85, h: 0.3, fontSize: 10.5, color: C.orange, fontFace: "Calibri", align: "center" });
  s.addShape(prs.ShapeType.rect, { x: 3.57, y: 3.78, w: 2.85, h: 1.22, fill: { color: "FFF0E8" } });
  const loxProd = [
    { text: "LTB4: chemotaxis of neutrophils (inflammatory)", options: { bullet: true, breakLine: true } },
    { text: "LTC4 / LTD4 / LTE4: cysteinyl leukotrienes — bronchoconstriction (asthma), ↑mucus secretion", options: { bullet: true, breakLine: true } },
    { text: "Blocked by: Zileuton (5-LOX inhibitor)", options: { bullet: true, breakLine: true } },
    { text: "Receptor blockers: Montelukast, Zafirlukast (CysLT1 receptor)", options: { bullet: true } },
  ];
  s.addText(loxProd, { x: 3.62, y: 3.8, w: 2.75, h: 1.18, fontSize: 9.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 2 });

  // CYP branch
  s.addShape(prs.ShapeType.rect, { x: 6.95, y: 3.0, w: 2.85, h: 0.42, fill: { color: C.red } });
  s.addText("CYP450 Pathway", { x: 6.95, y: 3.0, w: 2.85, h: 0.42, fontSize: 11, bold: true, color: C.white, align: "center", valign: "middle", fontFace: "Calibri" });
  s.addText("→ EETs, 20-HETE", { x: 6.95, y: 3.45, w: 2.85, h: 0.3, fontSize: 10.5, color: C.red, fontFace: "Calibri", align: "center" });
  s.addShape(prs.ShapeType.rect, { x: 6.95, y: 3.78, w: 2.85, h: 1.22, fill: { color: "FFE8E6" } });
  const cypProd = [
    { text: "EETs (epoxyeicosatrienoic acids): vasodilation, anti-inflammatory", options: { bullet: true, breakLine: true } },
    { text: "20-HETE: vasoconstriction, ↑Na+ reabsorption (renal)", options: { bullet: true, breakLine: true } },
    { text: "Role in: cardiovascular regulation, renal function", options: { bullet: true, breakLine: true } },
    { text: "Less clinically targeted but pharmacologically important", options: { bullet: true } },
  ];
  s.addText(cypProd, { x: 7.0, y: 3.8, w: 2.75, h: 1.18, fontSize: 9.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 2 });

  // Connect lines (dashed-style: thin colored bars)
  s.addShape(prs.ShapeType.rect, { x: 1.62, y: 2.47, w: 0.15, h: 0.53, fill: { color: C.navy } });
  s.addShape(prs.ShapeType.rect, { x: 5.0, y: 2.47, w: 0.15, h: 0.53, fill: { color: C.orange } });
  s.addShape(prs.ShapeType.rect, { x: 8.37, y: 2.47, w: 0.15, h: 0.53, fill: { color: C.red } });
  s.addShape(prs.ShapeType.rect, { x: 1.62, y: 2.47, w: 6.9, h: 0.12, fill: { color: C.text } });

  footerNote(s, "Glucocorticoids → ↑Annexin-1 (lipocortin) → inhibit PLA2 → broad eicosanoid suppression. NSAIDs → inhibit COX. | Katzung Ch 18");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 16 — PROSTAGLANDINS: EFFECTS & CLINICAL USE
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Prostaglandins & Thromboxane — Effects & Therapeutic Use");

  const rows = [
    [
      { text: "Eicosanoid", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Main Source", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Key Pharmacological Effects", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Drug / Therapeutic Use", options: { bold: true, color: C.white, fill: C.navy } },
    ],
    [
      { text: "PGE2", options: { bold: true, color: C.teal } },
      { text: "Ubiquitous; COX-1/2", options: {} },
      { text: "Vasodilation, ↑pain sensitivity (sensitizes nociceptors), fever (↑PGE2 in hypothalamus), uterine contraction at term, cytoprotection (gastric)", options: {} },
      { text: "Misoprostol (PGE1 analog): NSAID-induced ulcer prophylaxis, cervical ripening, PPH, medical abortion", options: {} },
    ],
    [
      { text: "PGI2 (Prostacyclin)", options: { bold: true, color: C.teal } },
      { text: "Vascular endothelium (COX-2)", options: {} },
      { text: "Potent vasodilator, ↓platelet aggregation (IP receptor → ↑cAMP), cytoprotection", options: {} },
      { text: "Epoprostenol, Iloprost, Treprostinil: pulmonary arterial hypertension (PAH)", options: {} },
    ],
    [
      { text: "TXA2", options: { bold: true, color: C.orange } },
      { text: "Platelets (COX-1)", options: {} },
      { text: "Potent vasoconstrictor + platelet aggregation promoter; balance with PGI2 determines thrombotic risk", options: {} },
      { text: "Aspirin (low-dose): irreversibly inhibits platelet COX-1 → ↓TXA2 → antiplatelet effect", options: {} },
    ],
    [
      { text: "PGF2α", options: { bold: true, color: C.orange } },
      { text: "Uterus, lungs", options: {} },
      { text: "Uterine/bronchial smooth muscle contraction, luteolysis", options: {} },
      { text: "Dinoprostone: labor induction; Latanoprost/Bimatoprost (PGF2α analogs): glaucoma (↑aqueous outflow via uveoscleral route)", options: {} },
    ],
    [
      { text: "PGD2", options: { bold: true, color: C.cyan } },
      { text: "Mast cells, brain (COX-1)", options: {} },
      { text: "Bronchoconstriction, vasodilation, sleep promotion (DP1 receptor in brain), allergic inflammation", options: {} },
      { text: "Laropiprant (DP1 antagonist): used with niacin (flushing). Fevipiprant (DP2/CRTH2): investigational for asthma", options: {} },
    ],
    [
      { text: "LTC4 / LTD4 / LTE4", options: { bold: true, color: C.red } },
      { text: "Mast cells, eosinophils (5-LOX)", options: {} },
      { text: "Cysteinyl LTs: bronchoconstriction (10-1000x > histamine), ↑mucus, ↑vascular permeability; slow-reacting substances of anaphylaxis (SRS-A)", options: {} },
      { text: "Montelukast, Zafirlukast (CysLT1 blockers): asthma (especially aspirin-exacerbated asthma, EIB, allergic rhinitis)", options: {} },
    ],
  ];

  s.addTable(rows, {
    x: 0.2, y: 1.25, w: 9.6,
    colW: [1.3, 1.8, 3.0, 3.5],
    border: { type: "solid", pt: 0.5, color: "C5D8E0" },
    fontSize: 10.5, fontFace: "Calibri",
    rowH: 0.58,
  });

  footerNote(s, "TXA2 : PGI2 = thrombus-promoting : thrombus-inhibiting. Selective COX-2 inhibitors ↓PGI2 (protective) but not TXA2 → ↑CV risk. | Katzung Ch 18");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 17 — NSAIDs & COX INHIBITION
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "NSAIDs — COX Inhibition, Selectivity & Clinical Implications");

  // left col
  addAccentBar(s, 0.25, 1.22, 4.55, 4.1, C.lightBg);
  s.addText("COX-1 vs COX-2: Key Distinction", {
    x: 0.35, y: 1.28, w: 4.35, h: 0.35,
    fontSize: 14, bold: true, color: C.navy, fontFace: "Calibri",
  });
  const cox = [
    { text: "COX-1 (Constitutive):", options: { bold: true, color: C.teal, breakLine: true } },
    { text: "- 'Housekeeping' enzyme — present in most cells", options: { bullet: true, breakLine: true } },
    { text: "- Produces PGE2/PGI2 for gastric mucosal protection", options: { bullet: true, breakLine: true } },
    { text: "- Platelet TXA2 synthesis (aggregation, hemostasis)", options: { bullet: true, breakLine: true } },
    { text: "- Renal prostaglandins (maintain GFR under stress)", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "COX-2 (Inducible):", options: { bold: true, color: C.orange, breakLine: true } },
    { text: "- Up-regulated by inflammation, growth factors, NFκB", options: { bullet: true, breakLine: true } },
    { text: "- Produces inflammatory prostaglandins (fever, pain, edema)", options: { bullet: true, breakLine: true } },
    { text: "- Also in vascular endothelium → PGI2 (cardioprotective)", options: { bullet: true, breakLine: true } },
    { text: "- Constitutive in kidney, brain, gut — not purely inducible", options: { bullet: true } },
  ];
  s.addText(cox, { x: 0.35, y: 1.68, w: 4.35, h: 3.55, fontSize: 12.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 4 });

  // right col
  addAccentBar(s, 5.1, 1.22, 4.65, 4.1, C.navy);
  s.addText("NSAID Classification & Side Effects", {
    x: 5.2, y: 1.28, w: 4.45, h: 0.35,
    fontSize: 14, bold: true, color: C.cyan, fontFace: "Calibri",
  });
  const nsaids = [
    { text: "Non-selective COX inhibitors:", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Aspirin (irreversible), Ibuprofen, Naproxen, Diclofenac, Indomethacin, Ketorolac (potent analgesic, short-term)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Selective COX-2 inhibitors (coxibs):", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Celecoxib (still available), Rofecoxib (WITHDRAWN — ↑MI risk), Etoricoxib", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Key Side Effects:", options: { bold: true, color: C.cyan, breakLine: true } },
    { text: "GI: peptic ulceration (↓mucosal PGE2) — COX-1 effect", options: { color: C.offWhite, breakLine: true } },
    { text: "Renal: ↓GFR, Na+ retention, hyperkalemia (COX-1/2)", options: { color: C.offWhite, breakLine: true } },
    { text: "Cardiovascular: ↑thrombotic risk (COX-2 selective)", options: { color: C.offWhite, breakLine: true } },
    { text: "Aspirin-exacerbated asthma: shunting to LOX pathway → ↑LTs", options: { color: C.offWhite, breakLine: true } },
    { text: "Reye syndrome: aspirin in viral illness (children — AVOID)", options: { color: C.red } },
  ];
  s.addText(nsaids, { x: 5.2, y: 1.68, w: 4.45, h: 3.55, fontSize: 12, fontFace: "Calibri", paraSpaceAfter: 4 });

  footerNote(s, "Aspirin 81mg: selectively acetylates platelet COX-1 (irreversibly). Platelets have no nucleus — cannot regenerate COX. Effect lasts platelet lifespan (~10 days). | Katzung");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 18 — SECTION DIVIDER: KININS & ANGIOTENSIN
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  sectionHeader(s, "KININS, ANGIOTENSIN & NITRIC OXIDE", "Bradykinin · Kallikrein-Kinin System · Angiotensin · NO", "⚗️");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 19 — BRADYKININ & KALLIKREIN-KININ SYSTEM
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Bradykinin & Kallikrein-Kinin System");

  // Info box 1
  addAccentBar(s, 0.25, 1.22, 4.55, 4.1, C.lightBg);
  s.addText("Kinin Synthesis & Metabolism", {
    x: 0.35, y: 1.28, w: 4.35, h: 0.35,
    fontSize: 14, bold: true, color: C.teal, fontFace: "Calibri",
  });
  const kinin = [
    { text: "Kininogens (plasma): High-MW (HMWK) and Low-MW (LMWK)", options: { bullet: true, breakLine: true } },
    { text: "Plasma kallikrein cleaves HMWK → Bradykinin (9 AA peptide)", options: { bullet: true, breakLine: true } },
    { text: "Glandular/tissue kallikrein cleaves LMWK → Lys-bradykinin (Kallidin)", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Metabolism:", options: { bold: true, color: C.navy, breakLine: true } },
    { text: "ACE (Kininase II / Peptidyl dipeptidase): inactivates bradykinin", options: { bullet: true, breakLine: true } },
    { text: "Kininase I (carboxypeptidase N): also degrades bradykinin", options: { bullet: true, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "ACE inhibitors block both Ang I → Ang II AND BK → inactive: this leads to ↑bradykinin accumulation → ACE inhibitor cough & angioedema", options: { italic: true, color: C.red } },
  ];
  s.addText(kinin, { x: 0.35, y: 1.68, w: 4.35, h: 3.55, fontSize: 12.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 4 });

  // Info box 2
  addAccentBar(s, 5.1, 1.22, 4.65, 4.1, C.navy);
  s.addText("Bradykinin Receptors & Effects", {
    x: 5.2, y: 1.28, w: 4.45, h: 0.35,
    fontSize: 14, bold: true, color: C.cyan, fontFace: "Calibri",
  });
  const brad = [
    { text: "Receptors: B1 (inducible — inflammation) and B2 (constitutive)", options: { bold: false, color: C.yellow, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Vascular Effects (B2 → Gq/Gi):", options: { bold: true, color: C.cyan, breakLine: true } },
    { text: "Potent vasodilation → ↓BP (via NO and PGI2 release)", options: { color: C.offWhite, breakLine: true } },
    { text: "↑Vascular permeability → edema", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Pain / Inflammation:", options: { bold: true, color: C.cyan, breakLine: true } },
    { text: "Direct activation of pain fibers (inflammatory pain, hyperalgesia)", options: { color: C.offWhite, breakLine: true } },
    { text: "Potentiates histamine + PGs in pain sensitization", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Clinical Relevance:", options: { bold: true, color: C.cyan, breakLine: true } },
    { text: "ICATIBANT (B2 antagonist): hereditary angioedema attacks", options: { color: C.offWhite, breakLine: true } },
    { text: "C1-esterase inhibitor (plasma kallikrein): Haegarda/Berinert for HAE prophylaxis", options: { color: C.muted } },
  ];
  s.addText(brad, { x: 5.2, y: 1.68, w: 4.45, h: 3.55, fontSize: 12, fontFace: "Calibri", paraSpaceAfter: 4 });

  footerNote(s, "Hereditary Angioedema (HAE): C1-inhibitor deficiency → ↑kallikrein → ↑bradykinin → subcutaneous/submucosal edema. NOT histamine-mediated. | Katzung");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 20 — ANGIOTENSIN & RENIN-ANGIOTENSIN SYSTEM
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Renin-Angiotensin System (RAS) — Key Pharmacology");

  // Pathway description box
  addAccentBar(s, 0.25, 1.22, 9.5, 0.65, C.teal);
  s.addText("Angiotensinogen (liver) → [Renin from JGA] → Ang I → [ACE (lung)] → Angiotensin II → Ang-(1-7) via ACE2 / Neprilysin (vasodilatory axis)", {
    x: 0.35, y: 1.24, w: 9.3, h: 0.63, fontSize: 12, color: C.white, fontFace: "Calibri", valign: "middle",
  });

  // Effects col
  addAccentBar(s, 0.25, 1.95, 4.55, 3.35, C.lightBg);
  s.addText("Angiotensin II Effects (AT1 receptor)", {
    x: 0.35, y: 2.0, w: 4.35, h: 0.38,
    fontSize: 13, bold: true, color: C.navy, fontFace: "Calibri",
  });
  const angII = [
    { text: "Potent vasoconstriction → ↑peripheral vascular resistance", options: { bullet: true, breakLine: true } },
    { text: "Adrenal cortex: ↑aldosterone secretion → Na+ & H2O retention", options: { bullet: true, breakLine: true } },
    { text: "Adrenal medulla: ↑catecholamine release", options: { bullet: true, breakLine: true } },
    { text: "Cardiac: hypertrophy, fibrosis (remodeling)", options: { bullet: true, breakLine: true } },
    { text: "Renal: efferent arteriole constriction → ↑GFR (early); Na+ reabsorption", options: { bullet: true, breakLine: true } },
    { text: "CNS: ↑ADH release, ↑sympathetic outflow, ↑thirst", options: { bullet: true } },
  ];
  s.addText(angII, { x: 0.35, y: 2.4, w: 4.35, h: 2.85, fontSize: 12.5, color: C.text, fontFace: "Calibri", paraSpaceAfter: 4 });

  // Drugs col
  addAccentBar(s, 5.1, 1.95, 4.65, 3.35, C.navy);
  s.addText("RAS-Targeting Drugs", {
    x: 5.2, y: 2.0, w: 4.45, h: 0.38,
    fontSize: 13, bold: true, color: C.cyan, fontFace: "Calibri",
  });
  const rasDrugs = [
    { text: "ACE inhibitors (ACEi): -prils (Enalapril, Lisinopril, Ramipril)", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Block Ang I → Ang II AND BK degradation. Side effects: Cough (↑BK), angioedema, ↑K+, contraindicated in pregnancy", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "ARBs (AT1 blockers): -sartans (Losartan, Valsartan, Olmesartan)", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Block AT1 receptors selectively. No BK effect → no cough. Preferred in ACEi cough. ↑AT2 receptor stimulation (beneficial: vasodilation)", options: { color: C.offWhite, breakLine: true } },
    { text: " ", options: { breakLine: true } },
    { text: "Renin inhibitor: Aliskiren — blocks renin directly → ↓Ang I & II", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "ARNI: Sacubitril (neprilysin inhibitor) + Valsartan (ARB) = Entresto — HFrEF treatment", options: { bold: true, color: C.yellow, breakLine: true } },
    { text: "Uses: Hypertension, HF, post-MI, diabetic nephropathy, CKD", options: { color: C.muted } },
  ];
  s.addText(rasDrugs, { x: 5.2, y: 2.4, w: 4.45, h: 2.85, fontSize: 11.5, fontFace: "Calibri", paraSpaceAfter: 4 });

  footerNote(s, "Do NOT combine ACEi + ARB + Aliskiren (↑hyperkalemia + AKI — ONTARGET trial). | Katzung Ch 17");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 21 — NITRIC OXIDE (NO)
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Nitric Oxide (NO) — An Endogenous Autocoid");

  twoColLayout(
    s,
    [
      { text: "Synthesis:", options: { bold: true, color: C.teal, breakLine: true } },
      { text: "L-Arginine + O2 → NO + L-Citrulline (via NOS enzymes)", options: { breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "NOS Isoforms:", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "eNOS (NOS3): Endothelial — constitutive, Ca2+-dependent; produces small amounts of NO for vasodilation", options: { bullet: true, breakLine: true } },
      { text: "nNOS (NOS1): Neuronal — constitutive; neurotransmission, LTP", options: { bullet: true, breakLine: true } },
      { text: "iNOS (NOS2): Inducible — cytokines/LPS → massive NO production → septic shock vasodilation", options: { bullet: true, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "Mechanism:", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "NO activates soluble guanylyl cyclase → ↑cGMP → PKG → vascular smooth muscle relaxation (VASODILATION)", options: { breakLine: true } },
    ],
    [
      { text: "Pharmacological Actions:", options: { bold: true, color: C.orange, breakLine: true } },
      { text: "Vasodilation (penile erection via cGMP — PDE5 inhibitors target this)", options: { bullet: true, breakLine: true } },
      { text: "Inhibits platelet aggregation and adhesion", options: { bullet: true, breakLine: true } },
      { text: "Neurotransmission (retrograde messenger in CNS)", options: { bullet: true, breakLine: true } },
      { text: "Bactericidal (iNOS — macrophage defense)", options: { bullet: true, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "Drugs Exploiting NO:", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "Nitrates (GTN, ISDN): Release NO → ↑cGMP → venodilation → ↓preload — angina", options: { bullet: true, breakLine: true } },
      { text: "Sildenafil/Tadalafil (PDE5 inhibitors): Prevent cGMP breakdown → prolonged NO effect — ED, PAH", options: { bullet: true, breakLine: true } },
      { text: "Sodium nitroprusside: Direct NO donor → acute hypertensive emergency", options: { bullet: true, breakLine: true } },
      { text: "Inhaled NO: Neonatal persistent pulmonary hypertension (PPHN)", options: { bullet: true } },
    ],
    "Synthesis & Mechanism",
    "Effects & Drugs"
  );

  footerNote(s, "NO half-life ~5 seconds. Rapidly inactivated by hemoglobin (forms methemoglobin). Classic: NO diffuses to muscle cell → binds sGC → ↑cGMP → relaxation. | Katzung");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 22 — PAF (Platelet Activating Factor)
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Platelet Activating Factor (PAF) & Natriuretic Peptides");

  twoColLayout(
    s,
    [
      { text: "Platelet Activating Factor (PAF)", options: { bold: true, color: C.red, breakLine: true } },
      { text: "Phospholipid mediator from membrane phosphatidylcholine", options: { breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "Actions:", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "↑Platelet aggregation (10,000x more potent than ADP)", options: { bullet: true, breakLine: true } },
      { text: "Bronchoconstriction, ↑vascular permeability, vasodilation", options: { bullet: true, breakLine: true } },
      { text: "Chemotaxis and activation of eosinophils, neutrophils", options: { bullet: true, breakLine: true } },
      { text: "Role in anaphylaxis, asthma, septic shock, ARDS", options: { bullet: true, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "PAF Receptor: GPCR (Gq) — present on platelets, lung, heart", options: { breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "Drug Relevance: No clinically established PAF antagonist yet; ginkgolides (from Ginkgo biloba) are natural PAF antagonists — under investigation", options: { italic: true, color: C.teal } },
    ],
    [
      { text: "Natriuretic Peptides", options: { bold: true, color: C.teal, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "ANP (Atrial Natriuretic Peptide):", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "Released from atria in response to ↑wall stretch (volume overload)", options: { bullet: true, breakLine: true } },
      { text: "↑Natriuresis, ↑diuresis, vasodilation, ↓aldosterone & renin", options: { bullet: true, breakLine: true } },
      { text: "Receptor: NPR-A → ↑cGMP (membrane guanylyl cyclase)", options: { bullet: true, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "BNP (Brain/B-type Natriuretic Peptide):", options: { bold: true, color: C.navy, breakLine: true } },
      { text: "Released from ventricles in heart failure — diagnostic biomarker", options: { bullet: true, breakLine: true } },
      { text: "Nesiritide (rh-BNP): acute decompensated HF (vasodilation + diuresis)", options: { bullet: true, breakLine: true } },
      { text: " ", options: { breakLine: true } },
      { text: "Sacubitril (ARNI): inhibits neprilysin → ↓BNP breakdown → ↑natriuresis. Combined with Valsartan (Entresto) — HFrEF first-line", options: { bullet: true, color: C.teal } },
    ],
    "PAF",
    "Natriuretic Peptides"
  );

  footerNote(s, "BNP > 100 pg/mL (or NT-proBNP > 300 pg/mL) supports diagnosis of heart failure. | Katzung / Harrison's");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 23 — CLINICAL PHARMACOLOGY SUMMARY TABLE
// ══════════════════════════════════════════════════════════════════
{
  const s = prs.addSlide();
  s.background = { color: C.offWhite };
  titleBar(s, "Quick-Reference: Autocoid Pharmacology Summary");

  const rows = [
    [
      { text: "Autocoid", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Key Enzymes / Synthesis", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Receptors", options: { bold: true, color: C.white, fill: C.navy } },
      { text: "Drugs Targeting It", options: { bold: true, color: C.white, fill: C.navy } },
    ],
    [
      { text: "Histamine", options: { bold: true, color: C.teal } },
      { text: "Histidine decarboxylase (L-histidine → histamine); metabolized by MAO/DAO", options: {} },
      { text: "H1, H2, H3, H4 (all GPCRs)", options: {} },
      { text: "H1-blockers (allergy), H2-blockers (PUD), Pitolisant (H3, narcolepsy)", options: {} },
    ],
    [
      { text: "Serotonin (5-HT)", options: { bold: true, color: C.teal } },
      { text: "Tryptophan hydroxylase + AAAD; metabolized by MAO-A → 5-HIAA", options: {} },
      { text: "5-HT1–7 (GPCRs), 5-HT3 (ion channel)", options: {} },
      { text: "Triptans (1B/1D), SSRIs (SERT), Setrons (5-HT3), Buspirone (5-HT1A)", options: {} },
    ],
    [
      { text: "Ergot alkaloids", options: { bold: true, color: C.orange } },
      { text: "Claviceps purpurea fungus (exogenous)", options: {} },
      { text: "5-HT, α-adrenergic, D2 receptors (partial agonist/antagonist)", options: {} },
      { text: "Ergotamine (migraine), Ergometrine (PPH), Bromocriptine (PD, prolactinoma)", options: {} },
    ],
    [
      { text: "Prostaglandins / TXA2 / PGI2", options: { bold: true, color: C.orange } },
      { text: "PLA2 → AA; COX-1/2 → PGH2; terminal synthases", options: {} },
      { text: "EP1–4, IP, TP, DP, FP receptors (GPCRs)", options: {} },
      { text: "NSAIDs / Aspirin (COX), Misoprostol (EP agonist), Latanoprost (FP), Epoprostenol (IP)", options: {} },
    ],
    [
      { text: "Leukotrienes", options: { bold: true, color: C.red } },
      { text: "5-LOX → LTA4 → LTB4 / LTC4 / LTD4 / LTE4", options: {} },
      { text: "BLT (LTB4), CysLT1, CysLT2", options: {} },
      { text: "Montelukast/Zafirlukast (CysLT1), Zileuton (5-LOX), Mepolizumab (anti-IL-5)", options: {} },
    ],
    [
      { text: "Bradykinin", options: { bold: true, color: C.cyan } },
      { text: "Kallikrein cleaves kininogens; degraded by ACE / kininase I", options: {} },
      { text: "B1 (inducible), B2 (constitutive) — Gq/Gi", options: {} },
      { text: "ACEi (↑BK → cough/angioedema), Icatibant (B2 antagonist — HAE)", options: {} },
    ],
    [
      { text: "Angiotensin II", options: { bold: true, color: C.cyan } },
      { text: "Renin (JGA) → Ang I; ACE (lung) → Ang II", options: {} },
      { text: "AT1 (Gq — vasoconstriction), AT2 (vasodilation)", options: {} },
      { text: "ACEi (-prils), ARBs (-sartans), Aliskiren (renin), Sacubitril+Valsartan (ARNI)", options: {} },
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      { text: "NOS (eNOS, nNOS, iNOS): L-Arg + O2 → NO", options: {} },
      { text: "sGC → ↑cGMP → PKG (no classic GPCR receptor)", options: {} },
      { text: "Nitrates (angina), Sildenafil (ED/PAH), SNP (hypertensive emergency), Inhaled NO (PPHN)", options: {} },
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  footerNote(s, "Comprehensive cross-reference of all major autocoid systems. Source: Katzung's Basic & Clinical Pharmacology, 16th Ed.");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 24 — HIGH-YIELD CLINICAL PEARLS
// ══════════════════════════════════════════════════════════════════
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    { icon: "💊", color: C.teal,   text: "ACE inhibitor cough is bradykinin-mediated (NOT histamine). Switch to ARB (e.g. losartan) — no cough." },
    { icon: "⚠️", color: C.red,    text: "Terfenadine/Astemizole (1st gen 2nd-gen antihistamines) WITHDRAWN: QT prolongation + CYP3A4 inhibitors → torsades de pointes." },
    { icon: "🩺", color: C.orange,  text: "Selective COX-2 inhibitors (coxibs) ↓PGI2 (protective) but not TXA2 → ↑CV thrombotic risk → rofecoxib withdrawn." },
    { icon: "🌡️", color: C.navy,   text: "Aspirin-exacerbated respiratory disease (AERD): COX inhibition shunts AA to 5-LOX → ↑cysteinyl LTs → bronchospasm. Use montelukast." },
    { icon: "🔬", color: C.cyan,   text: "5-HIAA in urine: marker for carcinoid syndrome (↑serotonin production from enterochromaffin cell tumors)." },
    { icon: "🏥", color: C.orange,  text: "Triptans (5-HT1B/1D agonists): CONTRAINDICATED in ischemic heart disease, uncontrolled hypertension, and within 24h of ergotamine (risk of coronary vasospasm)." },
    { icon: "💉", color: C.teal,   text: "Misoprostol (PGE1 analog): used for NSAID-induced ulcer prevention, cervical ripening, management of PPH, and medical abortion." },
    { icon: "🧬", color: C.red,    text: "Hereditary Angioedema (HAE): C1-esterase inhibitor deficiency → ↑bradykinin. Icatibant (B2 antagonist) or C1-INH concentrates for acute attacks. NOT responsive to antihistamines/steroids." },
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  footerNote(s, "High-yield exam & clinical pearls. Katzung's Basic & Clinical Pharmacology, 16th Ed.");
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 25 — CLOSING / THANK YOU
// ══════════════════════════════════════════════════════════════════
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  const summary = [
    "Autocoids = local hormones — act near their site of synthesis via specific receptors",
    "Histamine: H1 (allergy/bronchospasm), H2 (gastric acid), H3 (CNS presynaptic), H4 (immunity)",
    "Serotonin: 5-HT1B/1D (triptans — migraine), 5-HT3 (setrons — CINV), 5-HT4 (prokinetics)",
    "Eicosanoids: COX pathway (NSAIDs target) → prostaglandins & TXA2; LOX pathway → leukotrienes (LT-blockers for asthma)",
    "Bradykinin: ACE inhibitors block its degradation → ↑bradykinin → cough/angioedema",
    "Angiotensin II: ACEi (-prils), ARBs (-sartans), Aliskiren, ARNI (Entresto) — RAS drugs",
    "Nitric Oxide: eNOS → vasodilation via cGMP; nitrates, PDE5 inhibitors, inhaled NO — clinical applications",
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// ── SAVE ──────────────────────────────────────────────────────────
prs.writeFile({ fileName: "/home/daytona/workspace/autocoids-pptx/Autocoids_Pharmacology.pptx" })
  .then(() => console.log("DONE: /home/daytona/workspace/autocoids-pptx/Autocoids_Pharmacology.pptx"))
  .catch(e => { console.error(e); process.exit(1); });
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