const pptxgen = require("pptxgenjs");

const pres = new pptxgen();
pres.layout = "LAYOUT_WIDE"; // 13.3" x 7.5"
pres.title = "Pharmacology: Autonomic NS, Sedatives & Alcohol";
pres.author = "Pharmacology Lecture";

// ─── COLOR PALETTE ───────────────────────────────────────────────
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// ─── HELPER FUNCTIONS ────────────────────────────────────────────
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// ═══════════════════════════════════════════════════════════════════
// SLIDE 1 – TITLE SLIDE
// ═══════════════════════════════════════════════════════════════════
{
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  sl.background = { color: C.navy };

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  const topics = [
    "Basics of Pharmacology",
    "Pharmacology of the Autonomic Nervous System",
    "Sedatives & Sleeping Pills: Benzodiazepines, Barbiturates & Newer Agents",
    "Clinical Pharmacology of Alcohol & Its Antagonists",
  ];
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  sl.addText("Sources: Katzung's Basic & Clinical Pharmacology 16e | Goodman & Gilman's | Guyton & Hall", {
    x: 0.5, y: 7.24, w: 12.3, h: 0.3,
    fontSize: 9, color: C.textDim, align: "center", fontFace: "Calibri",
  });
}

// ═══════════════════════════════════════════════════════════════════
// SECTION 1 DIVIDER – BASICS OF PHARMACOLOGY
// ═══════════════════════════════════════════════════════════════════
sectionDivider(pres, "01", "Basics of Pharmacology", "Pharmacokinetics · Pharmacodynamics · Drug-Receptor Interactions");

// ─── SLIDE: What is Pharmacology? ────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "What is Pharmacology?", "Definition, Scope & Core Branches");

  addCard(sl, 0.3, 1.3, 6.1, 2.5, "Definition", [
    "Pharmacology: the science of how drugs interact with living systems",
    "Covers all aspects: absorption, distribution, metabolism, excretion (ADME)",
    "Distinguishes pharmacokinetics (what body does to drug) from pharmacodynamics (what drug does to body)",
    "Clinical pharmacology applies these principles to therapeutics",
  ]);

  addCard(sl, 6.7, 1.3, 6.1, 2.5, "Core Branches", [
    "Pharmacokinetics (PK): ADME — time-course of drug in body",
    "Pharmacodynamics (PD): dose-response relationships, receptor theory",
    "Toxicology: adverse & toxic effects",
    "Chemotherapy: drugs used against microorganisms/cancer",
    "Pharmacogenomics: genetic variation in drug response",
  ]);

  addCard(sl, 0.3, 4.0, 12.5, 2.85, "Key Terminology", [
    "Drug: any chemical agent that affects living processes",
    "Agonist: binds receptor and activates it | Antagonist: binds receptor but does NOT activate it",
    "Efficacy: maximum effect a drug can produce | Potency: amount of drug needed to produce 50% maximal effect (EC₅₀)",
    "Therapeutic index (TI): LD₅₀/ED₅₀ — measure of drug safety margin (higher = safer)",
    "Half-life (t½): time for plasma concentration to fall by 50%; determines dosing interval",
  ], { fontSize: 11 });
}

// ─── SLIDE: Pharmacokinetics ─────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Pharmacokinetics (PK)", "Absorption · Distribution · Metabolism · Excretion");

  // 4 PK boxes
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    {
      title: "ABSORPTION", bg: "102840", accent: C.accent,
      pts: [
        "Routes: oral (most common), IV (100% bioavailability), IM, SC, sublingual, transdermal",
        "First-pass effect: hepatic metabolism reduces oral bioavailability",
        "Bioavailability (F): fraction reaching systemic circulation",
        "Lipophilicity ↑ → faster absorption through membranes",
        "pKa & pH affect ionization → non-ionized forms cross membranes better",
      ]
    },
    {
      title: "DISTRIBUTION", bg: "102840", accent: C.gold,
      pts: [
        "Volume of distribution (Vd): theoretical volume at measured plasma concentration",
        "Plasma protein binding: albumin binds acidic drugs; only free drug is active",
        "Blood-brain barrier: tight junctions — only lipophilic / small molecules cross",
        "Placental transfer: lipophilic drugs cross easily — teratogenicity risk",
        "Highly perfused organs (brain, heart) equilibrate first",
      ]
    },
    {
      title: "METABOLISM", bg: "102840", accent: "E67E22",
      pts: [
        "Phase I: oxidation, reduction, hydrolysis (CYP450 enzymes — liver microsomes)",
        "Phase II: conjugation (glucuronidation, sulfation, acetylation) → water-soluble",
        "CYP3A4 metabolises ~50% of all drugs; CYP2D6 highly polymorphic",
        "Enzyme inducers (rifampin, phenytoin) speed metabolism → lower drug levels",
        "Enzyme inhibitors (azole antifungals, grapefruit) raise drug levels → toxicity risk",
      ]
    },
    {
      title: "EXCRETION", bg: "102840", accent: "27AE60",
      pts: [
        "Renal: glomerular filtration + tubular secretion − reabsorption",
        "Hepatic/biliary: large MW drugs → bile → enterohepatic recirculation",
        "Pulmonary: volatile anesthetics, ethanol (breathalyser)",
        "Creatinine clearance predicts renal drug clearance — dose-adjust in renal failure",
        "Clearance (CL): volume of plasma cleared of drug per unit time",
      ]
    },
  ];

  pkData.forEach((pk, i) => {
    const col = i % 2, row = Math.floor(i / 2);
    const x = col === 0 ? 0.25 : 6.8;
    const y = row === 0 ? 1.35 : 4.1;
    addCard(sl, x, y, 6.15, 2.55, pk.title, pk.pts, { accent: pk.accent, fontSize: 10, titleSize: 13 });
  });
}

// ─── SLIDE: Pharmacodynamics ─────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Pharmacodynamics (PD)", "Receptors · Dose-Response · Drug-Target Interactions");

  addCard(sl, 0.3, 1.3, 4.0, 5.5, "Receptor Types", [
    "Ionotropic (ligand-gated): fast (ms) — GABA-A, nAChR, NMDA",
    "Metabotropic (GPCR): slower (s) — adrenergic, muscarinic, opioid",
    "Enzyme-linked: RTKs — insulin, growth factors",
    "Nuclear / intracellular: steroid hormones, thyroid hormones",
    "Binding is reversible (mostly); obeys law of mass action",
    "KD = concentration at 50% receptor occupancy",
  ], { fontSize: 10.5 });

  addCard(sl, 4.55, 1.3, 4.25, 5.5, "Agonist / Antagonist Concepts", [
    "Full agonist: maximal intrinsic activity (Emax = 100%)",
    "Partial agonist: submaximal response even at 100% occupancy",
    "Inverse agonist: produces effect opposite to agonist",
    "Competitive antagonist: reversible; shifts dose-response curve RIGHT",
    "Non-competitive: irreversible; depresses Emax (insurmountable)",
    "Allosteric modulators: change receptor function without occupying orthosteric site",
    "Spare receptors: maximal effect before all receptors occupied",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 9.05, 1.3, 4.0, 5.5, "Key PD Concepts", [
    "Therapeutic index = LD₅₀ / ED₅₀",
    "High TI (e.g., penicillin) = safe; Low TI (digoxin, lithium, warfarin) = dangerous",
    "Tolerance: diminished response with repeated dosing",
    "Tachyphylaxis: rapid onset tolerance (receptor downregulation)",
    "Desensitisation: receptor unresponsiveness despite continued agonist",
    "Sensitisation: enhanced response after repeated low-dose exposure",
    "Drug synergism: additive (1+1=2) vs potentiation (1+1>2)",
  ], { fontSize: 10, titleSize: 12 });
}

// ═══════════════════════════════════════════════════════════════════
// SECTION 2 DIVIDER – AUTONOMIC NERVOUS SYSTEM
// ═══════════════════════════════════════════════════════════════════
sectionDivider(pres, "02", "Autonomic Nervous System", "Sympathetic · Parasympathetic · Drug Targets");

// ─── SLIDE: ANS Overview ─────────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Autonomic Nervous System — Overview", "Structural & Functional Organisation");

  addCard(sl, 0.3, 1.35, 6.0, 2.8, "Sympathetic Division ('Fight or Flight')", [
    "Pre-ganglionic: short, myelinated from T1–L2 (thoracolumbar outflow)",
    "Post-ganglionic: long, unmyelinated to effector organs",
    "Neurotransmitters: preganglionic → ACh (nAChR); postganglionic → Norepinephrine (NE)",
    "Adrenal medulla → EPI (80%) + NE (20%) directly to blood",
    "Receptors: α1, α2, β1, β2, β3 adrenoceptors on effectors",
  ], { fontSize: 10.5 });

  addCard(sl, 6.65, 1.35, 6.0, 2.8, "Parasympathetic Division ('Rest & Digest')", [
    "Pre-ganglionic: long, myelinated from CN III, VII, IX, X + S2–S4 (craniosacral)",
    "Post-ganglionic: short, unmyelinated — ganglia near/within target organ",
    "Neurotransmitters: both pre & post-ganglionic → ACh",
    "Post-ganglionic receptors: muscarinic (M1–M5) on effectors",
    "Vagus nerve (CN X) mediates 75% of all parasympathetic activity",
  ], { fontSize: 10.5 });

  addCard(sl, 0.3, 4.35, 12.4, 2.6, "Neurotransmitter Synthesis & Degradation", [
    "ACh synthesis: choline + acetyl-CoA → ACh (enzyme: ChAT) | Degradation: AChE → choline + acetate (fast, synaptic cleft)",
    "NE synthesis: Tyrosine → DOPA (TH) → Dopamine → NE (DBH) | Stored in vesicles | MAO & COMT degrade NE",
    "Reuptake: NE re-enters nerve terminal via NET (norepinephrine transporter) — major inactivation pathway",
    "Second messengers: α1 → IP3/DAG (Gq); α2 → ↓cAMP (Gi); β1/β2 → ↑cAMP (Gs); M2 → ↓cAMP (Gi); M1 → IP3 (Gq)",
  ], { fontSize: 11, titleSize: 13 });
}

// ─── SLIDE: Sympathomimetics ─────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Sympathomimetic Drugs", "Direct, Indirect & Mixed-Acting Adrenergic Agonists");

  addCard(sl, 0.3, 1.35, 4.1, 5.55, "Direct-Acting Agonists", [
    "Epinephrine (Adrenaline): α1, α2, β1, β2 — used in anaphylaxis, cardiac arrest",
    "Norepinephrine: α1, α2, β1 (no β2) — vasopressor in shock",
    "Phenylephrine: selective α1 — nasal decongestant, mydriasis",
    "Isoproterenol: β1 + β2 — bronchodilation, heart block (historical)",
    "Albuterol (Salbutamol): selective β2 — bronchodilator (asthma)",
    "Dobutamine: β1 selective — positive inotrope in heart failure",
    "Clonidine: α2 agonist (central) — antihypertensive, sedation",
  ], { fontSize: 10 });

  addCard(sl, 4.65, 1.35, 4.0, 5.55, "Indirect & Mixed Acting", [
    "Ephedrine: releases NE + direct — bronchodilator, nasal decongestant",
    "Tyramine: displaces NE from vesicles — dietary (aged cheese risk with MAOIs)",
    "Amphetamine: NE/DA release + uptake inhibition — stimulant",
    "Cocaine: blocks NET (NE reuptake) — local anaesthetic + sympathomimetic",
    "Key concept: indirect agents require endogenous NE — ineffective after reserpine",
  ], { fontSize: 10.5 });

  addCard(sl, 8.9, 1.35, 4.1, 5.55, "α & β Adrenoceptor Effects", [
    "α1: vasoconstriction (↑BP), mydriasis, GI/bladder relaxation",
    "α2 (presynaptic): inhibit NE release (autoreceptor); antihypertensive",
    "β1: ↑HR, ↑contractility (heart), ↑renin release (kidney)",
    "β2: bronchodilation, vasodilation, uterine relaxation, ↑glycogenolysis",
    "β3: lipolysis in adipose tissue",
    "Epinephrine at low dose → β2 (↓BP); high dose → α1 (↑BP)",
    "NE → predominant α effect → ↑BP → reflex bradycardia",
  ], { fontSize: 10 });
}

// ─── SLIDE: Sympatholytics & Adrenergic Blockers ─────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Adrenergic Blocking Drugs (Sympatholytics)", "Alpha-Blockers · Beta-Blockers · Ganglionic Blockers");

  addCard(sl, 0.3, 1.35, 6.3, 2.8, "Alpha (α) Blockers", [
    "Phenoxybenzamine: irreversible non-selective α1+α2 — phaeochromocytoma",
    "Phentolamine: reversible non-selective α — hypertensive crisis",
    "Prazosin / Terazosin: selective α1 — hypertension, BPH",
    "Yohimbine: selective α2 — research tool, erectile dysfunction",
    "Side effects: postural hypotension, reflex tachycardia, nasal stuffiness",
  ], { fontSize: 10.5 });

  addCard(sl, 6.85, 1.35, 6.1, 2.8, "Beta (β) Blockers", [
    "Propranolol: non-selective β1+β2 — angina, arrhythmia, hypertension, hyperthyroidism",
    "Atenolol / Metoprolol / Nebivolol: cardioselective β1 — hypertension, MI",
    "Carvedilol: α1 + β1 + β2 — heart failure, hypertension",
    "Labetalol: α1 + β — hypertensive emergencies, pregnancy hypertension",
    "Contraindicated in asthma (β2 blockade → bronchoconstriction), acute decompensated HF",
  ], { fontSize: 10.5 });

  addCard(sl, 0.3, 4.35, 6.3, 2.6, "Reserpine & Guanethidine", [
    "Reserpine: blocks vesicular monoamine transporter (VMAT) → depletes NE storage granules",
    "Guanethidine: blocks NE release from nerve endings",
    "Both used historically for hypertension; severe CNS side-effects limit use",
    "Reserpine → depression, nasal congestion, GI hypermotility",
  ], { fontSize: 10.5 });

  addCard(sl, 6.85, 4.35, 6.1, 2.6, "Ganglionic Blockers & Clinical Notes", [
    "Hexamethonium, Pentolinium: nAChR blockers at both sympathetic & parasympathetic ganglia",
    "Block ALL autonomic outflow — orthostatic hypotension, dry mouth, urinary retention",
    "Mainly used in research; trimethaphan (historical surgical hypotension)",
    "Remember: adrenergic blockers → unopposed parasympathetic activity",
  ], { fontSize: 10.5 });
}

// ─── SLIDE: Parasympathomimetics & Anticholinergics ──────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Cholinergic Drugs — Parasympathomimetics & Anticholinergics", "ACh Agonists & Antagonists");

  addCard(sl, 0.3, 1.35, 6.1, 2.7, "Direct-Acting Cholinomimetics", [
    "Pilocarpine: muscarinic — glaucoma (miosis + ↓IOP), Sjögren's syndrome",
    "Methacholine: muscarinic — bronchial challenge test (asthma diagnosis)",
    "Carbachol: muscarinic + nicotinic — glaucoma, bladder atony",
    "Bethanechol: selective muscarinic (M3) — urinary retention, GERD",
    "Muscarine: non-selective muscarinic — toxicology (mushroom poisoning)",
  ], { fontSize: 10.5 });

  addCard(sl, 6.65, 1.35, 6.3, 2.7, "Anticholinesterases (Indirect Cholinomimetics)", [
    "Neostigmine, Pyridostigmine: reversible AChE inhibitors — myasthenia gravis, NMB reversal",
    "Physostigmine: tertiary amine — crosses BBB — anticholinergic poisoning antidote",
    "Organophosphates (irreversible): nerve agents, pesticides → SLUDGE syndrome",
    "SLUDGE: Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis",
    "Treatment of OP poisoning: Atropine + Pralidoxime (reactivates AChE if given early)",
  ], { fontSize: 10.5 });

  addCard(sl, 0.3, 4.25, 12.6, 2.7, "Muscarinic Antagonists (Anticholinergics)", [
    "Atropine: competitive muscarinic antagonist — bradycardia, organophosphate poisoning, pre-op (dry secretions), ophthalmology (mydriasis/cycloplegia)",
    "Scopolamine: CNS penetrant — motion sickness, pre-op sedation",
    "Ipratropium / Tiotropium: inhaled — COPD, asthma (bronchodilation); minimal systemic effect",
    "Oxybutynin / Tolterodine: selective M3 — overactive bladder",
    "Side effects mnemonic — 'Dry as a bone, blind as a bat, red as a beet, hot as a hare, mad as a hatter, full as a flask'",
    "Contraindicated: narrow-angle glaucoma, BPH, pyloric stenosis",
  ], { fontSize: 10.5, titleSize: 12 });
}

// ═══════════════════════════════════════════════════════════════════
// SECTION 3 DIVIDER – SEDATIVES & SLEEPING PILLS
// ═══════════════════════════════════════════════════════════════════
sectionDivider(pres, "03", "Sedatives & Sleeping Pills", "Benzodiazepines · Barbiturates · Newer Hypnotics");

// ─── SLIDE: GABA-A Receptor & Mechanism ──────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "GABA-A Receptor — The Key Target of Sedative-Hypnotics", "Molecular Basis of CNS Depression");

  addCard(sl, 0.3, 1.35, 6.3, 5.5, "GABA-A Receptor Structure & Function", [
    "Pentameric ligand-gated Cl⁻ channel: most commonly α₂β₃γ₂ subunits",
    "GABA binds at β subunit interface → Cl⁻ influx → membrane hyperpolarisation → CNS inhibition",
    "Benzodiazepine site: at α-γ subunit interface (allosteric modulator)",
    "Barbiturate site: on β subunit transmembrane domain",
    "Neurosteroid site (e.g., allopregnanolone): separate allosteric site",
    "GABA-A diversity: α1 subunit mediates sedation/amnesia; α2 mediates anxiolysis/muscle relaxation",
    "Picrotoxin blocks the Cl⁻ channel (convulsant) — used in research",
    "GABA-B: metabotropic, coupled to Gi/K⁺ channels — baclofen target",
  ], { fontSize: 10.5 });

  addCard(sl, 6.85, 1.35, 6.1, 2.65, "How Benzodiazepines Work", [
    "Positive allosteric modulators — do NOT directly open the Cl⁻ channel",
    "Require GABA to be present — potentiate (↑frequency of) Cl⁻ channel opening",
    "Shift GABA dose-response curve LEFT (increase GABA sensitivity)",
    "Cannot cause maximal receptor activation alone — hence high safety margin vs barbiturates",
    "Subunit selectivity: α1 = sedation, α2/α3 = anxiolysis, α5 = memory",
  ], { fontSize: 10.5 });

  addCard(sl, 6.85, 4.2, 6.1, 2.65, "How Barbiturates Work", [
    "Also potentiate GABA-A, but at a different binding site",
    "At low concentrations: ↑DURATION of Cl⁻ channel opening (vs BZD ↑frequency)",
    "At high concentrations: directly activate Cl⁻ channel (without GABA) → overdose danger",
    "Also block AMPA/kainate (glutamate) receptors → additional CNS depression",
    "Steeper dose-response curve → narrow therapeutic index → lethal overdose easier",
  ], { fontSize: 10.5 });
}

// ─── SLIDE: Benzodiazepines ───────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Benzodiazepines (BZDs)", "Pharmacology, Classification & Clinical Uses");

  addCard(sl, 0.3, 1.35, 4.1, 5.5, "Pharmacokinetics", [
    "All highly lipid-soluble; oral absorption generally good",
    "Extensive plasma protein binding (albumin)",
    "Most undergo CYP3A4 hepatic metabolism → active/inactive metabolites",
    "Triazolam / Midazolam: ultra-short t½ (<6 h)",
    "Alprazolam / Lorazepam / Oxazepam: short-to-intermediate t½ (6–20 h)",
    "Diazepam / Clonazepam / Chlordiazepoxide: long t½ (20–100 h including active metabolites)",
    "Lorazepam / Oxazepam / Temazepam (LOT): conjugation only — safe in liver disease/elderly",
    "Clorazepate: prodrug → converted to desmethyldiazepam in stomach",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 4.65, 1.35, 4.5, 5.5, "Pharmacological Effects & Uses", [
    "Anxiolytic: panic disorder, GAD, social phobia",
    "Sedative-hypnotic: insomnia (short-term only)",
    "Anticonvulsant: diazepam IV (status epilepticus), clonazepam (absence/myoclonic)",
    "Muscle relaxant: spasticity (diazepam)",
    "Pre-operative sedation + amnesia: midazolam (most common)",
    "Alcohol withdrawal: chlordiazepoxide, diazepam, lorazepam",
    "Anterograde amnesia: therapeutically useful (procedures)",
    "All BZDs: cross placental barrier; teratogenic (cleft palate risk) in 1st trimester",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 9.4, 1.35, 3.6, 5.5, "ADRs & Dependence", [
    "CNS depression: sedation, psychomotor impairment, ↓driving ability",
    "Anterograde amnesia",
    "Respiratory depression: mild; severe with opioid co-use",
    "Paradoxical disinhibition: rage, aggression (elderly/paediatric)",
    "Physical dependence: ↑with dose & duration",
    "Withdrawal syndrome: anxiety, insomnia, tremors, seizures — taper slowly",
    "Tolerance: sedation > anxiolytic > anticonvulsant",
    "ANTIDOTE: Flumazenil (competitive BZD antagonist) — short t½ 0.7–1.3 h → re-sedation risk",
  ], { fontSize: 10, titleSize: 12 });
}

// ─── SLIDE: Barbiturates ──────────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Barbiturates", "Classification, Mechanism & Clinical Uses");

  addCard(sl, 0.3, 1.35, 4.1, 5.5, "Classification by Duration", [
    "Ultra-short acting (IV): Thiopental, Methohexital",
    "  – IV anaesthesia induction; t½ 5–10 min (redistribution)",
    "Short acting: Secobarbital, Pentobarbital",
    "  – Sedation/sleep; t½ 15–40 h",
    "Intermediate: Amobarbital",
    "  – Anxiety, insomnia; t½ 20–40 h",
    "Long-acting: Phenobarbital",
    "  – Epilepsy (grand mal, partial); t½ 80–120 h",
    "Very long-acting: Primidone",
    "  – Prodrug → phenobarbital; epilepsy",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 4.65, 1.35, 4.5, 5.5, "Pharmacokinetics & Metabolism", [
    "Absorbed well orally; thiopental IV for rapid CNS entry",
    "High lipid solubility → rapid brain penetration (thiopental)",
    "Redistribution from brain → fat/muscle → anaesthesia wears off quickly",
    "Hepatic metabolism by CYP2C9/CYP2C19/CYP3A4",
    "Phenobarbital: potent CYP enzyme inducer → numerous drug interactions",
    "Induces metabolism of: oral contraceptives, warfarin, corticosteroids, tricyclics",
    "Alkalinisation of urine (NaHCO₃) accelerates renal excretion in overdose",
    "Crosses placenta & breast milk; neonatal depression",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 9.4, 1.35, 3.6, 5.5, "Toxicity & Comparison with BZDs", [
    "Severe CNS depression → coma, respiratory arrest",
    "NO antidote available (unlike BZDs → flumazenil)",
    "Low therapeutic index — lethal overdose common",
    "Classic method of self-poisoning (Monroe, Marilyn reference)",
    "Tolerance develops rapidly; profound physical dependence",
    "Withdrawal: dangerous (seizures, death) — must taper",
    "Porphyria: barbiturates induce ALA synthase → contraindicated in porphyria",
    "Largely replaced by BZDs for anxiety/insomnia (safer); phenobarbital retained for epilepsy",
  ], { fontSize: 10, titleSize: 12 });
}

// ─── SLIDE: Newer Sleeping Pills ─────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Newer Sleeping Pills (Non-Benzodiazepine Hypnotics)", "Z-Drugs · Melatonin Agonists · Orexin Antagonists");

  addCard(sl, 0.3, 1.35, 6.2, 2.7, "Z-Drugs (Non-BZD BZD-Receptor Agonists)", [
    "Zolpidem (Ambien): selective for GABA-A α1 subunit — short t½ ~2.5 h; sedation > anxiolysis",
    "Zaleplon: ultra-short t½ 1 h; minimal residual sedation; take just before sleep",
    "Eszopiclone: longer t½ ~6 h; approved for chronic insomnia",
    "Zopiclone (racemic parent of eszopiclone): widely used in Europe",
    "All antagonised by flumazenil; less dependence than BZDs; complex sleep behaviours (sleep-walking, sleep-driving) reported",
  ], { fontSize: 10.5 });

  addCard(sl, 6.75, 1.35, 6.2, 2.7, "Melatonin & Ramelteon", [
    "Melatonin: endogenous hormone from pineal gland; regulates circadian rhythm; MT1/MT2 receptors",
    "Ramelteon: MT1/MT2 agonist — approved for sleep-onset insomnia; no abuse potential; no dependence",
    "No next-day sedation at therapeutic doses; safe in the elderly",
    "Melatonin supplements: jet-lag, shift-work sleep disorder",
    "Tasimelteon: MT1/MT2 agonist — non-24-hour sleep-wake disorder (blind patients)",
  ], { fontSize: 10.5 });

  addCard(sl, 0.3, 4.2, 6.2, 2.7, "Orexin (Hypocretin) Receptor Antagonists", [
    "Suvorexant (Belsomra): dual orexin receptor antagonist (DORA) — blocks OX1R & OX2R",
    "Lemborexant: newer DORA; approved for chronic insomnia disorder",
    "Mechanism: orexin promotes wakefulness; blocking it promotes sleep (natural)")  ,
    "Advantages: no dependence, minimal respiratory depression, no abuse liability",
    "Side effects: next-day impairment, abnormal dreams, sleep paralysis",
  ], { fontSize: 10.5 });

  addCard(sl, 6.75, 4.2, 6.2, 2.7, "Other Agents & Clinical Comparison", [
    "Doxylamine / Diphenhydramine: antihistamine OTC sleep aids; muscarinic blockade — tolerance develops quickly",
    "Trazodone: antidepressant; widely used off-label for insomnia (5-HT2 block)",
    "Melatonin: low-dose (0.5–3 mg) most effective; timing matters more than dose",
    "Ideal hypnotic: fast onset, appropriate duration, no residual sedation, no dependence",
    "CBT-I (cognitive behavioural therapy for insomnia) = first-line treatment by guidelines",
  ], { fontSize: 10.5 });
}

// ─── SLIDE: Flumazenil (BZD Antagonist) ──────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Benzodiazepine Antagonist — Flumazenil", "Pharmacology & Clinical Use");

  addCard(sl, 0.3, 1.35, 8.4, 5.5, "Flumazenil", [
    "Competitive antagonist at the BZD binding site of GABA-A receptor",
    "Blocks actions of BZDs, zolpidem, zaleplon, eszopiclone — does NOT block barbiturates, ethanol, opioids",
    "Route: IV only; onset: 1–2 min; duration 30–60 min; t½ 0.7–1.3 h",
    "Hepatic clearance is rapid → re-sedation common with long-acting BZDs → repeated dosing required",
    "Indications: BZD overdose reversal; reversal post-procedural sedation",
    "CAUTION — precipitates withdrawal seizures in BZD-dependent patients",
    "In tricyclic overdose + BZDs: may unmask cardiac arrhythmias and seizures — use with extreme caution",
    "Respiratory depression reversal is less predictable than sedation reversal",
    "Does NOT reverse amnesia if already consolidated",
  ], { fontSize: 11 });

  addCard(sl, 9.0, 1.35, 4.0, 5.5, "Clinical Pearls", [
    "Always observe for re-sedation — flumazenil wears off BEFORE most BZDs",
    "Dose: 0.2 mg IV over 30 sec; max 3 mg total",
    "Not recommended for routine reversal of procedural sedation",
    "Does NOT reverse BZD-induced anterograde amnesia",
    "No role in empirical treatment of unknown coma (misleading results)",
    "Naloxone for opioids; flumazenil for BZDs — remember the pair",
  ], { fontSize: 11 });
}

// ═══════════════════════════════════════════════════════════════════
// SECTION 4 DIVIDER – ALCOHOL
// ═══════════════════════════════════════════════════════════════════
sectionDivider(pres, "04", "Clinical Pharmacology of Alcohol", "Ethanol · Withdrawal · Treatment of AUD");

// ─── SLIDE: Pharmacology of Ethanol ──────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Pharmacology of Ethanol (Alcohol)", "Mechanism of Action & Acute Effects");

  addCard(sl, 0.3, 1.35, 6.2, 5.5, "Mechanism of CNS Action", [
    "Ethanol is a CNS DEPRESSANT — classified as sedative-hypnotic",
    "Enhances GABA-A receptor function (like BZDs/barbiturates) — ↑Cl⁻ influx",
    "Inhibits NMDA glutamate receptors (excitatory) → sedation, ataxia, amnestic blackouts",
    "Inhibits voltage-gated Ca²⁺ channels; enhances glycine receptors",
    "Low doses: apparent stimulation = disinhibition (inhibits inhibitory neurons)",
    "Cross-tolerance with benzodiazepines, barbiturates, and general anaesthetics",
    "Potent inhibitor of adenylyl cyclase via Gi coupling",
    "Chronic use: upregulation of NMDA receptors + downregulation of GABA-A → neuroadaptation → withdrawal syndrome",
  ], { fontSize: 10.5 });

  addCard(sl, 6.75, 1.35, 6.2, 2.8, "Blood Alcohol Concentration (BAC) & Effects", [
    "20–50 mg/dL: mild relaxation, ↑sociability",
    "50–100 mg/dL: ↓coordination, impaired judgment, euphoria",
    "100–150 mg/dL: ataxia, slurred speech, legally impaired in most countries",
    "150–250 mg/dL: staggering gait, nausea, marked cognitive impairment",
    "250–350 mg/dL: stupor, possible coma",
    ">400 mg/dL: potentially lethal — respiratory depression",
    "Acquired tolerance: alcoholics tolerate >300 mg/dL without gross sedation",
  ], { fontSize: 10 });

  addCard(sl, 6.75, 4.35, 6.2, 2.55, "Pharmacokinetics of Ethanol", [
    "Absorption: rapid oral → stomach + small intestine; food slows absorption",
    "Distribution: Vd ~0.6 L/kg (similar to total body water); crosses BBB & placenta freely",
    "Metabolism: zero-order kinetics at drinking doses — ~10 mL/hour",
    "Alcohol dehydrogenase (ADH): ethanol → acetaldehyde (toxic)",
    "Aldehyde dehydrogenase (ALDH): acetaldehyde → acetate",
    "CYP2E1 (MEOS): induced by chronic ethanol use; metabolises at high BAC",
    "Genetic variation: Asian ALDH2 deficiency → 'Asian flush' (↑acetaldehyde)",
  ], { fontSize: 10 });
}

// ─── SLIDE: Alcohol Withdrawal ────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Alcohol Withdrawal Syndrome", "Pathophysiology, Timeline & Management");

  addCard(sl, 0.3, 1.35, 4.3, 5.5, "Pathophysiology", [
    "Chronic alcohol use → neuroadaptation:",
    "  ↓GABA-A receptor function (downregulation)",
    "  ↑NMDA receptor upregulation + ↑excitatory tone",
    "On cessation: loss of GABAergic inhibition + unmasked excitation",
    "CNS becomes hyperexcitable → withdrawal symptoms",
    "Similar mechanism to BZD withdrawal",
    "Severity correlates with duration and amount of drinking",
    "Prior withdrawal episodes worsen subsequent ones ('kindling' effect)",
  ], { fontSize: 10.5 });

  addCard(sl, 4.85, 1.35, 4.3, 5.5, "Timeline of Withdrawal", [
    "0–6 hours: tremor, irritability, nausea, tachycardia, hypertension",
    "6–48 hours: withdrawal seizures (generalised tonic-clonic)",
    "12–48 hours: alcoholic hallucinosis (visual > auditory > tactile)",
    "48–96 hours: Delirium Tremens (DT) — peak danger",
    "DT features: severe agitation, confusion, fever, profuse sweating, tachycardia, dilated pupils",
    "DT mortality: 1–5% (historically up to 20%) — medical emergency",
    "CIWA-Ar scale: quantifies withdrawal severity for treatment decisions",
  ], { fontSize: 10.5 });

  addCard(sl, 9.4, 1.35, 3.6, 5.5, "Treatment", [
    "Benzodiazepines: FIRST-LINE for alcohol withdrawal",
    "Diazepam or chlordiazepoxide (long t½) — symptom-triggered or fixed schedule",
    "Lorazepam / Oxazepam: preferred in liver disease (no active metabolites)",
    "IV thiamine (B1) FIRST before glucose — prevent Wernicke's encephalopathy",
    "Fluid & electrolyte correction: Mg²⁺, K⁺, PO₄",
    "Anticonvulsants: carbamazepine — effective in mild/moderate withdrawal",
    "Beta-blockers (propranolol), clonidine: adjuncts to reduce autonomic symptoms",
    "ICU for DT: diazepam IV, antipsychotics if hallucinations persist",
  ], { fontSize: 10, titleSize: 12 });
}

// ─── SLIDE: Alcohol-Related Disorders ────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Chronic Alcohol Use — Organ Toxicity & Nutritional Deficiencies", "Systemic Complications of AUD");

  const compData = [
    { title: "CNS", pts: ["Wernicke's encephalopathy: thiamine deficiency → ophthalmoplegia, ataxia, confusion", "Korsakoff's syndrome: irreversible amnesia, confabulation (thiamine-prevent)", "Peripheral neuropathy: demyelination (B1, B6, folate deficiency)", "Cerebellar degeneration: truncal ataxia", "Alcohol-related dementia"] },
    { title: "Liver", pts: ["Fatty liver (steatosis): reversible", "Alcoholic hepatitis: AST:ALT >2:1", "Cirrhosis: irreversible fibrosis; portal hypertension", "Hepatocellular carcinoma: long-term risk"] },
    { title: "Cardiovascular", pts: ["Dilated cardiomyopathy (alcoholic)", "Holiday heart syndrome: arrhythmias (AF) after binge", "Moderate intake: ↑HDL — J-shaped mortality curve"] },
    { title: "GI & Pancreas", pts: ["Acute/chronic pancreatitis", "Mallory-Weiss tear: oesophageal tears", "Oesophageal varices (cirrhosis)", "Gastritis, duodenal ulceration"] },
    { title: "Metabolic", pts: ["Hypoglycaemia: blocks gluconeogenesis", "Hyperuricaemia → gout attack", "↑Triglycerides; ketoacidosis", "Hypomagnesaemia, hypophosphataemia"] },
    { title: "Reproductive", pts: ["Fetal Alcohol Spectrum Disorder (FASD)", "Facial abnormalities, cognitive impairment", "Growth retardation — no safe dose in pregnancy", "In males: gonadal atrophy, ↓testosterone, gynaecomastia"] },
  ];

  compData.forEach((c, i) => {
    const col = i % 3;
    const row = Math.floor(i / 3);
    const x = 0.3 + col * 4.35;
    const y = 1.35 + row * 2.9;
    addCard(sl, x, y, 4.1, 2.7, c.title, c.pts, { fontSize: 10, titleSize: 12, accent: C.gold });
  });
}

// ─── SLIDE: Alcohol Antagonists / Treatment of AUD ───────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Treatment of Alcohol Use Disorder (AUD)", "FDA-Approved Pharmacotherapies & Adjuncts");

  addCard(sl, 0.3, 1.35, 4.1, 5.5, "Disulfiram (Antabuse)", [
    "Mechanism: irreversibly inhibits ALDH → acetaldehyde accumulates",
    "Disulfiram-ethanol reaction (DER): flushing, nausea, vomiting, palpitations, hypotension, chest pain",
    "Deterrence-based approach — patient must CHOOSE to take it",
    "Dose: 250–500 mg/day orally",
    "Onset of effect: alcohol must be avoided for 2+ weeks after stopping disulfiram",
    "Drug interactions: warfarin potentiation (↓metabolism), metronidazole (psychosis)",
    "Contraindications: heart disease, severe hepatic disease, psychosis",
    "Not proven effective in RCTs — poor compliance is the main limitation",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 4.65, 1.35, 4.5, 5.5, "Naltrexone", [
    "Mechanism: opioid receptor antagonist (μ, κ, δ) — blocks endorphin-mediated reward of drinking",
    "Reduces craving and relapse to heavy drinking",
    "Oral: 50 mg/day; Extended-release IM (Vivitrol): 380 mg/month",
    "IM formulation: improves compliance, avoids first-pass",
    "Evidence: consistent reduction in heavy drinking days (multiple RCTs)",
    "Side effects: nausea, hepatotoxicity (rare at therapeutic doses), insomnia",
    "Contraindicated in current opioid use — precipitates acute withdrawal",
    "Most effective combined with behavioural therapy",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 9.4, 1.35, 3.6, 5.5, "Acamprosate & Other Agents", [
    "Acamprosate (Campral):",
    "  NMDA antagonist + GABA modulator",
    "  Reduces glutamate-driven craving & anxiety during abstinence",
    "  Dose: 666 mg TID; renal excretion (safe in liver disease)",
    "  Best for: already abstinent patients with cravings",
    "Nalmefene: opioid antagonist; as-needed dosing; ↓heavy drinking days (EU-approved)",
    "Gabapentin: off-label; reduces withdrawal/cravings; esp. for insomnia in AUD",
    "Baclofen: GABA-B agonist; some evidence in AUD; liver-safe; controversial",
    "Ondansetron: 5-HT3 antagonist; early-onset AUD (<25 years) — reduces drinking",
  ], { fontSize: 10, titleSize: 11.5 });
}

// ─── SLIDE: Methanol & Ethylene Glycol Poisoning ─────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Methanol & Ethylene Glycol Toxicity — Alcohol-Related Toxicology", "Antidotes & Mechanism");

  addCard(sl, 0.3, 1.35, 6.2, 5.5, "Methanol Poisoning", [
    "Source: industrial solvent, illicit alcohol ('moonshine')",
    "Metabolism: ADH converts methanol → formaldehyde → formic acid (TOXIC)",
    "Formic acid: inhibits cytochrome c oxidase → severe metabolic acidosis + optic nerve toxicity",
    "Clinical: latent period 12–24 h; then visual disturbance ('snowfield' vision), blindness, severe anion-gap acidosis",
    "Treatment: Fomepizole (4-MP) — competitive ADH inhibitor; FIRST-LINE antidote",
    "Ethanol IV: also ADH competitor (historical); now replaced by fomepizole",
    "Folinic acid (leucovorin): enhances formate metabolism",
    "Haemodialysis: for severe acidosis or visual impairment",
  ], { fontSize: 10.5 });

  addCard(sl, 6.75, 1.35, 6.2, 5.5, "Ethylene Glycol Poisoning", [
    "Source: antifreeze — sweet taste → accidental/intentional ingestion",
    "Metabolism: ADH → glycolic acid → oxalic acid → calcium oxalate crystals",
    "Clinical stages:",
    "  Stage 1 (0–12 h): apparent intoxication (no ethanol smell)",
    "  Stage 2 (12–24 h): cardiopulmonary — HF, ARDS",
    "  Stage 3 (24–72 h): renal failure — calcium oxalate crystal nephropathy",
    "Lab: severe anion-gap acidosis, hypocalcaemia, oxalate crystals in urine",
    "Treatment: Fomepizole (inhibits ADH); IV ethanol (if fomepizole unavailable)",
    "Pyridoxine (B6) + thiamine (B1) + magnesium: redirect metabolism away from oxalate",
    "Haemodialysis: definitive treatment",
  ], { fontSize: 10 });
}

// ─── SLIDE: Summary Table ─────────────────────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Comparative Summary — Sedative-Hypnotics & Alcohol Antagonists", "Quick Reference Table");

  const rows = [
    ["Drug Class", "Mechanism", "Main Uses", "Antidote / Treatment", "Key Concern"],
    ["Benzodiazepines", "GABA-A ↑ (↑freq Cl⁻)", "Anxiety, insomnia, seizures, withdrawal", "Flumazenil", "Dependence, re-sedation"],
    ["Barbiturates", "GABA-A ↑ (↑duration Cl⁻) + direct", "Epilepsy (phenobarb), anaesthesia", "None", "Low TI, lethal OD"],
    ["Z-Drugs (Zolpidem etc.)", "GABA-A α1 selective", "Insomnia (short-term)", "Flumazenil (partial)", "Sleep behaviours"],
    ["Ramelteon", "MT1/MT2 agonist", "Sleep-onset insomnia", "N/A", "Minimal — no abuse"],
    ["Suvorexant", "Orexin (OX1R/OX2R) blocker", "Chronic insomnia", "N/A", "Sleep paralysis, dreams"],
    ["Ethanol (acute)", "GABA-A ↑, NMDA ↓", "—", "Supportive", "Respiratory depression"],
    ["Disulfiram", "ALDH inhibitor", "AUD deterrence", "Avoid EtOH; vitamin C", "DER, compliance poor"],
    ["Naltrexone", "Opioid receptor antagonist", "AUD, opioid use disorder", "Opioid agonist (if needed)", "Liver toxicity, opioid CI"],
    ["Acamprosate", "NMDA antagonist / GABA mod.", "AUD abstinence maintenance", "N/A", "Renally excreted"],
    ["Fomepizole", "ADH inhibitor", "Methanol / EG poisoning", "N/A (IS the antidote)", "Expensive"],
  ];

  const colW = [2.2, 2.5, 2.8, 2.3, 2.3];
  const colX = [0.2, 2.42, 4.92, 7.72, 10.02];
  const rowH = 0.48;
  const rowY0 = 1.3;

  rows.forEach((row, ri) => {
    const bg = ri === 0 ? C.midBlue : (ri % 2 === 0 ? C.lightBg : C.cardBg);
    const textColor = ri === 0 ? C.accent : C.white;
    const isBold = ri === 0;

    row.forEach((cell, ci) => {
      sl.addShape(pres.ShapeType.rect, {
        x: colX[ci], y: rowY0 + ri * rowH, w: colW[ci], h: rowH,
        fill: { color: bg },
        line: { color: C.midBlue, width: 0.5 },
      });
      sl.addText(cell, {
        x: colX[ci] + 0.05, y: rowY0 + ri * rowH, w: colW[ci] - 0.1, h: rowH,
        fontSize: ri === 0 ? 10 : 9, bold: isBold, color: textColor,
        valign: "middle", fontFace: "Calibri", margin: 2,
        wrap: true,
      });
    });
  });
}

// ─── SLIDE: Key Mnemonics & Exam Points ──────────────────────────
{
  const sl = pres.addSlide();
  darkSlide(sl);
  addTitle(sl, "Key Mnemonics & High-Yield Exam Points", "Memory Aids for Pharmacology");

  addCard(sl, 0.3, 1.35, 4.1, 5.5, "Mnemonics", [
    "SLUDGE (cholinergic toxicity): Salivation, Lacrimation, Urination, Defecation, GI cramps, Emesis",
    "LOT (BZDs safe in liver disease): Lorazepam, Oxazepam, Temazepam",
    "ABC of alcohol Rx: Acamprosate, disulfiram (B sounds like antaBuse), Craving→Naltrexone",
    "MNEMONIC for anticholinergic OD: Dry as bone, Blind as bat, Red as beet, Hot as hare, Mad as hatter, Full as flask",
    "Wernicke's = COAT: Confusion, Ophthalmoplegia, Ataxia, Thiamine-responsive",
  ], { fontSize: 10.5 });

  addCard(sl, 4.65, 1.35, 4.5, 5.5, "High-Yield Comparisons", [
    "BZD vs Barbiturate: BZD potentiates GABA (safe); Barb also activates directly (dangerous)",
    "BZD vs Z-drug: Z-drugs are BZD-receptor agonists — all blocked by flumazenil",
    "Disulfiram vs Naltrexone: disulfiram deters (aversive); naltrexone reduces reward/craving",
    "Methanol vs Ethylene glycol: both treated by ADH inhibition (fomepizole); MeOH → blindness; EG → renal failure",
    "Lorazepam in liver disease (no active metabolites); diazepam has active desmethyldiazepam",
    "Flumazenil short t½ → re-sedation; NEVER use in chronic BZD users (seizure risk)",
  ], { fontSize: 10, titleSize: 12 });

  addCard(sl, 9.4, 1.35, 3.6, 5.5, "Clinical Pearls", [
    "Thiamine BEFORE glucose in alcoholics — prevents Wernicke's",
    "Alcohol cross-tolerant with BZDs — need higher BZD doses in severe withdrawal",
    "Phenobarbital: strong CYP inducer — lowers OCP, warfarin, antiretroviral levels",
    "Orexin antagonists: no respiratory depression — safer in COPD/sleep apnoea",
    "Acamprosate: renal excretion — safe in liver disease (unlike naltrexone)",
    "Fetal Alcohol Syndrome: most preventable cause of intellectual disability",
    "Propranolol contraindicated in asthma — use cardioselective β1 blocker instead",
  ], { fontSize: 10, titleSize: 12 });
}

// ─── FINAL SLIDE ─────────────────────────────────────────────────
{
  const sl = pres.addSlide();
  sl.background = { color: C.darkBlue };

  sl.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 13.3, h: 0.2, fill: { color: C.accent }, line: { color: C.accent } });
  sl.addShape(pres.ShapeType.rect, { x: 0, y: 7.3, w: 13.3, h: 0.2, fill: { color: C.gold }, line: { color: C.gold } });

  sl.addText("THANK YOU", {
    x: 0.5, y: 1.2, w: 12.3, h: 1.4,
    fontSize: 72, bold: true, color: C.accent, align: "center", fontFace: "Calibri", charSpacing: 10,
  });

  sl.addText("Pharmacology Lecture Series", {
    x: 0.5, y: 2.7, w: 12.3, h: 0.6,
    fontSize: 24, color: C.gold, align: "center", italic: true, fontFace: "Calibri",
  });

  sl.addShape(pres.ShapeType.rect, { x: 3, y: 3.45, w: 7.3, h: 0.05, fill: { color: C.midBlue }, line: { color: C.midBlue } });

  const sources = [
    "Katzung's Basic & Clinical Pharmacology, 16th Edition",
    "Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 14th Edition",
    "Guyton & Hall Textbook of Medical Physiology",
    "Tintinalli's Emergency Medicine | The Maudsley Prescribing Guidelines, 15th Edition",
  ];
  const sItems = sources.map((s, i) => ({
    text: `• ${s}`,
    options: { breakLine: i < sources.length - 1, fontSize: 13, color: C.gray, fontFace: "Calibri" }
  }));
  sl.addText("Key References:", {
    x: 2, y: 3.6, w: 9.3, h: 0.4,
    fontSize: 14, bold: true, color: C.textDim, align: "center", fontFace: "Calibri",
  });
  sl.addText(sItems, {
    x: 2, y: 4.1, w: 9.3, h: 2.5, align: "center", valign: "top",
  });
}

// ─── WRITE FILE ───────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/pharmacology-pptx/Pharmacology_Complete.pptx" })
  .then(() => console.log("✅ Presentation saved successfully!"))
  .catch(e => { console.error("❌ Error:", e); process.exit(1); });

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/pharmacology-pptx/build.js'