const pptxgen = require("pptxgenjs");
const pres = new pptxgen();
pres.layout = 'LAYOUT_16x9';
pres.title = 'Haem Metabolism, Metabolic Cycles & Vitamins';
pres.author = 'PGIMS Biochemistry Department';

// ─── COLOR PALETTE ───────────────────────────────────────────────────────────
const C = {
  darkBg:    '0D1B2A',  // Deep navy (title/section slides)
  midBg:     '1B2A3B',  // Slightly lighter navy
  cardBg:    '162032',  // Card background
  accent1:   'E63946',  // Red accent (haem = blood)
  accent2:   '2EC4B6',  // Teal accent
  accent3:   'F4A261',  // Warm orange accent (vitamins)
  accent4:   '8338EC',  // Purple (metabolic cycles)
  white:     'FFFFFF',
  offWhite:  'E8EEF4',
  yellow:    'FFD166',
  lightBlue: 'A8DADC',
  green:     '06D6A0',
  subtext:   'B0C4D8',
};

// ─── HELPER FUNCTIONS ─────────────────────────────────────────────────────────
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// ══════════════════════════════════════════════════════════════════════════════
// SLIDE 1 — TITLE
// ══════════════════════════════════════════════════════════════════════════════
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// ══════════════════════════════════════════════════════════════════════════════
// SLIDE 2 — TABLE OF CONTENTS
// ══════════════════════════════════════════════════════════════════════════════
{
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    {n:'SECTION 1', label:'HAEM METABOLISM', color:C.accent1, desc:'Synthesis · Porphyrias · Degradation · Jaundice · Bilirubin'},
    {n:'SECTION 2', label:'METABOLIC CYCLES', color:C.accent4, desc:'TCA Cycle · Urea Cycle · Cori Cycle · Glucose-Alanine Cycle'},
    {n:'SECTION 3', label:'VITAMINS', color:C.accent3, desc:'Fat-Soluble (A, D, E, K) · Water-Soluble (B-complex, C)'},
    {n:'SECTION 4', label:'EXAM QUESTIONS', color:C.green, desc:'MCQs · Short Answer · Clinical Scenarios'},
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// ══════════════════════════════════════════════════════════════════════════════
// SECTION 1 — HAEM METABOLISM
// ══════════════════════════════════════════════════════════════════════════════
addSectionSlide('HAEM METABOLISM', C.accent1);

// Slide — Structure of Haem
addContentSlide('Structure of Haem', [
  {text:'KEY CONCEPT', isHeader:true},
  {text:'Haem = Iron-containing porphyrin compound (Protoporphyrin IX + Fe²⁺)', color:C.lightBlue},
  {text:'Four pyrrole rings linked by methene bridges → porphyrin ring system', color:C.offWhite},
  {text:'Iron held in centre by coordinate bonds — can be Fe²⁺ (ferrous) or Fe³⁺ (ferric)', color:C.offWhite},
  {text:''},
  {text:'FUNCTIONS OF HAEM', isHeader:true},
  {text:'Haemoglobin — O₂/CO₂ transport (α₂β₂ tetramer, 4 haem groups)'},
  {text:'Myoglobin — O₂ storage in muscle (single haem)'},
  {text:'Cytochromes — Electron transport chain (ETC)'},
  {text:'Catalase & Peroxidase — Antioxidant enzymes'},
  {text:'Cytochrome P450 — Drug metabolism (liver)'},
  {text:''},
  {text:'MNEMONIC: "HMCCP" = Haemoglobin, Myoglobin, Cytochromes, Catalase, P450', color:C.yellow, isHeader:false},
], {headerColor:C.accent1});

// Slide — Haem Synthesis Overview
addContentSlide('Haem Synthesis — Step-by-Step Pathway', [
  {text:'SITE: Erythroid cells (80%) + Liver (20%)', isHeader:true},
  {text:'Mitochondria (steps 1 & last 3) ↔ Cytosol (middle steps)', color:C.accent2},
  {text:''},
  {text:'STEP 1 (Mitochondria): Succinyl-CoA + Glycine → ALA', isHeader:true},
  {text:'Enzyme: ALA Synthase (rate-limiting enzyme, requires PLP = Vit B6)'},
  {text:'Inhibited by: Haem (feedback), Glucose, Steroids; Induced by: Lead, Drugs (barbiturates)'},
  {text:''},
  {text:'STEP 2 (Cytosol): 2 ALA → Porphobilinogen (PBG)', isHeader:true},
  {text:'Enzyme: ALA Dehydratase (PBG Synthase) — most sensitive to LEAD poisoning'},
  {text:''},
  {text:'STEP 3–5 (Cytosol): PBG → Uroporphyrinogen III → Coproporphyrinogen III', isHeader:true},
  {text:'PBG Deaminase (HMBS) → Uroporphyrinogen III synthase → Uroporphyrinogen III decarboxylase'},
  {text:''},
  {text:'STEP 6–7 (Mitochondria): Coproporphyrinogen III → Protoporphyrin IX', isHeader:true},
  {text:'Coproporphyrinogen oxidase → Protoporphyrinogen oxidase'},
  {text:''},
  {text:'STEP 8 (Mitochondria): Protoporphyrin IX + Fe²⁺ → HAEM', isHeader:true},
  {text:'Enzyme: Ferrochelatase (Haem Synthase) — also inhibited by LEAD'},
], {headerColor:C.accent1});

// Slide — Lead Poisoning & Porphyrias summary table
addTableSlide('Regulation of Haem Synthesis & Lead Poisoning',
  ['Enzyme', 'Reaction', 'Inhibited By', 'Clinical Relevance'],
  [
    ['ALA Synthase', 'Succinyl-CoA + Gly → ALA', 'Haem (feedback), Glucose', 'Rate-limiting; induced by barbiturates'],
    ['ALA Dehydratase', '2 ALA → PBG', 'LEAD (most sensitive)', 'Basophilic stippling; ↑ urinary ALA'],
    ['PBG Deaminase', 'PBG → Hydroxymethylbilane', 'Deficient in AIP', 'Acute Intermittent Porphyria'],
    ['Ferrochelatase', 'Proto IX + Fe²⁺ → Haem', 'LEAD', '↑ free protoporphyrin in RBCs'],
  ],
  {headerColor:C.accent1, colW:[2.2,2.7,2.2,2.6]}
);

// Slide — Porphyrias
addContentSlide('Porphyrias — Classification & Key Features', [
  {text:'HEPATIC PORPHYRIAS (Mostly acute neurovisceral symptoms)', isHeader:true},
  {text:'Acute Intermittent Porphyria (AIP): PBG Deaminase deficient | ↑ ALA + PBG in urine | No photosensitivity | Rx: Haematin (IV) + High glucose'},
  {text:'Variegate Porphyria (VP): Protoporphyrinogen oxidase deficient | Acute attacks + photosensitivity'},
  {text:'Hereditary Coproporphyria: Coproporphyrinogen oxidase deficient'},
  {text:'Porphyria Cutanea Tarda (PCT): Uroporphyrinogen decarboxylase deficient | Photosensitivity, fragile skin | Commonest porphyria'},
  {text:''},
  {text:'ERYTHROPOIETIC PORPHYRIAS (Skin symptoms only)', isHeader:true},
  {text:'Congenital Erythropoietic Porphyria (CEP / Günther disease): Uroporphyrinogen III synthase deficient | Severe photosensitivity, haemolysis'},
  {text:'Erythropoietic Protoporphyria (EPP): Ferrochelatase deficient | Mild photosensitivity'},
  {text:''},
  {text:'MNEMONIC for AIP attacks: "5 Ps" = Painful abdomen, Polyneuropathy, Psychosis, Pink urine, Precipitated by drugs', color:C.yellow},
], {headerColor:C.accent1});

// Slide — Haem Degradation
addContentSlide('Haem Degradation — Bilirubin Metabolism', [
  {text:'SITE: Reticuloendothelial System (Spleen, Liver, Bone Marrow)', isHeader:true},
  {text:''},
  {text:'STEP 1: Haem → Biliverdin', isHeader:true},
  {text:'Enzyme: Haem Oxygenase (rate-limiting, produces CO + Fe²⁺ released)'},
  {text:'Biliverdin is green — responsible for greenish colour of bruises'},
  {text:''},
  {text:'STEP 2: Biliverdin → Bilirubin (Unconjugated = Indirect)', isHeader:true},
  {text:'Enzyme: Biliverdin Reductase | Bilirubin is water-INSOLUBLE, lipid-soluble'},
  {text:'Transported in blood bound to ALBUMIN (cannot be filtered by kidneys)'},
  {text:''},
  {text:'STEP 3 (Liver): Unconjugated → Conjugated Bilirubin (Direct)', isHeader:true},
  {text:'Hepatic uptake via LIGANDIN (Y protein) | UDP-Glucuronosyltransferase (UGT1A1) adds 2 glucuronate'},
  {text:'Conjugated bilirubin = water-soluble, can be excreted in bile'},
  {text:''},
  {text:'STEP 4 (Gut): Conjugated → Urobilinogen → Urobilin/Stercobilin', isHeader:true},
  {text:'Intestinal bacteria reduce bilirubin → Urobilinogen'},
  {text:'Stercobilin: excreted in faeces (brown colour) | Urobilin: excreted in urine (yellow colour)'},
], {headerColor:C.accent1});

// Slide — Jaundice types table
addTableSlide('Types of Jaundice — Differential Diagnosis',
  ['Feature', 'Pre-hepatic (Haemolytic)', 'Hepatic (Hepatocellular)', 'Post-hepatic (Obstructive)'],
  [
    ['Serum Bilirubin', '↑ Unconjugated', 'Both ↑', '↑ Conjugated'],
    ['Urine Bilirubin', 'Absent (acholuric)', 'Present', 'Present (dark urine)'],
    ['Urine Urobilinogen', '↑↑ (Increased)', '↓ Variable', 'Absent'],
    ['Stool Colour', 'Dark (normal/↑)', 'Pale', 'Clay/pale (acholic)'],
    ['Serum AST/ALT', 'Normal', '↑↑↑', 'Mildly ↑'],
    ['Serum ALP', 'Normal', 'Mild ↑', '↑↑↑'],
    ['Cause', 'Haemolysis, G6PD', 'Hepatitis, Cirrhosis', 'Gallstones, Ca head pancreas'],
  ],
  {headerColor:C.accent1, colW:[2.3,2.5,2.5,2.4]}
);

// Slide — Neonatal Jaundice & Kernicterus
addContentSlide('Neonatal Jaundice & Kernicterus', [
  {text:'PHYSIOLOGICAL NEONATAL JAUNDICE', isHeader:true},
  {text:'Appears: Day 2–3 | Disappears: Day 7–10 (term), Day 14 (preterm)'},
  {text:'Cause: Immature UGT1A1 + increased RBC breakdown (HbF → HbA transition) + reduced albumin'},
  {text:'Bilirubin < 12 mg/dL (term) — normal physiological range'},
  {text:''},
  {text:'PATHOLOGICAL NEONATAL JAUNDICE', isHeader:true},
  {text:'Appears < 24 hours OR bilirubin > 12 mg/dL (term) / > 15 mg/dL (preterm)'},
  {text:'Causes: Rh/ABO incompatibility, G6PD deficiency, Crigler-Najjar syndrome, Sepsis'},
  {text:''},
  {text:'KERNICTERUS', isHeader:true},
  {text:'Unconjugated bilirubin crosses blood-brain barrier → deposits in basal ganglia (especially subthalamic nuclei, hippocampus)'},
  {text:'Features: Hypotonia → Opisthotonus, High-pitched cry, Seizures, Sensorineural deafness, Choreoathetosis'},
  {text:''},
  {text:'TREATMENT: Phototherapy (converts bilirubin to lumirubin/photo-bilirubin) | Exchange transfusion if severe', color:C.yellow},
  {text:'Crigler-Najjar Type I: No UGT1A1 → fatal without liver transplant; Type II (Arias): Some UGT1A1 → responds to phenobarbitone', color:C.lightBlue},
], {headerColor:C.accent1});

// ══════════════════════════════════════════════════════════════════════════════
// SECTION 2 — METABOLIC CYCLES
// ══════════════════════════════════════════════════════════════════════════════
addSectionSlide('METABOLIC CYCLES', C.accent4);

// Slide — TCA Cycle intro
addContentSlide('TCA (Krebs / Citric Acid) Cycle — Overview', [
  {text:'LOCATION: Mitochondrial matrix (aerobic)', isHeader:true},
  {text:'Function: Final common pathway for oxidation of carbohydrates, fats, and amino acids'},
  {text:'One turn of cycle → 2 CO₂, 3 NADH, 1 FADH₂, 1 GTP (= 10 ATP per acetyl-CoA)'},
  {text:''},
  {text:'ENTRY POINT: Acetyl-CoA (2C) + Oxaloacetate (4C) → Citrate (6C)', isHeader:true},
  {text:'Enzyme: Citrate Synthase (irreversible, rate-limiting in fed state)'},
  {text:''},
  {text:'MNEMONIC — 8 Steps: "Citrate Is Krebs\' Starting Substrate For Making Oxaloacetate"', color:C.yellow, isHeader:false},
  {text:'C=Citrate, I=Isocitrate, K=α-Ketoglutarate, S=Succinyl-CoA, S=Succinate, F=Fumarate, M=Malate, O=Oxaloacetate'},
  {text:''},
  {text:'3 REGULATED/IRREVERSIBLE STEPS (rate-limiting enzymes):', isHeader:true},
  {text:'1. Isocitrate Dehydrogenase: Isocitrate → α-Ketoglutarate (+ CO₂, NADH) | Activated by ADP/Ca²⁺; Inhibited by ATP/NADH'},
  {text:'2. α-Ketoglutarate Dehydrogenase: α-KG → Succinyl-CoA (+ CO₂, NADH) | Same cofactors as PDH; inhibited by NADH, succinyl-CoA'},
  {text:'3. Citrate Synthase: OAA + Acetyl-CoA → Citrate | Inhibited by ATP, NADH, Citrate'},
  {text:''},
  {text:'SUBSTRATE-LEVEL PHOSPHORYLATION: Succinyl-CoA → Succinate | Enzyme: Succinyl-CoA Synthetase → GTP', color:C.lightBlue},
], {headerColor:C.accent4});

// Slide — TCA energy yield table
addTableSlide('TCA Cycle — Steps, Enzymes & Energy Yield',
  ['Step', 'Reaction', 'Enzyme', 'Product/Cofactor'],
  [
    ['1', 'Acetyl-CoA + OAA → Citrate', 'Citrate Synthase', 'Citrate'],
    ['2', 'Citrate → Isocitrate', 'Aconitase (Fe-S; inhibited by fluoroacetate)', 'Isocitrate'],
    ['3★', 'Isocitrate → α-Ketoglutarate', 'Isocitrate Dehydrogenase', 'NADH + CO₂'],
    ['4★', 'α-KG → Succinyl-CoA', 'α-KG Dehydrogenase (B1,B2,B3,B5,Lipoate)', 'NADH + CO₂'],
    ['5', 'Succinyl-CoA → Succinate', 'Succinyl-CoA Synthetase', 'GTP (substrate level)'],
    ['6', 'Succinate → Fumarate', 'Succinate Dehydrogenase (Complex II, ETC)', 'FADH₂'],
    ['7', 'Fumarate → Malate', 'Fumarase (hydration)', 'Malate'],
    ['8', 'Malate → OAA', 'Malate Dehydrogenase', 'NADH (regenerates OAA)'],
  ],
  {headerColor:C.accent4, colW:[0.5,3.0,3.0,3.2]}
);

// Slide — Urea Cycle
addContentSlide('Urea Cycle (Ornithine / Krebs–Henseleit Cycle)', [
  {text:'LOCATION: Liver (ONLY) — Steps 1–2 in Mitochondria, Steps 3–5 in Cytosol', isHeader:true},
  {text:'Function: Detoxify NH₃ → Urea (2 nitrogens per urea: 1 from NH₃, 1 from aspartate)'},
  {text:''},
  {text:'STEPS (MNEMONIC: "Ordinarily Careless Crappers Are Also Frivolous About Urination")', color:C.yellow, isHeader:false},
  {text:'MITOCHONDRIA:'},
  {text:'1. NH₃ + CO₂ + 2ATP → Carbamoyl Phosphate | Enzyme: CPS-I (activated by N-Acetylglutamate—NAG)', isSub:true},
  {text:'2. Carbamoyl Phosphate + Ornithine → Citrulline | Enzyme: OTC (Ornithine Transcarbamylase) — most common urea cycle enzyme deficiency; X-linked', isSub:true},
  {text:'CYTOSOL:'},
  {text:'3. Citrulline + Aspartate + ATP → Argininosuccinate | Enzyme: Argininosuccinate Synthetase (ASS)', isSub:true},
  {text:'4. Argininosuccinate → Arginine + Fumarate | Enzyme: Argininosuccinate Lyase (ASL) | Fumarate links to TCA!', isSub:true},
  {text:'5. Arginine → Ornithine + Urea | Enzyme: Arginase (Mn²⁺-dependent)', isSub:true},
  {text:''},
  {text:'ENERGY COST: 3 ATP per urea synthesized', isHeader:true},
  {text:'HYPERAMMONAEMIA: ↑ NH₃ → α-KG consumed → TCA cycle impaired → Cerebral oedema, Tremor, Encephalopathy'},
  {text:'Rx of hyperammonaemia: Low protein diet, Lactulose, Rifaximin, Sodium benzoate/phenylacetate (alternative NH₃ removal)'},
], {headerColor:C.accent4});

// Slide — Cori Cycle & Glucose-Alanine Cycle
addTwoColumnSlide('Cori Cycle & Glucose-Alanine Cycle',
  [
    {text:'CORI CYCLE', isHeader:true},
    {text:'Also called: Lactic Acid Cycle'},
    {text:'MUSCLE: Glucose → Pyruvate → Lactate (anaerobic)'},
    {text:'LIVER: Lactate → Pyruvate → Glucose (gluconeogenesis)'},
    {text:'Glucose sent back to muscle'},
    {text:''},
    {text:'PURPOSE: Regenerate glucose when O₂ limited'},
    {text:'Energy: Muscle uses 2 ATP; Liver consumes 6 ATP'},
    {text:'Net "energy debt" = 4 ATP paid by liver'},
    {text:'Key enzyme in liver: Lactate Dehydrogenase (LDH), then PEPCK'},
    {text:'Clinical: Metformin → lactic acidosis (blocks Complex I → ↑ lactate)'},
  ],
  [
    {text:'GLUCOSE-ALANINE CYCLE', isHeader:true},
    {text:'Also called: Cahill Cycle'},
    {text:'MUSCLE: Glucose → Pyruvate → Alanine (transamination with glutamate; enzyme: ALT/GPT)'},
    {text:'Alanine carries amino group safely to liver'},
    {text:'LIVER: Alanine → Pyruvate → Glucose (gluconeogenesis) + NH₃ → Urea Cycle'},
    {text:''},
    {text:'PURPOSE: Transfer amino groups from muscle to liver without toxic free NH₃'},
    {text:'Important in prolonged fasting & starvation'},
    {text:'Key enzyme: Alanine Aminotransferase (ALT/SGPT)'},
    {text:'Clinical: ↑ serum ALT = liver damage marker'},
  ],
  {headerColor:C.accent4}
);

// Slide — HMP Shunt
addContentSlide('Hexose Monophosphate (HMP) Shunt / Pentose Phosphate Pathway', [
  {text:'LOCATION: Cytosol | Active in: Liver, Adrenal cortex, RBCs, Lactating mammary gland, Gonads', isHeader:true},
  {text:''},
  {text:'TWO PHASES:', isHeader:true},
  {text:'Oxidative phase (irreversible): G6P → 6-Phosphogluconate → Ribulose-5-P | Generates 2 NADPH per G6P'},
  {text:'Non-oxidative phase (reversible): Interconverts pentose phosphates ↔ glycolytic intermediates'},
  {text:''},
  {text:'KEY PRODUCTS & FUNCTIONS:', isHeader:true},
  {text:'NADPH — Reductive biosynthesis (fatty acids, steroids, cholesterol), Glutathione reduction (antioxidant), NADPH oxidase (neutrophil burst), Cytochrome P450'},
  {text:'Ribose-5-Phosphate — Nucleotide/Nucleic acid synthesis'},
  {text:''},
  {text:'RATE-LIMITING ENZYME: G6PD (Glucose-6-Phosphate Dehydrogenase)', isHeader:true},
  {text:'G6PD DEFICIENCY: X-linked recessive | Most common enzyme deficiency of RBCs'},
  {text:'↓ NADPH → ↓ Reduced Glutathione → Oxidative stress → Heinz bodies (denatured Hb) → Haemolysis'},
  {text:'Precipitants: Primaquine, Dapsone, Nitrofurantoin, Fava beans, Infections'},
  {text:'Lab: ↑ MCV, reticulocytosis, ↑ LDH, ↑ indirect bilirubin, Heinz bodies on crystal violet stain'},
  {text:'Protective against: Falciparum malaria (common in Africa, India, Mediterranean)', color:C.yellow},
], {headerColor:C.accent4});

// Slide — Fatty Acid Oxidation & Synthesis overview
addTwoColumnSlide('Fatty Acid Metabolism — Key Concepts',
  [
    {text:'β-OXIDATION (Catabolism)', isHeader:true},
    {text:'Site: Mitochondrial matrix'},
    {text:'Steps: Activation (FA → Acyl-CoA, requires 2 ATP), Transport (Carnitine shuttle — CPTI), β-oxidation spiral'},
    {text:'Each cycle: 1 Acetyl-CoA + 1 NADH + 1 FADH₂'},
    {text:'Palmitate (16C): 7 cycles → 8 Acetyl-CoA → 106 ATP (net)'},
    {text:'Carnitine deficiency → Muscle weakness, Hypoglycaemia'},
    {text:'Odd-chain FA: Last product = Propionyl-CoA → Succinyl-CoA (requires B12)'},
    {text:'MCAD deficiency: Most common FA oxidation disorder'},
  ],
  [
    {text:'FATTY ACID SYNTHESIS', isHeader:true},
    {text:'Site: Cytosol (liver, adipose, mammary)'},
    {text:'Acetyl-CoA → Malonyl-CoA → Palmitate (16C)'},
    {text:'Rate-limiting enzyme: Acetyl-CoA Carboxylase (ACC) — requires Biotin'},
    {text:'Activated by: Insulin, Citrate'},
    {text:'Inhibited by: Glucagon, Epinephrine, Palmitoyl-CoA'},
    {text:'Each cycle adds 2C, uses 1 NADPH (HMP shunt link!)'},
    {text:'Fatty Acid Synthase (FAS) is a multifunctional enzyme'},
    {text:'ACP (Acyl Carrier Protein) — requires Pantothenic acid (Vit B5)'},
  ],
  {headerColor:C.accent4}
);

// ══════════════════════════════════════════════════════════════════════════════
// SECTION 3 — VITAMINS
// ══════════════════════════════════════════════════════════════════════════════
addSectionSlide('VITAMINS', C.accent3);

// Slide — Fat-Soluble Vitamins overview
addContentSlide('Fat-Soluble Vitamins — Overview (A, D, E, K)', [
  {text:'CHARACTERISTICS', isHeader:true},
  {text:'Stored in liver & adipose tissue | Absorbed with dietary fat (need bile salts)'},
  {text:'Toxicity possible with excess intake (especially Vit A & D)'},
  {text:'Malabsorption (Celiac, Crohn\'s, cholestasis) → All four deficient'},
  {text:''},
  {text:'VITAMIN A (Retinol)', isHeader:true, color:C.accent3},
  {text:'Active forms: Retinol (transport), Retinal (vision), Retinoic acid (gene expression/differentiation)'},
  {text:'Function: Vision (rhodopsin = retinal + opsin), Epithelial differentiation, Immune function, Spermatogenesis'},
  {text:'Deficiency: Night blindness (1st sign) → Bitot\'s spots → Xerophthalmia → Keratomalacia (corneal ulceration/blindness)'},
  {text:'          Also: Follicular hyperkeratosis (toad skin), Impaired immunity'},
  {text:'Toxicity (Hypervitaminosis A): Raised ICP (pseudotumor cerebri), Hepatotoxicity, Teratogenic (contraindicated in pregnancy!)'},
  {text:'Provitamin: β-Carotene (no toxicity — skin yellowing only)'},
  {text:''},
  {text:'VITAMIN D (Calciferol)', isHeader:true, color:C.yellow},
  {text:'D₂ (ergocalciferol, plant) / D₃ (cholecalciferol, skin via UV from 7-dehydrocholesterol)'},
  {text:'Activation: Liver (25-hydroxylation by 25-hydroxylase) → Kidney (1α-hydroxylation by 1α-hydroxylase → 1,25-(OH)₂D₃ = Calcitriol = active form)'},
  {text:'Function: ↑ Ca²⁺ absorption (intestine), ↑ renal Ca²⁺ reabsorption, bone mineralisation, immunomodulation'},
  {text:'Deficiency: Rickets (children — craniotabes, rachitic rosary, bow legs) | Osteomalacia (adults) | Hypocalcaemia → tetany'},
  {text:'Toxicity: Hypercalcaemia → metastatic calcification, renal stones, polyuria'},
], {headerColor:C.accent3});

// Slide — Vit E & K
addContentSlide('Fat-Soluble Vitamins — Vitamin E & K', [
  {text:'VITAMIN E (Tocopherol)', isHeader:true, color:C.green},
  {text:'Most potent fat-soluble antioxidant — protects polyunsaturated fatty acid membranes from lipid peroxidation'},
  {text:'Also protects RBCs from haemolysis, protects Vit A'},
  {text:'Deficiency: Rare | Premature neonates: Haemolytic anaemia + Thrombocytosis'},
  {text:'Adults: Spinocerebellar ataxia, Progressive muscle weakness, ↓ Deep tendon reflexes, Posterior column degeneration'},
  {text:'Abetalipoproteinaemia (MTP gene) → Cannot absorb Vit E → Neuromuscular disease'},
  {text:''},
  {text:'VITAMIN K (Phylloquinone K₁, Menaquinone K₂)', isHeader:true, color:C.accent3},
  {text:'K₁: Green leafy vegetables | K₂: Synthesised by gut bacteria | K₃: Menadione (synthetic)'},
  {text:'Function: Cofactor for γ-Carboxylation of glutamate residues (by Vit K-dependent carboxylase)'},
  {text:'Vit K-dependent clotting factors: II (Prothrombin), VII, IX, X + Protein C & S (anticoagulants)'},
  {text:'Mnemonic: "1972" = Factors II, VII, IX, X dependent on Vit K'},
  {text:''},
  {text:'Deficiency: Bleeding diathesis, Prolonged PT (extrinsic pathway affected first) + aPTT'},
  {text:'Neonates at risk (no gut flora + poor transfer across placenta) → Haemorrhagic disease of newborn'},
  {text:'Prevention: Vit K₁ 0.5–1 mg IM at birth'},
  {text:'Warfarin: Vit K antagonist → inhibits VKOR (Vit K Epoxide Reductase) → Rx with Vit K₁ (fresh frozen plasma for emergency)', color:C.yellow},
], {headerColor:C.accent3});

// Slide — Water-soluble vitamins B-complex table
addTableSlide('Water-Soluble Vitamins — B Complex Summary',
  ['Vitamin', 'Active Form/Coenzyme', 'Key Function', 'Deficiency Disease'],
  [
    ['B1 (Thiamine)', 'TPP (Thiamine Pyrophosphate)', 'PDH, α-KG DH, Transketolase (HMP)', 'Wernicke–Korsakoff, Dry/Wet Beriberi'],
    ['B2 (Riboflavin)', 'FMN, FAD', 'Oxidoreductases (ETC Complex I & II)', 'Cheilosis, Corneal vascularisation, Glossitis'],
    ['B3 (Niacin)', 'NAD⁺, NADP⁺', 'Energy metabolism (>400 reactions)', 'Pellagra: Dermatitis, Diarrhoea, Dementia, Death (4Ds)'],
    ['B5 (Pantothenic acid)', 'CoA, ACP', 'Fatty acid synthesis, TCA (Succinyl-CoA)', 'Burning feet syndrome (rare)'],
    ['B6 (Pyridoxine)', 'PLP (Pyridoxal Phosphate)', 'Transaminases, ALA Synthase, Decarboxylases, Glycogen Phosphorylase', 'Seborrhoeic dermatitis, Peripheral neuropathy, Sideroblastic anaemia'],
    ['B7 (Biotin)', 'Biocytin', 'Carboxylation (ACC, PC, PCC, MCC)', 'Dermatitis, Alopecia, Neurological changes (raw egg whites/avidin)'],
    ['B9 (Folate)', 'THF (Tetrahydrofolate)', 'One-carbon transfers, Purine synthesis, dTMP synthesis', 'Megaloblastic anaemia, Neural tube defects (NTD)'],
    ['B12 (Cobalamin)', 'Methylcobalamin, Adenosylcobalamin', 'Methyl-malonyl-CoA mutase, Methionine synthase', 'Megaloblastic anaemia + Subacute combined degeneration of cord'],
  ],
  {headerColor: C.accent3, colW:[1.7,2.0,3.2,2.8]}
);

// Slide — Vitamin B1, B3, B12 in detail
addContentSlide('Key B Vitamins — Clinical High-Yield Points', [
  {text:'VITAMIN B1 (Thiamine) — "The ENERGY vitamin"', isHeader:true},
  {text:'Coenzyme: TPP | Used by: PDH (pyruvate → Acetyl-CoA), α-KGDH, Transketolase (HMP shunt), Branched-chain α-KA dehydrogenase'},
  {text:'Beriberi: Dry (peripheral neuropathy) | Wet (High-output cardiac failure, dilated cardiomyopathy)'},
  {text:'Wernicke\'s encephalopathy: Ophthalmoplegia, Ataxia, Confusion (triad) — Thiamine FIRST before glucose in alcoholics!'},
  {text:'Korsakoff\'s psychosis: Anterograde amnesia + Confabulation (irreversible, mammillary body damage)'},
  {text:''},
  {text:'VITAMIN B3 (Niacin) — Pellagra: 3Ds → 4Ds', isHeader:true},
  {text:'Pellagra: Dermatitis (photosensitive, Casal\'s necklace), Diarrhoea, Dementia → Death'},
  {text:'Can be synthesised from Tryptophan (60 mg Trp = 1 mg Niacin); Hartnup disease & Carcinoid → Niacin deficiency despite adequate diet'},
  {text:'Pharmacological doses of Nicotinic acid → ↓ LDL, ↓ VLDL, ↑ HDL | Side effect: Cutaneous flushing (prostaglandin-mediated)'},
  {text:''},
  {text:'VITAMIN B12 (Cobalamin) — "Neural Protector"', isHeader:true},
  {text:'Only animal-source vitamin | Absorbed as IF-B12 complex via ileal cubilin receptors'},
  {text:'Deficiency causes: Pernicious anaemia (anti-IF Ab), Strict veganism, Ileal resection, Metformin, Prolonged PPI use'},
  {text:'Subacute combined degeneration (SCD): Dorsal (posterior) columns (vibration/proprioception) + Lateral corticospinal tracts'},
  {text:'Schilling test: Distinguishes IF deficiency from malabsorption | ↑ MMA + Homocysteine in B12 deficiency', color:C.yellow},
], {headerColor:C.accent3});

// Slide — Vitamin C and summary
addContentSlide('Vitamin C (Ascorbic Acid) & Summary Points', [
  {text:'VITAMIN C (Ascorbic Acid) — Water-soluble', isHeader:true},
  {text:'Antioxidant (reduces oxidative stress), cofactor for hydroxylation reactions'},
  {text:'Key roles: Collagen synthesis (prolyl & lysyl hydroxylase require Vit C) | Iron absorption (reduces Fe³⁺ → Fe²⁺) | Norepinephrine synthesis | Carnitine synthesis'},
  {text:'Deficiency (Scurvy):'},
  {text:'Perifollicular haemorrhage (corkscrew hairs) → Purpura', isSub:true},
  {text:'Bleeding gums (gingivitis), Loose teeth', isSub:true},
  {text:'Poor wound healing (↓ collagen cross-linking)', isSub:true},
  {text:'Anaemia (↓ Fe absorption), Haemarthrosis, Pseudoparalysis in infants', isSub:true},
  {text:'Woody oedema of legs', isSub:true},
  {text:'X-ray: Trümmerfeld zone, Pelkan spurs, Ground-glass cortex, Frankel\'s line', isSub:true},
  {text:''},
  {text:'VITAMIN INTERACTIONS (High-Yield)', isHeader:true},
  {text:'B12 deficiency → ↑ Homocysteine → Folate trap (↓ active THF available) → Combined megaloblastic picture'},
  {text:'Folate supplements MASK B12 deficiency neurological signs — always check B12 before giving folate alone'},
  {text:'Vit D + Calcium: Synergistic for bone density | Vit K: Needed for osteocalcin (bone protein) carboxylation'},
  {text:'Vit E spares Vit A and Vit C (antioxidant protection)'},
  {text:'Fat-soluble deficiencies cluster in fat malabsorption (Celiac, Short bowel, Biliary atresia, CF)', color:C.yellow},
], {headerColor:C.accent3});

// Vitamins deficiency table
addTableSlide('Fat-Soluble Vitamins — Deficiency & Toxicity Reference',
  ['Vitamin', 'Storage', 'Deficiency', 'Key Sign', 'Toxicity'],
  [
    ['A (Retinol)', 'Liver (stellate cells)', 'Night blindness → Xerophthalmia → Keratomalacia', 'Bitot\'s spots', 'Pseudo-tumour cerebri, Teratogen'],
    ['D (Calciferol)', 'Adipose/Liver', 'Rickets (child), Osteomalacia (adult), Tetany', 'Rachitic rosary, Craniotabes', 'Hypercalcaemia, Metastatic Ca²⁺'],
    ['E (Tocopherol)', 'Adipose', 'Haemolytic anaemia (neonate), Ataxia, Neuropathy', 'Posterior column signs', 'None significant'],
    ['K (Phylloquinone)', 'Liver', 'Prolonged PT, Haemorrhagic disease of newborn', '↑ PT/INR, Bruising', 'Haemolysis (Vit K3)'],
  ],
  {headerColor:C.accent3, colW:[1.6,1.6,2.8,2.2,1.5]}
);

// ══════════════════════════════════════════════════════════════════════════════
// SECTION 4 — EXAM QUESTIONS (MCQs)
// ══════════════════════════════════════════════════════════════════════════════
addSectionSlide('EXAM QUESTIONS', C.green);

addQSlide(1,
  'A 2-year-old child presents with photophobia, skin blistering after sun exposure, and pink-red urine. ALA-Synthase activity is normal. Which enzyme is most likely deficient?',
  ['A. ALA Dehydratase','B. PBG Deaminase','C. Uroporphyrinogen III Synthase','D. Ferrochelatase'],
  'C',
  'Congenital Erythropoietic Porphyria (CEP/Günther): URO III synthase deficiency — earliest onset, severe photosensitivity'
);

addQSlide(2,
  'Which enzyme of the urea cycle is located ONLY in the mitochondria AND is activated by N-Acetylglutamate?',
  ['A. OTC (Ornithine Transcarbamylase)','B. CPS-I (Carbamoyl Phosphate Synthetase-I)','C. Argininosuccinate Synthetase','D. Arginase'],
  'B',
  'CPS-I: Mitochondrial, activated by NAG (allosteric activator), catalyses first committed step of urea cycle'
);

addQSlide(3,
  'A 35-year-old alcoholic man presents with confusion, horizontal nystagmus, and ataxia. Before giving IV glucose, which vitamin must be administered FIRST?',
  ['A. Vitamin B12','B. Vitamin B6 (PLP)','C. Vitamin B1 (Thiamine)','D. Vitamin B3 (Niacin)'],
  'C',
  'Wernicke\'s encephalopathy: Give Thiamine BEFORE glucose to prevent precipitating/worsening encephalopathy (glucose depletes remaining B1)'
);

addQSlide(4,
  'In haem degradation, which enzyme catalyses the RATE-LIMITING step and also produces carbon monoxide (CO)?',
  ['A. Biliverdin Reductase','B. Haem Oxygenase','C. ALA Synthase','D. UDP-Glucuronosyltransferase'],
  'B',
  'Haem Oxygenase: Rate-limiting in degradation, produces Biliverdin + Fe²⁺ + CO (CO is a signalling molecule)'
);

addQSlide(5,
  'A young man develops haemolytic anaemia and Heinz bodies after taking primaquine for malaria prophylaxis. The metabolic pathway MOST impaired is:',
  ['A. Glycolysis','B. TCA cycle','C. HMP shunt / Pentose Phosphate Pathway','D. β-Oxidation'],
  'C',
  'G6PD deficiency → ↓ NADPH → ↓ Glutathione reductase → Oxidative damage to Hb → Heinz bodies → Haemolysis'
);

addQSlide(6,
  'Which metabolic cycle transfers amino groups from skeletal muscle to the liver WITHOUT releasing free ammonia into the bloodstream?',
  ['A. Cori Cycle (Lactic Acid Cycle)','B. Glucose-Alanine Cycle (Cahill Cycle)','C. Urea Cycle','D. Uronic Acid Pathway'],
  'B',
  'Glucose-Alanine (Cahill) Cycle: Amino group transferred as non-toxic alanine; in liver, alanine → pyruvate + NH₃ (→ urea)'
);

addQSlide(7,
  'A neonate develops jaundice on day 1 of life with rapidly rising bilirubin. Van den Bergh test shows predominantly indirect (unconjugated) bilirubin. The MOST likely cause is:',
  ['A. Biliary atresia','B. Neonatal hepatitis','C. Rh-incompatibility haemolytic disease','D. Choledochal cyst'],
  'C',
  'Early-onset haemolytic jaundice (< 24h) with indirect hyperbilirubinaemia = Rh/ABO incompatibility. Biliary atresia → conjugated (direct) jaundice'
);

addQSlide(8,
  'A 4-year-old child has bowed legs, craniotabes, rachitic rosary, and a low serum calcium. Serum 25-OH Vitamin D is normal, but 1,25-(OH)₂D₃ (Calcitriol) is low. The defect is most likely in the:',
  ['A. Liver (25-hydroxylase deficiency)','B. Kidney (1α-hydroxylase deficiency)','C. Intestinal vitamin D receptor mutation','D. Dietary calcium deficiency only'],
  'B',
  'Vitamin D-Dependent Rickets Type I: 1α-hydroxylase (CYP27B1) deficiency in kidney → cannot convert 25-OH D₃ → 1,25-(OH)₂D₃'
);

addQSlide(9,
  'Which TCA cycle enzyme is shared with the electron transport chain (Complex II) and is located on the INNER mitochondrial membrane?',
  ['A. Isocitrate Dehydrogenase','B. Malate Dehydrogenase','C. Succinate Dehydrogenase','D. Citrate Synthase'],
  'C',
  'Succinate Dehydrogenase = Complex II of ETC (embedded in inner mitochondrial membrane). Produces FADH₂; inhibited by malonate.'
);

addQSlide(10,
  'A pregnant woman with pernicious anaemia is given only folic acid supplementation. Her haematological picture improves but she develops progressive neurological deficits. This is because:',
  ['A. Folate depletes Vitamin B12 stores','B. Folate therapy masks B12 deficiency but does not correct the methylmalonyl-CoA mutase deficiency causing neurological damage','C. Folate is toxic to neurons','D. Folate competes with B12 for intrinsic factor binding'],
  'B',
  'Folate corrects megaloblastic anaemia (repairs DNA synthesis) but does NOT fix the neurological damage caused by ↓ adenosylcobalamin (needed for odd-chain FA metabolism via methylmalonyl-CoA mutase)'
);

// ══════════════════════════════════════════════════════════════════════════════
// FINAL SLIDE — SUMMARY & THANK YOU
// ══════════════════════════════════════════════════════════════════════════════
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  const boxes = [
    {x:0.2,y:0.8,color:C.accent1,title:'HAEM METABOLISM',pts:['ALA Synthase = Rate-limiting (synthesis)','Haem Oxygenase = Rate-limiting (degradation)','Lead → ALA Dehydratase + Ferrochelatase','AIP → PBG Deaminase deficiency','Jaundice types: Pre/Hepatic/Post-hepatic']},
    {x:3.55,y:0.8,color:C.accent4,title:'METABOLIC CYCLES',pts:['TCA: 3 irreversible steps (CS, IsoD, αKGD)','Urea: CPS-I activated by NAG | OTC = commonest defect','Cori: Lactate shuttle (2 vs 6 ATP)','Cahill: Alanine shuttle — safe NH₃ transport','HMP: G6PD → NADPH → antioxidant defense']},
    {x:6.9,y:0.8,color:C.accent3,title:'VITAMINS',pts:['Fat-soluble: A,D,E,K stored in liver/fat','Vit A: Night blindness → Xerophthalmia','Vit D: 1α-hydroxylase (kidney) → Calcitriol','B1: Wernicke — Thiamine BEFORE glucose!','B12: Posterior column + megaloblastic anaemia']},
  ];
  boxes.forEach(b=>{
    sl.addShape(pres.ShapeType.rect, {x:b.x,y:b.y,w:3.15,h:4.5,fill:{color:C.cardBg},line:{color:b.color,pt:1.5}});
    sl.addShape(pres.ShapeType.rect, {x:b.x,y:b.y,w:3.15,h:0.45,fill:{color:b.color}});
    sl.addText(b.title, {x:b.x+0.08,y:b.y,w:3.0,h:0.45,fontSize:11,bold:true,color:C.white,valign:'middle',fontFace:'Calibri',align:'center'});
    const items = b.pts.map((p,i)=>({text:p,options:{bullet:{indent:10},color:C.offWhite,fontSize:9.5,breakLine:i<b.pts.length-1}}));
    sl.addText(items, {x:b.x+0.08,y:b.y+0.52,w:3.0,h:3.8,valign:'top',fontFace:'Calibri',lineSpacingMultiple:1.3});
  });
  sl.addText('All the best for your examinations! — PGIMS Biochemistry Department', {x:0.3,y:5.22,w:9.4,h:0.3,fontSize:10.5,color:C.subtext,italic:true,align:'center',fontFace:'Calibri'});
}

// Write file
pres.writeFile({ fileName: '/home/daytona/workspace/haem-metabolism-ppt/Haem_Metabolic_Cycles_Vitamins_PGIMS.pptx' })
  .then(() => console.log('SUCCESS: Presentation saved!'))
  .catch(e => { console.error('ERROR:', e); process.exit(1); });