USMLE Step 1 Biochemistry - High-Yield Master Review

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// ══════════════════════════════════════════════════════════════
// SLIDE 1 – TITLE
// ══════════════════════════════════════════════════════════════
titleSlide(
  "USMLE Step 1\nBiochemistry\nHigh-Yield Review",
  "Concepts · Pathways · Mnemonics · MCQ Traps"
);

// ══════════════════════════════════════════════════════════════
// SLIDE 2 – OVERVIEW / TABLE OF CONTENTS
// ══════════════════════════════════════════════════════════════
{
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  const topics = [
    ["01", "The Big Picture", "Catabolism vs. Anabolism, hub molecules"],
    ["02", "Carbohydrate Metabolism", "Glycolysis, PDH, TCA, Gluconeogenesis, Glycogen"],
    ["03", "Amino Acids", "Essential, glucogenic/ketogenic, derivatives, diseases"],
    ["04", "Lipid Metabolism", "FA synthesis/oxidation, ketone bodies, lipoproteins"],
    ["05", "Vitamins", "Water-soluble B vitamins, fat-soluble ADEK"],
    ["06", "Enzyme Kinetics", "Km, Vmax, competitive vs. noncompetitive inhibition"],
    ["07", "Molecular Biology", "DNA replication, transcription, translation antibiotics"],
    ["08", "Urea Cycle", "Nitrogen disposal, OTC deficiency, hyperammonemia"],
    ["09", "Quick MCQ Guide", "Classic case-to-diagnosis table"],
  ];
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// ══════════════════════════════════════════════════════════════
// SECTION 1 – BIG PICTURE
// ══════════════════════════════════════════════════════════════
sectionHeader("01", "The Big Picture", "Understanding the flow of metabolism");

{
  const s = contentSlide("The Central Metabolic Chain", ACCENT);
  // Flow diagram
  const steps = ["Glucose", "Pyruvate", "Acetyl-CoA", "TCA Cycle", "ATP (via ETC)"];
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    "Produces ATP, NADH, FADH2",
    "Oxidative reactions (uses NAD+, FAD)",
    "Examples: glycolysis, beta-oxidation, TCA",
    "Convergent – many inputs, few outputs",
    "Dominant in fasting/exercise states",
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    "Consumes ATP and NADPH",
    "Reductive reactions (uses NADPH)",
    "Examples: fatty acid synthesis, gluconeogenesis",
    "Divergent – few inputs, many outputs",
    "Dominant in fed (insulin-high) state",
  ], ACCENT);
}

// ══════════════════════════════════════════════════════════════
// SECTION 2 – CARBOHYDRATE METABOLISM
// ══════════════════════════════════════════════════════════════
sectionHeader("02", "Carbohydrate Metabolism", "Glycolysis · PDH · TCA · Gluconeogenesis · Glycogen");

// Slide: Glycolysis
{
  const s = contentSlide("Glycolysis – Key Facts for USMLE", ACCENT2);
  card(s, 0.3, 1.0, 3.0, 3.9, "BASICS", [
    "Location: Cytoplasm",
    "Input: 1 Glucose (6C)",
    "Output: 2 Pyruvate + 2 ATP (net) + 2 NADH",
    "Occurs in ALL cells (incl. RBCs – only source!)",
    "Anaerobic: works without O₂",
  ], ACCENT2);

  card(s, 3.5, 1.0, 3.2, 3.9, "3 IRREVERSIBLE STEPS", [
    "① Hexokinase/Glucokinase → G-6-P",
    "② PFK-1 → F-1,6-BP  ← RATE-LIMITING",
    "③ Pyruvate Kinase → Pyruvate",
    "",
    "PFK-1 Activated by: AMP, F-2,6-BP",
    "PFK-1 Inhibited by: ATP, Citrate",
    "Mnemonic: 'AMP hits the GAS, ATP hits BRAKES'",
  ], ACCENT3);

  card(s, 6.85, 1.0, 2.85, 1.8, "MCQ TRAP ⚠️", [
    "PFK-1 deficiency (Tarui) =",
    "Exercise cramps +",
    "Hemolytic anemia",
  ], ACCENT3);

  card(s, 6.85, 2.95, 2.85, 1.95, "CORI CYCLE", [
    "Lactate (muscle) →",
    "→ Glucose (liver)",
    "Liver 'recycles' lactate",
    "Key in exercise/fasting",
  ], ACCENT);
}

// Slide: PDH Complex
{
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  s.addText("Pyruvate  →  Acetyl-CoA  (IRREVERSIBLE – you CANNOT make glucose from fat!)", {
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  card(s, 0.3, 1.65, 4.3, 2.4, "5 COFACTORS: 'Tender Loving Care For Nancy'", [
    "T – Thiamine (B1) → TPP",
    "L – Lipoic acid",
    "C – CoA (Pantothenic acid / B5)",
    "F – FAD (Riboflavin / B2)",
    "N – NAD+ (Niacin / B3)",
  ], ACCENT);

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    "↓ Energy state:",
    "High AMP",
    "High CoA",
    "High NAD+",
    "(Low products)",
  ], ACCENT);

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    "↑ Energy state:",
    "High ATP",
    "High NADH",
    "High Acetyl-CoA",
    "(Product inhibition)",
  ], ACCENT3);

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}

// Slide: TCA Cycle
{
  const s = contentSlide("TCA Cycle – Energy Accounting", ACCENT);

  s.addText("Per Acetyl-CoA turn: 3 NADH + 1 FADH₂ + 1 GTP + 2 CO₂", {
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  card(s, 0.3, 1.6, 4.5, 2.5, "KEY INTERMEDIATES", [
    "Oxaloacetate (OAA) – entry/exit for Acetyl-CoA",
    "Succinyl-CoA – used for HEME synthesis",
    "α-Ketoglutarate – connects to amino acid metabolism",
    "Citrate – exported for fatty acid synthesis",
    "Rate-limiting enzyme: Isocitrate dehydrogenase",
  ], ACCENT);

  card(s, 5.0, 1.6, 4.7, 2.5, "REGULATION", [
    "Inhibited by: ATP, NADH (energy replete)",
    "Activated by: ADP, NAD+ (energy needed)",
    "",
    "Anaplerosis = replenishing TCA intermediates",
    "Pyruvate carboxylase makes OAA (biotin needed)",
    "Muscle uses PC for anaplerosis only (not gluconeogenesis)",
  ], ACCENT2);

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  s.addText("⚠️  MCQ TRAP – Alcoholism: High NADH from alcohol dehydrogenase → inhibits TCA cycle, depletes OAA → gluconeogenesis blocked → hypoglycemia + lactic acidosis + fatty liver + ↑ uric acid (gout).", {
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    fontSize: 11, color: ACCENT3, fontFace: "Calibri"
  });
}

// Slide: Gluconeogenesis
{
  const s = contentSlide("Gluconeogenesis – Making Glucose from Scratch", ACCENT2);
  s.addText("Occurs in: LIVER and KIDNEY (fasting/starvation). Uses same enzymes as glycolysis EXCEPT 3 irreversible steps.", {
    x: 0.3, y: 1.0, w: 9.4, h: 0.42,
    fontSize: 11, color: LIGHT_TXT, fontFace: "Calibri", italic: true
  });
  addTable(s,
    ["Glycolysis (blocked)", "Gluconeogenesis bypass", "Cofactor needed"],
    [
      ["Pyruvate Kinase", "Pyruvate Carboxylase → PEPCK", "Biotin + GTP"],
      ["PFK-1", "Fructose-1,6-bisphosphatase", "—"],
      ["Hexokinase", "Glucose-6-phosphatase", "— (liver/kidney only!)"],
    ],
    0.3, 1.55, 9.4
  );

  card(s, 0.3, 3.45, 4.5, 1.95, "SUBSTRATES: 'GOAL'", [
    "G – Glycerol (from fat breakdown)",
    "O – Odd-chain fatty acids (propionyl-CoA)",
    "A – Amino acids (glucogenic ones)",
    "L – Lactate (from muscle via Cori cycle)",
  ], ACCENT2);

  card(s, 5.0, 3.45, 4.7, 1.95, "KEY CONCEPT", [
    "Even-chain fatty acids → Acetyl-CoA ONLY",
    "Acetyl-CoA CANNOT make glucose (PDH irreversible)",
    "So: FAT → cannot become GLUCOSE (in mammals)",
    "BUT: Glucose CAN become FAT (Acetyl-CoA → FA)",
  ], ACCENT3);
}

// Slide: Glycogen Storage Diseases
{
  const s = contentSlide("Glycogen Storage Diseases – 'Very Poor Carb Metabolism'", ACCENT3);
  addTable(s,
    ["Mnemonic", "Type", "Deficient Enzyme", "Key Features"],
    [
      ["Very", "I – Von Gierke", "Glucose-6-phosphatase", "Severe hypoglycemia, lactic acidosis, ↑ uric acid, hepatomegaly"],
      ["Poor", "II – Pompe", "Acid maltase (lysosomal)", "Cardiomegaly, hypotonia ('floppy baby'), early death"],
      ["Carb", "III – Cori", "Debranching enzyme", "Mild Von Gierke-like, hepatomegaly"],
      ["Metabolism", "V – McArdle", "Muscle phosphorylase", "Exercise cramps, NO lactate rise after exercise"],
    ],
    0.3, 1.05, 9.4
  );

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  s.addText([
    { text: "MCQ KEY: ", options: { bold: true, color: ACCENT2, fontSize: 12, fontFace: "Calibri" } },
    { text: "McArdle (Type V) → forearm ischemic exercise test shows NO rise in lactate (muscle can't break down glycogen → no pyruvate → no lactate). Pompe → only glycogen storage disease involving lysosomes.", options: { color: LIGHT_TXT, fontSize: 11, fontFace: "Calibri" } },
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}

// ══════════════════════════════════════════════════════════════
// SECTION 3 – AMINO ACIDS
// ══════════════════════════════════════════════════════════════
sectionHeader("03", "Amino Acids", "Essential · Glucogenic/Ketogenic · Derivatives · Diseases");

// Slide: Essential AAs
{
  const s = contentSlide("Essential Amino Acids & Glucogenic/Ketogenic Classification", ACCENT);
  card(s, 0.3, 1.0, 4.5, 2.2, "ESSENTIAL AAs – 'PVT TIM HaLL'", [
    "P – Phenylalanine",
    "V – Valine",
    "T – Threonine",
    "T – Tryptophan",
    "I – Isoleucine",
    "M – Methionine",
    "H – Histidine",
    "L – Leucine",
    "L – Lysine",
  ], ACCENT);

  card(s, 5.0, 1.0, 4.7, 1.05, "PURELY KETOGENIC (only 2!)", [
    "Leucine & Lysine → 'Lucky Lemons are Keto'",
  ], ACCENT2);

  card(s, 5.0, 2.15, 4.7, 1.05, "BOTH (glucogenic + ketogenic) – 'PITTT'", [
    "Phenylalanine, Isoleucine, Threonine, Tryptophan, Tyrosine",
  ], ACCENT3);

  card(s, 5.0, 3.3, 4.7, 1.1, "ALL OTHERS", [
    "Purely glucogenic → feed into TCA cycle intermediates or pyruvate",
  ], GREY);

  s.addShape(pres.shapes.ROUNDED_RECTANGLE, { x: 0.3, y: 3.35, w: 4.5, h: 2.0, fill: { color: CARD_BG }, line: { color: ACCENT, width: 1 }, rectRadius: 0.07 });
  s.addText("KEY CONCEPT", { x: 0.45, y: 3.43, w: 4.0, h: 0.3, fontSize: 10, bold: true, color: ACCENT, fontFace: "Calibri" });
  s.addText([
    { text: "Glucogenic AAs → can make GLUCOSE\n", options: { breakLine: true } },
    { text: "Ketogenic AAs → can make KETONE BODIES or FA\n", options: { breakLine: true } },
    { text: "Only Leu & Lys are PURELY ketogenic\n", options: { breakLine: true } },
    { text: "(They CANNOT contribute to glucose — classic MCQ!)", options: {} },
  ], { x: 0.45, y: 3.78, w: 4.1, h: 1.5, fontSize: 9.5, color: LIGHT_TXT, fontFace: "Calibri" });
}

// Slide: AA Derivatives
{
  const s = contentSlide("Key Amino Acid Derivatives – Extremely High-Yield!", ACCENT2);
  addTable(s,
    ["Amino Acid", "Product(s)", "Clinical Relevance"],
    [
      ["Tryptophan", "Serotonin, Niacin (B3), Melatonin", "Carcinoid → excess serotonin; pellagra if low tryptophan"],
      ["Phenylalanine", "Tyrosine", "PKU = can't convert Phe → Tyr"],
      ["Tyrosine", "Dopamine, Epi, NE, T3/T4, Melanin", "Albinism = tyrosinase deficiency"],
      ["Histidine", "Histamine", "Allergy, anaphylaxis"],
      ["Glycine", "Heme, Purines, Creatine", "Heme synthesis: Glycine + Succinyl-CoA (ALA synthase, B6)"],
      ["Glutamate", "GABA, Glutathione", "GABA deficiency → seizures"],
      ["Arginine", "Nitric oxide, Urea, Creatine", "Urea cycle; NO vasodilation"],
      ["Methionine", "SAM (universal methyl donor)", "Homocysteine metabolism; B12 + folate needed"],
    ],
    0.3, 1.0, 9.4
  );
}

// Slide: PKU & Homocystinuria
{
  const s = contentSlide("Classic Amino Acid Disorders – PKU & Homocystinuria", ACCENT3);
  card(s, 0.3, 1.0, 4.5, 4.35, "PKU – Phenylketonuria", [
    "Deficient enzyme: Phenylalanine hydroxylase",
    "(or BH4 cofactor deficiency)",
    "",
    "Result: Phe accumulates, Tyr becomes deficient",
    "",
    "Presentation:",
    "• Intellectual disability",
    "• Fair skin and hair (↓ melanin)",
    "• Musty / 'mousy' odor",
    "• Seizures",
    "",
    "Detected by: Newborn screening (Guthrie test)",
    "Treatment: Low-phenylalanine diet",
    "Add tyrosine (now essential!)",
  ], ACCENT3);

  card(s, 5.0, 1.0, 4.7, 4.35, "HOMOCYSTINURIA", [
    "Deficient: Cystathionine beta-synthase (CBS) – B6",
    "",
    "High homocysteine accumulates",
    "",
    "Presentation:",
    "• Intellectual disability",
    "• Marfanoid habitus (TALL)",
    "• Lens dislocation DOWNWARD ← key!",
    "  (Marfan = upward; Homocystinuria = downward)",
    "• Premature atherosclerosis, DVT, thrombosis",
    "",
    "B vitamin causes of high homocysteine:",
    "• B12↓ → Hcy↑ + methylmalonic acid↑",
    "• Folate↓ → Hcy↑ + MMA normal",
    "• B6↓ → Hcy↑ (can't make cysteine)",
  ], ACCENT2);
}

// ══════════════════════════════════════════════════════════════
// SECTION 4 – LIPID METABOLISM
// ══════════════════════════════════════════════════════════════
sectionHeader("04", "Lipid Metabolism", "FA Synthesis · Beta-Oxidation · Ketone Bodies · Lipoproteins");

{
  const s = contentSlide("Fatty Acid Synthesis vs. Beta-Oxidation", ACCENT);
  addTable(s,
    ["Feature", "FA SYNTHESIS (fed)", "BETA-OXIDATION (fasting)"],
    [
      ["Location", "Cytoplasm", "Mitochondria"],
      ["Key enzyme", "Acetyl-CoA Carboxylase (ACC) – rate-limiting", "Carnitine Acyltransferase I (CAT-I) – rate-limiting"],
      ["Activated by", "Insulin, Citrate", "Low malonyl-CoA, fasting state"],
      ["Inhibited by", "Glucagon, epinephrine, palmitoyl-CoA", "Malonyl-CoA (fed state shuts down oxidation!)"],
      ["Reducing power", "NADPH consumed", "NADH + FADH₂ produced"],
      ["Net direction", "Glucose → Fat", "Fat → Acetyl-CoA → ATP"],
    ],
    0.3, 1.0, 9.4
  );

  s.addShape(pres.shapes.ROUNDED_RECTANGLE, { x: 0.3, y: 4.3, w: 4.5, h: 1.1, fill: { color: "0D1B2A" }, line: { color: ACCENT3, width: 1.5 }, rectRadius: 0.07 });
  s.addText("⚠️  MCAD deficiency: Fasting hypoketotic hypoglycemia in infants. No ketones because can't oxidize medium-chain FAs. Dicarboxylic aciduria in urine.", {
    x: 0.45, y: 4.38, w: 4.15, h: 0.95, fontSize: 10, color: ACCENT3, fontFace: "Calibri"
  });

  s.addShape(pres.shapes.ROUNDED_RECTANGLE, { x: 5.0, y: 4.3, w: 4.7, h: 1.1, fill: { color: "0D1B2A" }, line: { color: ACCENT2, width: 1.5 }, rectRadius: 0.07 });
  s.addText("⚠️  Carnitine deficiency: Can't transport long-chain FAs into mitochondria → muscle weakness, hypoglycemia, fatty liver. Treat with L-carnitine.", {
    x: 5.15, y: 4.38, w: 4.4, h: 0.95, fontSize: 10, color: ACCENT2, fontFace: "Calibri"
  });
}

// Slide: Lipoproteins
{
  const s = contentSlide("Lipoproteins – 'Know Your Apolipoproteins!'", ACCENT2);
  addTable(s,
    ["Lipoprotein", "Made In", "Carries", "Key Apo"],
    [
      ["Chylomicron", "Intestine", "Dietary triglycerides (TGs)", "ApoB-48, ApoC-II, ApoE"],
      ["VLDL", "Liver", "Endogenous TGs", "ApoB-100, ApoC-II, ApoE"],
      ["IDL", "Blood (from VLDL)", "TGs + Cholesterol", "ApoB-100, ApoE"],
      ["LDL", "Blood (from IDL)", "Cholesterol to tissues", "ApoB-100"],
      ["HDL", "Liver + Intestine", "Reverse cholesterol transport", "ApoA-I"],
    ],
    0.3, 1.0, 9.4
  );

  card(s, 0.3, 3.45, 4.5, 2.0, "KEY APOLIPOPROTEINS", [
    "ApoC-II → activates LPL (releases TG)",
    "ApoB-100 → LDL receptor ligand",
    "ApoB-48 → chylomicron ID (intestinal)",
    "ApoE → receptor-mediated remnant uptake",
    "ApoA-I → activates LCAT (cholesterol esterification)",
  ], ACCENT2);

  card(s, 5.0, 3.45, 4.7, 2.0, "FAMILIAL HYPERCHOLESTEROLEMIA", [
    "Defect: LDL receptor (ApoB-100 ligand)",
    "Result: LDL cannot be taken up → sky-high LDL",
    "Features: Tendon xanthomas, xanthelasma",
    "Premature MI (even in 20s-30s)",
    "Treatment: High-dose statins, PCSK9 inhibitors",
  ], ACCENT3);
}

// Slide: Ketone Bodies
{
  const s = contentSlide("Ketone Bodies – Starvation Fuel", ACCENT);
  card(s, 0.3, 1.0, 4.5, 4.35, "KETONE BODY BASICS", [
    "Made from: Acetyl-CoA (liver only)",
    "",
    "Types:",
    "• Acetoacetate (main ketone body)",
    "• Beta-hydroxybutyrate (most in DKA)",
    "• Acetone (fruity breath – volatile)",
    "",
    "Made in: LIVER",
    "Used in: brain, muscle, heart – NOT liver",
    "(Liver lacks thiophorase/succinyl-CoA transferase)",
    "",
    "Brain uses ketones after ~3 days of starvation",
    "(glucose-sparing for RBCs that need glucose)",
  ], ACCENT);

  card(s, 5.0, 1.0, 4.7, 4.35, "DKA LOGIC (MCQ Favorite)", [
    "No insulin → cells can't take up glucose",
    "→ Glucagon high → lipolysis ↑↑",
    "→ Massive Acetyl-CoA from beta-oxidation",
    "→ TCA overwhelmed",
    "→ Ketone body production ↑↑",
    "→ Metabolic acidosis (↓ HCO₃⁻, ↓ pH)",
    "→ High anion gap",
    "",
    "Lab clues:",
    "• Blood glucose: very high",
    "• Urine: ketones + glucose",
    "• Serum: ↑ beta-hydroxybutyrate",
    "• pH < 7.3, HCO₃⁻ < 15",
    "• Fruity breath (acetone)",
  ], ACCENT3);
}

// ══════════════════════════════════════════════════════════════
// SECTION 5 – VITAMINS
// ══════════════════════════════════════════════════════════════
sectionHeader("05", "Vitamins", "B vitamins · Fat-soluble ADEK · Deficiency & Toxicity");

{
  const s = contentSlide("Water-Soluble B Vitamins – Deficiency Diseases", ACCENT);
  addTable(s,
    ["Vitamin", "Coenzyme", "Deficiency", "Classic MCQ Clue"],
    [
      ["B1 – Thiamine", "TPP", "Beriberi / Wernicke-Korsakoff", "Alcoholic + confusion + ataxia + nystagmus"],
      ["B2 – Riboflavin", "FAD, FMN", "Cheilosis, corneal vascularization", "'2 lips + 2 eyes' (angular stomatitis)"],
      ["B3 – Niacin", "NAD+, NADP+", "Pellagra (3Ds: Diarrhea, Dermatitis, Dementia)", "Sun-exposed skin rash + dementia"],
      ["B5 – Pantothenate", "CoA", "Rare – dermatitis, enteritis", "Needed for ALL CoA-requiring reactions"],
      ["B6 – Pyridoxine", "PLP", "Sideroblastic anemia, neuropathy", "INH (TB drug) causes B6 deficiency!"],
      ["B7 – Biotin", "Carboxylation rxns", "Dermatitis, alopecia, neurological", "Raw egg whites → avidin binds biotin"],
      ["B9 – Folate", "THF", "Megaloblastic anemia, neural tube defects", "NO methylmalonic acid rise"],
      ["B12 – Cobalamin", "Methylmalonyl-CoA", "Megaloblastic anemia + subacute combined degeneration", "↑ Methylmalonic acid + ↑ homocysteine"],
    ],
    0.3, 1.0, 9.4
  );
}

{
  const s = contentSlide("B12 vs Folate & Fat-Soluble Vitamins (ADEK)", ACCENT);
  card(s, 0.3, 1.0, 4.5, 2.5, "B12 vs FOLATE – How to Distinguish", [
    "BOTH cause: megaloblastic anemia, hypersegmented neutrophils",
    "",
    "B12 ONLY: neurological symptoms",
    "(posterior column + lateral column demyelination)",
    "↑ Methylmalonic acid",
    "Found only in animal products",
    "",
    "FOLATE ONLY: associated with pregnancy,",
    "MTX toxicity, phenytoin use",
    "Normal methylmalonic acid",
  ], ACCENT);

  addTable(s,
    ["Vitamin", "Function", "Deficiency", "Toxicity"],
    [
      ["A (Retinol)", "Vision, epithelial integrity, immunity", "Night blindness, xerophthalmia", "Teratogenic! Pseudotumor cerebri"],
      ["D (Calcitriol)", "Ca²⁺ + phosphate absorption", "Rickets (kids), Osteomalacia (adults)", "Hypercalcemia, nephrolithiasis"],
      ["E (Tocopherol)", "Antioxidant, protects RBC membranes", "Hemolytic anemia, ataxia", "Potentiates warfarin"],
      ["K", "Clotting factors II, VII, IX, X, Prot C&S", "Bleeding; neonates at risk", "Warfarin antagonism"],
    ],
    5.0, 1.0, 4.7
  );

  s.addShape(pres.shapes.ROUNDED_RECTANGLE, { x: 0.3, y: 3.65, w: 4.5, h: 1.7, fill: { color: "0D1B2A" }, line: { color: ACCENT2, width: 1.5 }, rectRadius: 0.07 });
  s.addText([
    { text: "⚠️  FAT-SOLUBLE vits (ADEK) are stored in fat and liver.\n", options: { bold: true, color: ACCENT2, breakLine: true, fontSize: 11, fontFace: "Calibri" } },
    { text: "Toxicity more likely than water-soluble vitamins.\n", options: { color: LIGHT_TXT, breakLine: true, fontSize: 10, fontFace: "Calibri" } },
    { text: "Vitamin A toxicity: teratogenic in pregnancy (avoid isotretinoin!).\n", options: { color: ACCENT3, breakLine: true, fontSize: 10, fontFace: "Calibri" } },
    { text: "Vitamin K: antagonized by warfarin (blocks gamma-carboxylation).", options: { color: LIGHT_TXT, fontSize: 10, fontFace: "Calibri" } },
  ], { x: 0.45, y: 3.73, w: 4.15, h: 1.55 });
}

// ══════════════════════════════════════════════════════════════
// SECTION 6 – ENZYME KINETICS
// ══════════════════════════════════════════════════════════════
sectionHeader("06", "Enzyme Kinetics", "Km · Vmax · Inhibition Types · Lineweaver-Burk");

{
  const s = contentSlide("Enzyme Kinetics – Concepts Only (No Math!)", ACCENT);
  card(s, 0.3, 1.0, 4.5, 2.0, "BASICS", [
    "Km = substrate [S] at half-Vmax",
    "LOW Km = HIGH affinity (enzyme 'likes' substrate)",
    "HIGH Km = LOW affinity",
    "",
    "Vmax = max rate at saturating [S]",
    "Lineweaver-Burk = double reciprocal plot",
  ], ACCENT);

  addTable(s,
    ["Inhibition Type", "Km", "Vmax", "How?"],
    [
      ["Competitive", "↑ Increases", "No change", "Competes at active site; outcompete with ↑ substrate"],
      ["Noncompetitive", "No change", "↓ Decreases", "Binds allosteric site; can't overcome with more substrate"],
      ["Uncompetitive", "↓ Decreases", "↓ Decreases", "Binds only enzyme-substrate complex; both decrease equally"],
    ],
    0.3, 3.1, 9.4
  );

  card(s, 5.0, 1.0, 4.7, 2.0, "MCQ EXAMPLES", [
    "Methotrexate → COMPETITIVE inhibitor of DHFR",
    "→ Give leucovorin (folinic acid) to rescue",
    "",
    "Statins → COMPETITIVE inhibitors of HMG-CoA reductase",
    "",
    "Penicillin → IRREVERSIBLE inhibitor of transpeptidase",
    "(covalent bond – cannot overcome with more substrate)",
  ], ACCENT2);
}

// ══════════════════════════════════════════════════════════════
// SECTION 7 – MOLECULAR BIOLOGY
// ══════════════════════════════════════════════════════════════
sectionHeader("07", "Molecular Biology", "DNA Replication · Transcription · Translation Antibiotics");

{
  const s = contentSlide("DNA Replication, Transcription & Translation Antibiotics", ACCENT);
  card(s, 0.3, 1.0, 4.5, 2.4, "DNA REPLICATION", [
    "Direction: always 5' → 3'",
    "Leading strand: continuous synthesis",
    "Lagging strand: Okazaki fragments (discontinuous)",
    "DNA Pol III: main replication enzyme (prokaryotes)",
    "DNA Pol I: removes RNA primers (prokaryotes)",
    "DNA Pol α, δ, ε: eukaryotes",
    "Telomerase: extends chromosome ends (uses RNA template)",
  ], ACCENT);

  card(s, 5.0, 1.0, 4.7, 2.4, "TRANSCRIPTION", [
    "RNA Pol II → transcribes mRNA (eukaryotes)",
    "TATA box → eukaryotic promoter element",
    "Pribnow box (−10) → prokaryotic promoter",
    "",
    "⚠️ Alpha-amanitin (Amanita mushroom):",
    "→ Inhibits RNA Pol II → severe liver failure",
    "",
    "Rifampin → inhibits prokaryotic RNA Pol",
    "(TB treatment)",
  ], ACCENT2);

  addTable(s,
    ["Antibiotic", "Target", "Mechanism"],
    [
      ["Aminoglycosides", "30S ribosome", "Misreading of mRNA codon"],
      ["Tetracyclines", "30S ribosome", "Block aminoacyl-tRNA entry"],
      ["Chloramphenicol", "50S ribosome", "Inhibits peptidyltransferase activity"],
      ["Macrolides (erythro)", "50S ribosome", "Block translocation"],
      ["Linezolid", "50S ribosome", "Blocks initiation complex formation"],
    ],
    0.3, 3.55, 9.4
  );

  s.addText("Mnemonic:  30S = 'AT' (Aminoglycosides, Tetracyclines)  |  50S = 'CCML' (Chloramphenicol, Clindamycin, Macrolides, Linezolid)", {
    x: 0.3, y: 5.25, w: 9.4, h: 0.32,
    fontSize: 10, bold: true, color: ACCENT2, fontFace: "Calibri", align: "center"
  });
}

// ══════════════════════════════════════════════════════════════
// SECTION 8 – UREA CYCLE
// ══════════════════════════════════════════════════════════════
sectionHeader("08", "Urea Cycle", "Nitrogen disposal · OTC deficiency · Hyperammonemia");

{
  const s = contentSlide("Urea Cycle – Getting Rid of Toxic Ammonia", ACCENT);
  card(s, 0.3, 1.0, 4.5, 4.35, "UREA CYCLE BASICS", [
    "Purpose: Convert NH4+ (ammonia) → urea (excreted)",
    "",
    "Location: Liver",
    "• Starts in mitochondria (carbamoyl phosphate step)",
    "• Finishes in cytoplasm",
    "",
    "Rate-limiting enzyme: CPS-I",
    "(Carbamoyl Phosphate Synthetase I)",
    "• Activated by: N-acetylglutamate (NAG)",
    "• NAG made from: Glutamate + Acetyl-CoA",
    "",
    "Urea cycle amino acids:",
    "Ornithine → Citrulline → Argininosuccinate",
    "→ Arginine → Ornithine + UREA",
  ], ACCENT);

  card(s, 5.0, 1.0, 4.7, 2.3, "OTC DEFICIENCY (Most Common Defect)", [
    "Enzyme: Ornithine transcarbamylase",
    "Inheritance: X-LINKED (most common X-linked metabolic disease)",
    "",
    "Accumulates: Carbamoyl phosphate → orotic acid",
    "→ HIGH orotic acid in urine ← classic finding!",
    "",
    "Triggers: High-protein meal, illness/stress",
    "Presentation: Hyperammonemia, encephalopathy",
  ], ACCENT3);

  card(s, 5.0, 3.45, 4.7, 1.9, "HYPERAMMONEMIA SYMPTOMS", [
    "Confusion, tremor, asterixis",
    "Slurred speech, cerebral edema, coma",
    "Same as hepatic encephalopathy!",
    "",
    "Treatment: Low-protein diet + arginine",
    "+ Sodium benzoate/phenylacetate",
    "(alternative nitrogen excretion routes)",
  ], ACCENT2);
}

// ══════════════════════════════════════════════════════════════
// SECTION 9 – QUICK MCQ GUIDE
// ══════════════════════════════════════════════════════════════
sectionHeader("09", "Quick MCQ Guide", "Classic presentations → instant diagnosis");

{
  const s = contentSlide("Classic Scenario → Diagnosis (MCQ Cheat Sheet)", ACCENT2);
  addTable(s,
    ["Clinical Scenario", "Diagnosis / Mechanism"],
    [
      ["Exercise + NO lactate rise on forearm ischemic test", "McArdle disease (muscle phosphorylase defect – Type V glycogenosis)"],
      ["Fasting hypoketotic hypoglycemia in infant", "MCAD deficiency (medium-chain acyl-CoA dehydrogenase)"],
      ["Alcoholic + confusion + nystagmus + ataxia", "Wernicke encephalopathy (Thiamine/B1 deficiency)"],
      ["High homocysteine + HIGH methylmalonic acid", "Vitamin B12 deficiency"],
      ["High homocysteine + NORMAL methylmalonic acid", "Folate deficiency"],
      ["Fair infant + musty/mousy odor + intellectual disability", "PKU (phenylalanine hydroxylase deficiency)"],
      ["Cardiomegaly + floppy baby", "Pompe disease (Type II – acid maltase, lysosomal)"],
      ["Severe hypoglycemia + lactic acidosis + ↑ uric acid", "Von Gierke (Type I – glucose-6-phosphatase deficiency)"],
      ["Tall + lens dislocation DOWNWARD + thrombosis", "Homocystinuria (CBS deficiency – B6)"],
      ["Tall + lens dislocation UPWARD + aortic root dilation", "Marfan syndrome (fibrillin-1 defect)"],
      ["Raw egg eater + hair loss + dermatitis", "Biotin (B7) deficiency – avidin binds biotin"],
      ["Child in developing country + night blindness", "Vitamin A deficiency"],
      ["Perifollicular hemorrhage + gum bleeding", "Scurvy (Vitamin C deficiency – collagen cross-linking)"],
    ],
    0.3, 1.0, 9.4
  );
}

// ══════════════════════════════════════════════════════════════
// SLIDE – PATHWAY CONNECTIONS
// ══════════════════════════════════════════════════════════════
{
  const s = contentSlide("The Big Picture – How Pathways Connect", ACCENT);

  // Fed state card
  card(s, 0.3, 1.0, 4.5, 2.1, "FED STATE (Insulin HIGH)", [
    "✓ Glycolysis ON",
    "✓ Fatty acid synthesis ON (ACC activated by citrate)",
    "✓ Glycogen synthesis ON",
    "✓ Protein synthesis ON",
    "✗ Gluconeogenesis OFF",
    "✗ Beta-oxidation OFF (malonyl-CoA inhibits CAT-I)",
  ], ACCENT);

  // Fasting state card
  card(s, 5.0, 1.0, 4.7, 2.1, "FASTING STATE (Glucagon HIGH)", [
    "✓ Glycogenolysis ON",
    "✓ Gluconeogenesis ON",
    "✓ Beta-oxidation ON",
    "✓ Ketogenesis ON",
    "✗ Glycogen synthesis OFF",
    "✗ Fatty acid synthesis OFF",
  ], ACCENT2);

  // Alcoholism box
  card(s, 0.3, 3.25, 9.4, 2.1, "⚠️ ALCOHOLISM – Disrupts Everything (High-Yield MCQ Pattern)", [
    "Alcohol → Acetaldehyde → Acetate (both steps use NAD+ → generate NADH)",
    "High NADH/NAD+ ratio → inhibits: gluconeogenesis (pyruvate → OAA blocked), TCA cycle, beta-oxidation",
    "Results: Hypoglycemia (can't make glucose), Lactic acidosis (pyruvate → lactate), Fatty liver (FA synthesis↑, oxidation↓)",
    "High uric acid (gout) – lactate competes with urate for renal excretion",
    "HIGH NADH also: pyruvate → lactate, OAA → malate (depletes TCA), acetyl-CoA → FA (fatty liver)",
  ], ACCENT3);
}

// ══════════════════════════════════════════════════════════════
// FINAL SLIDE – STUDY TIPS
// ══════════════════════════════════════════════════════════════
{
  const s = pres.addSlide();
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  s.addText("Top 5 USMLE Biochemistry Study Tips", {
    x: 0.5, y: 0.3, w: 9, h: 0.7,
    fontSize: 22, bold: true, color: WHITE, fontFace: "Calibri", align: "center"
  });

  const tips = [
    ["1", ACCENT,  "Learn the RATE-LIMITING ENZYME of each pathway", "Know what activates it and what inhibits it. Every pathway question tests this."],
    ["2", ACCENT2, "ALWAYS ask: what is blocked?", "Disease questions describe enzyme deficiency. Ask: what accumulates? What is deficient downstream?"],
    ["3", ACCENT3, "Master the fed vs. fasting switch", "Insulin = fed (build). Glucagon = fasting (break down). Every organ obeys this rule."],
    ["4", "5BC0EB", "Connect B vitamins to their cofactor role", "B1→PDH, B3→NAD+, B6→transamination, B12→methylmalonyl-CoA. Know the coenzyme form."],
    ["5", "B39DBC", "Practice MCQs from FA + Kaplan", "Biochem is pattern recognition. The same 20 clinical vignettes appear repeatedly."],
  ];

  tips.forEach(([num, col, heading, body], i) => {
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  });
}

// ══════════════════════════════════════════════════════════════
// WRITE FILE
// ══════════════════════════════════════════════════════════════
pres.writeFile({ fileName: "/home/daytona/workspace/biochem-usmle-ppt/USMLE_Biochemistry_HighYield.pptx" })
  .then(() => console.log("SUCCESS: PPTX written."))
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