const pptxgen = require("pptxgenjs");
const { execSync } = require("child_process");

// ─── Fetch images ─────────────────────────────────────────────────────────────
const imgUrls = [
  "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_09c4761b1c4dcfc1ed149f3f7dcb1e685afc10b3eb50c0f77460459e58eecf50.jpg",  // T2DM hyperglycemia pathophysiology
  "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_941c21066dfd3864f40b5622a42c85b1791757b3d5bc203e73b2853099bfe1a8.jpg",  // Insulin signaling GLUT-4
  "https://cdn.orris.care/cdss_images/GLGCA_3094724_1763331160817_d5c1f005-88e2-415b-bd53-3321ea5ff15d.png",                    // DM Classification table
  "https://cdn.orris.care/cdss_images/HARRISON_1763035986492_e2de3a37-3e6e-4ec4-9178-bf8624edacba.png",                        // DKA/HHS lab values table
];

let imgs = [];
try {
  const raw = execSync(
    `node /home/daytona/skills/shared/scripts/fetch_images.js ${imgUrls.map(u => `"${u}"`).join(" ")}`,
    { timeout: 60000 }
  ).toString();
  imgs = JSON.parse(raw);
} catch(e) {
  console.error("Image fetch error:", e.message);
  imgs = imgUrls.map(url => ({ url, base64: null, error: e.message }));
}

// ─── Theme ────────────────────────────────────────────────────────────────────
const DARK_BLUE  = "0A2647";   // dominant background on title/section slides
const MID_BLUE   = "144272";   // card backgrounds
const ACCENT     = "205295";   // accent headers
const LIGHT_BLUE = "2C74B3";   // highlight bars
const WHITE      = "FFFFFF";
const NEAR_WHITE = "E8F4FD";
const GOLD       = "F4A927";
const SOFT_GRAY  = "D6E8FA";
const TEXT_DARK  = "0A2647";

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Diabetes Mellitus & Diabetic Emergencies";
pres.author = "Medical Education";

// ─── Helper: slide background ─────────────────────────────────────────────────
function setBg(slide, color) {
  slide.background = { color };
}

// ─── Helper: section title slide ──────────────────────────────────────────────
function addSectionSlide(pres, num, title, subtitle) {
  const s = pres.addSlide();
  setBg(s, DARK_BLUE);
  // left accent bar
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 0.18, h: 5.625, fill: { color: GOLD } });
  // section number
  s.addText(`0${num}`, { x: 0.3, y: 0.8, w: 1.2, h: 1, fontSize: 52, bold: true, color: GOLD, fontFace: "Calibri" });
  // title
  s.addText(title, { x: 0.3, y: 1.9, w: 9.2, h: 1.2, fontSize: 34, bold: true, color: WHITE, fontFace: "Calibri" });
  if (subtitle) {
    s.addText(subtitle, { x: 0.3, y: 3.1, w: 9.2, h: 0.8, fontSize: 18, color: SOFT_GRAY, fontFace: "Calibri", italic: true });
  }
  return s;
}

// ─── Helper: content slide with title bar ─────────────────────────────────────
function addContentSlide(pres, title, bgColor) {
  const s = pres.addSlide();
  setBg(s, bgColor || NEAR_WHITE);
  // title bar
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 10, h: 0.72, fill: { color: DARK_BLUE } });
  s.addText(title, { x: 0.18, y: 0.05, w: 9.4, h: 0.62, fontSize: 20, bold: true, color: WHITE, fontFace: "Calibri", valign: "middle" });
  // bottom accent line
  s.addShape(pres.ShapeType.rect, { x: 0, y: 5.42, w: 10, h: 0.2, fill: { color: LIGHT_BLUE } });
  s.addText("Diabetes Mellitus & Diabetic Emergencies  |  Medical Education", {
    x: 0.2, y: 5.42, w: 9.6, h: 0.2, fontSize: 8, color: WHITE, fontFace: "Calibri", valign: "middle"
  });
  return s;
}

// ─── Helper: two-column layout ────────────────────────────────────────────────
function addTwoColSlide(pres, title, leftTitle, leftItems, rightTitle, rightItems) {
  const s = addContentSlide(pres, title);
  // Left card
  s.addShape(pres.ShapeType.rect, { x: 0.15, y: 0.85, w: 4.65, h: 4.45, fill: { color: MID_BLUE }, line: { color: MID_BLUE } });
  s.addText(leftTitle, { x: 0.25, y: 0.88, w: 4.45, h: 0.42, fontSize: 13, bold: true, color: GOLD, fontFace: "Calibri" });
  const leftBullets = leftItems.map((t, i) => ({ text: t, options: { bullet: true, breakLine: i < leftItems.length - 1, fontSize: 11, color: WHITE, fontFace: "Calibri" } }));
  s.addText(leftBullets, { x: 0.25, y: 1.32, w: 4.45, h: 3.8 });
  // Right card
  s.addShape(pres.ShapeType.rect, { x: 5.2, y: 0.85, w: 4.65, h: 4.45, fill: { color: ACCENT }, line: { color: ACCENT } });
  s.addText(rightTitle, { x: 5.3, y: 0.88, w: 4.45, h: 0.42, fontSize: 13, bold: true, color: GOLD, fontFace: "Calibri" });
  const rightBullets = rightItems.map((t, i) => ({ text: t, options: { bullet: true, breakLine: i < rightItems.length - 1, fontSize: 11, color: WHITE, fontFace: "Calibri" } }));
  s.addText(rightBullets, { x: 5.3, y: 1.32, w: 4.45, h: 3.8 });
  return s;
}

// ─── Helper: bullet slide ─────────────────────────────────────────────────────
function addBulletSlide(pres, title, items, noteText) {
  const s = addContentSlide(pres, title);
  const bullets = items.map((item, i) => {
    if (typeof item === "string") {
      return { text: item, options: { bullet: true, breakLine: i < items.length - 1, fontSize: 13, color: TEXT_DARK, fontFace: "Calibri" } };
    } else {
      // { text, bold, indent, color }
      return { text: item.text, options: { bullet: !item.indent, indentLevel: item.indent ? 1 : 0, breakLine: i < items.length - 1, fontSize: item.bold ? 14 : 12, bold: item.bold || false, color: item.color || TEXT_DARK, fontFace: "Calibri" } };
    }
  });
  s.addText(bullets, { x: 0.3, y: 0.85, w: 9.4, h: 4.5 });
  return s;
}

// ─── Helper: card grid (2x2 or 1x4) ─────────────────────────────────────────
function addCardGrid(pres, title, cards) {
  // cards: [{title, items[]}]  max 4
  const s = addContentSlide(pres, title);
  const positions = [
    { x: 0.15, y: 0.82 }, { x: 5.1, y: 0.82 },
    { x: 0.15, y: 3.1  }, { x: 5.1, y: 3.1  }
  ];
  const colors = [MID_BLUE, ACCENT, LIGHT_BLUE, "1B4F8A"];
  cards.forEach((card, i) => {
    const p = positions[i];
    const col = colors[i];
    s.addShape(pres.ShapeType.rect, { x: p.x, y: p.y, w: 4.75, h: 2.15, fill: { color: col } });
    s.addText(card.title, { x: p.x + 0.1, y: p.y + 0.05, w: 4.55, h: 0.38, fontSize: 12, bold: true, color: GOLD, fontFace: "Calibri" });
    const bItems = card.items.map((t, j) => ({ text: t, options: { bullet: true, breakLine: j < card.items.length - 1, fontSize: 10, color: WHITE, fontFace: "Calibri" } }));
    s.addText(bItems, { x: p.x + 0.1, y: p.y + 0.44, w: 4.55, h: 1.65 });
  });
  return s;
}

// ─── Slide 1: TITLE ───────────────────────────────────────────────────────────
{
  const s = pres.addSlide();
  setBg(s, DARK_BLUE);
  // Decorative circles
  s.addShape(pres.ShapeType.ellipse, { x: 7.6, y: -0.8, w: 4.0, h: 4.0, fill: { color: MID_BLUE }, line: { color: MID_BLUE } });
  s.addShape(pres.ShapeType.ellipse, { x: 8.2, y: 3.2, w: 2.5, h: 2.5, fill: { color: ACCENT }, line: { color: ACCENT } });
  // Gold accent bar
  s.addShape(pres.ShapeType.rect, { x: 0, y: 2.55, w: 10, h: 0.08, fill: { color: GOLD } });
  // Main title
  s.addText("DIABETES MELLITUS", { x: 0.5, y: 0.5, w: 7.5, h: 1.1, fontSize: 40, bold: true, color: WHITE, fontFace: "Calibri", charSpacing: 2 });
  s.addText("& DIABETIC EMERGENCIES", { x: 0.5, y: 1.55, w: 7.5, h: 0.9, fontSize: 28, bold: true, color: GOLD, fontFace: "Calibri", charSpacing: 1 });
  // Sub
  s.addText("Physiology · Pathophysiology · Clinical Features · Investigations · Management", {
    x: 0.5, y: 2.72, w: 8.5, h: 0.6, fontSize: 14, color: SOFT_GRAY, fontFace: "Calibri", italic: true
  });
  // bottom info
  s.addText("Goldman-Cecil Medicine  |  Harrison's Principles  |  Medical Education 2026", {
    x: 0.5, y: 5.1, w: 9, h: 0.35, fontSize: 11, color: SOFT_GRAY, fontFace: "Calibri"
  });
}

// ─── Slide 2: AGENDA ─────────────────────────────────────────────────────────
{
  const s = addContentSlide(pres, "Agenda");
  setBg(s, DARK_BLUE);
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 10, h: 0.72, fill: { color: LIGHT_BLUE } });
  s.addText("Agenda", { x: 0.18, y: 0.05, w: 9.4, h: 0.62, fontSize: 20, bold: true, color: WHITE, fontFace: "Calibri", valign: "middle" });
  const topics = [
    ["01", "Essential Physiology", "Insulin synthesis, glucose homeostasis, counter-regulatory hormones"],
    ["02", "Definitions & Classification", "WHO/ADA criteria, types of diabetes mellitus"],
    ["03", "Pathophysiology", "Type 1 (autoimmune), Type 2 (insulin resistance + β-cell failure)"],
    ["04", "Clinical Features & Natural History", "Symptoms, complications, disease progression"],
    ["05", "Investigations", "Diagnosis, HbA1c, OGTT, monitoring"],
    ["06", "Management", "Lifestyle, pharmacotherapy, targets"],
    ["07", "Diabetic Emergencies", "DKA, HHS, Hypoglycemia — recognition & management"],
  ];
  topics.forEach((t, i) => {
    const col = i % 2 === 0 ? MID_BLUE : ACCENT;
    const yp = 0.82 + i * 0.64;
    s.addShape(pres.ShapeType.rect, { x: 0.2, y: yp, w: 9.6, h: 0.58, fill: { color: col } });
    s.addText(t[0], { x: 0.3, y: yp + 0.05, w: 0.55, h: 0.48, fontSize: 14, bold: true, color: GOLD, fontFace: "Calibri", valign: "middle" });
    s.addText(t[1], { x: 0.9, y: yp + 0.05, w: 2.8, h: 0.48, fontSize: 13, bold: true, color: WHITE, fontFace: "Calibri", valign: "middle" });
    s.addText(t[2], { x: 3.75, y: yp + 0.05, w: 5.9, h: 0.48, fontSize: 11, color: SOFT_GRAY, fontFace: "Calibri", valign: "middle", italic: true });
  });
}

// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 01: ESSENTIAL PHYSIOLOGY
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 1, "Essential Physiology", "Insulin synthesis, glucose homeostasis & counter-regulatory hormones");

// Slide: Insulin — Structure & Synthesis
addTwoColSlide(pres,
  "Insulin — Structure & Synthesis",
  "Biosynthesis",
  [
    "Produced by pancreatic β-cells in islets of Langerhans",
    "Gene on chromosome 11; mRNA → preproinsulin",
    "Preproinsulin → proinsulin (ER) → insulin + C-peptide (Golgi)",
    "Stored as hexameric zinc complex in secretory granules",
    "Glucose-stimulated secretion: biphasic (early ~1–3 min; sustained ~2 h)",
    "C-peptide: equimolar to insulin; marker of endogenous secretion",
  ],
  "Structure & Key Actions",
  [
    "51 amino acids: A-chain (21 aa) + B-chain (30 aa) connected by 2 disulfide bonds",
    "Binds insulin receptor tyrosine kinase → IRS-1/2 → PI3K/AKT",
    "GLUT-4 translocation → glucose uptake in muscle & adipose",
    "Promotes glycogen synthesis, protein synthesis, lipogenesis",
    "Inhibits gluconeogenesis, glycogenolysis, lipolysis, ketogenesis",
    "Half-life: ~5 min; degraded by liver (50%) and kidney",
  ]
);

// Slide: Glucose Homeostasis
{
  const s = addContentSlide(pres, "Glucose Homeostasis");
  // Left image area
  if (imgs[1] && imgs[1].base64) {
    s.addImage({ data: imgs[1].base64, x: 5.5, y: 0.82, w: 4.3, h: 3.5 });
  }
  const bullets = [
    { text: "Normal fasting plasma glucose: 70–100 mg/dL (3.9–5.6 mmol/L)", bold: true },
    { text: "Postprandial glucose peak: <140 mg/dL at 2 h" },
    { text: "Renal threshold for glycosuria: ~180–200 mg/dL", bold: false },
    { text: "After a meal: ↑ glucose → ↑ insulin, ↓ glucagon" },
    { text: "Fasting state: ↓ insulin → hepatic glucose output via gluconeogenesis + glycogenolysis" },
    { text: "Counter-regulatory hormones (glucagon, cortisol, GH, catecholamines) raise glucose" },
    { text: "Insulin:glucagon ratio governs hepatic glucose output" },
    { text: "Glucose enters cells via GLUT transporters (GLUT-2 in liver/pancreas; GLUT-4 in muscle/fat)" },
  ];
  const bItems = bullets.map((b, i) => ({
    text: b.text,
    options: { bullet: true, breakLine: i < bullets.length - 1, fontSize: b.bold ? 13 : 12, bold: b.bold || false, color: TEXT_DARK, fontFace: "Calibri" }
  }));
  s.addText(bItems, { x: 0.3, y: 0.85, w: 5.1, h: 4.45 });
}

// Slide: Counter-regulatory Hormones
addCardGrid(pres, "Counter-Regulatory Hormones", [
  { title: "Glucagon (α-cells)", items: ["Secreted in response to hypoglycemia & amino acids", "Stimulates glycogenolysis & gluconeogenesis", "Increases hepatic ketone production", "Suppressed by insulin and hyperglycemia"] },
  { title: "Epinephrine & Norepinephrine", items: ["Rapid response to hypoglycemia (<3.8 mmol/L)", "Inhibit insulin secretion", "Stimulate glucagon secretion & hepatic glucose output", "Cause adrenergic symptoms (palpitations, tremor, sweating)"] },
  { title: "Cortisol", items: ["Increases gluconeogenesis substrates (amino acids)", "Promotes insulin resistance in muscle", "Impairs GLUT-4 translocation", "Elevated in stress, Cushing syndrome → hyperglycemia"] },
  { title: "Growth Hormone", items: ["Stimulates IGF-1 in liver", "Anti-insulin: promotes lipolysis & gluconeogenesis", "Dawn phenomenon: GH surge overnight → AM hyperglycemia in T1DM", "Acromegaly → secondary diabetes"] },
]);


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 02: DEFINITIONS & CLASSIFICATION
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 2, "Definitions & Classification", "WHO/ADA diagnostic criteria and disease taxonomy");

// Slide: Definition of Diabetes
addBulletSlide(pres, "Definition of Diabetes Mellitus", [
  { text: "Diabetes mellitus (DM) is a group of metabolic diseases characterized by:", bold: true },
  { text: "Hyperglycemia resulting from defects in insulin secretion, insulin action, or both", indent: true },
  { text: "Chronic hyperglycemia is associated with long-term damage to multiple organs", indent: true },
  { text: "Affects >500 million people worldwide; 7th leading cause of death in the USA", indent: true },
  { text: "WHO Diagnostic Criteria (any one of the following):", bold: true, color: ACCENT },
  { text: "Fasting plasma glucose (FPG) ≥ 7.0 mmol/L (126 mg/dL)  [8-h fast]", indent: true },
  { text: "2-hour plasma glucose ≥ 11.1 mmol/L (200 mg/dL) during 75g OGTT", indent: true },
  { text: "HbA1c ≥ 6.5% (48 mmol/mol) — confirmed by repeat testing if asymptomatic", indent: true },
  { text: "Random plasma glucose ≥ 11.1 mmol/L + classic hyperglycaemic symptoms", indent: true },
  { text: "Pre-diabetes thresholds:", bold: true, color: ACCENT },
  { text: "Impaired fasting glucose (IFG): FPG 6.1–6.9 mmol/L  |  HbA1c 5.7–6.4%", indent: true },
  { text: "Impaired glucose tolerance (IGT): 2-h OGTT 7.8–11.0 mmol/L", indent: true },
]);

// Slide: Classification
{
  const s = addContentSlide(pres, "Classification of Diabetes Mellitus (ADA/WHO)");
  if (imgs[2] && imgs[2].base64) {
    s.addImage({ data: imgs[2].base64, x: 5.5, y: 0.82, w: 4.3, h: 4.55 });
  }
  const items = [
    { text: "TYPE 1 — Immune-mediated β-cell destruction", bold: true, color: DARK_BLUE },
    { text: "Absolute insulin deficiency; autoimmune (HLA-DR3/DR4, anti-GAD, anti-IA2)", indent: true },
    { text: "TYPE 2 — Progressive β-cell failure + insulin resistance", bold: true, color: DARK_BLUE },
    { text: "Relative insulin deficiency; obesity-related; accounts for ~90% of cases", indent: true },
    { text: "GESTATIONAL DIABETES MELLITUS (GDM)", bold: true, color: DARK_BLUE },
    { text: "Diagnosed in 2nd/3rd trimester; resolves after delivery; ↑ T2DM risk later", indent: true },
    { text: "OTHER SPECIFIC TYPES", bold: true, color: DARK_BLUE },
    { text: "MODY (monogenic), pancreatic disease, endocrinopathies (Cushing, acromegaly)", indent: true },
    { text: "Drug-induced (corticosteroids, clozapine, SGLT2i → euDKA)", indent: true },
    { text: "Infections (rubella, CMV — rare)", indent: true },
  ];
  const bItems = items.map((item, i) => ({
    text: item.text,
    options: { bullet: !item.indent, indentLevel: item.indent ? 1 : 0, breakLine: i < items.length - 1, fontSize: item.bold ? 13 : 11.5, bold: item.bold || false, color: item.color || TEXT_DARK, fontFace: "Calibri" }
  }));
  s.addText(bItems, { x: 0.3, y: 0.85, w: 5.0, h: 4.5 });
}

// Slide: Type 1 vs Type 2 Comparison
{
  const s = addContentSlide(pres, "Type 1 vs Type 2 Diabetes — Key Differences");
  const headers = ["Feature", "Type 1", "Type 2"];
  const rows = [
    ["Age of onset", "Usually <30 yrs (peak: childhood)", "Usually >40 yrs (increasingly younger)"],
    ["Body habitus", "Normal / underweight", "Overweight / obese (>85%)"],
    ["Onset", "Acute / subacute", "Insidious (years)"],
    ["Pathogenesis", "Autoimmune β-cell destruction", "Insulin resistance + β-cell dysfunction"],
    ["Insulin level", "Absent / very low", "Normal, elevated, or low (late)"],
    ["C-peptide", "Undetectable", "Detectable"],
    ["Autoantibodies", "Anti-GAD, anti-IA2, anti-ZnT8", "Absent"],
    ["Ketosis", "Prone (DKA)", "Resistant (until late)"],
    ["Treatment", "Insulin mandatory", "Lifestyle → oral agents → insulin"],
    ["HLA association", "DR3, DR4", "No strong HLA link"],
  ];
  const colW = [2.1, 3.7, 3.7];
  const colX = [0.12, 2.24, 5.96];
  // header
  headers.forEach((h, ci) => {
    s.addShape(pres.ShapeType.rect, { x: colX[ci], y: 0.78, w: colW[ci], h: 0.38, fill: { color: DARK_BLUE } });
    s.addText(h, { x: colX[ci] + 0.05, y: 0.78, w: colW[ci] - 0.1, h: 0.38, fontSize: 11, bold: true, color: GOLD, fontFace: "Calibri", valign: "middle" });
  });
  rows.forEach((row, ri) => {
    const yp = 1.18 + ri * 0.40;
    const bg = ri % 2 === 0 ? SOFT_GRAY : WHITE;
    row.forEach((cell, ci) => {
      s.addShape(pres.ShapeType.rect, { x: colX[ci], y: yp, w: colW[ci], h: 0.38, fill: { color: ci === 0 ? ACCENT : bg }, line: { color: "CCCCCC", pt: 0.5 } });
      s.addText(cell, { x: colX[ci] + 0.05, y: yp, w: colW[ci] - 0.1, h: 0.38, fontSize: 10, bold: ci === 0, color: ci === 0 ? WHITE : TEXT_DARK, fontFace: "Calibri", valign: "middle" });
    });
  });
}


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 03: PATHOPHYSIOLOGY
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 3, "Pathophysiology", "Mechanisms of hyperglycemia in Type 1 and Type 2 DM");

// Type 1 pathophysiology
addBulletSlide(pres, "Pathophysiology — Type 1 Diabetes Mellitus", [
  { text: "Autoimmune Destruction of β-cells (Immune-Mediated)", bold: true, color: ACCENT },
  { text: "Genetic susceptibility: HLA class II alleles (HLA-DR3, HLA-DR4) on chromosome 6p21" },
  { text: "Environmental triggers: enteroviruses (Coxsackievirus B), dietary antigens (early cow's milk)" },
  { text: "Molecular mimicry: viral antigens resemble islet cell proteins → autoreactive T-cells" },
  { text: "CD4+ & CD8+ T-lymphocyte-mediated destruction of β-cells (insulitis)" },
  { text: "Circulating autoantibodies: anti-GAD65, anti-IA2, anti-insulin (ICA), anti-ZnT8" },
  { text: "Progressive β-cell loss over months to years before clinical diagnosis" },
  { text: "Absolute insulin deficiency → unopposed catabolic state", bold: true, color: ACCENT },
  { text: "↑ Glucagon → glycogenolysis + gluconeogenesis → hyperglycemia" },
  { text: "↑ Lipolysis → free fatty acids → hepatic ketogenesis (acetoacetate, β-hydroxybutyrate, acetone)" },
  { text: "Osmotic diuresis (glycosuria) → dehydration, electrolyte loss → DKA if untreated" },
  { text: "~90% β-cell mass must be destroyed before clinical hyperglycemia appears" },
]);

// Type 2 pathophysiology
{
  const s = addContentSlide(pres, "Pathophysiology — Type 2 Diabetes Mellitus");
  if (imgs[0] && imgs[0].base64) {
    s.addImage({ data: imgs[0].base64, x: 5.5, y: 0.82, w: 4.3, h: 3.6 });
    s.addText("Multi-organ contribution to hyperglycemia in T2DM", { x: 5.5, y: 4.42, w: 4.3, h: 0.35, fontSize: 9, color: ACCENT, fontFace: "Calibri", italic: true, align: "center" });
  }
  const items = [
    { text: "The 'Ominous Octet' (DeFronzo) — Multiple organ defects:", bold: true },
    { text: "Insulin resistance (muscle): reduced GLUT-4 translocation; IRS-1 phosphorylation impaired by lipids", indent: true },
    { text: "β-cell failure (pancreas): progressive loss of first-phase insulin secretion; glucolipotoxicity; amyloid deposition (IAPP)", indent: true },
    { text: "Liver: excessive gluconeogenesis; resistance to insulin suppression of hepatic glucose output", indent: true },
    { text: "α-cell dysfunction: paradoxical hyperglucagonemia in hyperglycaemic state", indent: true },
    { text: "Brain: impaired satiety signalling, insulin resistance centrally", indent: true },
    { text: "Kidney: increased glucose reabsorption via SGLT2 (upregulated in T2DM)", indent: true },
    { text: "Risk factors amplifying pathophysiology:", bold: true },
    { text: "Obesity (BMI ≥30): visceral fat → proinflammatory cytokines (TNF-α, IL-6), ↓ adiponectin, ↑ FFA" },
    { text: "Genetic: TCF7L2, KCNJ11 polymorphisms impair insulin secretion" },
    { text: "Metabolic progression: normoglycaemia → pre-diabetes → overt T2DM over years-decades" },
  ];
  const bItems = items.map((item, i) => ({
    text: item.text,
    options: { bullet: !item.indent, indentLevel: item.indent ? 1 : 0, breakLine: i < items.length - 1, fontSize: item.bold ? 13 : 11, bold: item.bold || false, color: item.color || TEXT_DARK, fontFace: "Calibri" }
  }));
  s.addText(bItems, { x: 0.3, y: 0.85, w: 5.0, h: 4.5 });
}


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 04: CLINICAL FEATURES & NATURAL HISTORY
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 4, "Clinical Features & Natural History", "Symptoms, complications, and disease trajectory");

// Clinical features
addTwoColSlide(pres,
  "Clinical Features of Diabetes Mellitus",
  "Classic Symptoms (\"3 Ps\")",
  [
    "Polyuria — osmotic diuresis once glucose >180–200 mg/dL",
    "Polydipsia — compensatory thirst from volume depletion",
    "Polyphagia — cellular energy deprivation despite hyperglycaemia",
    "Weight loss — catabolism; glycosuria; loss of calories in urine",
    "Fatigue — poor glucose utilization in cells",
    "Blurred vision — hyperosmolar lens swelling",
    "Recurrent infections — impaired neutrophil function in hyperglycaemia",
    "Acanthosis nigricans — insulin resistance marker (Type 2)",
    "Candidal infections (genital, oral) — glucose-rich mucosa",
  ],
  "Type 1-Specific Presentation",
  [
    "Acute onset, often presenting in DKA",
    "Kussmaul breathing (deep, sighing respirations) in DKA",
    "Fruity breath (acetone)",
    "Nausea, vomiting, abdominal pain",
    "Age: typically <30 years",
    "\"Honeymoon phase\": partial β-cell recovery 3–6 months after diagnosis; reduced insulin need",
    "Lipoatrophy / lipohypertrophy at injection sites",
    "Type 2: often asymptomatic for years; identified on routine screening",
  ]
);

// Microvascular complications
addCardGrid(pres, "Chronic Complications — Microvascular", [
  { title: "Diabetic Retinopathy", items: [
    "Most common cause of blindness in working-age adults",
    "Non-proliferative (NPDR): microaneurysms, haemorrhages, exudates",
    "Proliferative (PDR): neovascularisation, vitreous haemorrhage, retinal detachment",
    "Screening: annual fundoscopy from diagnosis (T2) or 5 yrs after (T1)",
    "Rx: laser photocoagulation, anti-VEGF (ranibizumab)",
  ]},
  { title: "Diabetic Nephropathy", items: [
    "Leading cause of end-stage renal disease globally",
    "Stages: microalbuminuria → macroalbuminuria → ↓ GFR → ESRD",
    "Kimmelstiel-Wilson nodules: pathognomonic on biopsy",
    "Glomerular basement membrane thickening; mesangial expansion",
    "Screening: urine ACR annually; ACEI/ARB for proteinuria",
    "SGLT2 inhibitors (empagliflozin) reduce progression",
  ]},
  { title: "Diabetic Neuropathy", items: [
    "Most common: distal symmetric sensorimotor polyneuropathy",
    "\"Glove & stocking\" pattern; loss of vibration/proprioception first",
    "Charcot arthropathy: bony destruction due to painless trauma",
    "Autonomic neuropathy: orthostatic hypotension, gastroparesis, ED",
    "Mononeuropathies: CN3 palsy (pupil spared), carpal tunnel",
    "Pain Rx: duloxetine, gabapentin, pregabalin",
  ]},
  { title: "Diabetic Foot", items: [
    "Combination of neuropathy + peripheral vascular disease",
    "Neuropathic ulcers: painless, punched out, pressure points (metatarsal heads)",
    "Ischaemic ulcers: painful, on toes/heels, poor pulses",
    "Annual foot exam; monofilament testing",
    "Leading cause of non-traumatic amputation",
    "Multidisciplinary care: podiatry, vascular surgery, orthotics",
  ]},
]);

// Macrovascular complications
addBulletSlide(pres, "Chronic Complications — Macrovascular & Natural History", [
  { text: "Macrovascular Disease (2–2.5× higher CV risk than non-diabetics)", bold: true, color: ACCENT },
  { text: "Coronary artery disease: commonest cause of death in T2DM; often \"silent\" MI" },
  { text: "Cerebrovascular disease: stroke risk 1.5–3× higher; lacunar infarcts common" },
  { text: "Peripheral arterial disease: ABI <0.9; claudication; critical limb ischaemia" },
  { text: "Heart failure: both HFrEF and HFpEF; SGLT2i reduce hospitalisation significantly" },
  { text: "Each 18 mg/dL (1 mmol/L) rise in fasting glucose → 17% ↑ cardiovascular event risk" },
  { text: "Natural History Trajectory", bold: true, color: ACCENT },
  { text: "T1DM: Rapid β-cell destruction → life-long insulin dependency from onset; complications appear ~5–10 yrs after diagnosis" },
  { text: "T2DM: Pre-diabetes (5–10 yrs) → early T2DM → progressive β-cell failure → complications over decades" },
  { text: "T2DM prognosis: life expectancy at 50 years is ~6 years lower than non-diabetics" },
  { text: "With optimal multi-factorial control (glucose + BP + lipids): risk of blindness, ESRD, amputation each <1%" },
]);


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 05: INVESTIGATIONS
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 5, "Investigations", "Diagnosis, monitoring and evaluation of complications");

// Diagnostic tests
addBulletSlide(pres, "Investigations — Diagnosis & Monitoring", [
  { text: "DIAGNOSTIC TESTS", bold: true, color: ACCENT },
  { text: "Fasting Plasma Glucose (FPG): ≥7.0 mmol/L (126 mg/dL) after 8-h fast; simple, cheap, reproducible" },
  { text: "Oral Glucose Tolerance Test (OGTT): 75 g glucose; 2-h PG ≥11.1 mmol/L (200 mg/dL)" },
  { text: "HbA1c: ≥6.5% (48 mmol/mol); reflects 3-month average glucose; not affected by short-term changes" },
  { text: "Random PG: ≥11.1 mmol/L + symptoms; no fasting required" },
  { text: "Note: Two abnormal results required if asymptomatic; one result if symptomatic hyperglycaemia" },
  { text: "MONITORING", bold: true, color: ACCENT },
  { text: "HbA1c: every 3 months if not at target; every 6 months if stable and at target" },
  { text: "Self-monitoring of blood glucose (SMBG): finger-prick capillary glucose; essential in insulin users" },
  { text: "Continuous glucose monitoring (CGM): interstitial glucose q5–15 min; TIR (time-in-range) 70–180 mg/dL target >70%" },
  { text: "Fructosamine: reflects 2–3 week average; useful in haemoglobinopathies, haemolysis, pregnancy" },
  { text: "C-peptide: low in T1DM; normal/high in T2DM; distinguishes T1 from T2 in uncertain cases" },
  { text: "COMPLICATION SCREENING (ANNUAL)", bold: true, color: ACCENT },
  { text: "Urine albumin:creatinine ratio (ACR); eGFR; lipid panel; fundoscopy; foot exam; BP; ECG" },
]);

// Lab interpretation table
{
  const s = addContentSlide(pres, "Glycaemic Targets & Key Lab Values");
  const tableData = [
    ["Parameter", "Normal", "Pre-diabetes", "Diabetes"],
    ["FPG (mmol/L)", "<5.6", "5.6–6.9", "≥7.0"],
    ["2-h OGTT (mmol/L)", "<7.8", "7.8–11.0", "≥11.1"],
    ["HbA1c (%)", "<5.7", "5.7–6.4", "≥6.5"],
    ["", "", "", ""],
    ["Treatment Target", "Most adults", "Tight control", "Relaxed"],
    ["HbA1c target (%)", "–", "<6.5", "7.0–8.0"],
    ["Fasting glucose (mmol/L)", "–", "4.4–7.2", "4.4–7.2"],
    ["Postprandial (mmol/L)", "–", "<10.0", "<10.0"],
    ["BP target (mmHg)", "–", "<130/80", "<130/80"],
    ["LDL-C target (mmol/L)", "–", "<1.8 (high CV risk)", "<1.8–2.6"],
  ];
  const colW = [3.0, 2.3, 2.2, 2.2];
  const colX = [0.12, 3.14, 5.46, 7.7];
  const hdrColors = [DARK_BLUE, MID_BLUE, ACCENT, LIGHT_BLUE];
  tableData.forEach((row, ri) => {
    const yp = 0.82 + ri * 0.42;
    row.forEach((cell, ci) => {
      const isHdr = ri === 0 || ri === 5;
      const bg = isHdr ? hdrColors[ci] : (ri % 2 === 0 ? SOFT_GRAY : WHITE);
      s.addShape(pres.ShapeType.rect, { x: colX[ci], y: yp, w: colW[ci], h: 0.40, fill: { color: bg }, line: { color: "CCCCCC", pt: 0.5 } });
      s.addText(cell, { x: colX[ci] + 0.05, y: yp, w: colW[ci] - 0.1, h: 0.40, fontSize: isHdr ? 11 : 10.5, bold: isHdr || ci === 0, color: isHdr ? WHITE : TEXT_DARK, fontFace: "Calibri", valign: "middle" });
    });
  });
}


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 06: MANAGEMENT
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 6, "Management", "Lifestyle, pharmacotherapy & cardiovascular risk reduction");

// T1 management
addBulletSlide(pres, "Management — Type 1 Diabetes", [
  { text: "Insulin is mandatory — no alternative", bold: true, color: ACCENT },
  { text: "Regimens:", bold: true },
  { text: "Basal-bolus (MDI): long-acting (glargine, detemir, degludec) once/twice daily + rapid-acting (lispro, aspart, glulisine) before meals" },
  { text: "Continuous subcutaneous insulin infusion (CSII/pump): most physiological; allows micro-dosing and temp basal rates" },
  { text: "DAFNE: Dose Adjustment For Normal Eating — carbohydrate counting framework" },
  { text: "Adjuncts:", bold: true },
  { text: "CGM with hybrid closed-loop (artificial pancreas) → automated insulin delivery" },
  { text: "Pramlintide (amylin analogue) — blunts postprandial glucose in select patients" },
  { text: "Monitoring:", bold: true },
  { text: "HbA1c target <7.0% (<53 mmol/mol) for most adults; individualised" },
  { text: "CGM Time-in-Range (TIR) 70–180 mg/dL: >70% target" },
  { text: "Sick-day rules: never stop insulin; increase monitoring; check ketones" },
  { text: "Transplantation:", bold: true },
  { text: "Pancreas or islet cell transplantation for brittle T1DM or concurrent kidney transplant" },
]);

// T2 management algorithm
{
  const s = addContentSlide(pres, "Management — Type 2 Diabetes: Stepwise Algorithm");
  // Step boxes
  const steps = [
    { n: "Step 1", title: "Lifestyle Modification (All patients)", items: ["Medical nutrition therapy: Mediterranean/DASH diet; ↓ refined carbs", "Physical activity: 150 min/week moderate intensity aerobic", "Weight loss: 5–10% reduces HbA1c 0.5–1.0%", "Smoking cessation; alcohol restriction", "Diabetes self-management education (DSME)"] },
    { n: "Step 2", title: "First-line Pharmacotherapy", items: ["Metformin: 1st-line (if eGFR ≥30); decreases hepatic glucose output; weight neutral/↓", "SGLT2 inhibitors: empagliflozin, dapagliflozin — prefer if HF or CKD", "GLP-1 RA: semaglutide, liraglutide — prefer if overweight + CVD risk"] },
    { n: "Step 3", title: "Add-on Agents", items: ["DPP-4 inhibitors: sitagliptin, saxagliptin — weight neutral; low hypoglycaemia risk", "Pioglitazone: if metabolic syndrome; caution: fluid retention, fracture risk", "Sulfonylureas: gliclazide, glimepiride — risk of hypoglycaemia; declining use"] },
    { n: "Step 4", title: "Insulin Initiation", items: ["When HbA1c persistently >10% or β-cell failure", "Start: basal insulin (glargine, NPH) bedtime or morning", "Intensify: premixed or basal-bolus regimen as needed", "Add GLP-1 RA to basal insulin to limit weight gain"] },
  ];
  const cols = [0.12, 5.06];
  const rows2 = [0.82, 3.12];
  const bgCols = [MID_BLUE, ACCENT, LIGHT_BLUE, "1B4F8A"];
  steps.forEach((step, i) => {
    const cx = cols[i % 2];
    const cy = rows2[Math.floor(i / 2)];
    s.addShape(pres.ShapeType.rect, { x: cx, y: cy, w: 4.8, h: 2.2, fill: { color: bgCols[i] } });
    s.addShape(pres.ShapeType.rect, { x: cx, y: cy, w: 4.8, h: 0.3, fill: { color: GOLD } });
    s.addText(`${step.n}: ${step.title}`, { x: cx + 0.1, y: cy, w: 4.6, h: 0.3, fontSize: 10, bold: true, color: DARK_BLUE, fontFace: "Calibri", valign: "middle" });
    const bItems = step.items.map((t, j) => ({ text: t, options: { bullet: true, breakLine: j < step.items.length - 1, fontSize: 9.5, color: WHITE, fontFace: "Calibri" } }));
    s.addText(bItems, { x: cx + 0.1, y: cy + 0.33, w: 4.6, h: 1.8 });
  });
}

// Drug table
{
  const s = addContentSlide(pres, "Pharmacotherapy Summary — Antidiabetic Agents");
  const headers = ["Drug Class", "Example", "Mechanism", "Key Benefit", "Caution"];
  const rows3 = [
    ["Metformin", "Metformin", "↓ Hepatic glucose output, ↑ insulin sensitivity", "Weight ↓, CV safe, cheap", "Lactic acidosis if eGFR<30"],
    ["SGLT2i", "Empagliflozin", "↓ Renal glucose reabsorption (glucosuria)", "HF, CKD protection; weight ↓", "UTI/genital fungal; DKA risk"],
    ["GLP-1 RA", "Semaglutide", "↑ Insulin, ↓ glucagon, ↑ satiety", "Weight ↓↓, CV & renal protection", "GI side-effects; pancreatitis"],
    ["DPP-4i", "Sitagliptin", "↑ Endogenous GLP-1 & GIP", "Weight neutral, low hypoglycaemia", "HF risk (saxagliptin)"],
    ["Sulfonylurea", "Gliclazide", "↑ Insulin secretion (β-cell K+ATP channel)", "Cheap; proven efficacy", "Hypoglycaemia, weight gain"],
    ["Thiazolidinedione", "Pioglitazone", "PPAR-γ agonist → ↑ insulin sensitivity", "Metabolic syndrome, NASH", "Fluid retention, fractures, HF"],
    ["Insulin", "Glargine/Aspart", "Direct glucose uptake via GLUT-4", "Unlimited efficacy ceiling", "Hypoglycaemia, weight gain"],
  ];
  const colW2 = [1.65, 1.45, 2.45, 2.2, 2.0];
  const colX2 = [0.1, 1.77, 3.24, 5.71, 7.93];
  // header row
  headers.forEach((h, ci) => {
    s.addShape(pres.ShapeType.rect, { x: colX2[ci], y: 0.78, w: colW2[ci], h: 0.34, fill: { color: DARK_BLUE } });
    s.addText(h, { x: colX2[ci] + 0.04, y: 0.78, w: colW2[ci] - 0.08, h: 0.34, fontSize: 10, bold: true, color: GOLD, fontFace: "Calibri", valign: "middle" });
  });
  rows3.forEach((row, ri) => {
    const yp = 1.14 + ri * 0.56;
    const bg = ri % 2 === 0 ? SOFT_GRAY : WHITE;
    row.forEach((cell, ci) => {
      s.addShape(pres.ShapeType.rect, { x: colX2[ci], y: yp, w: colW2[ci], h: 0.54, fill: { color: ci === 0 ? ACCENT : bg }, line: { color: "CCCCCC", pt: 0.5 } });
      s.addText(cell, { x: colX2[ci] + 0.04, y: yp, w: colW2[ci] - 0.08, h: 0.54, fontSize: 9.5, bold: ci === 0, color: ci === 0 ? WHITE : TEXT_DARK, fontFace: "Calibri", valign: "middle", wrap: true });
    });
  });
}

// CV risk reduction
addBulletSlide(pres, "Cardiovascular Risk Reduction in Diabetes", [
  { text: "Diabetics are treated as 'CVD-equivalent' — aggressive risk factor management mandatory", bold: true },
  { text: "Blood Pressure:", bold: true, color: ACCENT },
  { text: "Target <130/80 mmHg for most; first-line: ACEi or ARB (especially with proteinuria)" },
  { text: "Avoid ACEi + ARB combination (↑ AKI, hyperkalaemia risk)" },
  { text: "Lipid Management:", bold: true, color: ACCENT },
  { text: "Statin therapy for all T2DM >40 years or with CVD; LDL-C target <1.8 mmol/L (high risk)" },
  { text: "Ezetimibe or PCSK9 inhibitors if statin-intolerant or target not reached" },
  { text: "Antiplatelet:", bold: true, color: ACCENT },
  { text: "Aspirin 75 mg: secondary prevention (established CVD); not routine for primary prevention" },
  { text: "Cardioprotective Medications:", bold: true, color: ACCENT },
  { text: "SGLT2 inhibitors (empagliflozin, canagliflozin): reduce HF hospitalisation, CV death, renal progression — EMPA-REG, CANVAS, CREDENCE trials" },
  { text: "GLP-1 RA (liraglutide, semaglutide): reduce MACE (LEADER, SUSTAIN-6 trials)" },
  { text: "Finerenone (non-steroidal MRA): reduces CKD progression and CV events in T2DM + CKD" },
]);


// ═══════════════════════════════════════════════════════════════════════════════
// SECTION 07: DIABETIC EMERGENCIES
// ═══════════════════════════════════════════════════════════════════════════════
addSectionSlide(pres, 7, "Diabetic Emergencies", "DKA · Hyperosmolar Hyperglycaemic State · Hypoglycaemia");

// DKA definition & precipitants
addBulletSlide(pres, "Diabetic Ketoacidosis (DKA) — Definition & Precipitants", [
  { text: "DKA Diagnostic Triad (the 'D-K-A'):", bold: true, color: ACCENT },
  { text: "D — Diabetes: glucose ≥13.9 mmol/L (250 mg/dL) OR known diabetes" },
  { text: "K — Ketones: urine ketones ≥2+ OR serum β-hydroxybutyrate ≥3.0 mmol/L" },
  { text: "A — Acidosis: arterial/venous pH <7.3 OR serum bicarbonate <15 mmol/L" },
  { text: "Predominantly Type 1 DM; increasingly seen in T2DM (esp. SGLT2i — euglycaemic DKA)", bold: false },
  { text: "Mortality: ~1–4%; higher at extremes of age and with severe precipitating illness" },
  { text: "Precipitants — MOST COMMON:", bold: true, color: ACCENT },
  { text: "Infections (pneumonia, UTI, cellulitis): ~30–40% of cases" },
  { text: "Inadequate insulin / non-adherence: ~20–30%" },
  { text: "New-onset T1DM (first presentation): ~10–15%" },
  { text: "Acute coronary syndrome / MI — always rule out in DKA" },
  { text: "Other precipitants: CVA, pulmonary embolism, acute pancreatitis, burns, drugs (corticosteroids, clozapine, SGLT2i), Cushing syndrome, thyrotoxicosis" },
]);

// DKA pathophysiology
{
  const s = addContentSlide(pres, "DKA — Pathophysiology");
  s.addShape(pres.ShapeType.rect, { x: 0.15, y: 0.82, w: 9.7, h: 0.38, fill: { color: ACCENT } });
  s.addText("Absolute insulin deficiency + counter-regulatory hormone excess (glucagon ↑↑, catecholamines ↑, cortisol ↑)", {
    x: 0.25, y: 0.82, w: 9.5, h: 0.38, fontSize: 12, bold: true, color: WHITE, fontFace: "Calibri", valign: "middle"
  });
  // Flow diagram with shapes
  const flowItems = [
    { x: 0.2, y: 1.28, w: 2.9, h: 0.7, bg: MID_BLUE, text: "↑ Glycogenolysis\n↑ Gluconeogenesis\n↑ Hepatic glucose output" },
    { x: 3.55, y: 1.28, w: 2.9, h: 0.7, bg: ACCENT, text: "↑ Lipolysis\n↑ Free fatty acids → liver\n↑ Ketone production" },
    { x: 6.9, y: 1.28, w: 2.9, h: 0.7, bg: LIGHT_BLUE, text: "Glucose & ketones\nin circulation ↑↑\n(↓ utilisation)" },
    { x: 0.2, y: 2.35, w: 4.2, h: 0.7, bg: "1B4F8A", text: "Hyperglycaemia → Osmotic diuresis\n→ ↓ Na, ↓ K, ↓ PO4, ↓ Mg\n→ Dehydration + hypovolaemia" },
    { x: 5.6, y: 2.35, w: 4.2, h: 0.7, bg: "6B3A8A", text: "Ketoacidosis (pH <7.3, HCO3 <15)\n→ Kussmaul breathing\n→ Anion gap metabolic acidosis" },
    { x: 0.2, y: 3.45, w: 9.6, h: 0.6, bg: DARK_BLUE, text: "Clinical: Nausea, vomiting, polyuria, polydipsia, abdominal pain, lethargy → coma | Fruity breath (acetone) | Kussmaul respirations" },
    { x: 0.2, y: 4.2, w: 9.6, h: 0.6, bg: "8B0000", text: "Complications: cerebral oedema (esp. children), hypokalaemia (life-threatening!), aspiration pneumonia, AKI, thromboembolism" },
  ];
  flowItems.forEach(f => {
    s.addShape(pres.ShapeType.rect, { x: f.x, y: f.y, w: f.w, h: f.h, fill: { color: f.bg } });
    s.addText(f.text, { x: f.x + 0.08, y: f.y + 0.04, w: f.w - 0.16, h: f.h - 0.08, fontSize: 10, color: WHITE, fontFace: "Calibri", valign: "middle", align: "center" });
  });
}

// DKA investigations
{
  const s = addContentSlide(pres, "DKA — Investigations");
  if (imgs[3] && imgs[3].base64) {
    s.addImage({ data: imgs[3].base64, x: 4.8, y: 0.82, w: 5.05, h: 4.55 });
    s.addText("Lab values in DKA, HHS, euglycaemic DKA", { x: 4.8, y: 5.25, w: 5.05, h: 0.2, fontSize: 8, color: ACCENT, fontFace: "Calibri", italic: true, align: "center" });
  }
  const items = [
    { text: "BEDSIDE", bold: true, color: ACCENT },
    { text: "Blood glucose (BM) — typically 13.9–33.3 mmol/L (250–600 mg/dL)" },
    { text: "Urinalysis: glycosuria, ketonuria (2+ or more)" },
    { text: "Capillary β-hydroxybutyrate: ≥3.0 mmol/L" },
    { text: "BLOOD TESTS", bold: true, color: ACCENT },
    { text: "ABG / VBG: pH <7.3; pCO2 low (compensatory); HCO3 <15 mmol/L" },
    { text: "U&E: Na (often falsely low), K (⚠️ may be ↑ despite total body K+ deficit — monitor closely!)" },
    { text: "Serum ketones (β-hydroxybutyrate); amylase (often raised non-specifically in DKA)" },
    { text: "FBC: WBC may be raised (stress response, not always infection)" },
    { text: "Blood cultures, CRP, chest X-ray (if precipitant suspected)" },
    { text: "ECG: tall peaked T-waves if hyperkalaemia; ST changes if ACS" },
    { text: "Anion Gap: elevated (>12 mmol/L) = hyperchloraemic + ketoacid anions" },
  ];
  const bItems = items.map((item, i) => ({
    text: item.text,
    options: { bullet: !item.bold, breakLine: i < items.length - 1, fontSize: item.bold ? 12 : 10.5, bold: item.bold || false, color: item.color || TEXT_DARK, fontFace: "Calibri" }
  }));
  s.addText(bItems, { x: 0.25, y: 0.85, w: 4.4, h: 4.45 });
}

// DKA management
{
  const s = addContentSlide(pres, "DKA — Management: The '5 Fs'");
  const fItems = [
    { f: "FLUIDS", color: LIGHT_BLUE, content: "0.9% NaCl: 1L over 1 h → 1L/2 h × 2 → 1L/4 h × 2 → 1L/8 h (titrate to response)\n⚠️ Add 10% dextrose when glucose <14 mmol/L (do NOT stop insulin!)" },
    { f: "FIXED-RATE INSULIN", color: ACCENT, content: "0.1 units/kg/h IV infusion (e.g. Actrapid in 0.9% NaCl)\nDo NOT give bolus insulin (risk of cerebral oedema in children)\nContinue until: pH >7.3, HCO3 >15, ketones <0.6 mmol/L" },
    { f: "POTASSIUM", color: MID_BLUE, content: "⚠️ K+ falls rapidly with insulin therapy — check before starting\nIf K+ 3.5–5.5: add 40 mmol/L KCl to IV fluids\nIf K+ <3.5: hold insulin; replace K+ urgently\nIf K+ >5.5: no KCl; reassess frequently" },
    { f: "FIND & TREAT PRECIPITANT", color: "1B4F8A", content: "Antibiotics if infection; ACS management; thrombolysis if PE\nReview all medications; check HbA1c, autoantibodies\nAvoid routine bicarbonate (only pH <6.9 under specialist guidance)" },
    { f: "FLUIDS — TRANSITION", color: "6B3A8A", content: "Switch to SC insulin when: eating & drinking; glucose <14; ketones <0.3 mmol/L; pH >7.3\nOverlap SC + IV insulin by 30–60 min before stopping IV infusion\nReview and optimise long-term insulin regimen before discharge" },
  ];
  fItems.forEach((item, i) => {
    const cy = 0.82 + i * 0.93;
    s.addShape(pres.ShapeType.rect, { x: 0.15, y: cy, w: 9.7, h: 0.87, fill: { color: item.color } });
    s.addText(item.f, { x: 0.25, y: cy + 0.04, w: 1.8, h: 0.79, fontSize: 12, bold: true, color: GOLD, fontFace: "Calibri", valign: "middle" });
    s.addText(item.content, { x: 2.1, y: cy + 0.04, w: 7.6, h: 0.79, fontSize: 10.5, color: WHITE, fontFace: "Calibri", valign: "middle" });
  });
}

// HHS
addTwoColSlide(pres,
  "Hyperosmolar Hyperglycaemic State (HHS)",
  "Definition & Pathophysiology",
  [
    "Glucose >33.3 mmol/L (600 mg/dL) — typically much higher than DKA",
    "Plasma osmolality >320 mOsm/kg",
    "pH usually >7.30; HCO3 >18 mmol/L (ketosis absent or mild)",
    "Insufficient oral intake + osmotic diuresis → profound dehydration",
    "Residual insulin suppresses ketogenesis (unlike DKA)",
    "Occurs mainly in elderly T2DM; insidious onset over days-weeks",
    "Often precipitated by: infection, MI, CVA, GI illness, diuretics",
    "Mortality up to 20% (much higher than DKA)",
    "Mixed HHS-DKA occurs in some T2DM patients",
  ],
  "Clinical Features & Management",
  [
    "Profound dehydration: fluid deficit 8–10 L",
    "Neurological: confusion, drowsiness → coma (hallmark)",
    "Seizures, focal neurological deficits",
    "No Kussmaul breathing, no fruity breath",
    "Thrombosis risk: DVT/PE — prophylactic LMWH mandatory",
    "MANAGEMENT:",
    "Cautious fluid replacement (slower than DKA) — 0.9% NaCl",
    "Avoid rapid osmolality correction (>3 mOsm/kg/h → cerebral oedema)",
    "Low-dose insulin ONLY after fluids (insulin alone → fatal ↓ osmolality)",
    "Potassium replacement as per DKA protocol",
    "Identify and treat precipitant urgently",
  ]
);

// Hypoglycaemia
addBulletSlide(pres, "Hypoglycaemia — Definition, Features & Management", [
  { text: "Definition: plasma glucose <4.0 mmol/L (72 mg/dL) in diabetic patients; <2.8 mmol/L non-diabetic", bold: true, color: ACCENT },
  { text: "Whipple's Triad: (1) symptoms of hypoglycaemia + (2) low glucose + (3) relief with glucose correction" },
  { text: "Neuroglycopenic symptoms (glucose <3.0 mmol/L):", bold: true },
  { text: "Confusion, difficulty concentrating, drowsiness, seizures, focal deficits, coma" },
  { text: "Adrenergic/autonomic symptoms (early warning, glucose ~3.5 mmol/L):", bold: true },
  { text: "Sweating, tremor, palpitations, hunger, anxiety, pallor" },
  { text: "Hypoglycaemia unawareness: loss of adrenergic symptoms (common in long-standing T1DM, recurrent hypoglycaemia, autonomic neuropathy, β-blocker use)" },
  { text: "Common causes:", bold: true, color: ACCENT },
  { text: "Excess insulin dose, delayed/missed meal, increased exercise, alcohol, renal failure (↓ insulin clearance)" },
  { text: "MANAGEMENT:", bold: true, color: ACCENT },
  { text: "Conscious & able to swallow: 15–20 g fast-acting glucose (glucose tabs, juice, regular soda); repeat BM after 15 min (Rule of 15)" },
  { text: "Impaired consciousness/IV access: 75–100 mL 20% dextrose IV OR glucagon 1 mg IM/SC/IN" },
  { text: "Inpatient: 10% dextrose infusion; identify and treat cause" },
  { text: "Discharge advice: sick-day rules; adjust insulin/medications; refer to diabetes team" },
]);

// Comparison DKA vs HHS
{
  const s = addContentSlide(pres, "DKA vs HHS — Comparison at a Glance");
  const headers2 = ["Feature", "DKA", "HHS", "Hypoglycaemia"];
  const rows4 = [
    ["Glucose (mmol/L)", "13.9–33.3", ">33.3 (often >50)", "<4.0"],
    ["pH", "<7.30", ">7.30", "Normal"],
    ["HCO3 (mmol/L)", "<15", ">18", "Normal"],
    ["Ketones", "+++", "+/−", "Absent"],
    ["Osmolality (mOsm/kg)", "300–320", ">320 (often >380)", "Normal"],
    ["Onset", "Hours", "Days–weeks", "Minutes"],
    ["LOC", "Variable", "Often coma", "Can seize/coma"],
    ["Dehydration", "Moderate (3–6 L)", "Profound (8–10 L)", "Absent"],
    ["Key treatment", "Insulin + fluids + K+", "Fluids first, then insulin", "Glucose/glucagon"],
    ["Mortality", "~1–4%", "~10–20%", "<1% (if treated)"],
  ];
  const colW3 = [2.3, 2.5, 2.5, 2.4];
  const colX3 = [0.12, 2.44, 4.96, 7.48];
  headers2.forEach((h, ci) => {
    const hCol = [DARK_BLUE, MID_BLUE, ACCENT, LIGHT_BLUE][ci];
    s.addShape(pres.ShapeType.rect, { x: colX3[ci], y: 0.78, w: colW3[ci], h: 0.36, fill: { color: hCol } });
    s.addText(h, { x: colX3[ci] + 0.04, y: 0.78, w: colW3[ci] - 0.08, h: 0.36, fontSize: 11, bold: true, color: ci === 0 ? GOLD : WHITE, fontFace: "Calibri", valign: "middle" });
  });
  rows4.forEach((row, ri) => {
    const yp = 1.16 + ri * 0.40;
    row.forEach((cell, ci) => {
      const bg = ci === 0 ? ACCENT : (ri % 2 === 0 ? SOFT_GRAY : WHITE);
      s.addShape(pres.ShapeType.rect, { x: colX3[ci], y: yp, w: colW3[ci], h: 0.38, fill: { color: bg }, line: { color: "CCCCCC", pt: 0.5 } });
      s.addText(cell, { x: colX3[ci] + 0.04, y: yp, w: colW3[ci] - 0.08, h: 0.38, fontSize: 10, bold: ci === 0, color: ci === 0 ? WHITE : TEXT_DARK, fontFace: "Calibri", valign: "middle" });
    });
  });
}

// ─── FINAL SLIDE: Key Take-Homes ─────────────────────────────────────────────
{
  const s = pres.addSlide();
  setBg(s, DARK_BLUE);
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 10, h: 0.72, fill: { color: GOLD } });
  s.addText("Key Take-Home Messages", { x: 0.2, y: 0.08, w: 9.6, h: 0.56, fontSize: 20, bold: true, color: DARK_BLUE, fontFace: "Calibri", valign: "middle" });
  const msgs = [
    "DM is a chronic metabolic disease driven by insulin deficiency and/or resistance — both T1 and T2 share the endpoint of hyperglycaemia-mediated organ damage.",
    "Diagnosis requires objective biochemical confirmation — HbA1c ≥6.5%, FPG ≥7.0 mmol/L, or 2h-OGTT ≥11.1 mmol/L.",
    "T1DM needs insulin from day 1; T2DM is stepwise — lifestyle → metformin → combinations with SGLT2i / GLP-1 RA preferred for CV/renal benefit.",
    "HbA1c target 7.0% (53 mmol/mol) for most; individualise based on age, comorbidities, hypoglycaemia risk.",
    "DKA: Insulin deficiency + counter-regulatory excess → hyperglycaemia + ketoacidosis + dehydration; treat with fluids, fixed-rate insulin, potassium. Never stop insulin even when glucose normalises.",
    "HHS: Profound hyperglycaemia, dehydration, hyperosmolality without significant ketosis; treat with cautious fluid replacement FIRST, then low-dose insulin — mortality up to 20%.",
    "Hypoglycaemia: BM <4.0 mmol/L; treat conscious patients with 15–20 g fast glucose; unconscious → IV dextrose or glucagon IM.",
  ];
  msgs.forEach((msg, i) => {
    const yp = 0.82 + i * 0.67;
    const bg = i % 2 === 0 ? MID_BLUE : ACCENT;
    s.addShape(pres.ShapeType.rect, { x: 0.15, y: yp, w: 0.52, h: 0.57, fill: { color: GOLD } });
    s.addText(`${i + 1}`, { x: 0.15, y: yp, w: 0.52, h: 0.57, fontSize: 18, bold: true, color: DARK_BLUE, fontFace: "Calibri", valign: "middle", align: "center" });
    s.addShape(pres.ShapeType.rect, { x: 0.69, y: yp, w: 9.16, h: 0.57, fill: { color: bg } });
    s.addText(msg, { x: 0.79, y: yp, w: 9.0, h: 0.57, fontSize: 10.5, color: WHITE, fontFace: "Calibri", valign: "middle" });
  });
}

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