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

// Fetch images as base64 using the helper script
function fetchImages(urls) {
  try {
    const result = execSync(
      `node /home/daytona/skills/shared/scripts/fetch_images.js ${urls.map(u => `"${u}"`).join(" ")}`,
      { timeout: 60000 }
    ).toString();
    return JSON.parse(result);
  } catch (e) {
    console.error("Image fetch error:", e.message);
    return urls.map(() => ({ base64: null, error: e.message }));
  }
}

// ---- Fetch all images from Robbins textbook ----
const imageUrls = [
  "https://cdn.orris.care/cdss_images/bf02fb0bd95d1bac53eac5cbd060dac52ffebe95cc6ccdab7e6fe1ca48ca4382.png", // Fig 3.23 Regeneration vs scar
  "https://cdn.orris.care/cdss_images/ed8a00daf55030584873f5bcbc08406914630e46d74af1318cccfbf2f18829a6.png", // Key concepts target
];

console.log("Fetching images...");
const imgs = fetchImages(imageUrls);
console.log("Images fetched:", imgs.map(i => i.error ? "FAILED: " + i.error : "OK"));

// ---- Color palette ----
// Deep teal/navy theme with orange accents - medical, professional
const C = {
  navy:    "0D2B45",
  teal:    "0A7E8C",
  teal2:   "0E9EB0",
  orange:  "E87722",
  amber:   "F5A623",
  white:   "FFFFFF",
  lightGray: "EEF2F7",
  midGray: "7A8FA6",
  darkText: "1A2A3A",
  green:   "2ECC71",
  red:     "E74C3C",
  purple:  "8E44AD",
  lightTeal: "D4F1F4",
  lightAmber: "FEF9E7",
};

// ---- Helper functions ----
function addTitleSlide(pres, title, subtitle) {
  const slide = pres.addSlide();
  // Full background navy
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.navy } });
  // Teal accent bar left
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 0.18, h: "100%", fill: { color: C.teal } });
  // Orange accent bar
  slide.addShape(pres.ShapeType.rect, { x: 0.18, y: 0, w: 0.06, h: "100%", fill: { color: C.orange } });
  // Top line accent
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.08, fill: { color: C.teal2 } });
  // Bottom line
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 5.545, w: "100%", h: 0.08, fill: { color: C.orange } });

  // Title
  slide.addText(title, {
    x: 0.55, y: 1.8, w: 9, h: 1.4,
    fontSize: 36, bold: true, color: C.white,
    fontFace: "Calibri", align: "center", valign: "middle",
  });
  // Subtitle
  slide.addText(subtitle, {
    x: 0.55, y: 3.4, w: 9, h: 0.7,
    fontSize: 18, color: C.amber, fontFace: "Calibri", align: "center", italic: true,
  });
  // Source tag
  slide.addText("Source: Robbins, Cotran & Kumar — Pathologic Basis of Disease", {
    x: 0.55, y: 4.8, w: 9, h: 0.4,
    fontSize: 11, color: C.midGray, fontFace: "Calibri", align: "center",
  });
  return slide;
}

function addSectionHeader(pres, sectionNum, sectionTitle, subtitle) {
  const slide = pres.addSlide();
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.teal } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.08, fill: { color: C.orange } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 5.545, w: "100%", h: 0.08, fill: { color: C.navy } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 1.8, w: "100%", h: 2.0, fill: { color: C.navy, transparency: 30 } });
  slide.addText(`SECTION ${sectionNum}`, {
    x: 0.5, y: 1.0, w: 9, h: 0.5,
    fontSize: 14, bold: true, color: C.amber, fontFace: "Calibri", align: "center", charSpacing: 5,
  });
  slide.addText(sectionTitle, {
    x: 0.5, y: 1.9, w: 9, h: 1.0,
    fontSize: 32, bold: true, color: C.white, fontFace: "Calibri", align: "center", valign: "middle",
  });
  if (subtitle) {
    slide.addText(subtitle, {
      x: 0.5, y: 3.2, w: 9, h: 0.6,
      fontSize: 16, color: C.lightTeal, fontFace: "Calibri", align: "center", italic: true,
    });
  }
  return slide;
}

function addContentSlide(pres, title, bullets, opts = {}) {
  const slide = pres.addSlide();
  // BG
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.lightGray } });
  // Header bar
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.85, fill: { color: C.navy } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0.85, w: "100%", h: 0.06, fill: { color: C.orange } });
  // Left accent strip
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0.91, w: 0.08, h: 4.72, fill: { color: C.teal } });
  // Slide number bottom right
  if (opts.slideNum) {
    slide.addText(`${opts.slideNum}`, {
      x: 9.2, y: 5.2, w: 0.6, h: 0.3, fontSize: 10, color: C.midGray, fontFace: "Calibri", align: "right",
    });
    slide.addText("Robbins Pathology", {
      x: 0.2, y: 5.2, w: 4, h: 0.3, fontSize: 9, color: C.midGray, fontFace: "Calibri", italic: true,
    });
  }
  // Title
  slide.addText(title, {
    x: 0.15, y: 0.1, w: 9.5, h: 0.65,
    fontSize: 22, bold: true, color: C.white, fontFace: "Calibri", valign: "middle", margin: 6,
  });
  // Bullets
  const textItems = bullets.map((b, i) => ({
    text: b.text || b,
    options: {
      bullet: b.sub ? { indent: 30 } : { indent: 15 },
      color: b.sub ? C.midGray : C.darkText,
      fontSize: b.sub ? 13 : (opts.fontSize || 15),
      bold: b.bold || false,
      breakLine: true,
      fontFace: "Calibri",
    }
  }));

  const contentW = opts.imageRight ? 5.6 : 9.5;
  slide.addText(textItems, {
    x: 0.25, y: 1.0, w: contentW, h: 4.4,
    fontFace: "Calibri", valign: "top", margin: 4,
  });

  if (opts.imageRight && opts.imageData) {
    slide.addShape(pres.ShapeType.rect, { x: 6.1, y: 0.95, w: 3.6, h: 4.35, fill: { color: C.white }, line: { color: C.teal, width: 1.5 } });
    slide.addImage({ data: opts.imageData, x: 6.15, y: 1.0, w: 3.5, h: 4.2 });
    if (opts.imageCaption) {
      slide.addText(opts.imageCaption, {
        x: 6.1, y: 5.2, w: 3.6, h: 0.3, fontSize: 9, color: C.midGray, fontFace: "Calibri", align: "center", italic: true,
      });
    }
  }
  return slide;
}

function addTwoColumnSlide(pres, title, leftBullets, rightBullets, leftHead, rightHead, opts = {}) {
  const slide = pres.addSlide();
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.lightGray } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.85, fill: { color: C.navy } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0.85, w: "100%", h: 0.06, fill: { color: C.orange } });
  slide.addText(title, {
    x: 0.15, y: 0.1, w: 9.5, h: 0.65, fontSize: 22, bold: true, color: C.white, fontFace: "Calibri", valign: "middle", margin: 6,
  });
  if (opts.slideNum) {
    slide.addText(`${opts.slideNum}`, { x: 9.2, y: 5.2, w: 0.6, h: 0.3, fontSize: 10, color: C.midGray, fontFace: "Calibri", align: "right" });
    slide.addText("Robbins Pathology", { x: 0.2, y: 5.2, w: 4, h: 0.3, fontSize: 9, color: C.midGray, fontFace: "Calibri", italic: true });
  }
  // Left column header
  slide.addShape(pres.ShapeType.rect, { x: 0.2, y: 0.93, w: 4.45, h: 0.38, fill: { color: C.teal } });
  slide.addText(leftHead, { x: 0.2, y: 0.93, w: 4.45, h: 0.38, fontSize: 14, bold: true, color: C.white, fontFace: "Calibri", align: "center", valign: "middle" });
  // Right column header
  slide.addShape(pres.ShapeType.rect, { x: 5.05, y: 0.93, w: 4.65, h: 0.38, fill: { color: C.orange } });
  slide.addText(rightHead, { x: 5.05, y: 0.93, w: 4.65, h: 0.38, fontSize: 14, bold: true, color: C.white, fontFace: "Calibri", align: "center", valign: "middle" });
  // Divider
  slide.addShape(pres.ShapeType.line, { x: 4.9, y: 0.93, w: 0, h: 4.5, line: { color: C.midGray, width: 1 } });

  const leftItems = leftBullets.map(b => ({ text: b, options: { bullet: { indent: 12 }, color: C.darkText, fontSize: 13.5, breakLine: true, fontFace: "Calibri" } }));
  const rightItems = rightBullets.map(b => ({ text: b, options: { bullet: { indent: 12 }, color: C.darkText, fontSize: 13.5, breakLine: true, fontFace: "Calibri" } }));
  slide.addText(leftItems, { x: 0.2, y: 1.35, w: 4.45, h: 3.9, valign: "top", margin: 4 });
  slide.addText(rightItems, { x: 5.05, y: 1.35, w: 4.65, h: 3.9, valign: "top", margin: 4 });
  return slide;
}

function addImageSlide(pres, title, imageData, caption, bullets, opts = {}) {
  const slide = pres.addSlide();
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.navy } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.75, fill: { color: C.teal } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0.75, w: "100%", h: 0.05, fill: { color: C.orange } });
  slide.addText(title, { x: 0.15, y: 0.08, w: 9.5, h: 0.58, fontSize: 20, bold: true, color: C.white, fontFace: "Calibri", valign: "middle", margin: 4 });
  if (opts.slideNum) {
    slide.addText(`${opts.slideNum}`, { x: 9.2, y: 5.2, w: 0.6, h: 0.3, fontSize: 10, color: C.midGray, fontFace: "Calibri", align: "right" });
    slide.addText("Robbins Pathology", { x: 0.2, y: 5.2, w: 4, h: 0.3, fontSize: 9, color: "#AAAAAA", fontFace: "Calibri", italic: true });
  }
  if (imageData) {
    const imgW = bullets && bullets.length > 0 ? 5.0 : 8.5;
    const imgX = bullets && bullets.length > 0 ? 0.2 : 0.75;
    slide.addShape(pres.ShapeType.rect, { x: imgX, y: 0.88, w: imgW, h: 3.8, fill: { color: C.white }, line: { color: C.teal2, width: 1.5 } });
    slide.addImage({ data: imageData, x: imgX + 0.05, y: 0.93, w: imgW - 0.1, h: 3.7 });
  }
  if (caption) {
    slide.addText(caption, {
      x: 0.2, y: 4.75, w: bullets ? 5.2 : 9.5, h: 0.4,
      fontSize: 10, color: C.amber, fontFace: "Calibri", align: "center", italic: true,
    });
  }
  if (bullets && bullets.length > 0) {
    const textItems = bullets.map(b => ({ text: b, options: { bullet: { indent: 12 }, color: C.lightGray, fontSize: 13, breakLine: true, fontFace: "Calibri" } }));
    slide.addText(textItems, { x: 5.45, y: 0.88, w: 4.35, h: 4.35, valign: "top", margin: 6 });
  }
  return slide;
}

function addTableSlide(pres, title, tableData, opts = {}) {
  const slide = pres.addSlide();
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: "100%", fill: { color: C.lightGray } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: "100%", h: 0.85, fill: { color: C.navy } });
  slide.addShape(pres.ShapeType.rect, { x: 0, y: 0.85, w: "100%", h: 0.06, fill: { color: C.orange } });
  slide.addText(title, { x: 0.15, y: 0.1, w: 9.5, h: 0.65, fontSize: 22, bold: true, color: C.white, fontFace: "Calibri", valign: "middle", margin: 6 });
  if (opts.slideNum) {
    slide.addText(`${opts.slideNum}`, { x: 9.2, y: 5.2, w: 0.6, h: 0.3, fontSize: 10, color: C.midGray, fontFace: "Calibri", align: "right" });
    slide.addText("Robbins Pathology", { x: 0.2, y: 5.2, w: 4, h: 0.3, fontSize: 9, color: C.midGray, fontFace: "Calibri", italic: true });
  }
  slide.addTable(tableData, {
    x: 0.2, y: 0.98, w: 9.6, h: 4.15,
    fontFace: "Calibri",
    border: { pt: 1, color: C.teal },
    fill: C.white,
    color: C.darkText,
    fontSize: 12,
  });
  return slide;
}

// =====================================================
// CREATE PRESENTATION
// =====================================================
const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.author = "Robbins Pathology";
pres.title = "Wound Healing & Tissue Repair";

const img1 = imgs[0] && !imgs[0].error ? imgs[0].base64 : null; // Fig 3.23 regeneration vs scar
const img2 = imgs[1] && !imgs[1].error ? imgs[1].base64 : null;

// ==================== SLIDE 1: TITLE ====================
addTitleSlide(pres,
  "WOUND HEALING & TISSUE REPAIR",
  "Regeneration · Scar Formation · Bone Healing · Factors Affecting Healing"
);

// ==================== SLIDE 2: OVERVIEW ====================
addContentSlide(pres, "Overview — What is Tissue Repair?", [
  { text: "Repair (also called healing) = restoration of tissue architecture and function after an injury", bold: true },
  { text: "The terms repair (for parenchymal/connective tissue) and healing (for surface epithelia) are used interchangeably — Robbins p.109", bold: false },
  { text: "Two fundamental processes:", bold: true },
  { text: "1. Regeneration — complete restitution of normal tissue structure", sub: false },
  { text: "2. Scar formation (scarring) — connective tissue deposition when regeneration is insufficient", sub: false },
  { text: "Both processes involve cell proliferation and cell-ECM interactions", bold: false },
  { text: "Inflammation and repair are closely linked — inflammatory response sets the stage for repair", bold: false },
  { text: "Critical to survival: the ability to repair damage from toxic insults and inflammation", bold: false },
], { slideNum: "2/25", fontSize: 14 });

// ==================== SLIDE 3: SECTION HEADER — CELL PROLIFERATION ====================
addSectionHeader(pres, "01", "Cell & Tissue Regeneration", "Proliferative Capacity · Growth Factors · Stem Cells");

// ==================== SLIDE 4: THREE TISSUE TYPES ====================
addContentSlide(pres, "Proliferative Capacity of Tissues (Robbins Classification)", [
  { text: "LABILE (Continuously Dividing) Tissues", bold: true },
  { text: "Continuously lost and replaced from stem cells + mature cell proliferation", sub: true },
  { text: "Examples: hematopoietic cells, skin, oral mucosa, GI tract epithelium, urinary tract (transitional)", sub: true },
  { text: "Can readily regenerate after injury if stem cell pool is preserved", sub: true },
  { text: "STABLE Tissues", bold: true },
  { text: "Quiescent (G0) in normal state; can proliferate in response to injury", sub: true },
  { text: "Examples: liver, kidney, pancreas parenchyma; endothelial cells, fibroblasts, smooth muscle cells", sub: true },
  { text: "Limited regeneration capacity except liver (robust regeneration)", sub: true },
  { text: "PERMANENT Tissues", bold: true },
  { text: "Terminally differentiated, nonproliferative in postnatal life", sub: true },
  { text: "Examples: neurons (most), cardiac muscle cells; skeletal muscle (satellite cells provide limited repair)", sub: true },
  { text: "Repair dominated by SCAR FORMATION", sub: true },
], { slideNum: "4/25", fontSize: 13 });

// ==================== SLIDE 5: GROWTH FACTORS & ECM ====================
addContentSlide(pres, "Growth Factors & ECM in Cell Proliferation", [
  { text: "Growth factors drive cell proliferation via signaling pathways (RAS-MAPK, PI3K-AKT)", bold: true },
  { text: "Epidermal Growth Factor (EGF) / TGF-α — receptor tyrosine kinase; stimulate hepatocytes, epithelial cells, fibroblasts", bold: false },
  { text: "Hepatocyte Growth Factor (HGF / scatter factor) — enhances cell motility and invasion during liver regeneration", bold: false },
  { text: "Vascular Endothelial Growth Factor (VEGF) — promotes angiogenesis; critical for repair", bold: false },
  { text: "Platelet-Derived Growth Factor (PDGF) — attracts and activates fibroblasts, smooth muscle cells, monocytes", bold: false },
  { text: "Fibroblast Growth Factors (FGF-1, FGF-2) — stimulate fibroblasts and angiogenesis; activate keratinocytes", bold: false },
  { text: "TGF-β — most potent fibrogenic agent; stimulates collagen and ECM synthesis; inhibits inflammation", bold: true },
  { text: "Integrins (ECM receptors) — connect ECM to cytoskeleton; transduce mechanical and biochemical signals into proliferative response", bold: false },
], { slideNum: "5/25", fontSize: 13 });

// ==================== SLIDE 6: SECTION HEADER — REPAIR BY SCAR ====================
addSectionHeader(pres, "02", "Repair by Scar Formation", "When Regeneration is Insufficient");

// ==================== SLIDE 7: REPAIR — OVERVIEW WITH IMAGE ====================
addImageSlide(pres,
  "Mechanisms of Tissue Repair: Regeneration vs. Scar (Robbins Fig. 3.23)",
  img1,
  "Fig. 3.23 — Mild injury → regeneration. Severe injury (connective tissue damage) → scar formation.\n(Robbins, Cotran & Kumar, Pathologic Basis of Disease)",
  [
    "Mild injury affecting only epithelium: heals by REGENERATION",
    "Severe injury damaging connective tissue framework: heals by SCAR FORMATION",
    "Fibrosis = collagen deposition in lungs, liver, kidney, myocardium (post-infarct)",
    "Organization = fibrosis in a space originally occupied by inflammatory exudate (e.g., organizing pneumonia)",
    "Both regeneration and scar formation contribute variably in most clinical injuries",
  ],
  { slideNum: "7/25" }
);

// ==================== SLIDE 8: STEPS OF SCAR FORMATION ====================
addContentSlide(pres, "Steps of Repair by Scar Formation", [
  { text: "Step 1 — Clot Formation: immediate haemostasis after injury; fibrin scaffold provides framework", bold: true },
  { text: "Step 2 — Inflammation: neutrophils → macrophages; clear debris; produce cytokines and growth factors", bold: true },
  { text: "Step 3 — Angiogenesis: VEGF-driven new vessel formation (leaky, immature capillaries) → granulation tissue", bold: true },
  { text: "Step 4 — Migration & Proliferation of Fibroblasts: PDGF, TGF-β, and FGF recruit and activate fibroblasts", bold: true },
  { text: "Step 5 — Collagen Synthesis: fibroblasts produce type I collagen (main structural protein); cross-linking provides tensile strength", bold: true },
  { text: "Step 6 — Connective Tissue Remodeling: MMPs (matrix metalloproteinases) degrade ECM; TIMPs inhibit MMPs — balance determines final scar", bold: true },
  { text: "Macrophages are CRITICAL orchestrators — eliminate agents, produce cytokines (TGF-β, TNF, IL-1, IL-13, PDGF)", sub: false, bold: false },
], { slideNum: "8/25", fontSize: 13.5 });

// ==================== SLIDE 9: GRANULATION TISSUE ====================
addContentSlide(pres, "Granulation Tissue — The Foundation of Wound Repair", [
  { text: "Definition: pink granular tissue at gross examination; hallmark of healing", bold: true },
  { text: "Histological features:", bold: false },
  { text: "Proliferating fibroblasts embedded in loose ECM", sub: true },
  { text: "New thin-walled capillaries (angiogenesis)", sub: true },
  { text: "Scattered inflammatory cells (mainly macrophages)", sub: true },
  { text: "Function: provides temporary structural support; source of collagen-producing fibroblasts", bold: false },
  { text: "Angiogenesis drivers: VEGF-A, VEGF-C, bFGF-2, angiopoietins", bold: false },
  { text: "Steps of angiogenesis:", bold: false },
  { text: "Vasodilation → increased permeability → endothelial cell migration → proliferation → tube formation → pericyte stabilization", sub: true },
  { text: "Eventually replaced by avascular fibrous scar (collagen type I dominant)", bold: false },
], { slideNum: "9/25", fontSize: 13.5 });

// ==================== SLIDE 10: COLLAGEN SYNTHESIS & REMODELING ====================
addContentSlide(pres, "Collagen Synthesis, Cross-Linking & Remodeling", [
  { text: "Type III collagen initially deposited (granulation tissue phase) → replaced by stronger Type I collagen", bold: true },
  { text: "Collagen synthesis requires:", bold: false },
  { text: "Proline and lysine hydroxylation (requires Vitamin C — deficiency = scurvy → impaired healing)", sub: true },
  { text: "Adequate protein, oxygen, zinc", sub: true },
  { text: "Cross-linking by lysyl oxidase gives tensile strength", sub: true },
  { text: "ECM Remodeling:", bold: true },
  { text: "MMPs (collagenases, gelatinases, stromelysins) — degrade collagen and other ECM components", sub: true },
  { text: "TIMPs (Tissue Inhibitors of Metalloproteinases) — inhibit MMP activity", sub: true },
  { text: "Balance between MMPs and TIMPs determines net ECM deposition", sub: true },
  { text: "Wound strength: reaches ~70-80% of normal at best (never 100%)", bold: false },
  { text: "Wound contraction: myofibroblasts (α-SMA positive) pull wound edges together", bold: false },
], { slideNum: "10/25", fontSize: 13.5 });

// ==================== SLIDE 11: SECTION HEADER — SKIN WOUND HEALING ====================
addSectionHeader(pres, "03", "Healing of Skin Wounds", "Primary Union · Secondary Union · Kinetics");

// ==================== SLIDE 12: FIRST vs SECOND INTENTION ====================
addTwoColumnSlide(pres,
  "Healing by First vs. Second Intention (Robbins Table 3.10)",
  [
    "Small, clean surgical incision",
    "Well-apposed wound margins",
    "Generally uninfected",
    "Limited inflammatory response",
    "Less granulation tissue",
    "Minimal wound contraction",
    "Short healing time",
    "Neat linear scar outcome",
    "Rare complications (epidermal inclusion cyst)",
    "Example: clean surgical incision",
  ],
  [
    "Large tissue defect",
    "Irregular wound margins",
    "Often infected",
    "Marked inflammatory reaction",
    "Exuberant granulation tissue",
    "Significant wound contraction",
    "Prolonged healing time",
    "Contracted, irregular scar",
    "Frequent complications (suppuration)",
    "Example: deep burns, pressure ulcers",
  ],
  "First Intention (Primary Union)",
  "Second Intention (Secondary Union)",
  { slideNum: "12/25" }
);

// ==================== SLIDE 13: KINETICS OF HEALING ====================
addTableSlide(pres, "Kinetics of Skin Wound Healing (Robbins Table 3.11)", [
  [
    { text: "Time", options: { bold: true, color: C.white, fill: C.navy, fontSize: 13 } },
    { text: "Key Events", options: { bold: true, color: C.white, fill: C.navy, fontSize: 13 } },
  ],
  [
    { text: "Immediate", options: { bold: true, color: C.navy, fontSize: 12 } },
    { text: "Blood clot (fibrin + platelets) fills wound space; hemostasis", options: { fontSize: 12 } },
  ],
  [
    { text: "24 hours", options: { bold: true, color: C.teal, fontSize: 12 } },
    { text: "Neutrophils appear at incision margins; epidermis begins to thicken", options: { fontSize: 12 } },
  ],
  [
    { text: "3 days", options: { bold: true, color: C.teal, fontSize: 12 } },
    { text: "Macrophages replace neutrophils; granulation tissue begins forming; collagen fibers appear", options: { fontSize: 12 } },
  ],
  [
    { text: "5 days", options: { bold: true, color: C.teal, fontSize: 12 } },
    { text: "Neovascularization peaks; granulation tissue fills incision; collagen bridges gap; epidermis covers surface", options: { fontSize: 12 } },
  ],
  [
    { text: "2nd week", options: { bold: true, color: C.orange, fontSize: 12 } },
    { text: "Collagen accumulates, leukocytes and edema diminish; blanching begins", options: { fontSize: 12 } },
  ],
  [
    { text: "1 month", options: { bold: true, color: C.orange, fontSize: 12 } },
    { text: "Scar of acellular collagen; lack of inflammatory infiltrate; epidermis normal thickness; tensile strength increases", options: { fontSize: 12 } },
  ],
], { slideNum: "13/25" });

// ==================== SLIDE 14: SECTION HEADER — BONE HEALING ====================
addSectionHeader(pres, "04", "Bone Healing & Fracture Repair", "Stages · Callus Formation · Remodeling");

// ==================== SLIDE 15: BONE HEALING — STAGES ====================
addContentSlide(pres, "Stages of Bone Fracture Healing", [
  { text: "Stage 1 — Hematoma Formation (Days 1-3):", bold: true },
  { text: "Bleeding from fractured bone ends and periosteum forms hematoma; fibrin scaffold; hypoxic environment activates HIF-1α", sub: true },
  { text: "Stage 2 — Soft Callus / Fibrocartilaginous Callus (Days 3–14):", bold: true },
  { text: "Periosteal and endosteal progenitor cells proliferate; chondroblasts produce type II collagen + fibrocartilage; stabilizes fracture", sub: true },
  { text: "Stage 3 — Hard (Bony) Callus / Woven Bone (Weeks 2–6):", bold: true },
  { text: "Chondrocytes undergo hypertrophy, matrix mineralizes; osteoblasts invade and replace cartilage with woven bone (primary bone)", sub: true },
  { text: "Stage 4 — Bone Remodeling (Months to Years):", bold: true },
  { text: "Woven bone replaced by lamellar bone; osteoclasts resorb excess callus; medullary canal restored; mechanical forces guide remodeling (Wolff's law)", sub: true },
  { text: "BMP-2, BMP-7 (Bone Morphogenetic Proteins) drive osteoblast differentiation — key growth factors in bone repair", bold: false },
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// ==================== SLIDE 16: PRIMARY vs SECONDARY BONE HEALING ====================
addTwoColumnSlide(pres,
  "Primary vs. Secondary Bone Healing",
  [
    "Rare — requires anatomic reduction + rigid fixation (ORIF)",
    "Occurs without hematoma or external callus",
    "Cutting cones (osteoclasts) tunnel across fracture",
    "Osteoblasts deposit new lamellar bone directly",
    "Faster union, less callus visible on X-ray",
    "Example: internal fixation plates, screws",
  ],
  [
    "Most common type of fracture healing",
    "Proceeds through hematoma → soft callus → hard callus → remodeling",
    "Requires some movement at fracture site",
    "Visible periosteal callus on X-ray",
    "Involves both intramembranous and endochondral ossification",
    "Example: non-operative fracture management",
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  "Primary Bone Healing",
  "Secondary Bone Healing",
  { slideNum: "16/25" }
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// ==================== SLIDE 17: FACTORS AFFECTING BONE HEALING ====================
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  { text: "Local Factors:", bold: true },
  { text: "Fracture type (comminuted fractures heal more slowly)", sub: true },
  { text: "Degree of displacement and immobilization (too much motion = non-union)", sub: true },
  { text: "Blood supply: avascular necrosis (e.g., femoral head, scaphoid) → poor healing", sub: true },
  { text: "Infection (osteomyelitis) — major cause of non-union and delayed union", sub: true },
  { text: "Periosteal integrity — periosteum is the primary source of osteogenic cells", sub: true },
  { text: "Systemic Factors:", bold: true },
  { text: "Age — children heal faster; elderly have reduced osteogenic activity", sub: true },
  { text: "Hormones — PTH, GH, estrogen, calcitonin support; glucocorticoids inhibit", sub: true },
  { text: "Nutrition — calcium, phosphorus, vitamin D, protein deficiency impair healing", sub: true },
  { text: "Diabetes — impaired vascularity, neuropathy, reduced immune response", sub: true },
  { text: "Anemia, hypoxia — reduce osteoblast activity and energy for repair", sub: true },
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// ==================== SLIDE 18: SECTION HEADER — FACTORS AFFECTING WOUND HEALING ====================
addSectionHeader(pres, "05", "Factors Affecting Tissue Repair", "Local · Systemic · Clinical Implications");

// ==================== SLIDE 19: LOCAL FACTORS ====================
addContentSlide(pres, "Local Factors Affecting Wound Healing (Robbins Fig. 3.28)", [
  { text: "Infection", bold: true },
  { text: "Most important local cause of delayed healing; prolongs inflammation; extends tissue injury; promotes suppuration", sub: true },
  { text: "Mechanical factors", bold: true },
  { text: "Increased local pressure → impaired vascular perfusion (pressure ulcers)", sub: true },
  { text: "Excessive motion → disrupts granulation tissue formation; non-union in bone", sub: true },
  { text: "Foreign bodies", bold: true },
  { text: "Fragments of bone, metal, suture material → elicit granulomatous reaction; prolong inflammation; prevent closure", sub: true },
  { text: "Size, location, type of wound", bold: true },
  { text: "Poor blood supply (lower limbs, diabetic foot) → impaired nutrient/O2 delivery", sub: true },
  { text: "Radiation injury", bold: true },
  { text: "Damages small blood vessels → chronic ischaemia → atrophic skin → impaired healing; fibrosis", sub: true },
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// ==================== SLIDE 20: SYSTEMIC FACTORS ====================
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  { text: "Diabetes Mellitus — Most important systemic cause", bold: true },
  { text: "Hyperglycemia impairs leukocyte function, angiopathy reduces blood supply, neuropathy → unnoticed trauma", sub: true },
  { text: "Nutritional Deficiencies", bold: true },
  { text: "Protein deficiency → impaired collagen synthesis; Vitamin C deficiency → collagen hydroxylation failure (scurvy)", sub: true },
  { text: "Zinc deficiency → impaired cell proliferation and collagen production", sub: true },
  { text: "Glucocorticoids (Steroids)", bold: true },
  { text: "Anti-inflammatory → impair collagen synthesis; reduce fibroblast function; reduce wound tensile strength", sub: true },
  { text: "Aging", bold: true },
  { text: "Reduced dermal thickness; diminished vascular supply; impaired inflammatory response; decreased collagen cross-linking", sub: true },
  { text: "Hematologic / Vascular Disorders", bold: true },
  { text: "Anemia → impaired O2 delivery; coagulation defects → failure of clot scaffold; atherosclerosis → ischaemia", sub: true },
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// ==================== SLIDE 21: SECTION HEADER — ABNORMAL HEALING ====================
addSectionHeader(pres, "06", "Abnormal Wound Healing & Fibrosis", "Keloids · Chronic Wounds · Pathological Fibrosis");

// ==================== SLIDE 22: ABNORMAL HEALING ====================
addContentSlide(pres, "Clinical Examples of Abnormal Wound Healing (Robbins)", [
  { text: "Deficient Scar Formation / Wound Dehiscence", bold: true },
  { text: "Inadequate granulation tissue formation → wound rupture (dehiscence); especially abdominal wounds", sub: true },
  { text: "Causes: infection, poor nutrition, steroid use, poor technique", sub: true },
  { text: "Excessive Scar Formation", bold: true },
  { text: "Hypertrophic scar: raised, red, confined to wound margins; collagen oriented in whorled pattern; usually regresses", sub: true },
  { text: "Keloid: exuberant scar beyond wound margins; does NOT regress; thick type I collagen bundles; more common in dark-skinned individuals; genetic predisposition", sub: true },
  { text: "Excessive Contraction (Contracture)", bold: true },
  { text: "Myofibroblast over-activity → severe deformity; common after burns (especially over joints)", sub: true },
  { text: "Pathological Fibrosis", bold: true },
  { text: "Liver cirrhosis, pulmonary fibrosis (IPF), renal fibrosis, systemic sclerosis — diffuse collagen deposition destroys organ architecture and function", sub: true },
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// ==================== SLIDE 23: ROLE OF MACROPHAGES ====================
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  { text: "Macrophages are the CENTRAL orchestrators of wound healing — Robbins", bold: true },
  { text: "M1 Macrophages (Classically Activated):", bold: false },
  { text: "Early phase: kill bacteria, phagocytose debris, produce TNF, IL-1, IL-12, ROS", sub: true },
  { text: "M2 Macrophages (Alternatively Activated):", bold: false },
  { text: "Later phase: produce TGF-β, IL-10, VEGF, PDGF, FGF → promote fibroblast proliferation, angiogenesis, collagen deposition", sub: true },
  { text: "Macrophage depletion experiments: profoundly impaired repair — wounds fail to progress beyond initial inflammatory stage", bold: false },
  { text: "Produce MMPs for remodeling AND TIMPs to control MMP activity", bold: false },
  { text: "Clinical relevance: chronic non-healing wounds often have persistent M1 polarization; impaired M1→M2 switch", bold: false },
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// ==================== SLIDE 24: KEY CONCEPTS SUMMARY ====================
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  { text: "Tissue repair occurs by REGENERATION (normal cells restored) and/or SCAR FORMATION (connective tissue replacement)", bold: true },
  { text: "Healing capacity depends on tissue type: Labile > Stable > Permanent", bold: false },
  { text: "Scar formation steps: clot → inflammation → angiogenesis/granulation tissue → fibroblast proliferation → collagen synthesis → remodeling", bold: false },
  { text: "TGF-β = most potent fibrogenic agent; MMP/TIMP balance governs ECM remodeling", bold: false },
  { text: "Skin healing: First intention (clean wound, minimal scar) vs. Second intention (large defect, more scarring)", bold: false },
  { text: "Bone healing: hematoma → fibrocartilaginous callus → bony callus → lamellar bone remodeling (4 stages)", bold: false },
  { text: "Key factors impairing healing: infection, diabetes, malnutrition (Vit C, Zn, protein), steroids, aging, ischaemia", bold: false },
  { text: "Abnormal healing: keloid/hypertrophic scar (excessive), dehiscence (deficient), contracture (excessive contraction)", bold: false },
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// ==================== SLIDE 25: REFERENCES / END ====================
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  { text: "Robbins, Cotran & Kumar — Pathologic Basis of Disease, 10th Edition", options: { color: C.white, breakLine: true, fontSize: 14 } },
  { text: "Chapter 3: Tissue Renewal, Regeneration, and Repair (pp. 107–136)", options: { color: C.lightGray, breakLine: true, fontSize: 13 } },
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  { text: "Chapter 2: Inflammation and Repair", options: { color: C.lightGray, breakLine: true, fontSize: 13 } },
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  { text: "All figures referenced directly from Robbins textbook illustrations (Fig. 3.23, Fig. 3.28, Tables 3.10, 3.11)", options: { color: C.midGray, breakLine: true, fontSize: 12, italic: true } },
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