mkdir -p /home/daytona/workspace/inflammation-ppt && ls /home/daytona/workspace/…

~/inflammation-ppt/create_ppt.js

const pptxgen = require("pptxgenjs");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Inflammation - Pathology";
pres.author = "Orris Medical";

// ─── COLOR PALETTE ───────────────────────────────────────────────────────────
const C = {
  bg_dark:   "12213A",   // deep navy – title / section dividers
  bg_mid:    "1A3057",   // mid-navy
  bg_light:  "F4F7FB",   // near-white – content slides
  accent1:   "E84545",   // red – inflammatory highlights
  accent2:   "F5A623",   // amber – warnings / outcomes
  accent3:   "2EC4B6",   // teal – chronic / resolution
  white:     "FFFFFF",
  text_dark: "1A1A2E",
  text_mid:  "2D3561",
  text_light:"B8C9E1",
  green:     "27AE60",
  purple:    "8E44AD",
};

// ─── HELPERS ────────────────────────────────────────────────────────────────
function titleSlide(pres) {
  const s = pres.addSlide();
  // dark full-bleed background
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_dark} });
  // red accent bar
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.08, h:"100%", fill:{color: C.accent1} });
  // subtle grid lines
  for(let i=1;i<6;i++) s.addShape(pres.ShapeType.rect, { x:0, y:i*0.94, w:"100%", h:0.005, fill:{color:"1D3560"}, line:{color:"1D3560"} });

  s.addText("INFLAMMATION", {
    x:0.5, y:1.0, w:9, h:1.4,
    fontSize:60, bold:true, color:C.white,
    fontFace:"Calibri", align:"left", charSpacing:8
  });
  s.addText("PATHOLOGY", {
    x:0.5, y:2.3, w:6, h:0.7,
    fontSize:28, bold:false, color:C.accent1,
    fontFace:"Calibri", align:"left", charSpacing:6
  });
  s.addShape(pres.ShapeType.rect, { x:0.5, y:3.1, w:5, h:0.04, fill:{color:C.accent2} });
  s.addText("A response of vascularized tissues to infection and damage\nthat mobilises host defence to eliminate offending agents.", {
    x:0.5, y:3.25, w:8.5, h:0.9,
    fontSize:16, color:C.text_light, italic:true, fontFace:"Calibri", align:"left"
  });
  s.addText("Source: Robbins & Kumar Basic Pathology", {
    x:0.5, y:5.1, w:8, h:0.3,
    fontSize:11, color:"4A6D9A", fontFace:"Calibri", align:"left"
  });
}

function sectionDivider(pres, number, title, subtitle) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_mid} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:0.08, fill:{color: C.accent1} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:2.6, h:"100%", fill:{color:"162A4A"} });
  s.addText(number, {
    x:0.1, y:1.8, w:2.4, h:2.0,
    fontSize:90, bold:true, color:C.accent1,
    fontFace:"Calibri", align:"center", valign:"middle"
  });
  s.addText(title, {
    x:2.9, y:1.5, w:6.8, h:1.3,
    fontSize:36, bold:true, color:C.white,
    fontFace:"Calibri", align:"left"
  });
  s.addText(subtitle, {
    x:2.9, y:2.8, w:6.8, h:1.2,
    fontSize:18, color:C.text_light, italic:true,
    fontFace:"Calibri", align:"left"
  });
}

function contentSlide(pres, title, bullets, opts={}) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_light} });
  // top bar
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:0.72, fill:{color: C.bg_dark} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.72, w:"100%", h:0.04, fill:{color: opts.accent||C.accent1} });
  s.addText(title, {
    x:0.4, y:0.05, w:9.2, h:0.62,
    fontSize:22, bold:true, color:C.white,
    fontFace:"Calibri", align:"left", valign:"middle", margin:0
  });
  // bullet items
  const items = bullets.map((b, i) => {
    if(typeof b === "string") return { text: b, options:{ bullet:{type:"bullet"}, breakLine: i<bullets.length-1, fontSize:17, color:C.text_dark, fontFace:"Calibri" } };
    return { text: b.text, options:{ bullet:{type:"bullet"}, breakLine: i<bullets.length-1, fontSize: b.size||17, color: b.color||C.text_dark, bold: b.bold||false, fontFace:"Calibri", indentLevel: b.indent||0 } };
  });
  s.addText(items, { x:0.5, y:0.9, w:9, h:4.55, valign:"top" });
  return s;
}

function twoColumnSlide(pres, title, leftTitle, leftItems, rightTitle, rightItems, accentL, accentR) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_light} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:0.72, fill:{color: C.bg_dark} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.72, w:"100%", h:0.04, fill:{color: accentL||C.accent1} });
  s.addText(title, { x:0.4, y:0.05, w:9.2, h:0.62, fontSize:22, bold:true, color:C.white, fontFace:"Calibri", align:"left", valign:"middle", margin:0 });

  // left column
  s.addShape(pres.ShapeType.rect, { x:0.3, y:0.95, w:4.4, h:4.5, fill:{color:C.white}, line:{color:"D0DCF0",pt:1} });
  s.addShape(pres.ShapeType.rect, { x:0.3, y:0.95, w:4.4, h:0.42, fill:{color: accentL||C.accent1} });
  s.addText(leftTitle, { x:0.35, y:0.97, w:4.3, h:0.38, fontSize:15, bold:true, color:C.white, fontFace:"Calibri", margin:4 });
  const lItems = leftItems.map((b,i)=>({ text:b.text||b, options:{ bullet:{type:"bullet"}, breakLine:i<leftItems.length-1, fontSize:15, color:C.text_dark, fontFace:"Calibri", bold:b.bold||false } }));
  s.addText(lItems, { x:0.35, y:1.42, w:4.3, h:3.9, valign:"top" });

  // right column
  s.addShape(pres.ShapeType.rect, { x:5.3, y:0.95, w:4.4, h:4.5, fill:{color:C.white}, line:{color:"D0DCF0",pt:1} });
  s.addShape(pres.ShapeType.rect, { x:5.3, y:0.95, w:4.4, h:0.42, fill:{color: accentR||C.accent2} });
  s.addText(rightTitle, { x:5.35, y:0.97, w:4.3, h:0.38, fontSize:15, bold:true, color:C.white, fontFace:"Calibri", margin:4 });
  const rItems = rightItems.map((b,i)=>({ text:b.text||b, options:{ bullet:{type:"bullet"}, breakLine:i<rightItems.length-1, fontSize:15, color:C.text_dark, fontFace:"Calibri", bold:b.bold||false } }));
  s.addText(rItems, { x:5.35, y:1.42, w:4.3, h:3.9, valign:"top" });
}

function imageSlide(pres, title, imageUrl, caption, notes) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color:"0F1B2D"} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:0.62, fill:{color: C.bg_dark} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.62, w:"100%", h:0.04, fill:{color:C.accent1} });
  s.addText(title, { x:0.4, y:0.05, w:9.2, h:0.56, fontSize:20, bold:true, color:C.white, fontFace:"Calibri", align:"left", valign:"middle", margin:0 });
  // image
  s.addImage({ path: imageUrl, x:2.5, y:0.8, w:5, h:3.5 });
  s.addText(caption, { x:0.4, y:4.45, w:9.2, h:0.9, fontSize:14, color:C.text_light, italic:true, fontFace:"Calibri", align:"center" });
  if(notes) s.addNotes(notes);
  return s;
}

function tableSlide(pres, title, headers, rows, accent) {
  const s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_light} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:0.72, fill:{color: C.bg_dark} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.72, w:"100%", h:0.04, fill:{color: accent||C.accent3} });
  s.addText(title, { x:0.4, y:0.05, w:9.2, h:0.62, fontSize:22, bold:true, color:C.white, fontFace:"Calibri", align:"left", valign:"middle", margin:0 });

  const tableRows = [
    headers.map(h => ({ text: h, options: { bold:true, color:C.white, fill: accent||C.accent3, align:"center", fontSize:14 } })),
    ...rows.map(row => row.map(cell => ({ text: cell, options: { color:C.text_dark, fontSize:13, align:"left" } })))
  ];
  s.addTable(tableRows, { x:0.3, y:0.88, w:9.4, colW: headers.map(()=>9.4/headers.length), rowH:0.45, border:{pt:0.5, color:"C8D8F0"}, fill:{color:C.white}, fontFace:"Calibri" });
}

// ═══════════════════════════════════════════════════════════════════════════
// SLIDE CREATION
// ═══════════════════════════════════════════════════════════════════════════

// 1. TITLE SLIDE
titleSlide(pres);

// 2. OVERVIEW / AGENDA
contentSlide(pres, "Overview", [
  { text:"01  Introduction & Definition of Inflammation", bold:true, color:C.accent1 },
  "02  Acute Inflammation",
  { text:"     • Vascular changes  •  Leukocyte recruitment  •  Phagocytosis", indent:1, color:"555555" },
  { text:"03  Mediators of Inflammation", bold:true, color:C.accent1 },
  "     • Vasoactive amines  •  Arachidonic acid metabolites  •  Cytokines  •  Complement",
  { text:"04  Morphologic Patterns of Acute Inflammation", bold:true, color:C.accent1 },
  "05  Outcomes of Acute Inflammation",
  { text:"06  Chronic Inflammation & Granulomatous Inflammation", bold:true, color:C.accent3 },
  "07  Systemic Effects of Inflammation",
  { text:"08  Summary & Key Points", bold:true, color:C.accent2 },
], { accent: C.accent2 });

// ─── SECTION 1: INTRODUCTION ─────────────────────────────────────────────
sectionDivider(pres, "01", "Introduction", "Definition, purpose, and cardinal signs of inflammation");

contentSlide(pres, "What is Inflammation?", [
  { text:"Definition (Robbins & Kumar):", bold:true, color:C.accent1 },
  '"A response of vascularized tissues to infections and tissue damage that brings cells and molecules of host defence from the circulation to the sites where they are needed."',
  "",
  { text:"Purpose:", bold:true, color:C.text_mid },
  "Eliminate the offending agent (microbe, toxin, necrotic tissue)",
  "Contain and confine the damage",
  "Set the stage for tissue repair",
  "",
  { text:"Two forms:", bold:true, color:C.text_mid },
  { text:"Acute inflammation  – rapid onset (min to days), neutrophil-predominant", color:C.accent1 },
  { text:"Chronic inflammation – slower onset (days to years), lymphocytes & macrophages", color:C.accent3 },
]);

contentSlide(pres, "Cardinal Signs of Inflammation (Celsus & Virchow)", [
  { text:"Rubor   – Redness", bold:true, color:C.accent1 },
  "  Caused by vasodilation and increased blood flow",
  { text:"Calor   – Heat", bold:true, color:C.accent2 },
  "  Due to vasodilation and hyperaemia",
  { text:"Tumor   – Swelling", bold:true, color:C.text_mid },
  "  Due to increased vascular permeability and oedema",
  { text:"Dolor   – Pain", bold:true, color:C.purple },
  "  Mediated by prostaglandins, bradykinin acting on nerve endings",
  { text:"Functio laesa – Loss of function", bold:true, color:C.text_mid },
  "  Consequence of pain and swelling (added by Virchow)",
], { accent: C.accent2 });

// ─── SECTION 2: ACUTE INFLAMMATION ──────────────────────────────────────
sectionDivider(pres, "02", "Acute Inflammation", "Vascular reactions, leukocyte recruitment, and phagocytosis");

contentSlide(pres, "Acute Inflammation – Three Major Components", [
  { text:"1.  Dilation of small vessels", bold:true, color:C.accent1 },
  "    → leads to increased blood flow (erythema and warmth)",
  "",
  { text:"2.  Increased permeability of microvasculature", bold:true, color:C.accent1 },
  "    → plasma proteins escape → oedema (exudate formation)",
  "    → Exudate: high protein, cellular debris (implies increased permeability)",
  "    → Transudate: low protein, osmotic/hydrostatic imbalance (no inflammation)",
  "",
  { text:"3.  Emigration of leukocytes from microcirculation", bold:true, color:C.accent1 },
  "    → especially neutrophils in early phase",
  "    → Reactions occur mainly in postcapillary venules",
]);

contentSlide(pres, "Vascular Changes in Acute Inflammation", [
  { text:"Vasodilation:", bold:true, color:C.accent1 },
  "• Earliest reaction; produces redness (rubor) and warmth (calor)",
  "• Key mediator: Histamine (from mast cells)",
  "• Also mediated by NO, bradykinin, prostaglandins",
  "",
  { text:"Increased Vascular Permeability:", bold:true, color:C.accent2 },
  "• Principal mechanism: contraction of endothelial cells → interendothelial gaps",
  "• Histamine, bradykinin, leukotrienes, substance P responsible",
  "• Occurs rapidly (15-30 min) after mediator exposure",
  "• Burns: direct endothelial injury → sustained leakage",
  "",
  { text:"Result: Exudate formation, oedema, increased blood viscosity (stasis)", color:C.text_mid, bold:true },
]);

contentSlide(pres, "Leukocyte Recruitment – Steps", [
  { text:"1. Margination", bold:true, color:C.accent1 },
  "   Leukocytes move to periphery of vessel (due to slowing of blood flow)",
  { text:"2. Rolling", bold:true, color:C.accent1 },
  "   Mediated by selectins (P-selectin, E-selectin on endothelium; L-selectin on leukocytes)",
  { text:"3. Adhesion", bold:true, color:C.accent1 },
  "   Firm adhesion via integrins (LFA-1, Mac-1) binding to ICAM-1 on endothelium",
  "   TNF & IL-1 upregulate ICAM-1 and E-selectin",
  { text:"4. Transmigration (Diapedesis)", bold:true, color:C.accent1 },
  "   Leukocytes crawl and squeeze between endothelial cells (PECAM-1 / CD31)",
  { text:"5. Chemotaxis", bold:true, color:C.accent1 },
  "   Movement along a chemical gradient toward site of injury",
  "   Chemotactic agents: bacterial products, C5a, LTB4, IL-8 (CXCL8)",
]);

contentSlide(pres, "Phagocytosis & Killing", [
  { text:"Recognition & Attachment:", bold:true, color:C.accent1 },
  "• Enhanced by opsonisation – coating with IgG, C3b",
  "• Receptors: Fc receptors (for IgG), complement receptors (CR1, CR3)",
  "",
  { text:"Engulfment:", bold:true, color:C.accent2 },
  "• Cytoplasmic pseudopods extend around particle",
  "• Phagosome formed → fuses with lysosome → phagolysosome",
  "",
  { text:"Killing & Degradation:", bold:true, color:C.accent3 },
  "• Oxygen-dependent: Reactive oxygen species (ROS) via NADPH oxidase",
  "  – Superoxide (O₂⁻) → H₂O₂ → HOCl (via myeloperoxidase)",
  "• Oxygen-independent: Lysozyme, defensins, lactoferrin, elastase (in granules)",
  "",
  { text:"Leukocyte-mediated tissue injury: bystander damage by ROS and lysosomal enzymes", color:C.accent1, bold:true },
]);

// ─── SECTION 3: MEDIATORS ────────────────────────────────────────────────
sectionDivider(pres, "03", "Mediators of Inflammation", "Chemical signals that orchestrate the inflammatory response");

contentSlide(pres, "Vasoactive Amines & Arachidonic Acid Metabolites", [
  { text:"Histamine (mast cells, basophils, platelets):", bold:true, color:C.accent1 },
  "• Causes vasodilation and increased vascular permeability",
  "• First mediator released in acute inflammation",
  "",
  { text:"Serotonin (5-HT) – platelets:", bold:true, color:C.accent2 },
  "• Similar effects to histamine",
  "",
  { text:"Arachidonic Acid (AA) pathway:", bold:true, color:C.text_mid },
  "• COX pathway → Prostaglandins (PGE2, PGI2) + Thromboxane A2",
  "  – PGE2 & PGI2: vasodilation, increased permeability, pain, fever",
  "  – TxA2: vasoconstriction, platelet aggregation",
  "• Lipoxygenase pathway → Leukotrienes",
  "  – LTB4: potent neutrophil chemotaxis",
  "  – LTC4, LTD4, LTE4: bronchospasm, vasoconstriction (important in asthma)",
  "  – Lipoxins: anti-inflammatory (inhibit neutrophil recruitment)",
  "• NSAIDs → inhibit COX; Corticosteroids → inhibit phospholipase A2",
], { accent: C.accent2 });

contentSlide(pres, "Cytokines, Chemokines & Complement", [
  { text:"TNF and IL-1 (key pro-inflammatory cytokines):", bold:true, color:C.accent1 },
  "• Produced by macrophages, dendritic cells, mast cells, T cells",
  "• Upregulate endothelial adhesion molecules (E-selectin, ICAM-1, VCAM-1)",
  "• Induce fever via hypothalamus (PGE2 as second messenger)",
  "• Stimulate acute-phase protein synthesis in liver",
  "",
  { text:"Chemokines (IL-8/CXCL8, MCP-1):", bold:true, color:C.accent2 },
  "• Stimulate leukocyte migration along concentration gradients",
  "• CXC chemokines act mainly on neutrophils; CC chemokines on monocytes/lymphocytes",
  "",
  { text:"Complement System:", bold:true, color:C.accent3 },
  "• C3a, C5a (anaphylatoxins): mast cell degranulation, increased permeability",
  "• C5a: potent chemotaxis for neutrophils; activates macrophages",
  "• C3b: opsonin for phagocytosis",
  "• MAC (C5b-9): direct lysis of microbes",
]);

tableSlide(pres, "Key Inflammatory Mediators – Summary",
  ["Mediator", "Source", "Key Actions"],
  [
    ["Histamine", "Mast cells, basophils", "Vasodilation, ↑ permeability"],
    ["PGE2 / PGI2", "Arachidonic acid (COX)", "Vasodilation, pain, fever"],
    ["TxA2", "Platelets (AA-COX)", "Vasoconstriction, platelet aggregation"],
    ["LTB4", "Neutrophils, macrophages (lipoxygenase)", "Neutrophil chemotaxis"],
    ["LTC4/D4/E4", "Mast cells (lipoxygenase)", "Bronchospasm, ↑ permeability"],
    ["TNF & IL-1", "Macrophages, mast cells", "Adhesion molecules, fever, acute phase"],
    ["IL-8 (CXCL8)", "Macrophages, endothelium", "Neutrophil chemotaxis"],
    ["C3b", "Complement", "Opsonisation"],
    ["C3a / C5a", "Complement", "Mast cell degranulation, chemotaxis"],
    ["C5b-9 (MAC)", "Complement", "Microbial lysis"],
  ],
  C.accent3
);

// ─── SECTION 4: MORPHOLOGIC PATTERNS ────────────────────────────────────
sectionDivider(pres, "04", "Morphologic Patterns", "Serous, fibrinous, purulent, and ulcerative inflammation");

twoColumnSlide(pres,
  "Morphologic Patterns of Acute Inflammation",
  "Serous Inflammation",
  [
    { text:"Watery, protein-poor effusion", bold:false },
    "Derived from plasma or mesothelial secretion",
    "Example: blister fluid (skin burn)",
    "Example: pleural effusion in early TB",
    "No significant cellular infiltrate",
    "Reversible with treatment",
  ],
  "Fibrinous Inflammation",
  [
    { text:"Large molecules (fibrinogen) escape → fibrin deposits", bold:false },
    "Indicates severe vascular injury",
    "Example: fibrinous pericarditis ('bread-and-butter' pericarditis)",
    "Example: fibrinous pleuritis",
    "Resolution: fibrinolysis OR organisation → scarring",
    "Organisation can obliterate pericardial space",
  ],
  C.accent2, C.accent1
);

contentSlide(pres, "Purulent (Suppurative) Inflammation & Abscess", [
  { text:"Purulent Inflammation:", bold:true, color:C.accent1 },
  "• Production of pus: neutrophils + liquefied necrotic cells + oedema fluid",
  "• Caused by pyogenic bacteria (e.g., Staphylococcus, Streptococcus)",
  "• Example: Acute appendicitis, bacterial pneumonia",
  "",
  { text:"Abscess:", bold:true, color:C.accent1 },
  "• Localised collection of pus within a tissue/organ/confined space",
  "• Central region: necrotic leukocytes and tissue cells",
  "• Rim: preserved neutrophils (inner), vascular congestion + fibroblasts (outer)",
  "• Walled off by connective tissue over time",
  "",
  { text:"Ulcer:", bold:true, color:C.accent2 },
  "• Local defect/excavation of surface epithelium or organ surface",
  "• Caused by sloughing of necrotic tissue",
  "• Example: peptic ulcer, diabetic foot ulcer",
]);

// ─── SECTION 5: OUTCOMES ─────────────────────────────────────────────────
sectionDivider(pres, "05", "Outcomes of Acute Inflammation", "Resolution, abscess, fibrosis, or progression to chronic");

contentSlide(pres, "Outcomes of Acute Inflammation", [
  { text:"1. Resolution (Complete Restoration):", bold:true, color:C.green },
  "   • Occurs when injury is limited and the tissue can regenerate",
  "   • Oedema resorbed via lymphatics; neutrophils undergo apoptosis",
  "   • Macrophages clear debris → normal architecture restored",
  "",
  { text:"2. Healing by Fibrosis (Scarring):", bold:true, color:C.accent2 },
  "   • Occurs when injury is severe or tissue cannot regenerate",
  "   • Fibroblast proliferation + collagen deposition → scar",
  "",
  { text:"3. Abscess Formation:", bold:true, color:C.accent1 },
  "   • Pyogenic infections → loculated pus cavity",
  "",
  { text:"4. Progression to Chronic Inflammation:", bold:true, color:C.accent3 },
  "   • Offending agent not eliminated (e.g., TB, parasites, autoimmune)",
  "   • Shift from neutrophils to macrophages/lymphocytes",
], { accent: C.green });

// ─── SECTION 6: CHRONIC INFLAMMATION ────────────────────────────────────
sectionDivider(pres, "06", "Chronic Inflammation", "Cells, causes, and granulomatous inflammation");

contentSlide(pres, "Chronic Inflammation – Overview & Causes", [
  { text:"Definition:", bold:true, color:C.accent3 },
  "Inflammation of prolonged duration (weeks to years) in which active inflammation, tissue destruction, and healing occur simultaneously.",
  "",
  { text:"Causes:", bold:true, color:C.accent3 },
  "1. Persistent infections – organisms resistant to phagocytosis (TB, fungi, parasites)",
  "2. Immune-mediated diseases – autoimmune (RA, SLE, IBD, MS)",
  "3. Prolonged exposure to toxic agents – silica (silicosis), cigarette smoke, atherosclerosis",
  "",
  { text:"Key cells of chronic inflammation:", bold:true, color:C.text_mid },
  "• Macrophages (dominant) – produce cytokines (TNF, IL-1, IL-12), ROS, tissue factors",
  "• Lymphocytes – T cells activate macrophages; B cells produce antibodies",
  "• Plasma cells – antibody production",
  "• Eosinophils – parasitic infections and IgE-mediated allergic reactions",
  "• Mast cells – in connective tissue, IgE-mediated responses",
], { accent: C.accent3 });

contentSlide(pres, "Role of Macrophages in Chronic Inflammation", [
  { text:"Central cell of chronic inflammation", bold:true, color:C.accent3 },
  "• Derived from blood monocytes (circulate 1-3 days, then enter tissues)",
  "• Activated by: IFN-γ (from Th1 cells), microbial products, foreign substances",
  "",
  { text:"Products of activated macrophages:", bold:true, color:C.text_mid },
  "• Proteases (collagenase, elastase) → tissue destruction",
  "• ROS, NO → microbial killing (and bystander injury)",
  "• Growth factors (TGF-β, VEGF, PDGF) → tissue repair & fibrosis",
  "• Cytokines (TNF, IL-1, IL-6, IL-12, IFN-α/β) → perpetuate inflammation",
  "• Arachidonic acid metabolites → vasoactive effects",
  "",
  { text:"M1 macrophages:", bold:true, color:C.accent1 },
  "  Classically activated; microbicidal; pro-inflammatory",
  { text:"M2 macrophages:", bold:true, color:C.accent3 },
  "  Alternatively activated; anti-inflammatory; promote repair",
], { accent: C.accent3 });

contentSlide(pres, "Granulomatous Inflammation", [
  { text:"Definition:", bold:true, color:C.accent3 },
  "A pattern of chronic inflammation characterised by aggregates of activated macrophages (epithelioid macrophages) ± multinucleated giant cells.",
  "",
  { text:"Formation:", bold:true, color:C.text_mid },
  "• Occurs when macrophages fail to eliminate the inciting agent",
  "• Macrophages → epithelioid cells (flattened, pale cytoplasm)",
  "• Epithelioid cells fuse → Langhans giant cells (nuclei at periphery)",
  "",
  { text:"Types of granulomas:", bold:true, color:C.accent2 },
  { text:"Caseating granuloma (TB):", bold:true, color:C.accent1 },
  "  Necrotic centre resembling cheese; indicates T-cell mediated immunity",
  { text:"Non-caseating granuloma (Sarcoidosis, Crohn's):", bold:true, color:C.accent3 },
  "  No central necrosis",
  "",
  { text:"Common causes: TB, leprosy, syphilis, sarcoidosis, Crohn's disease, fungal infections, schistosomiasis, foreign body reaction", color:C.text_mid },
], { accent: C.accent3 });

// ─── SECTION 7: SYSTEMIC EFFECTS ────────────────────────────────────────
sectionDivider(pres, "07", "Systemic Effects", "Fever, acute-phase proteins, and leukocytosis");

contentSlide(pres, "Systemic Effects of Inflammation (Acute-Phase Response)", [
  { text:"Fever:", bold:true, color:C.accent1 },
  "• Induced by exogenous pyrogens (LPS) → macrophages release IL-1, TNF, IL-6",
  "• These cytokines stimulate PGE2 production in hypothalamus → raises temperature set point",
  "• NSAIDs reduce fever by blocking COX and PGE2 synthesis",
  "",
  { text:"Acute-Phase Proteins (liver synthesis stimulated by IL-6, IL-1, TNF):", bold:true, color:C.accent2 },
  "• C-Reactive Protein (CRP): opsonin; activates complement",
  "• Fibrinogen: ↑ ESR (causes RBC rouleaux formation)",
  "• Serum Amyloid A (SAA): replaces HDL apoprotein",
  "• Complement proteins, hepcidin",
  "",
  { text:"Other systemic effects:", bold:true, color:C.text_mid },
  "• Leukocytosis: neutrophilia (bacterial infection), lymphocytosis (viral), eosinophilia (allergy/parasites)",
  "• Leukemoid reaction: extreme leukocytosis (>40,000/µL)",
  "• Tachycardia, hypertension, decreased sweating",
  "• Severe/prolonged: septic shock, anorexia, somnolence, IL-6 → cachexia",
], { accent: C.accent2 });

// ─── SECTION 8: SUMMARY ──────────────────────────────────────────────────
sectionDivider(pres, "08", "Summary & Key Points", "High-yield revision for exams");

contentSlide(pres, "High-Yield Summary – Acute Inflammation", [
  { text:"REDNESS + HEAT + SWELLING + PAIN + LOSS OF FUNCTION", bold:true, color:C.accent1 },
  "",
  "• Vascular events: vasodilation → erythema/warmth; ↑ permeability → oedema/exudate",
  "• Main early cell: NEUTROPHIL (polymorphonuclear leukocyte)",
  "• Chemotaxis: C5a, LTB4, IL-8, bacterial products",
  "• Opsonins: IgG (Fc receptor), C3b (complement receptor)",
  "• Killing: ROS (NADPH oxidase), HOCl (myeloperoxidase), defensins",
  "",
  { text:"Key mediators:", bold:true, color:C.accent2 },
  "• Histamine – immediate vasodilation/permeability",
  "• PGE2 – pain + fever; inhibited by NSAIDs",
  "• LTB4 – neutrophil chemotaxis",
  "• TNF + IL-1 – adhesion molecules + fever + acute-phase response",
  "• C5a – chemotaxis + anaphylatoxin",
], { accent: C.accent1 });

contentSlide(pres, "High-Yield Summary – Chronic & Granulomatous Inflammation", [
  { text:"Main cell of chronic inflammation: MACROPHAGE", bold:true, color:C.accent3 },
  "  Activated by IFN-γ (Th1 cells)",
  "",
  { text:"Main cell of granuloma: EPITHELIOID MACROPHAGE (+ Langhans giant cells)", bold:true, color:C.accent3 },
  "",
  { text:"Caseating granuloma → TB (classic)", bold:true, color:C.accent1 },
  { text:"Non-caseating granuloma → Sarcoidosis, Crohn's disease, foreign body", bold:true, color:C.accent2 },
  "",
  { text:"Systemic features:", bold:true, color:C.text_mid },
  "• Fever: IL-1, TNF, IL-6 → PGE2 → hypothalamus reset",
  "• CRP, fibrinogen ↑ → useful clinical markers",
  "• Leukocytosis: neutrophilia (bacteria), lymphocytosis (virus)",
  "",
  { text:"Outcomes of acute inflammation: Resolution → Abscess → Fibrosis → Chronic", bold:true, color:C.accent2 },
], { accent: C.accent3 });

// CLOSING SLIDE
const closing = pres.addSlide();
closing.addShape(pres.ShapeType.rect, { x:0, y:0, w:"100%", h:"100%", fill:{color: C.bg_dark} });
closing.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.08, h:"100%", fill:{color: C.accent3} });
closing.addShape(pres.ShapeType.rect, { x:0, y:5.3, w:"100%", h:0.325, fill:{color:"0D1A2E"} });
closing.addText("Thank You", {
  x:0.5, y:1.3, w:9, h:1.4,
  fontSize:54, bold:true, color:C.white,
  fontFace:"Calibri", align:"left", charSpacing:6
});
closing.addShape(pres.ShapeType.rect, { x:0.5, y:2.75, w:4.5, h:0.04, fill:{color:C.accent3} });
closing.addText("\"Without inflammation there is no healing, but unchecked inflammation is the basis of chronic disease.\"", {
  x:0.5, y:2.9, w:9, h:1.1,
  fontSize:17, color:C.text_light, italic:true,
  fontFace:"Calibri", align:"left"
});
closing.addText("Robbins & Kumar Basic Pathology | Robbins, Cotran & Kumar Pathologic Basis of Disease", {
  x:0.5, y:5.25, w:9, h:0.3,
  fontSize:11, color:"3A5A80", fontFace:"Calibri", align:"left"
});

// ── WRITE FILE ────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/inflammation-ppt/Inflammation_Pathology.pptx" })
  .then(() => console.log("✅  Saved: Inflammation_Pathology.pptx"))
  .catch(e => { console.error("Error:", e); process.exit(1); });

cd /home/daytona/workspace/inflammation-ppt && node create_ppt.js

ls -lh /home/daytona/workspace/inflammation-ppt/