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    children: [new TextRun({ text: "Based on Johari Pathology | Pathology (General & Systemic)", size: 20, font: "Calibri", italics: true, color: "666666" })],
  }),

  spacer(),

  // ===================== SECTION 1: VIRAL HEPATITIS =====================
  heading1("1. VIRAL HEPATITIS"),
  body("Viral hepatitis = viral infection of hepatocytes → necrosis + inflammation of liver."),
  boldBullet("Causative agents", "Hepatotropic viruses: A, B, C, D, E"),
  boldBullet("RNA viruses", "HAV, HCV, HDV, HEV (ALL except HBV)"),
  boldBullet("DNA virus", "HBV (Hepadnaviridae) — only hepatotropic DNA virus"),

  spacer(),
  heading2("1.1 Hepatitis A Virus (HAV)"),
  keyFact("HAV = Most common viral cause of jaundice"),
  heading3("Virology"),
  bullet("Non-enveloped, 27 nm, ssRNA virus"),
  bullet("Has outer capsid protein (HAVAg)"),
  bullet("Replicates mainly in liver"),
  heading3("Transmission & Epidemiology"),
  bullet("Route: Fecal-oral (contaminated food/water)"),
  bullet("Incubation period: 3–6 weeks"),
  bullet("Most infectious just BEFORE onset of jaundice"),
  bullet("Virus excreted in stool ~2 weeks before symptoms"),
  heading3("Outcome"),
  bullet("Mild, benign, SELF-LIMITED acute hepatitis"),
  bullet("NO chronic hepatitis, NO carrier state"),
  bullet("Fulminant hepatitis — rare"),
  heading3("Lab & Serological Markers"),
  boldBullet("IgM anti-HAV", "Appears at onset of symptoms; reliable marker of ACUTE infection; peaks 2–3 weeks, disappears after 3–4 months"),
  boldBullet("IgG anti-HAV", "Follows IgM; persists for years → lifelong immunity"),
  boldBullet("Serum AST/ALT", "Raised; peaks within 1–2 days of jaundice, may rise >500 IU/L"),
  boldBullet("Serum ALP", "Usually <300 IU/L"),
  examTip("IgM anti-HAV = diagnosis of ACUTE HAV. IgG anti-HAV = past infection / immunity."),

  spacer(),
  heading2("1.2 Hepatitis B Virus (HBV)"),
  keyFact("HBV = Only hepatotropic DNA virus; belongs to family Hepadnaviridae"),
  heading3("Structure of HBV"),
  bullet("Spherical, double-layered virion"),
  bullet("Genome: partially double-stranded circular DNA"),
  bullet("4 genes: S (surface), C (core), P (polymerase), X"),

  spacer(),
  makeTable(
    ["Gene", "Antigen", "Details"],
    [
      ["S gene", "HBsAg (Surface Ag)", "Secreted into blood in large amounts; immunogenic"],
      ["C gene", "HBcAg (Core Ag)", "Remains intracellular — NOT detectable in serum"],
      ["C gene", "HBeAg (e Antigen)", "Secreted into serum; surrogate marker for HIGH viral replication"],
      ["P gene", "HBV Polymerase", "DNA polymerase enzyme; needed for replication"],
      ["X gene", "HBxAg", "Needed for virus infectivity; implicated in liver cancer pathogenesis"],
    ]
  ),

  spacer(),
  heading3("Mode of Transmission"),
  bullet("Vertical/congenital: Mother → child (in utero, during delivery, after birth)"),
  bullet("Horizontal: Dominant mode — percutaneous / mucous membrane exposure"),
  bullet("Parenteral: IV drug use, blood transfusion"),
  bullet("Sexual: Unprotected hetero/homosexual intercourse; virus in semen & saliva"),

  heading3("Serological Markers — Sequence"),
  boldBullet("HBsAg", "FIRST virologic marker; appears BEFORE symptoms; peaks during disease; undetectable in 3–6 months"),
  boldBullet("HBeAg + HBV-DNA", "Appear soon after HBsAg; persistence >6 weeks = high infectivity → likely chronic hepatitis B"),
  boldBullet("Anti-HBc (IgM)", "Marker during WINDOW PERIOD (HBsAg gone, anti-HBs not yet appeared); HBcAg NOT found in serum"),
  boldBullet("Anti-HBs", "Appears after clearance of HBsAg; confers immunity"),
  examTip("Window period = HBsAg negative + Anti-HBs negative. ONLY IgM anti-HBc is detectable → diagnoses acute HBV."),

  spacer(),
  heading2("1.3 Hepatitis C Virus (HCV)"),
  keyFact("HCV = Most common cause of CHRONIC hepatitis worldwide; highest risk of cirrhosis"),
  bullet("ssRNA virus, parenteral transmission"),
  bullet("Incubation: 7–8 weeks"),
  bullet("~80% develop CHRONIC hepatitis (highest among all hepatitis viruses)"),
  bullet("Marker: Anti-HCV antibody, HCV RNA"),
  examTip("HCV: No vaccine available. 80% chronicity. Common cause of post-transfusion hepatitis."),

  spacer(),
  heading2("1.4 Hepatitis D Virus (HDV)"),
  keyFact("HDV is a DEFECTIVE RNA virus — requires HBV for replication"),
  bullet("Circular defective ssRNA; parenteral transmission"),
  bullet("HDV infection only in HBsAg-positive patients (needs HBV coat)"),
  heading3("Co-infection vs Superinfection"),
  makeTable(
    ["Feature", "Co-infection", "Superinfection"],
    [
      ["Definition", "HDV + HBV acquire simultaneously", "HDV infects existing chronic HBsAg carrier"],
      ["Common outcome", "80% recovery + immunity", "Chronic HBV-HDV hepatitis (majority)"],
      ["Fulminant hepatitis", "Rare", "More common"],
      ["Chronicity", "Rarely develops", "Common (>70%)"],
      ["Markers", "IgM anti-HBc + IgM anti-HD", "IgG anti-HBc + IgG anti-HD"],
    ]
  ),
  examTip("Superinfection = worse outcome. Chronicity in >70%. Accelerates cirrhosis."),

  spacer(),
  heading2("1.5 Hepatitis E Virus (HEV)"),
  keyFact("HEV: Fecal-oral. MOST DANGEROUS in PREGNANCY (mortality up to 20%)"),
  bullet("ssRNA virus; fecal-oral transmission"),
  bullet("Incubation: 4–5 weeks"),
  bullet("NEVER causes chronic hepatitis"),
  bullet("Marker: IgM/IgG anti-HEV"),
  examTip("HEV in pregnancy → high mortality (20%). No carrier state."),

  spacer(),
  heading2("1.6 Summary Table — Hepatitis Viruses"),
  makeTable(
    ["Feature", "HAV", "HBV", "HCV", "HDV", "HEV"],
    [
      ["Genome", "ssRNA", "Partially dsDNA", "ssRNA", "Circular defective ssRNA", "ssRNA"],
      ["Transmission", "Fecal-oral", "Parenteral, sexual, perinatal", "Parenteral", "Parenteral (needs HBV)", "Fecal-oral"],
      ["Incubation", "2–4 weeks", "1–4 months", "7–8 weeks", "Same as HBV", "4–5 weeks"],
      ["Chronic liver disease", "Never", "10%", "~80%", "5% (coinfection); ~70% (superinfection)", "Never"],
      ["Key marker", "IgM anti-HAV", "HBsAg", "Anti-HCV, HCV RNA", "Anti-HDV, HDV RNA", "IgM/IgG anti-HEV"],
      ["Carrier state", "No", "Yes", "Yes", "Yes (if HBV chronic)", "No"],
    ]
  ),

  spacer(),

  // ===================== SECTION 2: ALCOHOLIC LIVER DISEASE =====================
  heading1("2. ALCOHOLIC LIVER DISEASE (ALD)"),
  body("ALD = spectrum of disorders from chronic/excessive ethanol consumption. Three overlapping lesions:"),
  bullet("(1) Hepatic steatosis (fatty liver)"),
  bullet("(2) Alcoholic hepatitis"),
  bullet("(3) Alcoholic cirrhosis"),

  heading2("2.1 Risk Factors"),
  boldBullet("Gender", "Females MORE susceptible — lower doses cause advanced disease. Estrogen ↑ gut permeability → ↑ endotoxins → ↑ pro-inflammatory cytokines from Kupffer cells"),
  boldBullet("Dose", "≥60–80 g ethanol/day for ≥10 years → alcoholic cirrhosis"),

  heading2("2.2 Metabolism of Ethanol"),
  body("Liver is the main organ for ethanol metabolism. Ethanol → Acetaldehyde by 3 enzyme systems:"),
  makeTable(
    ["Enzyme System", "Location", "Notes"],
    [
      ["Alcohol dehydrogenase (ADH)", "Cytoplasm of liver", "Main system at LOW alcohol concentrations"],
      ["Cytochrome P450 2E1 (CYP2E1)", "Smooth ER (microsomes)", "Activated at HIGH blood alcohol; generates ROS (free radicals)"],
      ["Catalase", "Peroxisomes", "Least important"],
    ]
  ),

  heading2("2.3 Hepatic Steatosis (Fatty Liver)"),
  keyFact("Steatosis = REVERSIBLE on alcohol cessation. Earliest and most common lesion."),
  heading3("Morphology"),
  boldBullet("Gross", "Enlarged, yellow (fat), greasy liver"),
  boldBullet("Micro", "Lipid vacuoles in hepatocyte cytoplasm"),
  bullet("Initially microvesicular steatosis → macrovesicular (large, single vacuole displacing nucleus to periphery)"),
  bullet("Primarily affects CENTRILOBULAR region (where ADH is located)"),
  bullet("No inflammation or fibrosis"),
  examTip("Fatty liver = COMPLETELY REVERSIBLE with abstinence."),

  heading2("2.4 Alcoholic Hepatitis (Alcoholic Steatohepatitis)"),
  keyFact("Alcoholic hepatitis may be PRECURSOR to cirrhosis"),
  heading3("Gross"),
  bullet("Liver enlarged, YELLOW (steatosis), FIRM (fibrosis)"),
  heading3("Microscopy — 4 Characteristic Features (Predominantly CENTRILOBULAR)"),
  makeTable(
    ["Feature", "Description"],
    [
      ["1. Ballooning degeneration", "Swollen hepatocytes with pale-stained, finely granular cytoplasm (due to accumulation of fat, water, proteins). Predominantly centrilobular."],
      ["2. Mallory bodies (Mallory-Denk bodies)", "Tangled skeins of cytokeratin intermediate filaments (CK 8 & 18) in cytoplasm of ballooned hepatocytes. HALLMARK of alcoholic hepatitis."],
      ["3. Neutrophilic infiltration", "Neutrophils commonly surround ballooned hepatocytes (esp. those with Mallory bodies)."],
      ["4. Alcoholic steatofibrosis", "Fibrosis starts as sclerosis of central veins → perisinusoidal fibrosis. Stellate cells and portal fibroblasts activated."],
    ]
  ),
  examTip("Mallory-Denk bodies = cytokeratin tangles. NOT specific to alcoholic hepatitis — also in PBC, Wilson's, NASH."),

  heading2("2.5 Alcoholic Cirrhosis"),
  keyFact("MOST COMMON (60–70%) and final irreversible stage of ALD"),
  bullet("Micronodular cirrhosis initially (nodules <3 mm)"),
  bullet("Later may become macronodular"),
  bullet("Bands of fibrosis surround nodules of regenerating hepatocytes"),

  spacer(),

  // ===================== SECTION 3: LIVER CIRRHOSIS =====================
  heading1("3. LIVER CIRRHOSIS"),
  keyFact("Cirrhosis = one of the TEN leading causes of death in Western world. IRREVERSIBLE end-stage."),
  heading3("Definition — 3 Key Features"),
  bullet("1. Involves the ENTIRE liver"),
  bullet("2. Normal lobular architecture is DISORGANIZED"),
  bullet("3. Formation of NODULES separated by irregular bands of FIBROSIS"),

  heading2("3.1 Classification"),
  makeTable(
    ["Morphologic", "Etiologic"],
    [
      ["Micronodular (nodules <3 mm)", "Alcoholic cirrhosis — MOST COMMON (60–70%)"],
      ["Macronodular (nodules >3 mm)", "Post-necrotic cirrhosis (10%)"],
      ["Mixed", "Biliary cirrhosis (5–10%)"],
      ["", "Pigment cirrhosis (haemochromatosis, 5%)"],
      ["", "Wilson's disease cirrhosis"],
      ["", "α-1 antitrypsin deficiency"],
      ["", "Cardiac cirrhosis"],
      ["", "Indian childhood cirrhosis (ICC)"],
      ["", "Autoimmune hepatitis"],
      ["", "Non-alcoholic steatohepatitis (NASH)"],
      ["", "Cryptogenic cirrhosis"],
    ]
  ),

  spacer(),

  // ===================== SECTION 4: PORTAL HYPERTENSION =====================
  heading1("4. PORTAL HYPERTENSION"),
  keyFact("Portal hypertension = hepatic venous pressure >7 mmHg"),
  body("MOST COMMON CAUSE: Cirrhosis (intrahepatic)"),

  heading2("4.1 Classification of Causes"),
  makeTable(
    ["Category", "Examples"],
    [
      ["PREHEPATIC (pre-sinusoidal)", "Obstructive thrombosis of portal vein before liver"],
      ["INTRAHEPATIC (sinusoidal)", "Cirrhosis (MAIN cause), schistosomiasis, massive fatty change, diffuse fibrosing conditions"],
      ["POSTHEPATIC (post-sinusoidal)", "Severe right-sided heart failure, constrictive pericarditis, Budd-Chiari syndrome"],
    ]
  ),

  heading2("4.2 Consequences / Clinical Features"),
  heading3("1. Varices (Esophageal/Gastric)"),
  bullet("Portal HTN → reversal of portal blood flow → collateral vessel dilation"),
  bullet("ESOPHAGEAL VARICES most important → risk of life-threatening hemorrhage"),
  bullet("Also: Hemorrhoidal varices, caput medusae"),
  examTip("Esophageal varices = most lethal complication of portal hypertension."),
  heading3("2. Ascites"),
  bullet("Accumulation of fluid in peritoneal cavity"),
  bullet("Due to: ↓ albumin (↓ oncotic pressure), ↑ aldosterone (Na/water retention), ↑ portal pressure"),
  heading3("3. Splenomegaly / Hypersplenism"),
  bullet("Long-standing congestion → congestive splenomegaly"),
  bullet("Massive splenomegaly → hypersplenism (pancytopenia)"),
  heading3("4. Hepatic Encephalopathy"),
  bullet("Due to failure to metabolize nitrogenous waste (NH3)"),
  bullet("Features: asterixis (flapping tremor), confusion, coma"),
  heading3("5. Hepatorenal Syndrome"),
  bullet("Functional renal failure in severe liver disease"),
  heading3("6. Spider Angiomata, Palmar Erythema"),
  bullet("Due to ↑ circulating estrogens (liver fails to metabolize)"),
  examTip("Complications mnemonic: VAHE-SH = Varices, Ascites, Hepatic encephalopathy, Esophageal varices, Splenomegaly, HRS"),

  spacer(),

  // ===================== SECTION 5: HEPATOCELLULAR CARCINOMA =====================
  heading1("5. HEPATOCELLULAR CARCINOMA (HCC)"),
  keyFact("HCC = Primary malignant tumor of hepatocytes. Alpha-fetoprotein (AFP) is the tumor marker."),

  heading2("5.1 Risk Factors"),
  bullet("Chronic viral hepatitis B and C (most important)"),
  bullet("Alcoholic cirrhosis"),
  bullet("Aflatoxin B1 (from Aspergillus flavus — contaminates peanuts/grains)"),
  bullet("Haemochromatosis"),
  bullet("Non-alcoholic steatohepatitis (NASH)"),
  examTip("HBV + Aflatoxin B1 = synergistic effect on HCC risk."),

  heading2("5.2 Gross Morphology"),
  bullet("Can be: solitary massive tumor, multinodular, or diffuse infiltrating"),
  bullet("Bile-stained (greenish) — bile production is hallmark"),
  bullet("Vascular invasion common → portal vein thrombosis"),

  heading2("5.3 Microscopic Grading"),
  makeTable(
    ["Grade", "Features"],
    [
      ["Well-differentiated HCC", "Recognizable hepatocytic origin; bile production (HALLMARK); trabecular and acinar pattern; large hyperchromatic nuclei with prominent nucleoli"],
      ["Moderately differentiated", "Solid, scirrhous, clear-cell patterns. Scirrhous: malignant cells in narrow bundles with fibrous stroma"],
      ["Poorly / Undifferentiated", "Pleomorphic cells; marked variation in cell size; bizarre anaplastic giant cells; bile production rare"],
    ]
  ),
  examTip("Bile production by tumor cells = HALLMARK of HCC (confirms hepatocytic origin)."),

  heading2("5.4 Clinical Features"),
  bullet("Ill-defined upper abdominal pain, malaise, fatigue, weight loss"),
  bullet("Enlarged, irregular, nodular liver"),

  heading2("5.5 Serum Marker"),
  keyFact("Alpha-fetoprotein (AFP) elevated in ~50% of HCC"),
  bullet("AFP >400 ng/mL is diagnostic when combined with imaging"),
  bullet("Also elevated in: hepatoblastoma, germ cell tumors, normal pregnancy"),
  examTip("AFP = serum tumor marker for HCC. Not 100% sensitive — only 50% HCC cases."),

  spacer(),

  // ===================== IMPORTANT EXAM POINTS SUMMARY =====================
  heading1("6. HIGH-YIELD EXAM SUMMARY"),

  heading2("Must-Know One-Liners"),
  bullet("HAV: fecal-oral, NEVER chronic, IgM anti-HAV = acute"),
  bullet("HBV: DNA virus, 10% chronic, window period → IgM anti-HBc"),
  bullet("HCV: 80% chronic, NO vaccine, parenteral"),
  bullet("HDV: defective RNA, needs HBV, superinfection = worse"),
  bullet("HEV: fecal-oral, high mortality in pregnancy, NEVER chronic"),
  bullet("Fatty liver: reversible, macrovesicular, centrilobular"),
  bullet("Mallory bodies: CK 8 & 18 tangles, hallmark of alcoholic hepatitis"),
  bullet("Cirrhosis: irreversible, entire liver, nodules + fibrosis bands"),
  bullet("Portal HTN: >7 mmHg, varices → hemorrhage is major killer"),
  bullet("HCC: AFP marker, bile production hallmark, HBV+HCV risk factors"),

  heading2("Common Long Questions (MUHS Pattern)"),
  makeTable(
    ["Topic", "Key Points to Cover"],
    [
      ["Viral hepatitis — HAV", "Definition, virus type, transmission, incubation, outcome, lab markers, serology"],
      ["Viral hepatitis — HBV", "Structure, genes/antigens, transmission, serological sequence, window period, outcome"],
      ["Alcoholic liver disease", "Three stages, risk factors, pathogenesis, morphology (steatosis, hepatitis — Mallory bodies, cirrhosis)"],
      ["Liver cirrhosis", "Definition, 3 features, morphologic + etiologic classification, complications"],
      ["Portal hypertension", "Definition, causes (pre/intra/post), pathogenesis of complications, clinical features"],
      ["Hepatocellular carcinoma", "Risk factors, gross + micro morphology, grading, tumor marker (AFP), clinical features"],
      ["Comparison of hepatitis viruses", "Table format: virus type, transmission, incubation, chronicity, markers"],
    ]
  ),

  spacer(),
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    children: [new TextRun({ text: "— END OF NOTES —", bold: true, size: 22, font: "Calibri", color: NAVY, italics: true })],
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