Opthalmology

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"age-related macular degeneration"[MeSH Terms] AND treatment

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"age-related macular degeneration" AND "anti-VEGF"

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I now have comprehensive material from Goldman-Cecil, Wills Eye Manual, Robbins, and Histology textbooks, plus fundus photos and the pathology diagram. Let me compile the full deep-dive.

Age-Related Macular Degeneration (AMD) - Full Deep-Dive


1. Overview & Epidemiology

AMD is a neurodegenerative disease primarily affecting the retinal pigment epithelium (RPE) of the macula. It is the most common cause of irreversible central vision loss in the elderly in industrialized countries, accounting for ~8.5% of global blindness.
  • Affects >1.75 million people in the United States
  • Prevalence increases sharply after age 55; cumulative incidence in those >75 years is approximately 8%
  • Both eyes are typically affected, though often asymmetrically
  • Peripheral vision is spared - only central/macular function is lost
Sources: Goldman-Cecil Medicine; Robbins, Cotran & Kumar Pathologic Basis of Disease

2. Pathophysiology

The RPE-Bruch Membrane-Choriocapillaris Unit

The key structural unit in AMD pathogenesis is the triad of:
  • Retinal Pigment Epithelium (RPE) - nourishes photoreceptors, phagocytoses spent outer segments
  • Bruch's Membrane - basement membrane of the RPE
  • Choriocapillaris - the innermost choroidal vasculature supplying oxygen/nutrients
Disturbance in any component of this unit leads to photoreceptor deterioration and vision loss.

Pathogenesis Diagram (Robbins)

Dry vs Wet AMD - pathogenesis diagram showing drusen formation, RPE damage, neovascularization
Risk factors drive both dry and wet AMD through complement activation, oxidative stress, and aging.

Dry (Atrophic) AMD

  • Drusen form as focal thickenings/abnormal lipoprotein deposits within Bruch's membrane
  • Lipofuscin (oxidation products of polyunsaturated fatty acids + vitamin A dimers) accumulates in stressed RPE cells
  • Chronic complement system activation leads to RPE geographic atrophy and choriocapillaris loss
  • Photoreceptors are secondarily lost overlying the atrophic RPE

Wet (Neovascular/Exudative) AMD

  • Choroidal neovascularization (CNV): new vessels from the choriocapillaris penetrate through a breach in Bruch's membrane into the subretinal space
  • These new vessels are fragile and leaky - they produce subretinal fluid (SRF), hemorrhage, and exudates
  • VEGF (vascular endothelial growth factor) is the principal driver of neovascularization
  • Blood may organize into a disciform scar (subretinal fibrosis), causing permanent photoreceptor loss
  • Wet AMD is a complication of dry AMD, though both can coexist as parallel processes
Sources: Robbins Pathologic Basis of Disease; Histology - A Text and Atlas

3. Genetics & Risk Factors

Genetic

GeneRole
CFH (Complement Factor H)Most strongly associated; abnormal CFH → unchecked complement activation
CFI (Complement Factor I)Complement regulatory gene
Other complement regulatory genesPolymorphisms increase risk

Environmental & Lifestyle Risk Factors

FactorNotes
SmokingStrongest modifiable risk factor; accelerates degeneration
Advanced ageRisk doubles each decade after 55
Family historyStrong genetic component
HyperopiaAssociated risk
Blue eyes/fair skinIncreased susceptibility
Systemic hypertensionVascular risk factor
High lipid levelsAccelerates disease
Uncontrolled blood sugarMetabolic risk
UV exposureEnvironmental oxidative stress
Sources: Goldman-Cecil Medicine; Wills Eye Manual

4. Clinical Features

Dry AMD

Symptoms:
  • Gradual, insidious loss of central vision (may be asymptomatic for years)
  • Amsler grid distortion (metamorphopsia may appear as the disease progresses)
  • Difficulty reading, recognizing faces
Fundus Signs:
  • Drusen - soft drusen >60 µm are most significant (deep, hypopigmented spots)
  • RPE mottling, depigmentation, hyperpigmentation clumps
  • Geographic atrophy - well-defined areas of RPE and photoreceptor loss in advanced disease
Fundus photo - dry AMD with fine drusen
Dry AMD with fine macular drusen - Wills Eye Manual

Wet AMD

Symptoms:
  • Sudden or rapid onset of central visual loss
  • Central or paracentral scotoma (blind spot)
  • Metamorphopsia (straight lines appear wavy) - hallmark symptom
  • Photopsias in the central visual field
Fundus Signs:
  • Subretinal fluid (SRF), macular edema (ME), or RPE detachment associated with CNV
  • Subretinal or intraretinal hemorrhage
  • Retinal exudates
  • Subretinal fibrosis / disciform scar (end-stage)
  • Retinal angiomatous proliferation (RAP) - intraretinal variant with telangiectatic vessels
Fundus photo - exudative (wet) AMD with hemorrhage and soft drusen
Exudative (wet) AMD - note hemorrhage, exudates, and soft drusen - Wills Eye Manual

A Key Clinical Pearl

Patients with peripheral retina intact can walk down a street without difficulty (peripheral function preserved), but cannot recognize faces of people they meet (macular function lost). - Goldman-Cecil Medicine

5. Diagnosis & Investigations

At the Slit-Lamp / Fundus Exam

  • Dilated fundus exam with indirect ophthalmoscopy
  • Soft drusen, RPE changes, CNV membranes, hemorrhage

Amsler Grid Testing

  • Home monitoring tool for detecting metamorphopsia
  • Patients with dry AMD at risk for CNV should perform daily Amsler grid testing and seek urgent attention if new distortion appears

Optical Coherence Tomography (OCT) - Gold Standard for Wet AMD

  • Identifies subretinal fluid, intraretinal fluid, RPE detachments, CNV membranes
  • Used for monitoring treatment response to anti-VEGF therapy

Fluorescein Angiography (FA)

  • Identifies classic vs. occult CNV
  • Classic CNV: well-defined, leaks early and progressively
  • Occult CNV: poorly defined, late leakage

Indocyanine Green Angiography (ICGA)

  • Better delineates occult CNV, polypoidal choroidal vasculopathy (PCV)

OCT Angiography (OCTA)

  • Non-invasive visualization of CNV without dye injection
  • Increasingly used in diagnosis and follow-up
Sources: Wills Eye Manual; Goldman-Cecil Medicine

6. Staging (AMD Classification)

StageFeatures
Early AMDSmall to medium drusen (<125 µm), no pigmentary changes
Intermediate AMDLarge drusen (>125 µm) or medium drusen with pigmentary changes
Advanced Dry AMDGeographic atrophy of RPE ± photoreceptors, not involving the fovea
Advanced Wet AMDCNV with subretinal fluid/hemorrhage, disciform scar

7. Differential Diagnosis

ConditionKey Distinguishing Feature
Myopic degenerationPeripapillary changes, macular changes without drusen, high myopia
Central serous chorioretinopathy (CSCR)Serous retinal elevation, usually <50 years, no drusen
Ocular histoplasmosisSmall white-yellow chorioretinal scars, peripapillary atrophy
Inherited macular dystrophies (Stargardt, Best disease)Usually <50 years, familial, no drusen
Chloroquine toxicityBull's eye maculopathy, drug history
Angioid streaksSub-retinal red-brown bands radiating from optic disc
IPCV (polypoidal choroidal vasculopathy)Polyp-like aneurysmal choroidal dilations on ICGA; common in Asian patients
Source: Wills Eye Manual

8. Management

Dry AMD - No Proven Curative Treatment

AREDS Supplementation (Age-Related Eye Disease Study):
The AREDS2 formula may retard progression from intermediate to advanced AMD:
  • Vitamin C (500 mg)
  • Vitamin E (400 IU)
  • Lutein (10 mg) + Zeaxanthin (2 mg) - replaces beta-carotene
  • Zinc (80 mg)
  • Copper (2 mg) - to prevent zinc-induced copper deficiency
Note: Beta-carotene is NOT recommended in smokers due to increased risk of lung cancer.
Behavioral Modifications:
  • Cessation of smoking (most important)
  • Control of blood pressure, blood sugar, and lipids
  • Dietary changes (green leafy vegetables rich in lutein/zeaxanthin)
Geographic Atrophy - Emerging Therapy:
  • Complement inhibitors are being investigated (target C3 or C5 pathway)
Low Vision Aids:
  • Special magnifying glasses
  • Video-based magnification aids
  • Allow patients to continue independent living

Wet AMD - Anti-VEGF Therapy (Mainstay)

Intravitreal injections of anti-VEGF agents are the standard of care for wet AMD. When administered promptly, they not only prevent vision loss but can result in gains in vision.
DrugClassNotes
Ranibizumab (Lucentis)Anti-VEGF-A fragment (Fab)FDA-approved, gold standard
Bevacizumab (Avastin)Full anti-VEGF antibodyOff-label, widely used; comparable efficacy in CATT trial
Aflibercept (Eylea)VEGF trap (VEGF-A + PlGF)Longer dosing intervals possible
Faricimab (Vabysmo)Dual inhibitor of VEGF-A + Angiopoietin-2Newest agent; longest dosing intervals (up to 16 weeks)
Recent Evidence Update (2025): A network meta-analysis (PMID: 40241463) comparing all intravitreal anti-VEGF therapies for neovascular AMD showed comparable efficacy across agents. A systematic review of faricimab (PMID: 39043575) confirmed non-inferiority to ranibizumab and aflibercept with extended dosing intervals.
Treatment Regimens:
  • Loading phase: Monthly injections for 3 months
  • Maintenance: Pro re nata (PRN), treat-and-extend (T&E), or fixed dosing depending on agent and response

Other Treatments for Wet AMD

  • Photodynamic therapy (PDT) with verteporfin - used in classic subfoveal CNV; less common since anti-VEGF era
  • Laser photocoagulation - for extrafoveal CNV lesions; risk of scotoma
  • Macular translocation surgery - retina detached, translocated away from CNV; then laser applied to destroy pathological vessels (advanced/salvage cases)
  • Vitrectomy - for advanced cases with vitreous hemorrhage or large subretinal hemorrhage

9. Prognosis & Follow-up

  • Dry AMD progresses slowly over months to decades; most patients retain some functional vision
  • Wet AMD without treatment: rapid central vision loss within months
  • With anti-VEGF treatment: ~33% gain >15 letters vision; 90%+ maintain or improve
  • Patients with wet AMD in one eye have 10-12% annual risk of CNV developing in the fellow eye
  • High-risk features for fellow eye: multiple/confluent soft drusen, RPE clumping

10. Summary Table

FeatureDry AMDWet AMD
Frequency90% of cases10% of cases
Vision lossGradual, over yearsSudden/rapid
Key findingDrusen, geographic atrophyCNV, subretinal fluid/hemorrhage
VEGF roleNot primary driverCentral driver (→ CNV)
TreatmentAREDS2 supplements, lifestyleAnti-VEGF injections
PrognosisVariable; can be severePoor if untreated; treatable if caught early

Sources:

Make a ppt

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mkdir -p /home/daytona/workspace/amd-ppt && node /home/daytona/skills/shared/scr…

Writing File

~/amd-ppt/amd.js

const pptxgen = require("pptxgenjs");
const fs = require("fs");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Age-Related Macular Degeneration (AMD)";
pres.author = "Orris Medical";

// Load images
const img0 = fs.readFileSync("/home/daytona/workspace/amd-ppt/img0.txt", "utf8"); // pathogenesis diagram dry vs wet
const img1 = fs.readFileSync("/home/daytona/workspace/amd-ppt/img1.txt", "utf8"); // fundus dry AMD
const img2 = fs.readFileSync("/home/daytona/workspace/amd-ppt/img2.txt", "utf8"); // fundus wet AMD

// ── Color Palette ──────────────────────────────────────────────
const DARK_BG   = "0D1B2A"; // deep navy
const MID_BG    = "1A2E42"; // slate navy
const ACCENT    = "1E90FF"; // clinical blue
const ACCENT2   = "E83030"; // alert red (wet AMD)
const ACCENT3   = "2ECC71"; // treatment green
const WHITE     = "FFFFFF";
const LIGHT_GRAY= "D0D8E4";
const GOLD      = "F4C430"; // soft gold for headers

// ── Helper: dark slide background ──────────────────────────────
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// ── Slide 2: Overview & Epidemiology ──────────────────────────
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// ── Slide 3: Pathophysiology ───────────────────────────────────
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// ── Slide 4: Types & Clinical Features ────────────────────────
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// ── Slide 5: Risk Factors & Genetics ─────────────────────────
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    { text: "CFH  ", options: { bold: true, color: GOLD } },
    { text: "(Complement Factor H) — strongest association\n", options: { color: LIGHT_GRAY } },
    { text: "CFI  ", options: { bold: true, color: GOLD } },
    { text: "(Complement Factor I) — regulatory gene\n", options: { color: LIGHT_GRAY } },
    { text: "Other complement regulatory gene polymorphisms\n", options: { color: LIGHT_GRAY } },
    { text: "→ Excess complement activity → RPE injury", options: { color: ACCENT, italic: true } }
  ], {
    x: 0.35, y: 1.45, w: 4.2, h: 1.9,
    fontSize: 10.5, fontFace: "Calibri", margin: 4
  });

  // Modifiable risk factors
  s.addShape(pres.shapes.ROUNDED_RECTANGLE, {
    x: 0.2, y: 3.6, w: 4.5, h: 1.8,
    fill: { color: "0A1628" }, line: { color: ACCENT2, width: 1.5 }, rectRadius: 0.08
  });
  s.addText("🚬  Modifiable Risk Factors", {
    x: 0.35, y: 3.67, w: 4.2, h: 0.4,
    fontSize: 13, bold: true, color: ACCENT2, fontFace: "Calibri", margin: 0
  });
  s.addText([
    { text: "• Smoking (strongest modifiable RF)\n", options: { bold: true, color: ACCENT2 } },
    { text: "• Hypertension  •  Dyslipidaemia\n• Poor glycaemic control\n• UV exposure", options: { color: LIGHT_GRAY } }
  ], {
    x: 0.35, y: 4.07, w: 4.2, h: 1.3,
    fontSize: 10.5, fontFace: "Calibri", margin: 4
  });

  // Non-modifiable risk factors
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    x: 5.2, y: 0.98, w: 4.5, h: 4.42,
    fill: { color: "0A1628" }, line: { color: GOLD, width: 1.5 }, rectRadius: 0.08
  });
  s.addText("Non-Modifiable Risk Factors", {
    x: 5.35, y: 1.05, w: 4.2, h: 0.4,
    fontSize: 13, bold: true, color: GOLD, fontFace: "Calibri", margin: 0
  });

  const nrfs = [
    ["Age", "Risk doubles every decade after 55; cumulative 8% at 75+"],
    ["Family history", "Strong genetic heritability"],
    ["Hyperopia", "Long-sighted individuals at higher risk"],
    ["Blue eyes / fair skin", "Lower macular pigment density"],
    ["Female sex", "Slightly higher prevalence in women"],
    ["Fellow eye involvement", "10–12% annual risk of CNV in second eye if first eye affected"]
  ];
  nrfs.forEach((r, i) => {
    s.addText([
      { text: r[0] + ": ", options: { bold: true, color: GOLD } },
      { text: r[1], options: { color: LIGHT_GRAY } }
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      fontSize: 10, fontFace: "Calibri", margin: 3
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        x: 5.35, y: 2.03 + i * 0.63, w: 4.2, h: 0.01,
        fill: { color: "2A3D55" }, line: { type: "none" }
      });
    }
  });
}

// ── Slide 6: Diagnosis & Investigations ───────────────────────
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    x: 0.3, y: 0.12, w: 9, h: 0.65,
    fontSize: 22, bold: true, color: WHITE, fontFace: "Calibri", margin: 0
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  const investigations = [
    {
      title: "Amsler Grid",
      body: "Home monitoring tool\nDetects metamorphopsia (wavy/distorted lines)\nDaily use mandatory for at-risk patients",
      color: "2ECC71", icon: "📊"
    },
    {
      title: "Dilated Fundus Exam",
      body: "First-line clinical exam\nIdentifies drusen, RPE changes, CNV, hemorrhage\nBilateral evaluation essential",
      color: ACCENT, icon: "👁"
    },
    {
      title: "OCT (Gold Standard)",
      body: "Detects SRF, IRF, RPE detachments, CNV\nQuantifies fluid for treatment monitoring\nOCT-A: non-invasive CNV mapping (no dye)",
      color: GOLD, icon: "🔬"
    },
    {
      title: "Fluorescein Angiography",
      body: "Classic CNV: early leakage, well-defined\nOccult CNV: late, poorly defined leakage\nStill gold standard for CNV characterisation",
      color: ACCENT2, icon: "💉"
    },
    {
      title: "ICGA",
      body: "Indocyanine green angiography\nBetter for occult CNV & polypoidal choroidal vasculopathy (PCV)\nEssential in Asian patients",
      color: "9B59B6", icon: "🩺"
    },
    {
      title: "AMD Staging (AREDS)",
      body: "Early: small/medium drusen\nIntermediate: large drusen ±pigment change\nAdvanced: geographic atrophy or wet AMD",
      color: "E67E22", icon: "📋"
    }
  ];

  investigations.forEach((inv, i) => {
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    const y = 0.98 + row * 2.25;

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      fontSize: 9.5, color: "333333", fontFace: "Calibri", margin: 3
    });
  });
}

// ── Slide 7: Management — Dry AMD ─────────────────────────────
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  });

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  });

  const areds = [
    ["Vitamin C", "500 mg"],
    ["Vitamin E", "400 IU"],
    ["Lutein", "10 mg"],
    ["Zeaxanthin", "2 mg"],
    ["Zinc", "80 mg"],
    ["Copper", "2 mg (prevents zinc-induced deficiency)"]
  ];
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      { text: a[0] + "  ", options: { bold: true, color: ACCENT3 } },
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      fontSize: 10.5, fontFace: "Calibri", margin: 2
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    fontSize: 10, fontFace: "Calibri", margin: 3
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    x: 6.2, y: 1.0, w: 3.6, h: 0.42,
    fill: { color: GOLD }, line: { type: "none" }
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    x: 6.3, y: 1.03, w: 3.4, h: 0.38,
    fontSize: 13, bold: true, color: DARK_BG, fontFace: "Calibri", margin: 2
  });

  const lifestyle = [
    ["Stop smoking", "Most important modifiable action"],
    ["Control BP", "Reduces vascular stress on RPE"],
    ["Control lipids", "Limit drusen progression"],
    ["Glycaemic control", "Prevents metabolic damage"],
    ["Diet", "Green leafy veg (lutein/zeaxanthin)"],
    ["Amsler grid", "Daily home monitoring for CNV onset"],
    ["Low vision aids", "Magnifiers, video aids for independence"]
  ];
  lifestyle.forEach((l, i) => {
    s.addText([
      { text: l[0] + ": ", options: { bold: true, color: GOLD } },
      { text: l[1], options: { color: LIGHT_GRAY } }
    ], {
      x: 6.3, y: 1.5 + i * 0.55, w: 3.4, h: 0.48,
      fontSize: 10, fontFace: "Calibri", margin: 3
    });
  });

  // Footer note
  s.addText("No curative treatment exists for dry AMD. Supplements retard progression from intermediate → advanced AMD.", {
    x: 0.2, y: 5.1, w: 9.6, h: 0.35,
    fontSize: 9, color: "5A8F70", italic: true, fontFace: "Calibri", margin: 0, align: "center"
  });
}

// ── Slide 8: Management — Wet AMD ─────────────────────────────
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    x: 0, y: 0, w: 0.08, h: 5.625,
    fill: { color: ACCENT2 }, line: { type: "none" }
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  s.addText("Management — Wet AMD (Anti-VEGF Therapy)", {
    x: 0.3, y: 0.12, w: 9, h: 0.65,
    fontSize: 22, bold: true, color: WHITE, fontFace: "Calibri", margin: 0
  });

  // Anti-VEGF drugs table
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    { name: "Ranibizumab", brand: "Lucentis", class: "Anti-VEGF-A Fab fragment", notes: "FDA-approved. Gold standard. Monthly injection.", color: ACCENT },
    { name: "Bevacizumab", brand: "Avastin", class: "Full anti-VEGF-A antibody", notes: "Off-label. Comparable efficacy (CATT trial). Lower cost.", color: "2E86AB" },
    { name: "Aflibercept", brand: "Eylea", class: "VEGF trap (VEGF-A + PlGF)", notes: "Longer dosing intervals possible (8 weeks).", color: "8E44AD" },
    { name: "Faricimab", brand: "Vabysmo", class: "Dual inhibitor: VEGF-A + Ang-2", notes: "Newest agent. Up to 16-week intervals. 2025 meta-analysis confirms non-inferiority.", color: ACCENT2 }
  ];

  drugs.forEach((d, i) => {
    const y = 0.98 + i * 1.12;
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      x: 0.2, y, w: 9.6, h: 1.05,
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      shadow: { type: "outer", color: "000000", blur: 3, offset: 1, angle: 135, opacity: 0.08 }
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      x: 0.2, y, w: 0.5, h: 1.05,
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    s.addText("(" + d.brand + ")", {
      x: 0.85, y: y + 0.48, w: 2.2, h: 0.3,
      fontSize: 9.5, color: "666666", italic: true, fontFace: "Calibri", margin: 0
    });
    s.addShape(pres.shapes.RECTANGLE, {
      x: 3.15, y: y + 0.18, w: 0.02, h: 0.7,
      fill: { color: "CCCCCC" }, line: { type: "none" }
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      x: 3.3, y: y + 0.05, w: 2.8, h: 0.95,
      fontSize: 10, color: "333333", fontFace: "Calibri", margin: 4, valign: "middle"
    });
    s.addShape(pres.shapes.RECTANGLE, {
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      fill: { color: "CCCCCC" }, line: { type: "none" }
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      fontSize: 10, color: "333333", fontFace: "Calibri", margin: 4, valign: "middle"
    });
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  // Footer regimen note
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    fill: { color: "EFF4F9" }, line: { color: ACCENT, width: 1 }
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    { text: "Treatment Regimen: ", options: { bold: true, color: ACCENT } },
    { text: "Loading phase (3 monthly injections) → Maintenance via PRN or treat-and-extend (T&E) protocol  |  ", options: { color: "333333" } },
    { text: "Early treatment = gains in vision (33% gain >15 letters)", options: { color: ACCENT2, bold: true } }
  ], {
    x: 0.3, y: 5.12, w: 9.4, h: 0.36,
    fontSize: 9.5, fontFace: "Calibri", margin: 2
  });
}

// ── Slide 9: Differential Diagnosis ───────────────────────────
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  const diffs = [
    { dx: "Myopic Degeneration", clue: "High myopia, peripapillary changes, macular changes WITHOUT drusen", color: ACCENT },
    { dx: "CSCR", clue: "Central serous chorioretinopathy. Serous elevation, usually <50 yrs, no drusen, often males", color: "27AE60" },
    { dx: "Ocular Histoplasmosis", clue: "White-yellow chorioretinal scars, peripapillary atrophy, CNV possible", color: GOLD },
    { dx: "Stargardt / Best Disease", clue: "Inherited macular dystrophies. Usually <50 yrs, familial, no drusen, variable atrophy", color: "9B59B6" },
    { dx: "Chloroquine Toxicity", clue: "Bull's-eye maculopathy — ring of hyperpigmentation. Drug history essential", color: ACCENT2 },
    { dx: "Angioid Streaks", clue: "Red-brown/gray bands radiating from optic disc. Associated with pseudoxanthoma elasticum", color: "E67E22" },
    { dx: "IPCV (Polypoidal Choroidal Vasculopathy)", clue: "Polyp-like aneurysmal choroidal dilations on ICGA. Common in Asian patients. Serosanguineous RPE detachments", color: "1ABC9C" }
  ];

  diffs.forEach((d, i) => {
    const col = i < 4 ? 0 : 1;
    const row = i < 4 ? i : i - 4;
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    const y = 0.98 + row * 1.17;
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// ── Slide 10: Prognosis & Summary ─────────────────────────────
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  // Summary table
  const rows = [
    ["", "DRY AMD", "WET AMD"],
    ["Frequency", "90% of cases", "10% of cases"],
    ["Vision loss", "Gradual (years to decades)", "Rapid / sudden"],
    ["Key finding", "Drusen, geographic atrophy", "CNV, hemorrhage, SRF"],
    ["VEGF role", "Not primary driver", "Central driver"],
    ["Treatment", "AREDS2 + lifestyle", "Anti-VEGF injections"],
    ["Prognosis", "Variable; can preserve vision", "Good if treated early; poor if not"]
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        bold: isHeader || isRowHeader,
        color: isHeader ? WHITE : (isRowHeader ? GOLD : LIGHT_GRAY),
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    fill: { color: ACCENT2 }, line: { type: "none" }
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// ── Write file ─────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/amd-ppt/AMD_Ophthalmology.pptx" })
  .then(() => console.log("SUCCESS: AMD_Ophthalmology.pptx written"))
  .catch(e => { console.error("ERROR:", e); process.exit(1); });
Running Command

cd /home/daytona/workspace/amd-ppt && node amd.js 2>&1

Running Command

ls -lh /home/daytona/workspace/amd-ppt/AMD_Ophthalmology.pptx

Your AMD presentation is ready (3.1 MB):

AMD Ophthalmology

Presentation · PPTX


What's inside — 10 slides with a deep navy/clinical blue theme and embedded fundus photos:
SlideContent
1Title slide — AMD with design accents
2Overview & Epidemiology — 4 stat boxes + key facts
3Pathophysiology — Robbins dry vs wet AMD diagram (embedded) + annotated mechanism boxes
4Types & Clinical Features — Side-by-side dry vs wet with real fundus photographs
5Risk Factors & Genetics — CFH/CFI genetics, modifiable vs non-modifiable RF
6Diagnosis & Investigations — 6 investigation cards (Amsler, OCT, FA, ICGA, staging)
7Management — Dry AMD — Full AREDS2 formula + lifestyle/monitoring column
8Management — Wet AMD — Anti-VEGF drug table (Ranibizumab, Bevacizumab, Aflibercept, Faricimab)
9Differential Diagnosis — 7 differentials with distinguishing features
10Prognosis & Summary — Comparison table + prognosis callouts
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