AMD Basics - Dotty Vision Drama
- Leading cause of irreversible blindness in elderly (>60 yrs).
- Types:
- Dry (Non-exudative/Atrophic): 80-90%; geographic atrophy.
- Wet (Exudative/Neovascular): 10-20%; choroidal neovascularization (CNV).
- Risk Factors: Age, smoking, genetics (CFH, ARMS2), HTN, āantioxidants.

ā Drusen accumulation between the RPE and Bruch's membrane is the earliest clinically detectable feature of AMD.
Pathophysiology - RPE's Ruin
- Chronic oxidative stress & inflammation primarily target the Retinal Pigment Epithelium (RPE).
- RPE dysfunction: Impaired phagocytosis of photoreceptor outer segments, ā intracellular lipofuscin, cytokine release, oxidative damage.
- Bruch's membrane: Thickens, accumulates lipids & collagen (basal laminar and linear deposits), ā nutrient & waste transport.
- Drusen formation: Extracellular debris (lipids, proteins) accumulates between RPE & inner collagenous layer of Bruch's; soft drusen indicate higher risk.
- Dry AMD (Non-exudative): Leads to geographic atrophy (RPE & photoreceptor cell death).
- Wet AMD (Exudative): Characterized by Choroidal Neovascularization (CNVM) through breaks in Bruch's membrane.
ā VEGF (Vascular Endothelial Growth Factor) is a key mediator in the development of choroidal neovascularization (CNVM) in wet AMD.

Clinical Features - Signs & Symptoms
- Symptoms:
- Gradual, painless, progressive bilateral ā central vision.
- Metamorphopsia (Amsler grid distortion): straight lines appear wavy.
- Central or paracentral scotoma (blind spot).
- Difficulty with reading, recognizing faces, needing brighter light.
- Signs (Dry AMD):
- Drusen (key finding):
- Hard: small, yellow, well-defined.
- Soft: larger, paler, indistinct borders (higher risk for CNV).
- RPE changes: hyperpigmentation or hypopigmentation.
- Geographic Atrophy (GA): advanced, sharply demarcated RPE/choriocapillaris atrophy.
- Drusen (key finding):
- Signs (Wet AMD):
- Choroidal Neovascularization (CNV) evidence.
- Subretinal/intraretinal fluid, hemorrhage; lipid exudates.
- Disciform scar (fibrovascular, end-stage).
ā Sudden onset of metamorphopsia or a central scotoma often indicates conversion to wet AMD.
Diagnostic Workup - Eye Spy Tech
- Fundoscopy: Drusen, RPE changes, exudates, hemorrhage.
- Amsler Grid: Metamorphopsia, scotoma screening.
- OCT (Optical Coherence Tomography): Detects fluid (SRF/IRF), drusen, RPE integrity; monitors therapy.
- FFA (Fundus Fluorescein Angiography): CNVM (classic/occult) detection, leakage patterns.
- ICG (Indocyanine Green Angiography): Occult CNVM with blood/pigment; choroidal circulation.

ā Fundus Fluorescein Angiography (FFA) is the gold standard for visualizing and classifying CNVM patterns, while OCT is crucial for detecting and monitoring fluid.
Management - Fighting Blindness
- Overall Goals: Preserve/improve vision, slow AMD progression.
- General Measures:
- Smoking cessation (critical).
- Healthy diet (green leafy veg, fish).
- UV protection.
- Dry AMD (Non-neovascular):
- Observation (early).
- AREDS2 (intermediate/advanced): Vit C (500mg), E (400IU), Lutein (10mg), Zeaxanthin (2mg), Zinc (80mg), Copper (2mg). š LZ-CEZ (Lutein, Zeaxanthin, Vit C, Vit E, Zinc).
- Wet AMD (Neovascular):
ā Intravitreal anti-VEGF injections (e.g., Ranibizumab, Bevacizumab, Aflibercept) are the mainstay of treatment for neovascular (wet) AMD.
- Photodynamic Therapy (PDT) with Verteporfin: Adjunctive, specific cases (e.g., PCV).
- Thermal Laser: Rare, extrafoveal CNVM.
- Low Vision Rehabilitation: Essential for advanced AMD.
HighāYield Points - ā” Biggest Takeaways
- AMD is a leading cause of irreversible vision loss in individuals >50 years.
- Dry AMD: Characterized by Drusen (yellow deposits) and geographic atrophy. More common.
- Wet AMD: Involves Choroidal Neovascularization (CNV), leading to exudation and hemorrhage. More severe.
- Metamorphopsia (distorted vision) is a key symptom, detected by Amsler grid.
- Anti-VEGF injections are first-line treatment for Wet AMD.
- Major risk factors: Age, smoking, positive family history, hypertension.
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