Macular Degeneration

What is the function of the macula?

Central vision, color vision, and fine detail.

What is age-related macular degeneration (AMD)?

Progressive degeneration of the macula causing central vision loss.

What is the fovea responsible for?

Highest-acuity vision; densely packed cone photoreceptors.

What are the major risk factors for AMD?

Age, genetics, smoking, Caucasian ancestry, obesity, and cardiovascular disease.

Which age group is most affected by AMD?

Adults older than 60 years.

What is the hallmark retinal finding of AMD?

Drusen deposits.

What do large drusen indicate?

Higher risk of progression to advanced AMD.

What are the two forms of advanced AMD?

Geographic atrophy (dry) and neovascular (wet) AMD.

What characterizes early AMD?

Small drusen and mild retinal pigment epithelium (RPE) changes.

What characterizes intermediate AMD?

Intermediate drusen and RPE pigment abnormalities.

What characterizes advanced dry AMD?

Geographic atrophy with loss of RPE and photoreceptors.

What characterizes wet AMD?

Choroidal neovascularization with fluid and blood leakage.

What drives abnormal blood vessel growth in wet AMD?

Increased vascular endothelial growth factor (VEGF).

Why can wet AMD cause rapid vision loss?

Fragile new vessels leak fluid and blood, damaging the macula.

What symptoms suggest AMD?

Blurred central vision, wavy lines, difficulty reading, and central dark spots.

What is metamorphopsia?

Distorted vision in which straight lines appear wavy.

What is the Amsler grid used for?

Home monitoring for central vision distortion or missing areas.

What should a patient do if straight lines suddenly appear wavy?

Seek prompt ophthalmic evaluation for possible wet AMD.

What examination helps identify drusen and RPE changes?

Dilated fundus examination.

What does optical coherence tomography (OCT) detect?

Retinal fluid, structural abnormalities, and RPE changes.

What does fluorescein angiography identify?

Abnormal retinal/choroidal blood vessels and leakage.

What is fundus autofluorescence useful for?

Evaluating RPE abnormalities and geographic atrophy.

Are routine laboratory tests needed to diagnose AMD?

No; diagnosis relies on eye examination and retinal imaging.

What are the main treatment approaches for AMD?

AREDS2 for eligible AMD, complement inhibitors for GA, anti-VEGF for wet AMD.

Which AMD stage benefits from AREDS2?

Intermediate AMD; also late AMD in one eye when the other remains at risk.

What is the purpose of AREDS2 supplementation?

Reduce progression to advanced AMD in appropriate patients.

Does AREDS2 prevent AMD from developing?

No; it reduces progression risk, not disease onset.

What is the AREDS2 vitamin C dose?

500 mg daily.

What is the AREDS2 vitamin E dose?

400 IU daily.

What is the AREDS2 zinc dose in the lecture?

80 mg daily.

What is the AREDS2 copper dose?

2 mg daily.

What is the AREDS2 lutein dose?

10 mg daily.

What is the AREDS2 zeaxanthin dose?

2 mg daily.

Which ingredient is excluded from AREDS2?

Beta-carotene.

Why should current or former smokers avoid original AREDS?

Its beta-carotene content is inappropriate for patients with a smoking history.

Can a standard multivitamin replace AREDS2?

No; it does not provide the studied AREDS2 formulation.

What is the usual PreserVision AREDS2 softgel dosing?

One softgel twice daily.

Which original AREDS ingredient was replaced in AREDS2?

Beta-carotene was replaced with lutein and zeaxanthin.

What is the key difference between AREDS and AREDS2?

Original AREDS contains beta-carotene; AREDS2 contains lutein and zeaxanthin.

What is geographic atrophy (GA)?

Advanced dry AMD with progressive RPE and photoreceptor loss.

What is the goal of complement inhibitors in GA?

Slow geographic atrophy lesion growth and disease progression.

What is the MOA of pegcetacoplan (Syfovre)?

Complement C3 inhibition.

What is the MOA of avacincaptad pegol (Izervay)?

Complement C5 inhibition.

What is the route of GA complement inhibitors?

Intravitreal injection.

Can complement inhibitors restore lost vision?

No; they slow progression but do not regenerate lost RPE or photoreceptors.

What monitoring is required with GA complement inhibitors?

Repeated retinal examinations and follow-up injections.

What is the first-line drug class for wet AMD?

Intravitreal anti-VEGF agents.

What is the MOA of anti-VEGF medications?

Inhibit abnormal blood vessel growth and vascular leakage.

What is the goal of anti-VEGF therapy in wet AMD?

Reduce fluid/leakage, suppress neovascularization, and stabilize or improve vision.

What is the route of anti-VEGF therapy for wet AMD?

Intravitreal injection.

What are examples of anti-VEGF agents?

Aflibercept, ranibizumab, faricimab, bevacizumab, and brolucizumab.

What is the brand name of aflibercept?

Eylea.

What is the brand name of ranibizumab?

Lucentis.

What is the brand name of bevacizumab in the older table?

Avastin.

What is the brand name of brolucizumab-dbll?

Beovu.

What is the brand name of ranibizumab-nuna?

Byooviz.

What is the brand name of pegaptanib?

Macugen.

What is the older table's bevacizumab dose for wet AMD?

1.25 mg intravitreally monthly for 3 months, then monthly or as needed.

What is the older table's ranibizumab dose?

0.5 mg intravitreally approximately every 28 days.

What is the older table's aflibercept regimen?

2 mg intravitreally every 4 weeks for 12 weeks, then every 8 weeks.

What is the older table's brolucizumab regimen?

6 mg monthly for 3 months, then every 8–12 weeks.

What is the older table's pegaptanib dose?

0.3 mg intravitreally every 6 weeks.

Is pegaptanib available in the U.S. according to the table?

No; the table identifies it as unavailable.

Which anti-VEGF medication has historically been used off-label?

Bevacizumab (Avastin).

Which bevacizumab product does the 2026 lecture identify as FDA-approved for wet AMD?

Bevacizumab-vikg (Lytenava).

What does TREX dosing refer to?

Treat-and-extend injection scheduling based on clinical response.

What is a major pharmacist counseling point for intravitreal therapy?

Maintain scheduled injections and retina follow-up appointments.

What is the most important modifiable AMD risk factor?

Smoking.

What lifestyle measures are emphasized for AMD prevention?

Avoid smoking, exercise, maintain healthy weight, and eat a healthy diet.

Why is cardiovascular disease management important in AMD?

Cardiovascular conditions are associated with increased AMD risk.

What should a pharmacist check before recommending an eye vitamin?

AMD stage, smoking history, and exact supplement ingredients.

A former smoker with intermediate AMD needs a supplement. Which one?

AREDS2 without beta-carotene.

A patient with wet AMD asks whether AREDS2 replaces injections. What is the answer?

No; wet AMD requires treatment directed at neovascularization, such as anti-VEGF.

Which AMD treatment targets complement C3?

Pegcetacoplan (Syfovre).

Which AMD treatment targets complement C5?

Avacincaptad pegol (Izervay).

Which AMD treatment targets VEGF-driven neovascularization?

Intravitreal anti-VEGF therapy.

What are the key AMD exam associations?

Drusen = AMD; AREDS2 = intermediate; C3/C5 = GA; anti-VEGF = wet AMD.