Ophthalmology · Glaucoma
The facts most likely to be tested
Primary open-angle glaucoma is a chronic, progressive optic neuropathy characterized by painless, bilateral peripheral vision loss that progresses to tunnel vision.
The classic physical exam finding is an increased cup-to-disc ratio (>0.5) on funduscopic examination due to optic nerve cupping.
Visual field testing typically reveals nasal scotomas that eventually progress to arcuate scotomas.
The primary mechanism is impaired aqueous humor drainage through the trabecular meshwork, leading to elevated intraocular pressure (IOP).
First-line pharmacologic therapy is topical prostaglandin analogs (e.g., latanoprost) which increase uveoscleral outflow.
Risk factors include advanced age, African American or Hispanic ethnicity, family history, and myopia.
Screening for asymptomatic patients is performed via tonometry and dilated funduscopy to assess the optic nerve head.
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A 68-year-old African American male presents for a routine physical examination. He reports no eye pain, redness, or acute vision changes, but mentions he feels like he is 'bumping into door frames' more often lately. On physical exam, his visual acuity is 20/20 bilaterally, but confrontation visual field testing reveals bilateral peripheral field constriction. Funduscopic examination demonstrates optic disc cupping with a cup-to-disc ratio of 0.8 in both eyes.
What is the most appropriate initial pharmacologic treatment for this patient?
Latanoprost
The patient presents with classic signs of primary open-angle glaucoma (peripheral vision loss and increased cup-to-disc ratio); prostaglandin analogs like latanoprost are the first-line treatment to lower intraocular pressure.
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High yield triage
Etiology / Epidemiology
Chronic, progressive optic neuropathy in African Americans and patients with elevated intraocular pressure (IOP).
Clinical Manifestations
Asymptomatic until late-stage peripheral vision loss; tunnel vision is the classic late finding.
Diagnosis
Goldmann applanation tonometry is the gold standard; IOP > 21 mmHg is diagnostic.
Treatment
Latanoprost is first-line; avoid beta-blockers in asthma/COPD.
Prognosis
Permanent optic nerve cupping leads to irreversible blindness if untreated.
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Epidemiology & Etiology
Most common form of glaucoma, characterized by a slow, insidious onset. Major risk factors include African American descent, family history, and age > 40.
Pertinent Anatomy
The trabecular meshwork remains open, but aqueous humor outflow is impaired. This leads to increased pressure on the optic nerve head.
Pathophysiology
Impaired drainage causes chronic elevation of IOP, resulting in mechanical compression and ischemia of the optic nerve axons. This leads to progressive retinal ganglion cell death and characteristic visual field defects.
Clinical Manifestations
Patients are typically asymptomatic until significant damage occurs. The hallmark is a painless, progressive loss of peripheral vision, eventually resulting in tunnel vision. Red flags include sudden vision loss or pain, which suggest acute angle-closure rather than open-angle.
Diagnosis
Diagnosis requires Goldmann applanation tonometry to measure IOP and dilated funduscopy to assess the cup-to-disc ratio. A ratio > 0.5 or asymmetry between eyes is highly suspicious. Automated perimetry is used to map visual field loss.
Treatment
Latanoprost (prostaglandin analog) is the first-line agent to increase uveoscleral outflow. Beta-blockers (e.g., timolol) are contraindicated in asthma, COPD, and heart block. If medical therapy fails, laser trabeculoplasty or surgical intervention is indicated.
Prognosis
Untreated disease leads to irreversible optic nerve cupping and blindness. Patients require lifelong monitoring of IOP and visual fields to prevent progression.
Differential Diagnosis
Acute Angle-Closure Glaucoma: sudden, painful, steamy cornea
Normal-Tension Glaucoma: optic nerve damage with normal IOP
Ocular Hypertension: elevated IOP without optic nerve damage
Retinal Detachment: sudden onset, painless, curtain coming down
Age-Related Macular Degeneration: central vision loss