Primary Open-Angle Glaucoma Flashcards

1
Q

What is primary open-angle glaucoma (POAG)?

A

A chronic, progressive condition characterised by optic neuropathy and visual field loss, associated with raised intraocular pressure.

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2
Q

What causes POAG?

A

Impaired drainage of aqueous humour through the trabecular meshwork, leading to increased intraocular pressure.

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3
Q

What are the risk factors for POAG?

A

Age, family history, African or Hispanic ethnicity, myopia, diabetes, and prolonged corticosteroid use.

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4
Q

What are the typical symptoms of POAG?

A

POAG is often asymptomatic in the early stages; later, peripheral vision loss occurs, leading to “tunnel vision.”

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5
Q

How is POAG typically detected?

A

During routine eye exams, with findings such as raised intraocular pressure, optic disc cupping, and visual field defects.

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6
Q

What is the pathophysiology of POAG?

A

Progressive optic nerve damage occurs due to mechanical compression or vascular insufficiency from elevated intraocular pressure.

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7
Q

What is the prevalence of POAG?

A

POAG is one of the leading causes of irreversible blindness worldwide, particularly in older adults.

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8
Q

What is the normal range for intraocular pressure (IOP)?

A

10–21 mmHg, but optic nerve damage can occur even at normal pressures in normal-tension glaucoma.

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9
Q

What are the characteristic fundoscopic findings in POAG?

A

Optic disc cupping (enlarged cup-to-disc ratio) and thinning of the neuroretinal rim.

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10
Q

What is the role of visual field testing in POAG?

A

It detects peripheral vision loss and maps visual field defects characteristic of glaucoma.

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11
Q

What is the role of optical coherence tomography (OCT) in POAG?

A

OCT measures retinal nerve fibre layer thickness to detect early optic nerve damage.

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12
Q

What are the first-line medications for POAG?

A

Prostaglandin analogues (e.g., latanoprost) to increase aqueous humour outflow.

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13
Q

What are the common side effects of prostaglandin analogues?

A

Eye redness, eyelash growth, and darkening of the iris or periocular skin.

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14
Q

What is the role of beta-blockers in POAG?

A

Beta-blockers (e.g., timolol) reduce aqueous humour production.

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15
Q

What is the role of carbonic anhydrase inhibitors in POAG?

A

These drugs (e.g., dorzolamide) decrease aqueous humour production.

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16
Q

What is the role of alpha agonists in POAG?

A

Alpha agonists (e.g., brimonidine) reduce aqueous humour production and increase uveoscleral outflow.

17
Q

What is selective laser trabeculoplasty (SLT)?

A

A laser treatment that improves aqueous humour drainage through the trabecular meshwork.

18
Q

What are the surgical options for POAG?

A

Trabeculectomy, aqueous shunt implants, or minimally invasive glaucoma surgeries (MIGS).

19
Q

What are potential complications of untreated POAG?

A

Progressive vision loss leading to blindness, optic nerve damage, and reduced quality of life.

20
Q

What is normal-tension glaucoma?

A

A subtype of POAG where optic nerve damage occurs despite normal intraocular pressure levels.

21
Q

What lifestyle modifications can help manage POAG?

A

Regular eye exams, avoiding smoking, maintaining a healthy weight, and controlling systemic conditions like diabetes.

22
Q

Why is POAG often called the “silent thief of sight”?

A

Because it progresses slowly and painlessly, causing significant damage before symptoms appear.

23
Q

What is the role of compliance in POAG management?

A

Adherence to prescribed medications and regular follow-ups is critical to prevent progression of the disease.

24
Q

How does POAG differ from acute angle-closure glaucoma?

A

POAG is chronic and painless with gradual vision loss, while acute angle-closure glaucoma is sudden, painful, and requires emergency treatment.

25
Q

Why is early detection important in POAG?

A

Early detection and treatment can prevent irreversible vision loss and preserve quality of life.