Primary Open-Angle Glaucoma Flashcards
What is primary open-angle glaucoma (POAG)?
A chronic, progressive condition characterised by optic neuropathy and visual field loss, associated with raised intraocular pressure.
What causes POAG?
Impaired drainage of aqueous humour through the trabecular meshwork, leading to increased intraocular pressure.
What are the risk factors for POAG?
Age, family history, African or Hispanic ethnicity, myopia, diabetes, and prolonged corticosteroid use.
What are the typical symptoms of POAG?
POAG is often asymptomatic in the early stages; later, peripheral vision loss occurs, leading to “tunnel vision.”
How is POAG typically detected?
During routine eye exams, with findings such as raised intraocular pressure, optic disc cupping, and visual field defects.
What is the pathophysiology of POAG?
Progressive optic nerve damage occurs due to mechanical compression or vascular insufficiency from elevated intraocular pressure.
What is the prevalence of POAG?
POAG is one of the leading causes of irreversible blindness worldwide, particularly in older adults.
What is the normal range for intraocular pressure (IOP)?
10–21 mmHg, but optic nerve damage can occur even at normal pressures in normal-tension glaucoma.
What are the characteristic fundoscopic findings in POAG?
Optic disc cupping (enlarged cup-to-disc ratio) and thinning of the neuroretinal rim.
What is the role of visual field testing in POAG?
It detects peripheral vision loss and maps visual field defects characteristic of glaucoma.
What is the role of optical coherence tomography (OCT) in POAG?
OCT measures retinal nerve fibre layer thickness to detect early optic nerve damage.
What are the first-line medications for POAG?
Prostaglandin analogues (e.g., latanoprost) to increase aqueous humour outflow.
What are the common side effects of prostaglandin analogues?
Eye redness, eyelash growth, and darkening of the iris or periocular skin.
What is the role of beta-blockers in POAG?
Beta-blockers (e.g., timolol) reduce aqueous humour production.
What is the role of carbonic anhydrase inhibitors in POAG?
These drugs (e.g., dorzolamide) decrease aqueous humour production.
What is the role of alpha agonists in POAG?
Alpha agonists (e.g., brimonidine) reduce aqueous humour production and increase uveoscleral outflow.
What is selective laser trabeculoplasty (SLT)?
A laser treatment that improves aqueous humour drainage through the trabecular meshwork.
What are the surgical options for POAG?
Trabeculectomy, aqueous shunt implants, or minimally invasive glaucoma surgeries (MIGS).
What are potential complications of untreated POAG?
Progressive vision loss leading to blindness, optic nerve damage, and reduced quality of life.
What is normal-tension glaucoma?
A subtype of POAG where optic nerve damage occurs despite normal intraocular pressure levels.
What lifestyle modifications can help manage POAG?
Regular eye exams, avoiding smoking, maintaining a healthy weight, and controlling systemic conditions like diabetes.
Why is POAG often called the “silent thief of sight”?
Because it progresses slowly and painlessly, causing significant damage before symptoms appear.
What is the role of compliance in POAG management?
Adherence to prescribed medications and regular follow-ups is critical to prevent progression of the disease.
How does POAG differ from acute angle-closure glaucoma?
POAG is chronic and painless with gradual vision loss, while acute angle-closure glaucoma is sudden, painful, and requires emergency treatment.
Why is early detection important in POAG?
Early detection and treatment can prevent irreversible vision loss and preserve quality of life.
