Glaucoma is a progressive optic neuropathy with characteristic cupping and field loss, usually with raised intraocular pressure; the angle decides whether it is a silent thief or an emergency.
How it's asked: Field defects of POAG in order, first-line drugs and their side effects, and the management of acute angle-closure.
Why this is true
Aqueous is produced by the ciliary body, flows through the pupil and drains through the trabecular meshwork in the angle. In primary open-angle glaucoma the angle is open but the meshwork resists outflow, so pressure rises slowly and painlessly, gradually damaging ganglion-cell axons at the optic disc — the arcuate fibres first, which is why the earliest field defects curve around fixation. In angle closure the peripheral iris is pushed forward against the meshwork (often when the pupil is mid-dilated in dim light), blocking drainage abruptly: pressure can exceed 50 mmHg within hours, causing pain, corneal oedema and haloes.
Key points
POAG vs acute PACG
| Feature | POAG | Acute PACG |
|---|---|---|
| Onset | Insidious, painless | Sudden, painful |
| Angle | Open | Closed |
| Pupil | Normal | Fixed, mid-dilated, vertically oval |
| Cornea | Clear | Oedematous (haloes) |
| Treatment | Drops, SLT, trabeculectomy | Lower IOP, then laser iridotomy (both eyes) |
Common traps
- Normal IOP doesn't exclude glaucoma — normal-tension glaucoma exists; diagnosis rests on disc and field.
- Treat the fellow eye with prophylactic iridotomy after an acute angle-closure attack.
Clinical case
A 60-year-old hypermetropic woman develops severe eye pain, blurred vision with coloured haloes and vomiting after watching a film in a dark hall. The pupil is fixed and mid-dilated, the cornea hazy.
High-yield
POAG fields: paracentral → Bjerrum's arcuate → nasal step → tubular. Acute angle-closure: fixed mid-dilated oval pupil, haloes; acetazolamide then iridotomy (both eyes).
Quick check
Q1.Earliest field defect in primary open-angle glaucoma:
Q2.Definitive treatment of acute angle-closure glaucoma: