Glaucoma
Core concepts
Build a framework around open-angle vs angle-closure, primary vs secondary, and the aqueous pathway (ciliary body → trabecular meshwork → Schlemm canal → episcleral veins). Understand IOP as a balance of production and outflow, and how each drug class acts on that balance: prostaglandins (uveoscleral outflow), beta-blockers (production), alpha-agonists (both), carbonic anhydrase inhibitors (production), cholinergics (outflow).
Know the optic nerve head features of glaucomatous damage: cupping, rim thinning (especially inferior and superior), disc haemorrhage, and retinal nerve fibre layer loss. Link structure to field defects: nasal step, arcuate scotoma, paracentral loss, and the rule that field loss respects the horizontal midline.
Traps
- Treating IOP alone without assessing the disc and field.
- Missing angle closure in a patient labelled open-angle (check gonioscopy and anterior chamber depth).
- Forgetting steroid-induced ocular hypertension.
- Confusing normal-tension glaucoma with ischaemic optic neuropathy (respects midline vs altitudinal).
Rule of thumb
Gonioscopy is mandatory before labelling glaucoma; and a field defect that crosses the horizontal midline is not glaucomatous.
Worked example
A 65-year-old with IOP 26 mmHg, cupping, and a superior arcuate defect respecting the midline. Gonioscopy shows open angles. This is primary open-angle glaucoma; target IOP is set at least 20–30% below baseline, and prostaglandin first-line is appropriate unless contraindicated.