Glaucoma
Core concepts
Know the open-angle vs. closed-angle framework and the mechanisms of each. For open-angle, understand the optic nerve head features (cupping, rim loss, RNFL thinning, disc hemorrhage) and the role of IOP, CCT, and gonioscopy. For angle-closure, know the plateau iris, pupillary block, and the role of laser peripheral iridotomy. Understand the glaucoma medications by class and side effects: prostaglandins (latanoprost - iris darkening, periorbital fat atrophy), beta-blockers (timolol - bronchospasm, bradycardia), alpha-agonists (brimonidine - fatigue, allergy), carbonic anhydrase inhibitors (topiramate - acute angle-closure, paresthesia), and pilocarpine.
Traps
A favorite trap is topiramate-induced acute angle-closure - a young patient on topiramate for migraine presents with bilateral angle-closure and myopia; the mechanism is ciliary body swelling, not pupillary block, so iridotomy does not help; treat by stopping the drug and cycloplegia. Another trap is normal-tension glaucoma vs. ischemic optic neuropathy. Also know that steroid response can mimic glaucoma.
Worked example
A 28-year-old on topiramate has bilateral blurred vision, shallow anterior chamber, and high IOP. Rule of thumb: bilateral angle-closure in a young patient on a sulfa-derived drug = topiramate; stop the drug, use cycloplegics and aqueous suppressants, and avoid iridotomy.