Ocular Pharmacology and Toxicology
This domain tests drug classes, ocular pharmacokinetics, therapeutic indications, and toxicities. Expect mechanism-based questions and contraindication recognition.
Core rules
- Topical drug penetration depends on lipophilicity, concentration, contact time, and corneal integrity; punctal occlusion reduces systemic absorption.
- Autonomic agents: pilocarpine is a muscarinic agonist causing miosis and increased trabecular outflow; timolol is a beta-blocker reducing aqueous production; brimonidine is an alpha-2 agonist; phenylephrine is an alpha-1 agonist causing mydriasis.
- Cycloplegics: atropine, cyclopentolate, tropicamide block muscarinic receptors; tropicamide is short-acting, atropine long-acting.
- Glaucoma: prostaglandin analogs increase uveoscleral outflow; beta-blockers and carbonic anhydrase inhibitors reduce production; pilocarpine increases trabecular outflow.
- Toxicities: hydroxychloroquine causes retinopathy; ethambutol causes optic neuropathy; topiramate can cause acute angle closure; methanol causes severe metabolic acidosis and visual loss.
Worked example
A patient with asthma and primary open-angle glaucoma needs topical therapy. Reasoning: nonselective beta-blockers such as timolol can cause bronchospasm and should be avoided. A prostaglandin analog such as latanoprost is a reasonable first-line alternative because it lowers IOP by increasing uveoscleral outflow with minimal pulmonary effect.
Traps that cost marks
- Expecting pilocarpine to dilate the pupil; it causes miosis and can cause brow ache.
- Using prostaglandins as first-line therapy in active uveitis; inflammation and cystoid macular edema risk matter.
- Overlooking systemic absorption of topical phenylephrine or beta-blockers.