Ocular Pharmacology and Toxicology
Ocular pharmacology and toxicology
This domain tests drug delivery, autonomic control, anti-inflammatory and anti-infective therapy, and adverse effects. Questions often ask why a topical drug causes a systemic effect or which drug is contraindicated.
Core rules
- Topical drops are absorbed through cornea and conjunctiva; nasolacrimal drainage increases systemic absorption. Punctal occlusion and eyelid closure reduce systemic exposure.
- Pilocarpine is a direct muscarinic agonist; tropicamide and cyclopentolate are antimuscarinics; phenylephrine is an alpha-1 agonist.
- Timolol reduces aqueous formation; latanoprost increases uveoscleral outflow; acetazolamide inhibits carbonic anhydrase.
- Corticosteroids suppress inflammation but can raise IOP, cause cataract, and mask infection. Steroid response is dose- and duration-dependent.
- Preservatives such as benzalkonium chloride can cause corneal epithelial toxicity and allergy.
Worked example
A 50 µL drop of 0.5% timolol contains 0.25 mg of drug. If 80% reaches the systemic circulation through nasolacrimal drainage, the systemic dose is 0.20 mg. That is small, but beta-blockade can still trigger bronchospasm in an asthmatic patient. Punctal occlusion for 1-2 minutes reduces drainage and is a practical way to lower systemic risk. This is why the route, not just the concentration, determines toxicity.
Traps
- Assuming topical means systemic safety.
- Mixing up alpha agonists and antimuscarinics.
- Forgetting that prostaglandin analogues can cause iris and eyelid hyperpigmentation.
- Using steroids without considering infection or IOP rise.