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PH9.7 | PH9.7 | Ocular Pharmacotherapy and Topical Delivery — SDL Guide — SDL Guide (Part 3)
Self-Assessment
Test your understanding of ocular pharmacology.
- Name the drug class, prototype, and mechanism for each of the following: (a) most potent single-agent IOP-reducing drug for open-angle glaucoma, (b) drug class contraindicated in asthma that is commonly used in glaucoma, (c) drug used for acute angle-closure emergency to reduce vitreous volume, (d) drug for herpes simplex keratitis.
- Why is brimonidine absolutely contraindicated in infants under 2 years? What adverse effect is specifically at risk?
- A patient with open-angle glaucoma is on timolol and presents with increasing fatigue and cold extremities. His heart rate is 48 bpm. Which drug class is responsible, and what alternative would you use that reduces the systemic beta-blocking risk?
- Explain the pharmacokinetic basis for systemic adverse effects from topical ocular timolol, and describe the technique to minimise them.
- What is the role of anti-VEGF injections in wet AMD, and why is bevacizumab used off-label in preference to ranibizumab in many settings?
SELF-CHECK
Latanoprost eye drops cause iris pigmentation as a side effect. Which mechanism explains this adverse effect?
A. Latanoprost causes melanocyte destruction leading to patchy iris depigmentation
B. Latanoprost stimulates prostaglandin FP receptors on iris melanocytes, increasing melanin synthesis and causing progressive irreversible darkening of the iris, especially in mixed-colour irides
C. Latanoprost causes corneal deposition of pigment that gives the iris a darker appearance
D. Latanoprost triggers an immune reaction that deposits haemosiderin in the iris stroma
Reveal Answer
Answer: B. Latanoprost stimulates prostaglandin FP receptors on iris melanocytes, increasing melanin synthesis and causing progressive irreversible darkening of the iris, especially in mixed-colour irides
Latanoprost (and other prostaglandin FP receptor agonists — bimatoprost, travoprost) stimulate melanocyte activity in the iris stroma via the FP receptor, increasing tyrosinase activity and melanin synthesis within iris melanocytes. This causes progressive darkening of the iris — particularly in patients with mixed-colour irides (hazel, green-brown). The change is irreversible. It affects iris pigmentation but not skin pigmentation. It is not an immune reaction and does not involve corneal deposition. This cosmetic side effect should be disclosed to patients before starting therapy, particularly in those who have different eye colours (the treated eye may become permanently darker than the untreated eye).