A 40-year-old woman started on prednisolone acetate drops four times daily for uveitis develops a rise in IOP from 16 to 34 mmHg after five weeks, with open angles and no other cause identified. The mechanism of this pressure rise is best described as:
- A Increased outflow resistance from accumulation of glycosaminoglycans in trabecular endothelial cells ✓
- B Deposition of corticosteroid-prostaglandin complexes in the trabecular meshwork
- C Increased aqueous humour production by the ciliary processes
- D Angle closure from forward rotation of the ciliary body
Explanation
Corticosteroid-induced glaucoma results from reduced facility of aqueous outflow, attributed to decreased trabecular endothelial phagocytosis and accumulation of extracellular matrix glycosaminoglycans in the meshwork. Susceptibility follows a population distribution, with POAG patients being the most frequent high responders. The angle remains open, aqueous secretion is unaffected, and the response reverses over weeks after stopping the steroid, distinguishing it from permanent forms of secondary open-angle glaucoma.
Reference: Yanoff & Duker, Ophthalmology, 5th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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