A patient on long-term topical corticosteroids for vernal keratoconjunctivitis develops elevated IOP. The mechanism by which corticosteroids elevate IOP in steroid responders is:
- A Pupillary block from posterior synechiae formation
- B Increased aqueous production by the ciliary body epithelium
- C Decreased aqueous outflow through the trabecular meshwork due to accumulation of glycosaminoglycans and inhibition of phagocytic activity of trabecular cells ✓
- D Neovascularization of the angle obstructing outflow
Explanation
Corticosteroid-induced ocular hypertension results from decreased aqueous outflow resistance at the trabecular meshwork. Corticosteroids inhibit phagocytosis by trabecular endothelial cells (reducing clearance of extracellular matrix debris), increase glycosaminoglycan deposition in the trabecular meshwork, and rearrange cytoskeletal actin in trabecular cells — collectively reducing outflow facility. The IOP rise is dose-dependent and more pronounced with potent steroids (dexamethasone, prednisolone) than with lower-potency preparations (fluorometholone, loteprednol). Aqueous production is not increased.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
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Written and medically reviewed by the StethoPrep medical team.