A patient using topical prednisolone acetate 1% for 6 weeks develops elevated IOP to 36 mmHg. The IOP rise is due to blockade of which pathway?
- A Increased prostaglandin synthesis leading to uveoscleral outflow reduction
- B Trabecular meshwork glycosaminoglycan accumulation reducing conventional outflow ✓
- C Ciliary body stimulation increasing aqueous production
- D Episcleral venous pressure elevation
Explanation
Corticosteroid-induced ocular hypertension results primarily from accumulation of glycosaminoglycans (GAGs) in the trabecular meshwork, reducing aqueous outflow through the conventional (trabecular) pathway. Steroids also reduce the phagocytic activity of trabecular endothelial cells, leading to further debris accumulation. The IOP rise is not from increased aqueous production; aqueous production is minimally affected. This is most pronounced with high-potency topical steroids like prednisolone acetate and dexamethasone.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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