A patient on topical dexamethasone drops for 6 weeks after corneal transplant develops elevated IOP of 32 mmHg in the treated eye. Which receptor mechanism explains steroid-induced ocular hypertension?

• A Blockade of prostaglandin synthesis reducing uveoscleral outflow
• B Mineralocorticoid receptor activation increasing aqueous secretion
• C Inhibition of carbonic anhydrase in ciliary epithelium
• D Glucocorticoid receptor-mediated increase in trabecular meshwork extracellular matrix glycosaminoglycans reducing aqueous outflow ✓

Explanation

Steroid-induced ocular hypertension results from glucocorticoid receptor (GR) activation in trabecular meshwork (TM) cells, leading to accumulation of extracellular matrix (fibronectin, laminin, collagen IV) and glycosaminoglycans in the juxtacanalicular TM, reducing aqueous humor outflow resistance. Additionally, steroids upregulate myocilin (MYOC) expression in TM cells. About 35% of the general population are 'steroid responders.' Uveoscleral outflow is actually reduced, not the primary pathway affected.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.