Netarsudil, a newer topical glaucoma drug, lowers IOP by which mechanism DISTINCT from all other anti-glaucoma classes?
- A Increasing uveoscleral outflow via prostaglandin receptors
- B Decreasing aqueous production by inhibiting carbonic anhydrase
- C Inhibiting Rho kinase to increase trabecular meshwork outflow and reduce episcleral venous pressure ✓
- D Stimulating adenylate cyclase to increase aqueous outflow
Correct answer: C. Inhibiting Rho kinase to increase trabecular meshwork outflow and reduce episcleral venous pressure
Explanation
Netarsudil is a Rho kinase (ROCK) inhibitor that relaxes the contractile actin-myosin cytoskeleton of trabecular meshwork cells, increasing conventional outflow facility. It also lowers episcleral venous pressure and inhibits norepinephrine transport, contributing to aqueous suppression. This triple mechanism is unique among anti-glaucoma agents. Prostaglandins act on FP receptors for uveoscleral outflow; CA inhibitors suppress aqueous; adenylate cyclase stimulation by catecholamines reduces aqueous production.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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