Which cholinesterase inhibitor is used as a glaucoma preventive agent?

Which cholinesterase inhibitor is used as a glaucoma preventive agent?

• A. Neostigmine
• B. Pyridostigmine
• C. Demecarium
• D. Carbamylcholine

Answer: (C)

Cholinesterase inhibitors raise acetylcholine levels at the muscarinic receptors in the eye, leading to ciliary muscle contraction and increased outflow of aqueous humor through the trabecular meshwork, which lowers intraocular pressure and helps prevent glaucoma. Demecarium bromide is a long-acting cholinesterase inhibitor formulated for topical ocular use. Its prolonged action provides sustained stimulation of muscarinic receptors in the eye, producing miosis and enhanced drainage of aqueous humor, making it suitable as a glaucoma preventive agent. The other options don’t fit this use. Neostigmine and pyridostigmine are mainly systemic agents for myasthenia gravis and aren’t used for glaucoma due to limited ocular penetration and systemic effects. Carbamylcholine (carbachol) is a direct-acting cholinergic agonist, not a cholinesterase inhibitor, and it achieves miosis through receptor activation rather than by inhibiting acetylcholinesterase.

Cholinesterase inhibitors raise acetylcholine levels at the muscarinic receptors in the eye, leading to ciliary muscle contraction and increased outflow of aqueous humor through the trabecular meshwork, which lowers intraocular pressure and helps prevent glaucoma.

Demecarium bromide is a long-acting cholinesterase inhibitor formulated for topical ocular use. Its prolonged action provides sustained stimulation of muscarinic receptors in the eye, producing miosis and enhanced drainage of aqueous humor, making it suitable as a glaucoma preventive agent.

The other options don’t fit this use. Neostigmine and pyridostigmine are mainly systemic agents for myasthenia gravis and aren’t used for glaucoma due to limited ocular penetration and systemic effects. Carbamylcholine (carbachol) is a direct-acting cholinergic agonist, not a cholinesterase inhibitor, and it achieves miosis through receptor activation rather than by inhibiting acetylcholinesterase.