Glaucoma: Pathophysiology, Drugs, and Adverse Effects

Glaucoma is a group of eye disorders characterized by progressive optic neuropathy, often associated with elevated intraocular pressure (IOP). The increase in IOP is due to an imbalance between the production and drainage of aqueous humor, leading to optic nerve damage and visual field loss.

• Open-angle Glaucoma: Blockage in the trabecular meshwork leads to reduced aqueous humor outflow.
• Angle-closure Glaucoma: The iris physically obstructs the trabecular meshwork, causing acute IOP elevation.

• Prostaglandin Analogues: Latanoprost, Travoprost, Bimatoprost
• Beta-blockers: Timolol, Betaxolol
• Carbonic Anhydrase Inhibitors: Acetazolamide, Dorzolamide
• Alpha-2 Agonists: Brimonidine, Apraclonidine
• Cholinergic Agonists: Pilocarpine, Carbachol
• Rho Kinase Inhibitors: Netarsudil

1. Prostaglandin Analogues

• Mechanism: Increase uveoscleral outflow of aqueous humor, reducing IOP.
• Adverse Effects: Iris pigmentation, eyelash growth, conjunctival hyperemia.

2. Beta-blockers

• Mechanism: Decrease aqueous humor production by blocking beta-adrenergic receptors in the ciliary body.
• Adverse Effects: Bradycardia, hypotension, bronchospasm, fatigue.

3. Carbonic Anhydrase Inhibitors

• Mechanism: Inhibit carbonic anhydrase in the ciliary epithelium, reducing aqueous humor production.
• Adverse Effects: Paresthesia, gastrointestinal upset, metabolic acidosis (systemic use).

4. Alpha-2 Agonists

• Mechanism: Reduce aqueous humor production and increase uveoscleral outflow.
• Adverse Effects: Allergic conjunctivitis, dry mouth, fatigue.

5. Cholinergic Agonists

• Mechanism: Stimulate muscarinic receptors, contracting the ciliary muscle to open the trabecular meshwork and increase aqueous outflow.
• Adverse Effects: Miosis, brow ache, retinal detachment (rare).

6. Rho Kinase Inhibitors

• Mechanism: Improve trabecular outflow by relaxing the cytoskeleton of the trabecular meshwork.
• Adverse Effects: Conjunctival hyperemia, corneal deposits, eye irritation.