Learning Objective

Explain the pathophysiology, clinical features, and pharmacologic management of open-angle glaucoma, including mechanisms of drugs that reduce intraocular pressure.

Open-Angle Glaucoma (Chronic Glaucoma)

• Caused by increased intraocular pressure (IOP) due to reduced reabsorption of aqueous humor.
• Presents with painless, progressive visual field loss.
• If untreated → optic nerve damage → irreversible blindness.

IOP Regulation

IOP depends on:

• Formation of aqueous humor (ciliary epithelium)
• Drainage via the trabecular meshwork and uveoscleral pathways

Pharmacologic Treatment Strategies

↓ Aqueous Humor Production

• β blockers (e.g., timolol, betaxolol)
  • Block β receptors on ciliary epithelium → ↓ aqueous humor formation

↑ Aqueous Humor Outflow

• PGF₂α analogs (e.g., latanoprost, travoprost)
  • Increase uveoscleral outflow
  • First-line therapy in many cases

Contraindications (VERY high yield)

• Antimuscarinic drugs
• α₁ agonists

These can worsen closed-angle (narrow-angle) glaucoma by causing mydriasis, which further obstructs the angle.

Activity