Learning Objective
Differentiate the pathophysiology and management of closed-angle glaucoma from open-angle glaucoma, and describe the mechanisms of drugs used to lower intraocular pressure.
Closed-Angle Glaucoma (Acute or Chronic)
- Acute form: Sudden, painful increase in IOP
- Chronic form: Often genetic, gradual narrowing of the angle.
- Caused by the blockage of the canal of Schlemm, preventing aqueous humor outflow
- Requires emergent management to lower IOP before definitive surgery
Emergency Medical Therapy
- Carbonic anhydrase inhibitors (e.g., acetazolamide) → ↓ aqueous humor formation
- Mannitol → osmotic diuresis → ↓ IOP rapidly
NEVER give antimuscarinics or α₁ agonists (cause mydriasis → worsen angle closure)
Mechanisms of Glaucoma Drugs
| Drug | Class | Mechanism of Action |
|---|---|---|
| Timolol | β-blocker | β₂ blockade → ↓ aqueous humor formation |
| Latanoprost | PGF₂α analog | ↑ Uveoscleral outflow |
| Apraclonidine | α₂ agonist | ↓ Aqueous humor production + ↑ drainage |
| Acetazolamide | Carbonic anhydrase inhibitor (CAI) | Inhibits CA → ↓ aqueous humor formation |
Cholinergic Effects on the Eye
Muscarinic Stimulation (Parasympathetic)
- Miosis (pupil constriction)
- Accommodation for near vision
- Ciliary muscle contraction
Muscarinic Antagonism (e.g., Atropine)
- Mydriasis (pupil dilation)
- Cycloplegia → paralysis of accommodation
- Vision fixed for far objects
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