13.3 Glaucoma, Anti-Infective, and Anti-Inflammatory Agents
Key Takeaways
- Glaucoma drops lower intraocular pressure by reducing aqueous production (beta-blockers, alpha agonists, carbonic anhydrase inhibitors) or increasing outflow (prostaglandins, miotics).
- Timolol is contraindicated in asthma, COPD, and bradycardia/heart block because of systemic beta-blockade.
- Prostaglandin analogs like latanoprost are first-line and can darken the iris and lengthen eyelashes.
- Fluoroquinolones, aminoglycosides, and macrolides treat bacterial infection; corticosteroids reduce inflammation but raise IOP and worsen herpes simplex keratitis.
13.3 Glaucoma, Anti-Infective, and Anti-Inflammatory Agents
Glaucoma medications
Glaucoma treatment lowers intraocular pressure (IOP) by one of two strategies: decreasing aqueous humor production or increasing aqueous outflow. Know which class does which.
| Class | Example | Mechanism | Key side effect |
|---|---|---|---|
| Prostaglandin analog | Latanoprost, bimatoprost | Increases uveoscleral outflow | Iris darkening, lash growth, redness |
| Beta-blocker | Timolol 0.5% | Decreases aqueous production | Bradycardia, bronchospasm |
| Alpha-2 agonist | Brimonidine | Decreases production + increases outflow | Drowsiness, dry mouth, allergy |
| Carbonic anhydrase inhibitor | Dorzolamide (drop), acetazolamide (oral) | Decreases production | Stinging; oral form causes tingling, kidney stones |
| Cholinergic (miotic) | Pilocarpine | Increases outflow, constricts pupil | Brow ache, dim vision, miosis |
Timolol is the most-tested contraindication: as a non-selective beta-blocker it can cause systemic bronchospasm and bradycardia, so it is avoided in asthma, COPD, and heart block. Always teach patients punctal occlusion to limit systemic absorption.
Anti-infectives
- Antibiotics: Fluoroquinolones (moxifloxacin, ofloxacin) are broad-spectrum and common for bacterial conjunctivitis and corneal ulcers; aminoglycosides (tobramycin, gentamicin) cover gram-negatives; macrolides (erythromycin ointment) are gentle and used in neonates.
- Antivirals: Trifluridine and ganciclovir gel treat herpes simplex keratitis (the classic dendritic ulcer).
- Antifungals: Natamycin is the standard for fungal keratitis, often after vegetable/plant trauma.
Anti-inflammatory agents
Corticosteroids (prednisolone acetate 1%, dexamethasone) powerfully reduce inflammation but carry three exam-critical risks: they can raise IOP (steroid responders), accelerate cataract formation, and dramatically worsen herpes simplex keratitis by promoting viral replication. NSAIDs (ketorolac, diclofenac) reduce inflammation and pain without raising IOP and are common after cataract surgery to prevent cystoid macular edema.
Antihistamines / mast-cell stabilizers
Drops such as olopatadine relieve allergic conjunctivitis itching by blocking histamine and stabilizing mast cells.
Worked scenario
A patient on chronic prednisolone for uveitis returns with a branching corneal lesion that stains with fluorescein in a dendritic pattern. This is herpes simplex keratitis, and continuing the steroid alone could be vision-threatening. The COA flags this immediately for the physician because steroids worsen active herpetic infection; antiviral therapy is needed. Recognizing the steroid/herpes interaction is a high-value exam point.
Production vs. outflow (a structuring framework)
The single most useful glaucoma concept is sorting drugs by what they do to aqueous humor. Aqueous is made by the ciliary body and drains chiefly through the trabecular meshwork into Schlemm's canal, with a smaller uveoscleral pathway. Drugs that reduce production are beta-blockers, alpha-2 agonists, and carbonic anhydrase inhibitors. Drugs that increase outflow are prostaglandin analogs (uveoscleral route) and miotics like pilocarpine (trabecular route). Brimonidine straddles both. If an exam item asks "which lowers IOP by decreasing aqueous production," timolol and dorzolamide are right and latanoprost is wrong.
Acetazolamide and systemic carbonic anhydrase inhibitors
Acetazolamide is an oral CAI used for acute IOP spikes and angle-closure crises. The COA should know its systemic side effects: paresthesias (tingling fingers and toes), metallic taste, malaise, and risk of kidney stones; it is a sulfonamide, so sulfa allergy matters. It is far more potent than topical dorzolamide but with more body-wide effects.
Steroid-response and ocular surface points
About one-third of patients are steroid responders whose IOP climbs on topical corticosteroids, which is why steroid use is monitored with pressure checks. NSAIDs avoid this but can rarely cause corneal melts in compromised eyes. For dry eye, artificial tears, cyclosporine, and lifitegrast reduce inflammation and improve the tear film. For allergic conjunctivitis, dual-action antihistamine/mast-cell stabilizers like olopatadine are preferred over decongestant drops, which cause rebound redness with chronic use. Matching the agent to the surface problem is a recurring exam theme.
Recognizing the infection picture
The COA should connect a clinical pattern to the likely drug class. Bacterial conjunctivitis or ulcer shows purulent discharge and responds to antibiotics (fluoroquinolone for an ulcer). Viral conjunctivitis (often adenoviral) is watery, highly contagious, and usually treated supportively, not with antibiotics; herpes simplex shows the dendritic ulcer needing antivirals. Fungal keratitis follows vegetable matter or plant trauma and needs natamycin. Allergic disease itches and is bilateral. When a stem describes the presentation, the antibiotic-versus-antiviral-versus-supportive choice is the point.
Treating a viral pink eye with antibiotics or steroids is a classic wrong answer.
Anti-VEGF and the modern injection clinic
Intravitreal anti-VEGF agents (ranibizumab, aflibercept, bevacizumab) treat wet age-related macular degeneration, diabetic macular edema, and retinal vein occlusion by blocking the vascular growth factor that drives leaky neovascular vessels. The COA assists by preparing the sterile field, confirming the correct eye and agent, and monitoring the patient afterward for endophthalmitis warning signs (increasing pain, redness, decreased vision). These injections are among the most common procedures in modern ophthalmology, so recognizing the drug class, its indications, and the post-injection red flags is increasingly exam-relevant.
A reconciliation scenario
A glaucoma patient lists "Cosopt and Xalatan" plus an over-the-counter redness reliever they use daily. You recognize Cosopt as dorzolamide-timolol (a beta-blocker contraindicated in their noted asthma) and Xalatan as latanoprost, and you flag both the asthma conflict and the rebound-redness habit for the physician. Accurate name reconciliation plus contraindication awareness is the defensible action.
A patient with a history of asthma is started on a glaucoma drop and reports new wheezing and shortness of breath. Which medication class is the most likely cause?