Glaucoma / Ophthalmic Agents

The goal is a number the team sets for this patient, not a universal target. Treatment aims at "preventing the progression of optic nerve head changes" and "preventing deterioration of the visual field," through the concept of target IOP — "below a certain upper limit of IOP, it is estimated that the visual field, the optic nerve head, and RNFL parameters will not deteriorate." That target is individual, set "depending on the severity of structural and functional damage, baseline IOP, age, race, family history, corneal thickness, hysteresis, and other risk factors," and revised as the disease behaves. When to start is genuinely debated, with "some clinicians initiating treatment of IOP when it reaches above only 21 mm Hg and others reserving treatment either until evidence of optic nerve or RNFL damage or if the patient is at high risk" — the sourced trigger being evidence of damage, or symptoms with an IOP consistently above 28 to 30 mm Hg. PROSTAGLANDIN ANALOGUES ARE FIRST-LINE, and the reasons are both pharmacologic and behavioural: each "reduces IOP 25% to 33% by increasing the UVEOSCLERAL OUTFLOW," the dose is daily, and the class "is preferred as initial therapy", and laser therapy and surgery are the other treatment families. The disorder-side counselling point is cosmetic and it costs adherence if unmentioned: lengthening of eyelashes and pigmentation of the lids or iris, plus possible exacerbation of uveitis or herpetic infection and cystoid macular oedema. The other four classes, by mechanism: alpha-2 agonists (brimonidine, apraclonidine) reduce IOP 20–25% by both decreasing production and increasing uveoscleral outflow — and cause apnoea, lethargy or bradycardia in children; beta-blockers (timolol and relatives) reduce IOP 20–25% by decreasing production, and non-selective agents must be avoided in COPD and asthma, with heart block, hypotension and bradycardia as further contraindications (betaxolol is the selective option with a "better safety profile about respiratory symptoms"); carbonic anhydrase inhibitors (dorzolamide, brinzolamide) reduce IOP 15–20% by decreasing production; and cholinergics (pilocarpine) reduce IOP 20–25% by increasing outflow but "are poorly tolerated and normally not considered first-line." THE ADMINISTRATION TEACHING IS THE NURSING HEART OF THIS CLASS: "closing eyelids after administration of drops with NASOLACRIMAL DUCT OCCLUSION may prevent SYSTEMIC ABSORPTION of the topical medication" — a drop drains into a highly vascular nasal mucosa, which is how a "topical" beta-blocker produces systemic beta-blockade. And when the disease worsens on therapy, check the patient before changing the drug: "if IOP, visual field, or optic nerve inflammation worsens while the patient is on medical therapy, COMPLIANCE TO TREATMENT MUST BE CHECKED. Systemic factors, including diabetes, smoking, and nocturnal hypotension, should be controlled." The class page owns each agent’s systemic adverse-effect profile.

Slow heart rate & lower BP by blocking β-adrenergic receptors. Watch for bradycardia.

Turn UP “rest-and-digest.” Used for urinary retention, myasthenia, dry mouth and the eye; methacholine tests airway reactivity and physostigmine reverses anticholinergic poisoning. Overdose = cholinergic crisis (SLUDGE).

Block "rest-and-digest." Atropine treats bradycardia; glycopyrrolate dries secretions with fewer CNS effects; tropicamide and cyclopentolate drops dilate pupils; classic toxidrome — can’t see/pee/spit/poop.