A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 65-year-old patient with a history of COPD and open-angle glaucoma in the left eye has had uncontrolled intraocular pressure (IOP) for the last few months. She is currently using latanoprost eye drops. Her ophthalmologist adds another eye drop to her regimen to further decrease her IOP. A week later, the patient returns because of persistent dim vision. On exam, she has a small fixed pupil in her left eye as well as a visual acuity of 20/40 in her left eye compared to 20/20 in her right eye. Which of the following is the mechanism of action of the medication most likely prescribed in this case?
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A
Inhibiting the production of aqueous humor by the ciliary epitheliumIncorrect. Inhibiting aqueous humor production is the mechanism of beta-blockers (timolol), alpha-2 agonists (brimonidine), and carbonic anhydrase inhibitors (dorzolamide) — not associated with miosis.
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B
Closing the trabecular mesh by relaxing the ciliary musclesIncorrect. Anticholinergics would relax the ciliary muscle and dilate the pupil — the opposite of the miosis seen here.
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C
Opening the canal of Schlemm by contracting the ciliary muscleCorrect. Pilocarpine (M3 muscarinic agonist) contracts the ciliary muscle, opens the trabecular meshwork/canal of Schlemm, and lowers IOP; muscarinic action also causes miosis and dim vision.
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D
Increasing the permeability of sclera to aqueous humorIncorrect. Increasing scleral permeability is the proposed mechanism of prostaglandin analogs (latanoprost) increasing uveoscleral outflow — these cause iris darkening and eyelash growth, not miosis.
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E
Decreasing the contraction of the dilator pupillaeIncorrect. Blocking the dilator muscle (alpha-1 antagonism) would cause miosis but is not the mechanism of any standard IOP-lowering glaucoma drop; the patient's findings fit cholinergic activation of the ciliary muscle.
↑ Tap an answer to reveal the reasoning
Answer: C. A glaucoma patient who develops a small fixed pupil (miosis) and dim vision after adding a second eye drop has been prescribed a muscarinic agonist, most likely pilocarpine. Pilocarpine directly stimulates M3 muscarinic receptors on the ciliary muscle, causing contraction. Contraction of the ciliary muscle pulls on the scleral spur, which OPENS the trabecular meshwork and the canal of Schlemm — increasing aqueous humor outflow and lowering IOP.
The side effects come from the same muscarinic action: miosis (sphincter pupillae contraction) causes the small fixed pupil and dim vision, and ciliary muscle contraction shifts the lens forward, causing accommodative spasm and blurred vision. Pilocarpine is now rarely used as first-line for chronic open-angle glaucoma but is invaluable in acute angle-closure glaucoma (where it pulls the iris away from the trabecular meshwork).
Differentiate from: timolol/brimonidine/dorzolamide (decrease aqueous PRODUCTION by ciliary epithelium); latanoprost (prostaglandin analog — increases uveoscleral outflow). Anticholinergics would DILATE the pupil and worsen angle-closure, the opposite of what was prescribed here.
**Why each option:**
**A.** Inhibiting aqueous humor production is the mechanism of beta-blockers (timolol), alpha-2 agonists (brimonidine), and carbonic anhydrase inhibitors (dorzolamide) — not associated with miosis.
**B.** Anticholinergics would relax the ciliary muscle and dilate the pupil — the opposite of the miosis seen here.
**C.** Pilocarpine (M3 muscarinic agonist) contracts the ciliary muscle, opens the trabecular meshwork/canal of Schlemm, and lowers IOP; muscarinic action also causes miosis and dim vision.
**D.** Increasing scleral permeability is the proposed mechanism of prostaglandin analogs (latanoprost) increasing uveoscleral outflow — these cause iris darkening and eyelash growth, not miosis.