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Glaucoma and its drugs flashcards

20 high-yield MRCP Part 1 cards from the Intellect Medicos Ophthalmology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. What is the first-line investigation in suspected acute angle-closure glaucoma?

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    Tonometry (measure the intraocular pressure).

    Why? A markedly raised IOP confirms the emergency quickly; it is what you act on.

  2. A 68-year-old long-sighted woman develops a severely painful red left eye with haloes around lights after watching TV in a dark room. The pupil is semi-dilated and unreactive and the cornea is hazy. What is the first-line medical treatment?

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    IV acetazolamide plus a combination of eye drops: pilocarpine, a topical beta-blocker (timolol) and an alpha-2 agonist (apraclonidine).

    Why? Acetazolamide, the beta-blocker and apraclonidine all cut aqueous production, and pilocarpine constricts the pupil to pull the iris off the angle. Hypermetropia (short eye, shallow anterior chamber) and dim light (mydriasis) are the classic triggers.

  3. What is the definitive treatment to prevent further attacks of acute angle-closure glaucoma?

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    Laser (YAG) peripheral iridotomy, usually to both eyes; surgical iridectomy is the alternative.

    Why? The hole in the iris lets aqueous bypass the pupil, relieving pupillary block. The fellow eye shares the same narrow-angle anatomy.

  4. Name three drug classes that can precipitate acute angle-closure glaucoma.

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    Any three of: tricyclic antidepressants (e.g. amitriptyline), antihistamines, antiparkinsonian (anticholinergic) drugs, antipsychotics, sulphonamides.

    Why? Anticholinergic effects dilate the pupil and crowd a narrow angle; sulphonamide-type drugs can swell the ciliary body and push the lens-iris forward.

  5. Which antiepileptic is classically linked to acute bilateral angle-closure glaucoma with sudden myopia?

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    Topiramate.

    Why? This sulphonamide-derived drug can cause ciliochoroidal effusion, rotating the lens-iris diaphragm forward; it usually happens in the first month of treatment.

  6. What is the first-line treatment for newly diagnosed primary open-angle glaucoma that is not advanced (NICE)?

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    360° selective laser trabeculoplasty (SLT).

    Why? NICE now offers SLT before drops; it improves trabecular outflow and avoids daily drop burden. Risk factors for POAG include age, family history, African-Caribbean descent, myopia and steroid use.

  7. How does latanoprost lower intraocular pressure?

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    It increases uveoscleral outflow of aqueous.

    Why? Prostaglandin analogues are the first-choice drops in open-angle glaucoma when SLT is not used, and are given once daily.

  8. What is the classic cosmetic side effect of latanoprost eye drops?

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    Permanent brown pigmentation of the iris (it may also lengthen and darken the eyelashes).

    Why? Prostaglandin analogues increase melanin in iris melanocytes; it matters most in one-eye treatment because the eyes become different colours.

  9. In which two conditions should timolol eye drops be avoided?

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    Asthma and heart block.

    Why? Timolol (a beta-blocker that reduces aqueous production) is absorbed systemically after draining down the nasolacrimal duct and can cause bronchospasm and bradycardia.

  10. Brimonidine eye drops should be avoided with which antidepressant classes?

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    MAOIs and tricyclic antidepressants.

    Why? Brimonidine is an alpha-2 agonist that reduces aqueous production and increases outflow; the interaction is through noradrenergic effects. Hyperaemia is a common side effect.

  11. How do dorzolamide and acetazolamide lower intraocular pressure?

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    They inhibit carbonic anhydrase in the ciliary body, reducing aqueous humour production.

    Why? Dorzolamide (and brinzolamide) are topical; acetazolamide is given IV then orally in acute angle closure. Both are sulphonamides (see the separate allergy card).

  12. How does pilocarpine lower intraocular pressure?

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    Muscarinic agonist: it contracts the ciliary muscle, opening the trabecular meshwork and increasing trabecular (conventional) outflow; it also constricts the pupil.

    Why? The miosis pulls the iris away from the angle, which is why it helps in angle closure. Side effects: small pupil, brow ache/headache and blurred vision.

  13. While awaiting emergency ophthalmology, how should a patient with acute angle-closure glaucoma be positioned?

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    Lying flat on their back (supine), without a pillow.

    Why? Lying face-up lets the lens fall back away from the iris, which may help open the angle. Give analgesia and an antiemetic as well, because attacks often cause vomiting.

  14. What is the gold-standard investigation to confirm that the drainage angle is closed?

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    Gonioscopy.

    Why? A mirrored contact lens at the slit lamp shows the angle between iris and cornea directly. In an acute attack, tonometry is the first test because the raised IOP is what you treat.

  15. What is the gold-standard method of measuring intraocular pressure?

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    Goldmann applanation tonometry.

    Why? It flattens a fixed area of cornea at the slit lamp. In suspected POAG it is combined with automated perimetry, optic disc assessment and gonioscopy.

  16. Netarsudil is combined with latanoprost in one drop for open-angle glaucoma. What is its mechanism of action?

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    Rho kinase (ROCK) inhibitor — it increases aqueous outflow through the trabecular meshwork.

    Why? This adds to latanoprost, which increases uveoscleral outflow, so the combination works on both drainage routes. NICE reserves it for when a PGA alone and then a fixed-dose combination have not lowered IOP enough (or a beta-blocker combination is unsuitable).

  17. In open-angle glaucoma, what drug option is next if a prostaglandin analogue does not lower IOP enough?

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    A drop from a different class — beta-blocker (e.g. timolol), carbonic anhydrase inhibitor or alpha-2 agonist — alone or combined.

    Why? NICE also allows further SLT or surgery at this stage. Check adherence and drop technique before escalating.

  18. How does timolol lower intraocular pressure?

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    It blocks beta receptors in the ciliary body, reducing aqueous humour production.

    Why? Systemic absorption via the nasolacrimal duct explains its cardiac and respiratory side effects (bradycardia, bronchospasm).

  19. Name two systemic side effects of oral acetazolamide.

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    Any two of: paraesthesia (tingling), hypokalaemia, metabolic acidosis, renal stones, nausea/taste disturbance.

    Why? Carbonic anhydrase inhibition in the kidney causes bicarbonate loss (acidosis) and potassium loss.

  20. Which drug allergy history matters before prescribing dorzolamide drops or acetazolamide?

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    Sulphonamide allergy — both drugs are sulphonamides.

    Why? Even topical dorzolamide is absorbed enough to cause sulphonamide-type reactions, as the course drug table notes.

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