OP7.1-5 | Glaucoma — Graded Quiz

Correct. Trabeculodysgenesis — an arrest of neural crest-derived trabecular meshwork development — is the fundamental pathology. The infant eye is distensible, so sustained raised IOP causes buphthalmos and corneal enlargement.

Primary congenital glaucoma results from trabeculodysgenesis — maldevelopment of the neural crest-derived trabecular meshwork and anterior chamber angle. This obstructs aqueous outflow from birth, causing raised IOP and secondary corneal enlargement (buphthalmos).

Incorrect. Primary congenital glaucoma is caused by trabeculodysgenesis — an embryological arrest of development of the neural crest-derived trabecular meshwork and anterior chamber angle. This creates obstruction to aqueous outflow from birth.

Correct. Adding a prostaglandin analogue (latanoprost, bimatoprost) is the appropriate next step when timolol monotherapy is insufficient in POAG. Prostaglandins provide the greatest additional IOP reduction. Miotics are not indicated in POAG.

When monotherapy fails to achieve target IOP in POAG, the next step is to add a prostaglandin analogue — the most potent IOP-lowering class (25-33% reduction). Miotics (pilocarpine) are not used in POAG. Oral acetazolamide is reserved for short-term or acute use due to systemic side effects. Surgery is not the next step when medical escalation is available.

Incorrect. When timolol monotherapy is insufficient for target IOP in POAG, the next step is adding a prostaglandin analogue — the most potent IOP-lowering class. Miotics such as pilocarpine are NOT used in POAG: they cause side effects and are reserved for acute angle-closure. Oral acetazolamide is not appropriate for chronic POAG management.

Correct. This is an acute PACG attack. The management is fundamentally different from POAG: emergency IV acetazolamide, IV mannitol (if IOP >50 mmHg), topical pilocarpine 2% (breaks pupil block by constricting the pupil), and topical timolol. Laser PI is definitive once the cornea clears. Prostaglandins are NOT used in the acute setting.

This is an acute primary angle-closure crisis (PACG), NOT POAG. The management differs fundamentally: PACG requires emergency multi-drug systemic IOP reduction (IV acetazolamide, IV mannitol if needed), topical pilocarpine 2% to mechanically break pupil block, and topical timolol. Prostaglandins are NOT appropriate as initial emergency treatment for PACG. Definitive treatment is laser peripheral iridotomy (PI) once the cornea is clear. In POAG: prostaglandins are first-line and miotics are not used.

Incorrect. This is an acute angle-closure crisis — NOT POAG. The management must be immediate and aggressive: IV acetazolamide 500 mg, IV mannitol 20% (if IOP >50 mmHg), topical pilocarpine 2% (to constrict the pupil and break the pupil block), topical timolol, and apraclonidine if available. Prostaglandins are NOT first-line here. Laser peripheral iridotomy is performed once IOP is controlled and the cornea clears. This is the critical POAG vs PACG management distinction: in POAG — prostaglandins first-line, miotics NOT used; in acute PACG — pilocarpine and systemic agents are the emergency, laser PI is definitive.

Correct. Dim lighting causes physiological pupil dilation, which maximises the contact zone between the iris and the lens in a predisposed eye, worsening pupil block and precipitating acute angle closure.

In a PACG-susceptible eye with a narrow angle, pupil dilation (triggered by dim light) maximises the pupillary block between iris and lens. This is why attacks occur in darkened environments such as cinemas. Similarly, mydriatic drops can precipitate an acute attack.

Incorrect. In PACG, dim lighting causes physiological pupil dilation. In a predisposed eye with a narrow angle, this dilation maximises the iris-lens contact (pupil block), elevating posterior chamber pressure and precipitating angle closure. This is why attacks occur in darkened environments (cinemas, movie theatres) and why mydriatic drops must be used with extreme caution in narrow-angle eyes.

Correct. Neovascular glaucoma results from VEGF-stimulated fibrovascular membrane formation over the angle. It evolves from open-angle (membrane covers trabecular meshwork) to closed-angle (membrane contracts, forming peripheral anterior synechiae).

Neovascular glaucoma (rubeosis iridis) is caused by retinal ischaemia (proliferative diabetic retinopathy, CRVO, ocular ischaemic syndrome) stimulating VEGF-driven new vessel formation over the angle. Initially open-angle (vessels cover the meshwork), then the membrane contracts to cause synechial angle closure. Treatment includes anti-VEGF and panretinal photocoagulation.

Incorrect. This is neovascular glaucoma — a secondary glaucoma caused by retinal ischaemia (here, proliferative diabetic retinopathy) driving VEGF production, which stimulates a fibrovascular membrane over the trabecular meshwork. Early phase: open-angle (membrane covers meshwork). Late phase: membrane contracts, forming peripheral anterior synechiae and closed-angle glaucoma. Treatment targets the underlying ischaemia with panretinal photocoagulation and anti-VEGF agents.

Correct. Pigmentary glaucoma is a secondary open-angle glaucoma managed similarly to POAG — prostaglandin analogues as first-line IOP reduction. Miotics have a theoretical role but are not first-line.

Pigmentary glaucoma is a secondary open-angle glaucoma and is managed like POAG — prostaglandin analogues are first-line. While miotics (pilocarpine) theoretically reduce iris-zonule contact and pigment shedding, they have significant side effects and are NOT first-line. Surgery is reserved for medically uncontrolled cases.

Incorrect. Pigmentary glaucoma is a secondary open-angle glaucoma. The first-line treatment follows POAG principles: topical prostaglandin analogues. Miotics (pilocarpine) theoretically reduce iris-lens zonule contact and pigment shedding, but are not first-line due to side effects. Trabeculectomy or lens extraction is not the first step.

Correct. Pilocarpine is a miotic that constricts the pupil — this breaks pupil block and relieves angle closure in PACG. In POAG the angle is open, so miotics are not used first-line. Prostaglandin analogues (latanoprost) are the first-line choice for POAG. This is the key POAG vs PACG management distinction.

Miotics (pilocarpine) work by constricting the pupil, which mechanically pulls the peripheral iris away from the angle — this is effective in angle-closure glaucoma. In POAG, the angle is already open; miotics are not first-line and cause troublesome side effects (dim vision, brow ache). This distinction is essential for patient counselling and OP7.5 competency.

Incorrect. Pilocarpine (a miotic) is specifically indicated in angle-closure glaucoma because pupil constriction pulls the peripheral iris away from the angle, breaking pupil block. In POAG, the iridocorneal angle is already open — miotics provide little benefit and cause side effects (miosis causing dim vision, accommodative spasm). The correct first-line for POAG is a prostaglandin analogue like latanoprost.

Correct. This patient has ocular hypertension with high-risk features (family history of glaucomatous blindness, mildly elevated IOP, borderline cup). Treatment to lower IOP and close monitoring are indicated to prevent POAG conversion.

An IOP of 24 mmHg, C:D ratio of 0.65, and a positive family history of glaucomatous blindness are high-risk features for conversion to POAG. Even without confirmed visual field defects, treatment (IOP-lowering drops) and close monitoring are indicated in high-risk ocular hypertension — this falls within the POAG management spectrum.

Incorrect. This patient has ocular hypertension with high-risk features: IOP above normal range, a C:D ratio of 0.65, and a first-degree relative with glaucomatous blindness. These features warrant IOP-lowering treatment (typically a prostaglandin analogue) and regular monitoring of optic disc and visual fields, as the risk of converting to POAG is significant.