OP7.1-5 | Glaucoma — Glossary

A carbonic anhydrase inhibitor given IV (500 mg) or orally to reduce aqueous production; used as emergency adjunct in acute PACG and as oral maintenance in chronic glaucoma.

Sudden, complete closure of the iridocorneal angle in a predisposed eye, causing IOP to rise rapidly to 50–80+ mmHg; an ophthalmic emergency requiring immediate intervention to prevent permanent vision loss.

The extent to which a patient uses prescribed treatment as instructed; in glaucoma, non-adherence to topical drops is the single most modifiable predictor of disease progression and vision loss.

Reduced visual acuity due to abnormal visual experience during the critical period of visual cortex development (birth to age 7-8); a major post-operative concern in congenital glaucoma requiring spectacles and patching.

A traumatic tear in the anterior face of the ciliary body between its longitudinal and circular muscle layers, visible on gonioscopy as a widened angle; leads to delayed open-angle glaucoma years after blunt ocular trauma.

A rare form of secondary glaucoma where aqueous is secreted into the vitreous cavity rather than the anterior chamber; the lens-iris diaphragm is pushed forward, closing the angle; occurs post-intraocular surgery.

A curved visual field defect following the path of the superior or inferior arcuate RNFL bundle; the characteristic perimetric finding of POAG.

Involuntary forceful closure of the eyelids; in congenital glaucoma, a reflex response to corneal pain and photophobia caused by elevated intraocular pressure.

Enlargement of the globe ('ox eye') due to raised intraocular pressure in infancy, when the sclera and cornea are distensible before collagen crosslinks mature (typically before age 3).

The thickness of the cornea at its centre (normally 520–540 µm); thin CCT underestimates IOP on applanation tonometry and is an independent risk factor for POAG development.

Phacoemulsification removal of the crystalline lens in angle closure disease (without significant cataract); removes a key cause of angle crowding; EAGLE trial demonstrated superiority over LPI in PAC/PACG.

The ratio of the optic cup diameter to the total optic disc diameter; C:D >0.6, asymmetry >0.2 between eyes, or violation of the ISNT rule are suspicious for glaucomatous optic neuropathy.

The ratio of the optic cup diameter to the total optic disc diameter; in infants, >0.3 suggests significant glaucomatous damage; uniquely, may reverse partially after IOP control (unlike adults).

Gene encoding cytochrome P450 1B1, expressed in developing anterior chamber angle structures; mutations are the commonest identified genetic cause of familial primary congenital glaucoma (autosomal recessive).

A 2016 randomised controlled trial demonstrating that early clear lens extraction was superior to laser peripheral iridotomy for IOP control and quality of life in primary angle closure and PACG patients.

Overflow of tears (watering eye) due to excess production or impaired drainage; in infants, a key symptom of congenital glaucoma when combined with photophobia and blepharospasm.

Examination of an infant under general anaesthesia to measure IOP, corneal diameter, perform gonioscopy, and assess the optic disc; required because infants cannot cooperate with standard clinical examination.

A secondary open-angle glaucoma caused by rigid, degenerated erythrocyte ghosts (from vitreous haemorrhage) clogging the trabecular meshwork; khaki-coloured cells visible in the anterior chamber.

Anterior subcapsular lens opacities (white, sector-shaped or scattered) caused by ischaemic damage to the lens epithelium during an acute PACG attack; a permanent marker of a previous acute episode.

The gold-standard method for measuring IOP; measures force required to flatten a 3.06 mm corneal area; results influenced by central corneal thickness.

Examination of the anterior chamber angle using a goniolens; in PCG performed under anaesthesia with a Koeppe lens to directly visualise the trabeculodysgenesis.

Surgical incision through the trabecular meshwork under direct gonioscopic visualisation; the preferred angle surgery for PCG when the cornea is clear.

Permanent horizontal or oblique breaks in Descemet's membrane of the cornea caused by physical stretching from elevated intraocular pressure; pathognomonic of previous congenital glaucoma episodes.

A patient's capacity to obtain, understand, and act on health information; highly variable in clinical populations; clinicians must adapt language, analogies, and visual aids to the individual patient's literacy level.

Long-sightedness due to a short axial length; the small anterior segment, shallow anterior chamber, and thick anteriorly situated lens predispose to angle closure.

Forward bowing of the peripheral iris toward the cornea, due to posterior chamber aqueous accumulation in pupil block; the iris then occludes the iridocorneal angle.

An irreversible increase in brown melanin pigmentation in the iris stroma caused by prostaglandin analogues; affects patients with hazel, blue-green, or heterochromic eyes; purely cosmetic but must be disclosed before starting therapy.

A vertical fusiform band of brown pigment on the central corneal endothelium, caused by iris pigment dispersal; the characteristic sign of pigmentary glaucoma.

Nd:YAG laser creation of a small full-thickness hole in the peripheral iris, providing an alternate route for aqueous flow from posterior to anterior chamber, eliminating the pupil block mechanism.

A multidisciplinary service for patients with irreversible visual impairment; provides magnifiers, mobility training, and adaptive techniques; relevant for advanced glaucoma patients who have lost significant field.

A 20% osmotic agent given IV (1–2 g/kg) to rapidly lower IOP in acute glaucoma by creating an osmotic gradient that draws fluid from the vitreous into the bloodstream.

Pressing the inner corner of the eyelid after eye drop instillation to block drainage into the nasolacrimal duct, reducing systemic absorption of topical medications (especially important for timolol).

Secondary glaucoma caused by rubeosis iridis (VEGF-driven iris neovascularisation from retinal ischaemia in PDR or CRVO); fibrovascular membrane first obstructs then closes the angle.

The tissue of the optic disc between the cup margin and the disc margin, containing retinal ganglion cell axons; progressive thinning or notching is the hallmark of glaucomatous optic neuropathy.

A variant of POAG where IOP is consistently within the normal range (≤21 mmHg) but glaucomatous optic neuropathy and field loss progress; vascular risk factors and optic nerve vulnerability are important.

India's government programme for prevention of blindness; provides glaucoma medicines and screening at district hospitals; a resource for patients who cannot afford branded medications.

IOP consistently >21 mmHg with a normal optic disc and visual field; a risk factor for POAG but not itself glaucoma; requires monitoring and sometimes prophylactic treatment.

Permanent adhesions between the peripheral iris and the trabecular meshwork/cornea, formed after prolonged angle closure; their presence upgrades PACS to PAC on the ISGEO spectrum.

A secondary open-angle glaucoma caused by lens proteins leaking from a hypermature (Morgagnian) cataract, together with macrophages, clogging the trabecular meshwork; treated by lens extraction.

A secondary closed-angle glaucoma caused by a swollen intumescent cataract physically pushing the iris forward to close the iridocorneal angle; mechanism is mechanical (not pupil block); treated by lens extraction.

Abnormal sensitivity to light; in congenital glaucoma, arises from corneal irritation due to elevated IOP and corneal oedema; drives the characteristic 'sun-shy' behaviour in affected infants.

A secondary open-angle glaucoma in young myopic males with a concave iris; iris pigment rubbed off by zonular contact deposits in the trabecular meshwork; Krukenberg spindle is the pathognomonic slit-lamp sign.

A muscarinic agonist (miotic) that constricts the pupil, pulling the peripheral iris away from the trabecular meshwork to open the angle; the key drug for acute PACG emergency management. NOT appropriate for POAG.

Conditions or drugs that cause pupil dilation and trigger an acute PACG attack in predisposed narrow-angle eyes: dim lighting, anticholinergic drugs (antihistamines, tricyclics, antispasmodics), adrenergic drugs (decongestants).

A glaucoma in which the iridocorneal angle is closed (peripheral iris obstructs the trabecular meshwork) due to pupil block, causing raised IOP and progressive optic nerve damage.

An eye with a narrow, occludable angle on gonioscopy but without raised IOP, PAS, or optic nerve damage; at risk of angle closure but has not yet closed.

A chronic, progressive optic neuropathy characterised by an open iridocorneal angle on gonioscopy, characteristic glaucomatous optic disc changes, and visual field loss, with or without elevated IOP.

The likely visual outcome: early/moderate POAG with good IOP control has an excellent prognosis for preserving vision; advanced glaucoma or NTG carries greater risk; vision already lost is irreversible but remaining vision is protectable.

First-line topical glaucoma drugs (latanoprost, travoprost, bimatoprost); lower IOP by 25–35% via increased uveoscleral outflow; administered once daily in the evening.

A class of once-daily glaucoma drops (e.g., latanoprost) that lower eye pressure by increasing a secondary drainage route; side effects include mild eye redness, eyelash thickening, and (irreversible) iris colour change.

The commonest secondary open-angle glaucoma worldwide; caused by fibrillar PXF material depositing in the trabecular meshwork, impairing outflow; associated with LOXL1 gene variants and white PXF deposits on the anterior lens capsule.

The fundamental mechanism of PACG: relative obstruction to aqueous flow at the pupillary aperture, causing pressure to build in the posterior chamber and the iris to bow forward.

The layer of retinal ganglion cell axons on the inner retinal surface; RNFL thinning on OCT precedes visual field defects in POAG by approximately 4–6 years.

New blood vessel growth on the iris surface (neovascularisation), driven by VEGF from ischaemic retina; the hallmark of neovascular glaucoma.

Circumferential venous sinus at the corneoscleral junction that collects aqueous humour from the trabecular meshwork and drains it into episcleral veins.

360-degree posterior synechiae between the entire pupil margin and the anterior lens capsule in uveitis, causing complete pupil block → iris bombe → secondary angle-closure glaucoma.

Glaucoma in which IOP elevation has an identifiable underlying cause (disease, drug, trauma, or structural change), distinguished from primary glaucoma where no such cause is found.

A laser procedure targeting pigmented trabecular meshwork cells to improve aqueous outflow; evidence-based first-line alternative to topical drops in POAG/OHT (LiGHT trial).

An evidence-based laser alternative to drops for POAG first-line therapy (LiGHT trial); uses 532 nm laser to stimulate trabecular outflow improvement; useful when drops are poorly tolerated or compliance is challenging.

An NMC CBME competency level indicating that the student must demonstrate the skill habitually in a simulated or real clinical environment, beyond knowledge alone.

An evidence-based consultation approach where the clinician provides information about options and consequences, and the patient expresses values and preferences, to reach a mutually agreed, concordant decision.

A secondary open-angle glaucoma caused by glucocorticoids reducing trabecular endothelial phagocytosis, allowing extracellular matrix accumulation and outflow resistance; typically reversible on stopping steroids.

A phakomatosis with a facial port-wine naevus (V1/V2), leptomeningeal angioma, and episcleral haemangioma causing raised episcleral venous pressure and post-trabecular secondary glaucoma.

A communication technique where the clinician asks the patient to explain back the key information in their own words; the gold-standard method for confirming comprehension and identifying misunderstandings.

Sieve-like tissue at the iridocorneal angle through which approximately 85-90% of aqueous humour drains; its maldevelopment (trabeculodysgenesis) is the structural defect in PCG.

Glaucoma filtering surgery creating a controlled fistula from the anterior chamber to a subconjunctival bleb; achieves greatest IOP reduction; reserved for inadequate medical/laser control.

Glaucoma filtering surgery creating a controlled drainage channel under the eyelid (a bleb); achieves the greatest IOP reduction; risks include infection, low eye pressure, and cataract acceleration.

Embryological maldevelopment or arrest of the trabecular meshwork and anterior chamber angle, leading to obstructed aqueous outflow; the primary defect in primary congenital glaucoma.

Ab externo surgical procedure using a trabeculotome to locate Schlemm's canal and tear through the trabecular meshwork; preferred when corneal haze prevents gonioscopic view.

Glaucoma complicating anterior uveitis, arising via direct trabeculitis (open-angle) or seclusio pupillae with pupil block (closed-angle), compounded by steroid therapy.

The unconventional aqueous humour drainage route across the ciliary body face and supraciliary space to the sclera; normally 10–15% of total outflow; enhanced by prostaglandin analogues.

A slit-lamp method to estimate the iridocorneal angle depth by comparing the peripheral anterior chamber depth to the corneal thickness; grades I–IV (I = narrowest, IV = widest).