OP6.1-4 | Iris, Uvea and Anterior Chamber — Practice Quiz

Correct. The combination of ciliary flush, fine KPs, aqueous cells and flare, miosis, and low IOP is classic for anterior uveitis (iridocyclitis). This distinguishes it from acute angle-closure glaucoma, which causes a raised IOP and a fixed mid-dilated pupil.

Iridocyclitis presents with ciliary flush, KPs, aqueous cells and flare, miotic pupil, and characteristically LOW IOP — the mnemonic CAMP (Ciliary flush, Aqueous cells/flare, Miosis, Posterior synechiae/KPs). Acute angle-closure glaucoma has a RAISED IOP with a fixed mid-dilated pupil.

This presentation describes anterior uveitis (iridocyclitis). The key features are ciliary flush, KPs on the corneal endothelium, cells and flare in the anterior chamber, miotic pupil, and LOW IOP — use the mnemonic CAMP. Acute angle-closure glaucoma causes raised IOP with a fixed mid-dilated pupil, not a miotic pupil.

Correct. Anterior uveitis = iridocyclitis = inflammation of the iris and ciliary body. The SUN classification (Standardization of Uveitis Nomenclature) is anatomical: anterior, intermediate, posterior, and panuveitis.

The SUN Working Group classifies uveitis anatomically: anterior (iris and ciliary body = iridocyclitis), intermediate (vitreous and pars plana = pars planitis), posterior (choroid and retina = chorioretinitis), and panuveitis (all layers). Anterior uveitis is the most common form.

Inflammation of the iris and ciliary body is anterior uveitis (iridocyclitis). The SUN classification: anterior = iris/ciliary body; intermediate = vitreous/pars plana; posterior = choroid/retina; panuveitis = all layers.

Correct. Mutton-fat KPs plus Koeppe/Busacca nodules define granulomatous iridocyclitis. Important causes include sarcoidosis, tuberculosis, sympathetic ophthalmitis, VKH syndrome, and leprosy.

Granulomatous iridocyclitis is characterised by large greasy mutton-fat KPs (composed of epithelioid cells and macrophages) and iris nodules (Koeppe at pupillary margin; Busacca on iris stroma). Non-granulomatous iridocyclitis has fine/stellate KPs. HLA-B27 disease is typically non-granulomatous.

Mutton-fat KPs and iris nodules (Koeppe/Busacca) are hallmarks of granulomatous iridocyclitis. Non-granulomatous iridocyclitis has fine or stellate KPs and no iris nodules. HLA-B27-associated uveitis is typically acute, unilateral, and non-granulomatous.

Correct. Seclusio pupillae causes pupil block: aqueous cannot traverse the pupil, builds up behind the iris, pushes it forward (iris bombe), and closes the angle — resulting in secondary angle-closure glaucoma. Treatment is a laser or surgical peripheral iridectomy to bypass the block.

Seclusio pupillae (360-degree posterior synechiae) blocks aqueous flow from the posterior chamber through the pupil (pupil block). Aqueous pressure builds behind the iris, bowing it forward (iris bombe). This closes the drainage angle, causing acute secondary angle-closure glaucoma with a markedly raised IOP.

360-degree posterior synechiae (seclusio pupillae) creates pupil block. Aqueous accumulates behind the iris, bowing it forward to create iris bombe, which closes the drainage angle and causes secondary angle-closure glaucoma. This is one of the most serious complications of chronic iridocyclitis.

Correct. A rise in IOP to 32 mmHg after starting topical steroids indicates a steroid responder. The appropriate response is to taper or switch to a weaker steroid preparation and add anti-glaucoma medication. Increasing steroids would worsen the pressure rise.

Steroid-induced ocular hypertension is a recognised complication of topical (and systemic) corticosteroids, especially in 'steroid responders'. The IOP must be checked at every visit. Management involves switching to a less potent steroid (e.g., loteprednol, fluorometholone), reducing frequency, and adding IOP-lowering drops if needed.

This patient is a steroid responder — topical corticosteroids have elevated the IOP to 32 mmHg. The correct response is to reduce or switch the steroid (to loteprednol or fluorometholone) and add IOP-lowering medication, not to increase steroids. This complication must be checked at every uveitis visit.

Correct. Blunt trauma causing a red fluid level in the anterior chamber is traumatic hyphema. The iris root vessels tear under the force of impact. Graded I to IV based on the proportion of anterior chamber filled. Key complication is rebleeding on days 2-5.

Hyphema is blood in the anterior chamber, appearing as a red/dark-red horizontal level. Blunt trauma is the most common cause (rupture of iris root vessels). Hypopyon is a white/cream fluid level from leucocytes and fibrin, seen in severe uveitis or endophthalmitis. The traumatic context and red colour confirm hyphema.

A red (not white) horizontal level in the anterior chamber after blunt ocular trauma is hyphema — blood in the anterior chamber. Hypopyon is a white/cream level caused by leucocytes (seen in uveitis, endophthalmitis, or corneal ulcer), not by trauma. The colour distinguishes them.

Correct. Hypopyon is a white/cream fluid level in the inferior anterior chamber composed of leucocytes and fibrin. In the setting of corneal ulcer, it forms due to intense anterior segment inflammation with breakdown of the blood-aqueous barrier. It is sterile unless the infection has penetrated the cornea.

Hypopyon is an accumulation of leucocytes (white cells), fibrin, and inflammatory protein in the inferior anterior chamber, appearing as a white or cream horizontal level. It forms when the blood-aqueous barrier is overwhelmed by severe infection or inflammation. Corneal ulcer, severe iridocyclitis, and endophthalmitis are common causes.

A white fluid level in the inferior anterior chamber is hypopyon — an accumulation of leucocytes and fibrin. This differs from hyphema (red/dark red, composed of blood). Hypopyon in the context of a corneal ulcer is usually sterile (reactive) but indicates severe infection with blood-aqueous barrier breakdown.

Correct. Rheumatoid arthritis is NOT an HLA-B27-associated disease. The HLA-B27 spondyloarthropathies causing anterior uveitis are: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and IBD-related arthropathy. RA causes scleritis or keratoconjunctivitis sicca, not typical acute anterior uveitis.

HLA-B27-associated anterior uveitis occurs with the seronegative spondyloarthropathies: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and IBD-related arthritis. Rheumatoid arthritis (RA) is a seropositive disease (anti-CCP, RF) NOT associated with HLA-B27. RA can cause scleritis but is NOT typically associated with acute anterior uveitis.

Rheumatoid arthritis is NOT associated with HLA-B27. HLA-B27-linked anterior uveitis occurs with seronegative spondyloarthropathies: ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and IBD-related arthritis. RA can cause scleritis but is a separate seropositive disease unrelated to HLA-B27.

Correct. Cycloplegics in iridocyclitis serve two key roles: preventing and breaking posterior synechiae (which can lead to seclusio pupillae and iris bombe if neglected), and relieving ciliary spasm that causes significant pain and photophobia. These effects are therapeutic, not merely diagnostic.

Cycloplegics (e.g., atropine, cyclopentolate) serve two purposes in iridocyclitis: (1) they dilate the pupil and paralyse the ciliary muscle, preventing and breaking posterior synechiae before they become fibrous and permanent; and (2) cycloplegia relieves the ciliary spasm that causes deep aching pain and photophobia.

Cycloplegics (atropine, cyclopentolate) in iridocyclitis dilate the pupil to prevent posterior synechiae formation and break early synechiae, and also paralyse the ciliary muscle to relieve the painful ciliary spasm and photophobia. They do not lower IOP or enhance steroid penetration.

Correct. The two steroid-specific counselling imperatives are: never stop steroids abruptly (taper as directed) and attend every follow-up so IOP can be monitored — silent steroid-induced glaucoma is one of the most dangerous complications. Attendance is not optional in uveitis management.

Two steroid-specific dangers must be emphasised: (1) IOP rise — steroid responders can develop silent glaucoma within weeks; IOP must be checked at every visit. (2) Rebound inflammation — abrupt steroid cessation causes flare-up. Patients must taper, attend follow-ups, and be aware of red-eye/vision-blur as an alarm symptom.

For a patient on long-term topical steroids for uveitis, the two critical counselling points are: (1) IOP must be checked at every visit because steroid-induced glaucoma can be silent and irreversible; (2) steroids must never be stopped abruptly — taper as instructed. Monitoring attendance is not optional.