# Gouty Arthritis > Gouty arthritis for NEET-PG Orthopaedics covers urate crystals, punched-out erosions with overhanging edges, acute flare treatment and urate-lowering therapy. - Canonical URL: https://prepelephant.com/topics/neet-pg/orthopaedics/gouty-arthritis - Exam / course: NEET-PG · Subject: Orthopaedics - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-14 - Last updated: 2026-10-14 - Reference basis: Harrison's Principles of Internal Medicine; Apley's System of Orthopaedics and Trauma - How to cite: "Gouty Arthritis", PrepElephant, https://prepelephant.com/topics/neet-pg/orthopaedics/gouty-arthritis ## Direct answer Gouty arthritis is an inflammatory arthritis caused by deposition of monosodium urate crystals in joints once serum urate stays above saturation, roughly 6.8 mg per decilitre. Negatively birefringent, needle-shaped crystals on polarised microscopy confirm it, and the first metatarsophalangeal joint is the classic site. Acute attacks respond to NSAIDs, low-dose colchicine or steroids, while urate-lowering therapy prevents recurrence and tophi. ## What you must remember - **Crystal identity:** monosodium urate needles are negatively birefringent, appearing yellow when aligned parallel to the compensator axis under polarised light. - **Podagra:** the first metatarsophalangeal joint is the classic site of an acute attack, with abrupt pain, redness and swelling, often at night. - **Radiology:** punched-out erosions with overhanging edges, joint space preserved until late, and soft-tissue tophi. - **Serum urate:** levels above about 6.8 mg per decilitre (about 400 µmol per litre) favour crystal formation, although attacks can occur at lower levels. - **Acute management:** NSAIDs, low-dose colchicine or steroids, chosen by kidney function and comorbidity, with urate-lowering drugs not started during the flare. - **Long-term control:** allopurinol, a xanthine oxidase inhibitor, is the usual first-line agent, titrated to a target below 6 mg per decilitre in established gout. - **Precipitants:** thiazide and loop diuretics, low-dose aspirin, alcohol, especially beer, and fructose-rich drinks raise urate levels or trigger attacks. ## From a red toe to a lowered urate A 48-year-old man wakes with a hot, red and exquisitely tender first toe joint after a night of beer and seafood. He has no fever, and his serum urate is raised. 1. **Aspirate and examine the fluid.** Polarised microscopy showing negatively birefringent needles confirms the crystal, although a typical picture with high urate can suffice when aspiration is impossible. 2. **Exclude septic arthritis.** Fever, a large effusion or an unusual joint raise the possibility of infection, so Gram stain and culture of the fluid are sent before steroids are given. 3. **Treat the attack.** NSAIDs, low-dose colchicine or a short steroid course are chosen according to kidney function, bleeding risk and comorbidity, with rest and ice. 4. **Hold urate-lowering during the flare.** Starting allopurinol in the middle of an attack can prolong or intensify it, so lowering begins only after the attack settles, with prophylaxis added as cover. 5. **Lower urate between attacks.** Allopurinol is started at a low dose and titrated against serum urate until it stays below about 6 mg per decilitre, with febuxostat or probenecid as alternatives in selected patients. 6. **Address drugs and lifestyle.** Diuretics, alcohol and fructose drinks are reviewed, and comorbidities such as hypertension, renal disease and obesity are managed. ## Gout in the examination room Gout traps usually concern the timing of drugs and the differential diagnosis. - **Trap:** starting allopurinol in the middle of an acute attack — **Correct:** it can prolong or intensify the flare, so urate lowering waits until the attack settles, with cover added. - **Trap:** reading punched-out erosions in a small-joint arthritis as rheumatoid — **Correct:** gout spares the joint space until late and gives overhanging edges, while rheumatoid arthritis narrows the space symmetrically with marginal erosions. - **Trap:** giving a thiazide diuretic for hypertension in a patient with gout — **Correct:** thiazide and loop diuretics raise serum urate, so a non-diuretic agent is preferred where appropriate. ## Frequently asked questions ### Which crystal causes gout, and what is its shape? Monosodium urate crystals cause gout, appearing as needle-shaped structures that are strongly negatively birefringent under polarised light. This pattern distinguishes them from the rhomboid, weakly positively birefringent crystals of pseudogout. ### Why is colchicine dose-limited in renal impairment? Colchicine toxicity, including bone marrow suppression and myopathy, rises with renal impairment and with interacting drugs such as clarithromycin. Its dose is therefore reduced or avoided when kidney function is poor, and interacting drugs are reviewed before it is given. ### How do gout and rheumatoid arthritis differ on radiographs? Gout produces punched-out erosions with overhanging edges and preserves the joint space until late, while rheumatoid arthritis causes marginal erosions with symmetric joint-space narrowing and juxta-articular osteopenia. The erosion shape and the joint-space pattern help separate the two. ### What target serum urate is used for established gout? A serum urate below 6 mg per decilitre, about 360 µmol per litre, is the usual target in established gout, particularly with tophi. Allopurinol is titrated towards this level, and treatment is continued long term to dissolve crystals and prevent flares. ### Should urate-lowering therapy be started during an acute gout attack? Traditionally, urate-lowering therapy is not started during an acute gout attack, because it can prolong or intensify the flare (newer guidelines allow starting it under anti-inflammatory cover). It is begun once the attack has settled, with prophylaxis such as low-dose colchicine added for several weeks.