Q: What is gout?
A: An inflammatory arthritis caused by monosodium urate crystal deposition due to hyperuricaemia.
Q: Causes of raised uric acid?
↓ Renal excretion (most common)
↑ Production (purine metabolism)
Drugs (thiazides, loop diuretics)
Q: How does gout develop?
A: Excess uric acid → crystal formation in joints → neutrophil-mediated inflammation.
Q: Risk factors for gout?
Male sex
Obesity
Alcohol
Hypertension
CKD
Diuretics
Q: Most common joint affected?
A: First metatarsophalangeal joint (podagra)
Q: Role of NSAIDs in gout?
A: Reduce inflammation and pain — use if no contraindications.(peptic ulcer,heart failure,hypertension)
Q: Features of acute gout?
Sudden severe pain
Red, hot, swollen joint
Often at night
Q: First-line treatment for acute gout?
NSAIDs
Colchicine
Corticosteroids
Q: Mechanism of colchicine?
A: Inhibits neutrophil migration and inflammatory response.
Q: Key lifestyle advice in gout?
Reduce alcohol
Avoid high-purine foods
Weight loss
Hydration
Major adverse effects of colchicine?
Diarrhoea
Nausea
Bone marrow suppression (rare)
Q: Target serum uric acid level?
A: < 0.3
Q: Mechanism of allopurinol?
A: Xanthine oxidase inhibition → ↓ uric acid production.
Q: Serious adverse effect of allopurinol?
A: Allopurinol hypersensitivity syndrome (rash, hepatitis, renal failure).
Q: When use febuxostat?
A: If allopurinol is contraindicated or not tolerated.
Q: When to start urate-lowering therapy?
A:
Recurrent attacks
Tophi
CKD
Very high uric acid
Q: Why give colchicine/NSAID when starting ULT?
A: Prevents acute gout flares during urate lowering.
Q: When are steroids used in gout?
A: When NSAIDs and colchicine are contraindicated.
Q: Should allopurinol be started during acute gout?
A: No — it can worsen the attack.