Gout
Pathophysiology & Risk Factors
Gout is a crystal arthropathy driven by hyperuricemia (serum uric acid above 6.8 mg/dL), causing monosodium urate crystals to deposit in joints. Attacks classically strike the great toe (first MTP joint) at night, triggered by purine load, alcohol, dehydration, or rapid urate shifts.
Signs & Symptoms
Diagnostics & Labs
Diagnostic
Monitor
Interventions & Priorities
Treatments & Medications
Two distinct goals: abort the acute flare with anti-inflammatories, then prevent recurrence with urate-lowering therapy once inflammation resolves. The classic NCLEX trap is starting allopurinol during a flare.
Acute flare vs chronic urate-lowering therapy
Acute flare
- Goal
- Abort inflammation
- Drugs
- NSAIDs, colchicine, corticosteroids
- Allopurinol
- Do NOT start during flare
- Timing
- Immediate
Chronic prevention
- Goal
- Lower serum urate < 6 mg/dL
- Drugs
- Allopurinol, febuxostat
- Allopurinol
- Start after flare resolves; titrate low to high
- Timing
- After inflammation subsides
Patient Teaching
Complications
Clinical Pearl
Purines up, uric acid up, crystals down — into the joint. Beer and steak tonight, screaming toe by morning. Treat the flare first; never START allopurinol mid-attack (but never STOP it either).