Gout on the NCLEX
Acute vs chronic management, colchicine and allopurinol timing, diet triggers.
Urate crystals in a joint, classically the great toe. The med timing rules are what get tested.
The acute attack
Sudden, severe pain, redness, and swelling, classically the first metatarsophalangeal joint (great toe), often at night. Even the bedsheet hurts. Treat the inflammation: NSAIDs (indomethacin is classic), colchicine, or corticosteroids. Rest the joint, no weight bearing during the flare.
The timing rule everyone misses
Do not START allopurinol during an acute attack. Shifting urate levels mid-flare can prolong or worsen it. A patient already taking allopurinol continues it through the flare. Colchicine works best started within 24 hours of flare onset. Diarrhea, nausea, and vomiting signal toxicity: stop the drug and report.
Chronic urate-lowering therapy
Allopurinol (xanthine oxidase inhibitor) blocks uric acid production. Teach: report any rash immediately (risk of severe hypersensitivity, including Stevens-Johnson syndrome), take with food, stay hydrated. Febuxostat is the alternative in the same class. Probenecid increases urate excretion: hydrate well and avoid aspirin, which blocks its effect. Goal: keep serum uric acid low enough that crystals dissolve, commonly cited as below 6 mg/dL.
Diet and lifestyle triggers
Limit organ meats, shellfish, red meat, beer and other alcohol, and high-fructose drinks. Weight loss helps; crash dieting and fasting can trigger flares. Fluids 2-3 L/day (unless restricted) to flush urate and protect the kidneys from stones. Untreated chronic gout deposits tophi and damages kidneys.
Frequently asked
Patient on allopurinol has a new flare. Stop the allopurinol?
No. Continue it and add an anti-inflammatory for the flare. Only starting it mid-flare is the problem.
Which cheeseburger-and-beer choice matters most?
The beer. Alcohol, especially beer, both raises urate production and blocks its excretion.
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