Gout Flashcards
Pathophysiology
Uric acid produced by purine metabolism: increased Ua assoc w/gout attacks, kidney damage, kidney stones; sx of gout due to deposition of monosodium urate crystals in joints, bones, and soft tissue; usual joints include 1st MTP (podagra)0, tarsal joint, ankle, knee, and sometimes fingers, but, may be anywhere; tophi (urate MSU deposits w/ granulomatous inflammation) are a pathognomonic feature of gout and can occur in many different tissues; presence of tophi indicative of chronic tophaceous gout
Asymptomatic hyperuricemia
Pts should be assessed for gout arthritis, urolithiasis, and kidney damage; most pts w/ asx hyperuricemia require no tx; indications for consideration of tx include:
- Uric acid >13 in males, >10 in females
- urinary uric acid excretion >1.1 g/d(increase risk of kidney stones)
- Planned XRT or chemo
Causes of increased uric acid (UA)
B12 deficiency
lymphoproliferative d/o
psoriasis
hemolysis
obesity
diet/etoh
CKD
hypothyroidism
Increase PTH
CHF
Volume depletion
Diuretics
Risk factors
Increase age
M>F
consumption of red meat, shellfish, alcohol
Medications; ASA, thiazide and loop diuretics
Trauma/surgery
infection
HTN
IV contrast
Epidemiology
Affects 8 million pts in US, approx. 10% of pts with hyperuricemia develop gout
History
Sudden onset of painful, erythematous, warm, swollen joint; can be polyarticular later in course; w/o active RX, tends to resolve in days to weeks; presence of fevers should prompt w/o of septic arthritis
Exam
Monoarticular inflammation, inspect for tophi (accumulations of urate in connective tissues +/- calcification)
Workup
Joint fluid w/3 C’s; cell count (WBCs often 2k-60k/ul, but can be >100k), Cx (-), and crystal analysis; fluid will often be cloudy and demonstrate strongly negatively birefringement needle-shaped crystals; ideally, Dx will be made based on joint aspirate, however clinical criteria exist; consider BUN/Cr for renal function, CBC for neutrophilia, serum UA.
Serum UA
Increase UA is supportive but not diagnostic; during acute flares, UA can be nl or even low; UA crystallizes >6.8mg/dl, but only 22% of pts w. UA >9 have sx so no specific; all pts w/gout as tomse point have Increase UA, however no all pts w/ elevated UA develop gout
Acute flair treatment
Treated ASAP to decrease duration of sx; urate-lowering Rx and low-dose ASA (81mg) should be continued in pts already on these meds; severe attacks may be treated with colchicine + NSAIDs or PO steroids + colchicine
NSAIDS
Typically 1st line; naproxen, indomethacin, or celexocib; continue 1-2 days after attack; use cautiously in pts w/ CKD, hx GIB, CVD, CHF, anticoagulant Rx
Colchicine
If pt cannot tolerate NSAIDs; then consider colchicine; 1.2 mg at onset -> 0.6mg an h later -> 0.6mg BID; continue for 2-3 days after attaxk ends; low dose 1.8mg/h and high dose 4.8mg/6 h equally effective, but low dose preffered due to less toxicity.
Steroid Injection
If monoarticular
First aspirate to verify crystals and r/o infection; use methylprednisolone or triamcinolone (10-80mg, depending on joint size) after numbing SC (2% lidocaine or 1% xylocaine); can inject up to 3X/year
Prednisone
Consider if multiple joints involved; many options for dosing, but can consider 20mg BID x 1week, then 10mg qd x 1 week; pts can reflare if tapered to quickly
Prevention
Start during acute flare if pt has had multiple attaxks; encourage hydration to prevent kidney stones; indications include >/- 2 attacks, erosive disease on radiographs, nephrolithiasis, CKD >/= stage 2, tophi, or urinary UA>1.1 g/d; Goal serum UA <6 and often <5 mg/dl; generally, initiate Ua lowering Rx 2 weeks after attack, although this is debated
