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
Diet/Lifestyle
Decrease meat, seafood, high-purine vegetables, EtOH, high-fructose corn syrup; avoid HCTZ and loop diuretics; ASA may exacerbate; cherry juice may prevent or decrease attacks
Prophylactic medications
Administer during intiation of urate lowering RX to decrease risk of triggering a flare when allopurinol, febuxostat, or probenecid are prescribed; colchicine (0.6mg QD-BID, decrease frequency in CKD); low dose nsaids (naproxen/ibuprofen/indomethacin) or prednisone (= 10mg/day) are alternatives (albeit with less supporting data); PPx should be continued for at least 6 or 3 months after achieving target serum UA (no tophi) or 6 months after achieving tarter serum UA (tophi present); pts unable to reach goal UA levels w/xanthine oxidase inhibitor may benefit from combination Rx w.uricosuric agent
Allopurinol
1st line prevention agent
Xanthine oxidase inhibitor; start 100mg QD X 2 wks (decrease dose in CKD), then 200mg QD X 2weeks; titrate to lower UA by 1mg/dl/wk; typically dose 300-800 mg/d; check LFTs at 1 mo and watch for toxicities (acute gouty attack, rash, diarrhea, cytopenies, fever); pts of Han chines, Tahi, and Korean pts w/ stage 3 CKd ancestry ate at increased risk of hypersensitivity reaction (consider PCR-based HLA-B5801 screening); warfarin interaction
Febuxostat
Prophylactic agent
Xanthine oxidase inhibitor; 40mg/d starting dose, up to 80mg/d; s/e include/ abnormal LFTs, nausea, rash, arthraligias; use prophylactic colchicine/NSAIDs; useful in CKD
Probenecid
Prophylactic agent
Promotes UA secretion (uricosuric); appropriate for pts w/ decrease renal UAn secrtion (verified by 24h urin UA); contraindications include CKD, nephrolithiasis, tophi; titrate to goal serum UA; losartan has a mild uricosuric effect
Refractory gout
Pegloticase (converts UA to allantoin, which is more soluble) indicated in pts who have contraindications to or who are refractory to above agents
Pseudogout (CPDD)
Pathophysiology
Mono- or oligoarthritis typically of knee (>50%), and also wrist, ankle; possible caused by excess pyrophosphate -> crystal formation
Pseudogout (CPDD)
Risk factors
Increase age, hyperthyroidism, hemochromatosis, epiphyseal dysplasias; assoc w/hyperparathyroidism, Mg/phosphate abnormalities, hypothyroidism, GH-secreting adenomas
Pseudogout (CPDD)
History
Presentation similar to gout-acute pain, inflammation of one to several joints; may be provoked by illness, trauma, surgery, or rapid decreases of calcium
Pseudogout (CPDD)
Workup
Synovial fluid shows crystals are rectangular/rod/rhomboid shaped w/ weak, + birefringence; radiograph can show chondrocalcinosis (calcification within the joint space/cartilage) and aid dx; chem-12, Mg, ferritin, iron, transferrin, TSH, PTH, IGF-1
Pseudogout (CPDD)
Acute flair treatment
Similar to gout; joint aspiration and injection (for dx and tx); NSAIDs or colchicine; oral and intraarticular steroids may be helpful; ice and immobilize joint
Pseudogout (CPDD)
Prophylaxis
Treat underlying condition and low-dose colchicine (0.6 mg PO BID-QOD)
