Gout Flashcards
What is gout?
inflammatory process in response to crystallization of monosodium urate in articular and non-articular tissues
hyperuricemia - uric acid level > 6.8 mg/dL AND symptomatic (can have hyperuricemia w/o sx or gout, so we don’t treat)
Epidemiology
men more likely to be affefcted
individual factors that may influence development of gout: genetics, dietary intake, socioeconomic factors
Pathophysiology
uric acid is main end product in purine degradation
allantoin is a soluble byproduct from uric acid breakdown
uric acid concentrations influenced by overproduction or underexcretion
Hyperuricemia -overproduction
regulatory enzyme variability, cytotoxic medications, increase dietary intake of purines, chronic alcohol intake
Hyperuricemia - underexcretion
dehydration, insulin resistance, acute alcohol intake, meds
Medications
diuretics (loops and thiazides), cytotoxic drugs, salicylates (<2g/day)
Risk factors
male, post-menopausal women (estrogen helps with excretion of uric acid), elderly, obesity, diet and alcohol intake, sedentary lifestyle, renal impairment
Acute gouty arthritis presentation
acute, inflammatory monoarthritis
podagra - first metatarsal joint often involved
uric acid can deposit elsewhere: fingers or wrist, cartilage or tendons, kidneys
s/sx: fever, intense pain, erythema, warmth, edema, and inflammation of affected joints
Lab tests
elevated uric acid > 6.8 mg/dL
WBC > 11,000cell/uL (could be an infection, use to rule out)
Complications
tophi - deposits of monosodium urate
nephrolithiasis - kidney stones
gouty nephropathy - acute and chronic kidney disease
Diagnosis
synovial fluid aspiration (not feasible)
in clinical practice use: monoarticular involvement, previous episodes, rapid onset of pain, swelling, and erythema, risk factors
Treatment goals
terminate acute attack
prevent recurrent attacks of gouty arthritis
prevent complications associated with chronic deposition or urate crystals in joints and tissues
patient education
Treatment approach
treatment of pain and inflammation (acute tx)
use of urate-lowering therapy to prevent recurrence (chronic treatment)
anti-inflammatory prophylaxis
Non-pharmacologic therapy
modification of risk factors over time
applying ice to the affected area to reduce pain
no supplements have shown benefit
Pharmacologic therapy for acute treatment
NSAIDs, corticosteroids, colchicine
NSAIDs
MOA: inhibits COX1 and 2 and decreases prostaglandin synthesis, thus decreasing inflammation
effective and have minimal toxicity short term
NSAIDs meds
indomethacin, naproxen, ibuprofen, sulindac
early initiation is key!
NSAID AEs
GI effects, kidney injury, CV effects, CNS effects, bleeding risk
Corticosteroids
MOA: decreases inflammation by suppression of leukocytes, reverses increased capillary permeability, and suppresses the immune system
Oral corticosteroids
methylprednisolone
prednisone
IM corticosteroids
triamcinolone
methylprednisolone
then follow with anti-inflammatory agent (NSAID, PO corticosteroid) b/c might have rebound pain
Intra-articular corticosteroids
triamcinolone
then follow with anti-inflammatory agent (NSAID, PO corticosteroid)