crystalline arthritis Flashcards
Gout overview
disease associated with hyperuricemia which causes deposition of monosodium urate crystals in and around joints.
casues a painful inflammatory, destructive arthropathy.
may also see salt accumulations in the soft tissue
may be due to insufficient uric acid excretion by the kidneys or overproduction of purines
natural hx of gout
begins as asymptomatic hyperuricemia. Then, pt will have a first attack- 3rd-5th decade for men, after menopause for women
attacks become more frequent
gradual deposition of urate crystals in tophi (yrs)
destructive arthropathy and exraarticular deposition.
Risk factors for gout
hyperuricemia, genetics, EtOH (effects kidney excretion of uric acid; beer is also rich in purines), metabolic syndrome, diuretic use, renal disease
Basically, anything that decreases removal of uric acid from the body by the kidneys or incr. input into the body.
Dietary factors that contribute to gout. What dietary foods help with gout?
high meat or seafood intake, beer.
low fat dairy consumption reduces incidence of gout. 1/2 cup cherries (10-12)/day reduces gout flares
Important complication of gout
gout is an INDEPENDENT risk factor for CV disease
significantly reduces quality of life
normal purine metabolism
basically, AMP (from adenosine) is made into hypoxanthine, and GMP is made into guanine. both result in the formation of xanthine.
xanthine made into urate by xanthine oxidase.
hypoxanthine and guanine can be salvaged (returned to AMP and GMP) by HRPT or HGPRT. missing in pts with Lesch-Nyhan syndrome- secondary gout.
What class of disease is gout (autoimmune? autoinflammatory?) What is the pathogenesis of gout?
autoinflammatory: activates the innate immune system
crystal motifs are irritants that cause frustrated phagocytosis, production of IL-1, and inflammasome initiation.
Dx of gout
joint aspiration and demonstration of MSU crystals. Crystals will be needle shaped and negative birefringence under polarized light (yellow when they lay flat or when under parallel light)
demonstration of hyperuricemia not helpful- sometimes ppl have normal levels during acute gout, and not everyone with high levels will get gout.
X-ray findngs with gout
soft tissue changes with slight radio-opacity near eroded joints, some calcification in soft tissue masses, erosions and bone production that create overhanging edges of cortex (rat bites). Rat bites are in contrast to rheumatoid arthritis, where you would NOT see new bone formation.
antiinflammatory tx of gout
NSAIDs at HIGH doses (naprosyn or indocin)
colchicine (which poisons microtubule formation/spindle formation and prevents ability to go through metaphase, causing high GI toxicity. therapeutically acts as an anti-inflammatory), corticosteroids, IL-1 antagonists (off-label)
Tx strategy for gout
treat inflammation FIRST
if necessary, begin urate lowering medication while still taking anti-inflammatory prophylaxis.
adjusting doses may precipitate gout: use prophylactic medication.
urate lowering therapies: indications
tophus, >2 arthritic attacks/yr, CKD stage 2 or worse, past urolithiasis. Do NOT give for asymptomatic hyperuricemia.
urate lowering therapies: types
allowpurinol (xanthine oxidase inhibitor), febuxostat (XO inhibitor), or uricosurics (probenecid directly; side effect of losartan, fenofibrate). targe serum urate under 6 mg/dl.
can give pegloticase- pig uricase. problems: not long term, requires recurrent infusions, can cause anaphylaxis.
What other crystals can cause crystalline arthritis?
CPPD: calcium pyrophosphate dihydrate (can cause pseudogout)
basic calcium hydroxyapatite (rarer)
oxalate crystals in dialysis pts
Pseudogout
caused by CPPD crystals
overproduction of excracellular pyrophaspate in abnormal cartilage matrix? (probably won’t learn this)
synovial fluid inorganic pyrophosphate (?) concentrations are elevated in jts with CPPD deposition. PPI is liberated by chonrocytes.
