25: Crystalline Arthropathies - Craig Flashcards
serum urate
formed in process of purine metabolism/degradation
hyperuricemia ***
serum urate values in excess of 6.8 mg/dl
higher levels = more risk
gout
inflammatory arthritis developing as a consequence of urate deposition in joint
4 stages of gout
asymptomatic hyperuricemia (elevated serum urate with no clinical manifestations)
acute flares (acute inflammationin joint caused by urate crystallization)
intercritical segments (intervals between flares)(progressively shorter)
advanced gout (long-term gouty complications of uncontrolled hyperuricemia)
why is incidence of gout rising?
- increased longevity
- increased comorbidity
- low dose ASA
- thiazides
- CSA (cyclosporine)
- fructose
- decreased HRT
catalyzes the final conversions to uric acid
xanthine oxidase
purine degradation to uric acid
medicines that are risk factors for gout
- diuretics [lead to increased uric acid reabsorption]
- low dose ASA [ over 6% increase in mean serum urate and 23% decrease in uric acid clearance]
- pyrazinamide, ethambutol, niacin [observed at higher incidence]
why is transplant pt a risk factor for gout?
- attributed to cyclosporine (azathiprine) use
- see an accelerated clinical course with polyarticular involvement and tophi
which foods are related to gout?
- red meat
- seafood
- dairy products are PROTECTIVE
- NOT purine-rich vegetables
which alcohol is worst for gout?
beer is worse than liquor or wine
what medical comorbidities are assoc with gout
- obesity
- metabolic syndrome
- DM
- heart failure
- hyperlipidemia
- hypertension
gold standard gout diagnosis ***
synovial fluid analysis - MSU crystals visible with compensated polarized light
ddx gout
- CPPD pseudogout
- septic arthritis
chronic gout xray
- overhanging edge **
- erosions demarcated round deficits with sclerotic margins
- very destructive
*** goals of gout therapy
- terminate acute attack**
- prevent recurrence while lowering serum urate
- prevent or reverse complications from deposition of monosodium urate or uric acid crystals (kidney disease, joint destruction)
- address comorbidity
- DO NO HARM
IV colchicine
NO don’t do it
acute tx gout
intraarticular corticosteroids
goal urate level
less than 6 mg/dL
uricosuric agents
probenecid
- pee out the uric acid
xanthine oxidase inhibtors
allopurinol and febuxostat (stop uric acid production)
advantage/disadvantage uricosurics
+ reverse most common physiological abnormality in gout = underexcretion
- BID to TID dosing
- dependent on renal function
- drug-drug interactions
number one side effect allopurinol ***
- precipitation of acute attack [lowering serum urate mobilizes deposited crystals]
important drug interactions with allopurinol
- azathioprine
- 6-mercaptopurine
(require xanthine oxidase for breakdown)
how long a protective med and allopurinol?
3-6 mo or longer!
12 mo is good
don’t start or stop allopurinol in the midst of an acute flare- allopurinol is a life-long drug
CPPD =
calcium pyrophosphate dihydrate deposition disease
- formation of CPPD crystals in articular hyaline and fibrocartilage
- when these crystals produce inflammatory arthrtisi = pseudogout
radiographs CPPD
chondrocalcinosis
clinical classifications of pseudogout
A: pseudogout B: pseudorheumatoid arthritis C: pseudoOA with acute attacks D: pseudoOA w/o inflammation E: asymptomatic/lathaic F: pseudoneurotrophic
when in life is pseudogout more likely?
strong age correlation, especially prevalent in 8th and 9th decades
4 Hs associated with pseudogout **
- only HEMOCHROMATOSIS assoc with structural arthropathy
- hypomagnesmia
- hyperparathyroidism
- hypophosphatasia
- hemochromatosis
most common cause of acute monoarthritis in eldery
pseudogout
