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45 Cards in this Set

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  • Back
what is the offending structure in gout?
monosodium urate crystals
why is gout exclusively a disease of humans?
b/c we lack uricase enzyme (seen in other animals) which breaks catabolizes uric acid (urate)
how is uric acid formed?
elimination of excess nucleic acid purines and nitrogenous waste productes
what is more important in the pathogenesis of hyperuricemia in gout: dietary sources of urate or endogenous overproduction?
endogenous overproduction
what is the rate-limiting rxn in urate formation? what enzyme catalyzes it? where does it occur?
PRPP + Glutamine --> Inosinic Acid
catalyzed bye PRPP aminotransferase
primarily in the liver
what is the defect in Lesch-Nyhan syndrome and what are the consequences?
HGPRTase deficiency --> no purine (really, hypoxanthine and guanine) salvage --> increased urate production
the biochemical hallmark of gout is __
in general terms what is primary hyperuricemia?
an idiopathic or inborn error of metabolism leading ONLY to hyperuricemia
in general terms, what is 2'ary hyperuricemia?
an acquired or inborn error of metabolism leading to a spectrum of diseases, one of which is gout
more than 95% of the pts w/ gout have __
primary hyperuricemia
T/F: In primary gout, there is a problem with renal excretion of urate
TRUE (but the main problem is overproduction of MSU)
what is the cause of saturnine gout?
lead nephropathy in "moonshine" drinkers leads to decreased urate excretion
what molecules compete w/ urate for secretion along the nephron with overingestion leading to hyperuricemia?
lactate (metabolic acidosis)
ketogenic acids (ketosis)
salicylate ingestion
after filtration in the glomerulus, how is urate resorbed?
by active transport, primarily in the proximal tubule
why are synovial joints a site of crystal formation?
uric acid becomes less soluble with:
lower body temps
repetitive trauma
increased or decreased hydrostatic pressure
rapid change in serum concentration
describe the acute inflammatory cascade in gout.
1. MSU crystals precipitate in joint
2. IgG binds to crystals
3. Complement binds to crystals or are activated by inflammatory response --> amplifier
4. PMNs bind to crystals via Fc receptor of immunoglobulin
5. PMNs phagocytize crystals
what happens after PMNs phagocytize the MSU crystals?
there is lysosomal mediated cell rupture, or the actual crystal pierces the membrane leading to spilling of the PMN cytoplasmic contents into the synovial fluid which amplifies the inflammatory response
what is crystal chemotactic factor?
a glycopeptide released from PMNs after exposure to MSU crystals --> attracts other PMNs to the synovial fluid
what is podagra?
gout of the first MTP joint
what is the typical presentation of gout?
severe monoarticular arthritis lasting days to weeks
T/F: Actue gout can be precipitated by physical stress
how do you dx gout?
observing negatively birefringent (yellow crystals), needle-shaped MSU crystals engulfed by PMNs in a synovial fluid aspirate
what is the major extraarticular manifestation of gout?
what are some common chronic diseases assoc w/ gout?
T/F: Extracellular MSU crystals seen in a joint aspirate are diagnostic of gout
T/F: elevated serum uric acid is pivotal in the diagnosis of gout
FALSE. It is of little value.
what are some supportive lab studies seen in gout?
CBC (left shift to PMNs)
what are typical ranges of WBC counts in synovial aspirates in gout?
can mimic septic arthritis
what are tophi?
cystalline deposits of urate (chalk-like)
how do tophi appear on x-ray?
what is the treatment of acute gout?
oral corticosteroid
intraarticular aspiration/steroid injection
in reality is ice used to treat acute gout?
no, b/c they can't stand pressure or moving the joint
what is the MOA of colchicine?
Inhibits PMN microtubular function and migration
what is the MOA of probenecid?
inhibits reabsorption of uric acid in the PCT
for whom is probenecid contraindicated?
pts w/ hx of renal stones or elevated urinary urate excretion rates b/c probenecid may promote stone formation
how does allopurinol block purine degradation?
it inhibits xanthine oxidase and blocks purine degradation at RLS.
what is pseudogout?
acute arthritis caused by calcium pyrophosphate deposition disease (CPPD) crystal induced inflammation
if you see pseudogout in a pt < 50, what should you do?
look for assoc disease such as:
ochronosis (pigmented cartilage from alkaptonuria)
how do you dx pseudogout?
rhomboid crystals that are weakly-postively birefringent (blue) engulfed by PMNs
T/F: attacks of pseudogout are slower in onset and not as severe as gout
what joints are commonly affected by pseudogout?
knee, wrist, elbow, shoulder, pubic symphysis
what is an x-ray finding in severe pseudogout?
chondrocalcinosis (linear or punctate radiodensities in the cartilage of tendons and ligaments)
Basically mineralization of fibrocartilage and articular cartilage (like meniscus)
how do you Rx pseudogout?
joint aspiration and NSAIDs
gout-like clinical pattern, periarticular calcium on radiograph, absence of other arthritic causes and observation of purple rounded inclusions in PMNs -->
apatite arthritis
how can you distinguish corticosteroid arithritis flare from iatrogeneic infection?
steroid flare will occur in hours, the infection won't manifest for a few days