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20 Cards in this Set
- Front
- Back
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what is the most important part of urate production
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- PRPP and glutamine
- the enzyme that controls them making iosinic acid, PRPP aminotransferase |
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what controls PRPP aminotransferase
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negative feedback by purine nucleosides
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what is the deal with purine salvage
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- when purines that would be converted to urate are lost for incorporation into nucleic acids
- the enzyme HGPRTase is what send them into this (so it sends them away from gout) |
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Lesch-Nyhan syndrome
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- decreased HGPRTase
- increased de novo urate synthesis from too much PRPP not used in salvaging purine bases |
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how do gout pts excrete urate as a group?
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- they tend to excrete 40% less, even thought their blood levels are high
- some 20% secrete more than average |
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how much urate does a gout person have in their system?
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- normal is 1 g
- w/out tophi is 4 g - w/ tophi, 15-30 g |
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2o causes of gout
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- increased nucleic acid turnover (myeloprolif disorders)
- Lesch-Nyhan syndrome - von Gierke's disease - renal failure - moonshine drinking - metabolic acidosis, ketoacidosis, salycylates competing for PT in kidney |
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how does the synovial fluid react with MSU?
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- The FC of IgG is available to the PNN FC-R, which leads to adherance and phagocytosis
- Haegmen Factor, C1, C3, and C4 can also be bound and activated |
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how do PMN's react with MSU?
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- MSU is way bigger, so more incomplete phagogenesis a membrane rupture --> lysosomes released
- if fully phagocytized, MSU destroys the membrane of the phagolysosome, so increased fluid levels of lysozymes - crystal chemotactic factor is released from PMN's which attracts other PMN's |
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podagra
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gout of 1st MTP
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gout labs
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- not diganostic!
- but, increased UA - leukocytosis w/ immature PMNs (left shift) - sed rate up - serum acute phase reactants (will look like infectious arthritis) - synovial viscocity is less than RA or ifectious A |
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colchicine
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- for acute tx of gout, or prophylacticaly to prevent multiple attacks
- inhibits PMN microtubular function (at super high doses) - inhibits MSU-incuded chemotactic factor release |
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allopurinol
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- purine antimetabolite to block purine degradation for that feedback inhibition of PRPP aminotransferase
- also blocks xanthine oxidase - high levels of oxypurinol |
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probenecid
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- uricosuric agent - blocks renal tubular reabsorption of uric acid, promotes urinary excretion
- not for people w/ high urine sed rate or increased urinary excretion, can cause nephrolithiasis |
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tumor lysis syndrome
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ARF from UA precipitates lodging in DT and CD
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pseudogout clinical
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- from CPPD
- older, more women than gout - less mild than gout - knees, wrists, elbows, shoulders, pubic symphysis - deposits not seen on PE |
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diseases associated w/ pseudogout
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- hyperPT, hypoT
- hemochromatosis - ochronosis - pagets - DM - OA - hypoMag |
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chondrocalcinosis
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CPPD depositis in cartilage of tendons and ligaments
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tx of pseudogout
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- rest
- NSAID (indomethacin) - joint aspiration |
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other crystals that can cause arthritis
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- Ca - can cause tophi, in inflamed joints and bursae
- apitate (mineral of bone) - purple rounded inclusions on PMN's |
