Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

20 Cards in this Set

  • Front
  • Back
what is the most important part of urate production
- PRPP and glutamine
- the enzyme that controls them making iosinic acid, PRPP aminotransferase
what controls PRPP aminotransferase
negative feedback by purine nucleosides
what is the deal with purine salvage
- 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)
Lesch-Nyhan syndrome
- decreased HGPRTase
- increased de novo urate synthesis from too much PRPP not used in salvaging purine bases
how do gout pts excrete urate as a group?
- they tend to excrete 40% less, even thought their blood levels are high
- some 20% secrete more than average
how much urate does a gout person have in their system?
- normal is 1 g
- w/out tophi is 4 g
- w/ tophi, 15-30 g
2o causes of gout
- 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
how does the synovial fluid react with MSU?
- 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
how do PMN's react with MSU?
- 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
gout of 1st MTP
gout labs
- 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
- 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
- purine antimetabolite to block purine degradation for that feedback inhibition of PRPP aminotransferase
- also blocks xanthine oxidase
- high levels of oxypurinol
- 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
tumor lysis syndrome
ARF from UA precipitates lodging in DT and CD
pseudogout clinical
- from CPPD
- older, more women than gout
- less mild than gout
- knees, wrists, elbows, shoulders, pubic symphysis
- deposits not seen on PE
diseases associated w/ pseudogout
- hyperPT, hypoT
- hemochromatosis
- ochronosis
- pagets
- DM
- OA
- hypoMag
CPPD depositis in cartilage of tendons and ligaments
tx of pseudogout
- rest
- NSAID (indomethacin)
- joint aspiration
other crystals that can cause arthritis
- Ca - can cause tophi, in inflamed joints and bursae
- apitate (mineral of bone) - purple rounded inclusions on PMN's