RT Book, Section
A1 Bottenberg, Michelle M.
A2 Sutton, S. Scott
SR Print(0)
ID 1158315786
T1 Gout
T2 McGraw-Hill's NAPLEX® Review Guide, 3e
YR 2019
FD 2019
PB McGraw-Hill Education
PP New York, NY
SN 9781260135923
LK accesspharmacy.mhmedical.com/content.aspx?aid=1158315786
RD 2024/04/19
AB Gout  is  characterized  by  acute  and  recurrent  arthritis  mediated  by  the  formation  of  monosodium  uric  acid  (MSU)  crystals  within  the  joints  and  surrounding  tissues.  This  results  in  pain,  erythema,  and  inflammation.  Elevated  serum  uric  acid  (SUA)  concentrations  are  a  result  of  a  defect  in  purine  metabolism,  a  decrease  in  uric  acid  excretion,  increased  nucleic  acid  turnover,  or  increased  purine  production.  Uric  acid  is  a  metabolic  by-product  of  purine  compounds  derived  from  dietary  sources  or  the  breakdown  of  DNA  within  the  body’s  cells.  Uric  acid  is  excreted  by  the  kidneys  and  can  accumulate  if  production  exceeds  excretion.  A  majority  of  patients  with  gout  accumulate  excessive  uric  acid  due  to  underexcretion  of  the  compound.  Regardless  of  the  cause,  excessive  intake  of  high  purine  foods  contributes  to  hyperuricemia  and  gout  exacerbations  (Table  48-1).