Create a 6 page essay paper that discusses Gout and Hyperuricemia.
Overproduction of uric acid leads to increased phosphoribosyl pyrophosphate (PRPP) synthetase activity and deficiency of hypoxanthine‐guanine phosphoribosyl transferase (HGPRT ), which is responsible for the conversion of hypoxanthine to ionsinic acid and guanine to guanylic acid. A deficiency of HGPRT is likely to cause hyperuricemia in healthy individuals (p.49). Uric acid elimination occurs in two ways: through urine (66%) and through the gastrointestinal tract. A decline in the level of uric acid urinary excretion results in an increase in sodium urate pool and hyperurecemia. Accumulation of uric acid in the urine is determined by glomerular filtration, tubular reabsorption, tubular secretion, and postsecretory reabsorption. Enhanced sodium reabsorption also means increased reabsorption of uric acid. Any factor that increases the production of uric acid and decreases its clearance results in elevated levels of serum urate concentration, causing gout and hyperuricemia (Teng, Nair and Saag, 2006, p. 1549) Acute gouty arthritis is characterized by the rapid onset of swelling, inflammation and excruciating pain in affected joints. The attack is normally monoarticular at the beginning and it affects the first metatarsophalangeal joint and then spreads to the insteps, ankles, heels, knees, wrists, fingers, and elbows. It is likely that the predilection of low extreme acute gout in peripheral joints is related to the high intraarticular urate concentration and low temperature of joints (Terkeltaub and Edwards, 2010, p.18).
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