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of complete
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gout and p. 473
for gout p. 473, 496
gout p. 724
treatment p. 724
acute gout attack p. 724
gout p. 473, 496
gout p. 249
gout exacerbation p. 473
in gout p. 496
gout p. 473, 496, 724
gout with p. 249
acute gout attack p. 724
gout p. 473, 496
as drug reaction p. 249
drug therapy for p. 495
kidney stones and p. 622
lab findings p. 728
Lesch-Nyhan syndrome p. 35
loop diuretics and p. 624
presentation p. 724
treatment p. 724
Von Gierke disease p. 85
gout p. 473
gout p. 473
acute gout drugs p. 497
gout p. 249
acute gout attack p. 724
gout p. 473, 497
gout p. 473
presentation p. 724
for gout p. 496, 724
gout p. 249
gout p. 249
gout p. 496
Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours.
When this happens, it’s called a gouty attack.
The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules.
Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.
To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles.
A heterocycle being any molecular ring or cycle with different types of atoms.
Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine.
Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL.
At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.
These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.
Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.
Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out.
Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are risk-factors for gout.
Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal rate.
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