Gout
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Similar nodules are present on the left elbow and right external pinna of the ear. Further evaluation of this patient will most likely reveal which of the following?
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First Aid
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Alcohol use
gout and p. 477
Allopurinol
for gout p. 477, 500
gout p. 726
Chronic gout
treatment p. 726
Colchicine
acute gout attack p. 726
gout p. 477, 500
Cyclosporine
gout p. 251
Dehydration
gout exacerbation p. 477
Diuretics
in gout p. 500
Febuxostat
gout p. 477, 500, 726
Furosemide p. 253, 632
gout with p. 251
Glucocorticoids
acute gout attack p. 726
gout p. 477, 500
Gout p. 477
as drug reaction p. 251
drug therapy for p. 499
kidney stones and p. 628
lab findings p. 722
Lesch-Nyhan syndrome p. 35
loop diuretics and p. 632
presentation p. 718
treatment p. 726
Von Gierke disease p. 85
Indomethacin p. 499
gout p. 477
Metatarsophalangeal (MTP) joints
gout p. 477
Naproxen p. 499
acute gout drugs p. 501
Niacin
gout p. 251
Nonsteroidal anti-inflammatory drugs (NSAIDs) p. 499
acute gout attack p. 726
gout p. 477, 501
Podagra
gout p. 477
presentation p. 718
Probenecid p. 253
for gout p. 500, 726
Pyrazinamide p. 194
gout p. 251
Thiazides p. 633
gout p. 251
Tophi in gout p. 718
Uric acid
gout p. 500
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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.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Gout" The Lancet (2016)
- "Update on gout: new therapeutic strategies and options" Nature Reviews Rheumatology (2010)
- "Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians" Annals of Internal Medicine (2016)
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