Gout pathophysiology
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Gout pathophysiology On the Web |
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American Roentgen Ray Society Images of Gout pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Defects in the kidney may cause uric acid to build up in the blood, leading to hyperuricemia, and the subsequent formation of gout crystals.
Pathophysiology
Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a hyperuricaemia, although it is 10 times more common without clinical gout than with it[1]
Purines can be generated by the body via breakdown of cells in normal cellular turnover, or can be ingested in purine-rich foods such as seafood. The kidneys are responsible for approximately one-third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.
Hyperuricemia is considered an aspect of metabolic syndrome, although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among obese individuals.
Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.[2] It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout,[3][4] which condition is then known as saturnine gout, because of its association with alcohol and excess.[5]
Gross Pathology
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Microscopic Pathology
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Sources
Copyleft images obtained courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, CA) Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology
References
- ↑ Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. (2007). "Levels of uric Acid in serum in patients with metabolic syndrome". Georgian Med News. 146: 34&ndash, 7. PMID 17595458.
- ↑ Robert S. Ivker, D.O. ; et al. (1999). The Complete Self-Care guide to Holistic Medicine. pp. 186&ndash, 8. ISBN0-87477-986-J.
- ↑ Lin JL, Huang PT. (1994). "Body lead stores and urate excretion in men with chronic renal disease". J Rheumatol. 21 (4): 705&ndash, 9. PMID 8035397.
- ↑ Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000). "Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study". J Rheumatol. 27 (7): 1708&ndash, 12. PMID 10914856.
- ↑ Ball GV. (1971). "Two epidemics of gout". Bull Hist Med. 45 (5): 401&ndash, 8. PMID 4947583.