Gout

Gout
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Introduction
Gout is a disease that results after crystals of monosodium urate (MSU) are found in soft tissues, joints, and bones. When gout gets into its advanced stage, it may result in tophaceous gout or acute arthritis. When urate concentration exceeds its solubility level in extracellular fluid, gout development becomes susceptible in that being. However, it is not easy to differentiate the clinical expression of chronic gouty arthropathy and self-limited attacks of acute gouty arthritis. There are chronic or acute inflammatory responses due to the presence of MSU crystal formation.
A brief Pathophysiology of Gout
MSU crystal deposition is a unique factor in gout. There is numerous pathophysiological checkpoints are needed to determine gout development. For instance, urate concentration is evaluated. Underexcretion and overproduction of urate contribute to the total urate balance. Alteration of degradation pathways and purine synthesis results in overproduction. Hyperuricaemia (elevated serum urate concentrations) is caused by the renal underexcretion (Teng, et al., 2006). Development of hyperuricemia is contributed by extrarenal urate underexcretion. The other checkpoint is the formation of MSU crystals. Structural joint damage occurs in some patients with advanced gout. Both indirect effects of joint inflammation and direct effects of MSU crystals on joint tissue are the key mediators of joint damage due to gout. Apart from their pathogenesis role, gout endangers immune surveillance.

Cultural Influences such as Dietary or Lifestyle Predisposed for Gout
High-level intake of liquor increases the risk for gout in an individual. It is evident that beer is associated with products such as guanosine, which is the cause of association. Nevertheless, the wine has no significant effect in the risk factor for gout. On the other hand, obesity is increasingly heightening at an alarming rate. Currently, over 55% of the total American population, is obese. As if this is not enough, childhood obesity is also rising. Holding to the fact that obesity has a positive relationship with body mass index (BMI). Consequently, obesity has been found to result in gout. Majority of people with obesity are also found to have gout. According to research found recently, serum urate is contributed by obesity. Weight loss is closely associated with reduced uric acid levels, and the contrary is true.
Aspects of the Purine Diet for Patients
In the USA, over 1% of the total population is affected by gout. This form inflammation arthritis is prevalent mostly in men. Gout is among the significant factors that are attributed to recent shifts in lifestyle and diet. Increase in seafood and meat intake is associated with high-level risk for gout. Protein and purine-rich vegetables do not contribute to gout disease (Lee & Lee, 2011). Consumption of dairy products such as low-fat milk and liver, lungs, and meat contribute to 50% in the reduction of gout. Alcohol consumption especially purine-rich alcoholic beverages have a positive correlation with the increase in hyperuricemia risk.
Medication for Gout and Possible Cultural Influences
Medication for gout is rooted in prevention through lifestyle choices. The past tested medical treatments have proven insufficient. However, new treatments are available for better living standards. These include a nonpurine inhibitor of xanthine oxidase, febuxostat, and investigational inhibitors of URAT. Uric acid homeostasis is efficient in the anion exchanger in the proximal tubule.
Conclusion
Gout ought to be dealt with since it has an advance effect regarding longevity, shifts in diet, age, and medical care. Sex and age are non-modifiable risk factors. The elderly suffer from gout mostly. Age-related disorders such as hypertension and metabolic syndrome are among the major causes of gout. Therefore, the urgent need to identify and treat patients with gout is necessary to control the prevalence of the illness. Hypertension control, weight loss, dietary changes, and changes in medication regimens are lifestyles that may provide adequate controls of gout.

References
Lee, K. H., & Lee, S. K. (2011). Pathophysiology of gout. The Korean Journal of Medicine, 80(3), 251-254.
Teng, G. G., Nair, R., & Saag, K. G. (2006). Pathophysiology, clinical presentation and treatment of gout. Drugs, 66(12), 1547-1563.