Both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms.

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Both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms.

Both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms.
Both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms.

· Decreased renal excretion is by far the most common cause of hyperuricemia.

It may be hereditary and also occurs in patients receiving diuretics, like this patient receiving hydrochlorothiazide diuretics. Increased production of urate may be caused by increased nucleoprotein turnover in hematologic conditions and in conditions with increased rates of cellular proliferation and cell death. Increased urate production may also occur as a primary hereditary abnormality and in obesity, because urate production correlates with body surface area.

· Neurological proceses account for the pain associated in gout. Pain is a central feature of the acute gout flare. This pain may be due to a number of factors, including local production of prostaglandins and bradykinin, and sensitization of nociceptors [51]. When unmyelinated nerve fibres are stimulated, there is release of neuropeptides such as substance P. Substance P results in vasodilatation, plasma extravasation, leucocyte recruitment, mast cell degranulation, and release of PGs and cytokines.

· The muskuloskeletal process in developing gout involves the precipitation of urate as needle-shaped monosodium urate (MSU) crystals, which are deposited extracellularly in avascular tissues (eg, cartilage) or in relatively avascular tissues (eg, tendons, tendon sheaths, ligaments, walls of bursae) and skin around cooler distal joints and tissues (eg, ears).