58-year-old obese white male

58-year-old obese white male

A 58-year-old obese white male presents to ED with chief complaint of fever, chills, pain, and swelling in the right great toe. He states the symptoms came on very suddenly and he cannot put any weight on his foot. Physical exam reveals exquisite pain on any attempt to assess the right first metatarsophalangeal (MTP) joint. Past medical history positive for hypertension and Type II diabetes mellitus. Current medications include hydrochlorothiazide 50 mg po q am, and metformin 500 mg po bid. CBC normal except for elevated sedimentation rate (ESR) of 33 mm/hr and C-reactive protein (CRP) 24 mg/L. Metabolic panel normal. Uric acid level 6.7 mg/dl.

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In your Case Study Analysis related to the scenario provided, explain the following:

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

· Any racial/ethnic variables that may impact physiological functioning.

· How these processes interact to affect the patient.

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).

Any racial/ethnic variables that may impact physiological functioning.

· Gout is reported more prevalent in African-American men than white men. Previous analyses have demonstrated that there are genetic differences in renal urate handling that increase the risk of hyperuricemia and gout. Furthermore, racial/ethnic minorities may share a higher burden of gout, due to higher prevalence of comorbidities (hypertension, obesity, renal failure etc.), the use of predisposing medications such as diuretics, and delay in diagnosis and/or treatment.

How these processes interact to affect the patient.

· Both the medical history of hypertension and diabetes mellitus already posed high risks for the patient to develop gouty arthritis secondary to increased uric acid levels. As previously mentioned, obesity and the patient’s recent intake of hydrochlorothiazide also play significant roles in the pathogenesis of the disease. The gout flare represents a sterile acute auto-inflammatory response to MSU crystals, characterized by heat, swelling, erythema, pain, and loss of joint movement- which explains the signs and symptoms found in the patient. Moreover, the first MTP joint is the most common location for gout attacks, as seen in this case. Although comprising the lesser population at risk in developing gout compared to blacks, the medical history of the patient already put him to a high probability of developing hyperuricemia- one that is a potential cause for gouty arthritis.

Step-by-step explanation


· https://www.merckmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/crystal-induced-arthritides/gout

· https://oxfordmedicine.com/view/10.1093/med/9780199668847.001.0001/med-9780199668847-chapter-39#:~:text=Initiation%20of%20the%20acute%20gout,to%20MSU%20crystals%20%5B58%5D.

· https://academic.oup.com/rheumatology/article/44/9/1090/1784320

· https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3545402/

· https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3927975/

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