Any racial/ethnic variable that may impact physiologic functioning. How these processes interact to affect the patient?

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Any racial/ethnic variable that may impact physiologic functioning. How these processes interact to affect the patient?

Any racial/ethnic variable that may impact physiologic functioning. How these processes interact to affect the patient?
Any racial/ethnic variable that may impact physiologic functioning. How these processes interact to affect the patient?

neurological and musculoskeletal pathophysiologic processes

Case study: 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 metatrasophalangeal joint. Past medical history positive for hypertension and type 2 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.

In your case study analysis related to the scenario provided, explain the following: Both neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms. Any racial/ethnic variable that may impact physiologic functioning. How these processes interact to affect the patient?

 

 

 

Answer:

 

 

With the patient’s presenting symptoms, it is high likely to consider the diagnosis of gouty arthritis. This type of arthritis is caused by the inflammatory reaction due to the deposition of monosodium urate (MSU) crystals into the joints of patient with hyperuricemia. The inflammation induced by MSU is driven by components of the innate immune system, thus provide normally with the initial nonspecific immune response to invading pathogens. The key players of the immune response, or the inflammatory mediators, for gouty arthritis include IL-1β, which regulates cell proliferation, differentiation, and apoptosis. IL-1β is a proinflammatory cytokine which induces the expression of a variety of inflammatory mediators. These mediators are then directly responsible for neutrophil influx in the patient’s synovium, which is the hallmark of gouty arthritis. Overtime, when the acute inflammation accompanies repeated flares of gouty arthritis, it can cause a pathologic joint damage, giving rise to what is called “tophi”, an accumulation of MSU crystals in the joint common in the great toe, and small phalangeal joints. In addition, overproduction of uric acid can involve neurological abnormalities such as dystonia, compulsive injurious behavior, cognitive dysfunction, and articular manifestations. With this pathogenesis explains the pathophysiologic processes that involve the neurologic and musculoskeletal systems of the patient as being presented by the symptoms.

 

With regards to racial/ethnic variability, gouty arthritis is more common on blacks than whites. African-american race in some genetic studies was found to have a genetic loci associated with hyperuricemia. However, a study was found out that racial/ethnic variables shared a higher burden of gout, for a reason that there is a higher prevalence of comorbidities, such as obesity, hypertension, and renal failure, among others. Also the use of predisposing medications such as diuretics, and delay in diagnosis and/or treatment could affect the pathophysiology of gout. With these being said, from the patient’s perspective, his comorbidity with hypertension and diabetes mellitus and his taking up with diuretics (hydrochlorothiazide) could potentially affect the prognosis of his gouty arthritis.