Case Study- Neurological and Musculoskeletal

Case Study- Neurological and Musculoskeletal

Neurological and musculoskeletal disorders are common companions of aging. They are a spectrum of disorders characterized by impairments in muscular, neurologic, skeletal, and cognitive functionalities. These disorders include but are not limited to Parkinson’s disease, multiple sclerosis, arthritic disorders, and osteoporosis. They remain one of the leading causes of functional disability, mortality, and deterioration in the quality of life. This paper analyzes a case presentation emphasizing the neurological and musculoskeletal pathophysiological processes and factors that may impact the physiological functioning of individuals with these disorders.

Case Analysis

The case study is of a 58-year-old male presenting to the ED with pain and swelling in his right great toe, fever, and chills. He notes that his symptoms came suddenly and that he cannot put any weight on his foot. A physical examination of the patient revealed pain on the right first metatarsophalangeal (MTP) joint. The patient has a history of hypertension and type 2 diabetes mellitus and is currently on hydrochlorothiazide and metformin. Laboratory findings revealed normal CBC except for elevated erythrocyte sedimentation rate (ESR) and C-reactive protein of 33mm/hr and 24mg/L, respectively. His metabolic panel was normal, and his uric acid level was 6.7mg/dL.

The patient’s manifestations are suggestive of acute gouty arthritis. Acute gouty arthritis is characterized by the sudden onset of severe pain and swelling on a joint. Acute gouty attacks are mostly monoarticular, affecting only one joint. The most commonly affected joints are those of the lower extremities, especially the first metatarsophalangeal joint. The ankle, talar, and subtalar joints may also be affected. Gouty attacks are often acute, manifesting as pain and swelling of the affected joint within 3-24 hours. The pain experienced in acute gout attacks is often severe and excruciatingly painful to even touch. Gout flares often elicit inflammatory responses. Erythema, warmth, and swelling are evident in the affected region (Yip & Berman, 2021). The patient in the case study presented with symptoms suggestive of acute gout attacks. He had a sudden onset swelling on his right great toe. Additionally, the swollen region was excruciatingly painful and could not bear any weight or touch. This is indicative of a gout attack on his great toe.

An acute gouty attack may also present with systemic features. These include fever, chills, malaise, and fatigue (Yip & Berman, 2021). These manifestations are attributed to the inflammatory responses that accompany gouty attacks and gout flares. The patient in the case study had a fever and chills. This further confirmed the acute gout diagnosis.

Gout has a multi-factorial etiology. Genetics, medical comorbidities such as type 2 diabetes mellitus, obesity/overweight, medications, and dietary factors such as consumption of high proteinaceous foods are risk factors for the disease (Yip & Berman, 2021). Individuals with type 2 DM have a higher chance of developing gout. Hypertension also increases an individual’s chances of developing gout (Evans et al., 2019). Hypertension causes glomerulosclerosis and damage to the glomerular arteriolar, lowering the efficiency of glomerular urate excretion. The consequent accumulation of urate predisposes individuals to hyperuricemia and, consequently, gout attacks (Evans et al., 2019). The patient in the case study had type 2 diabetes mellitus and hypertension. These may have contributed to his presentation. He was also obese. Obesity increases an individual’s chances of developing gout and other forms of arthritis. According to Evans et al. (2019), obesity lessens the work efficiency of the kidneys, lowering the kidney’s ability to excrete urate effectively. This may lead to hyperuricemia and gout. The patient in the case study was obese. This may have contributed to his suffering. The patient was also on hydrochlorothiazide for the management of his hypertension. Thiazide diuretics predispose individuals to hyperuricemia and gout (Evans et al., 2019). This may have contributed to this disease.

Although acute gout is sometimes self-limiting, the pain that often accompanies inflammatory responses may warrant therapeutic interventions. Physical examination aligned with subjective findings on the patients is critical in accurately diagnosing the disease. Laboratory findings are also critical in this regard. Lab findings in gout attacks revealed elevated ESR and C-reactive proteins. While hyperuricemia is highly predictive of gout, acute gouty attacks may occur even in normal uric acid levels. Laboratory findings in the patient, accompanied by subjective findings, pointed towards an acute gout diagnosis. Lab work revealed elevations of ESR and C-reactive protein. This is confirmatory of the gout diagnosis.

Neurological and Musculoskeletal Pathophysiologic Processes Accounting for the Patient Symptoms

Gouty attacks are often present with swelling, pain, erythema, and warmth of the affected joint. It results from tissue deposition of mono-sodium urate salt crystals. Deposition of uric acid crystals on the joints triggers an inflammatory response. Initially, monocytes and mast cells are activated, followed by the activation of neutrophils (Towiwat et al., 2019). Before the initial attack and in the inter-critical period, macrophages will engulf the deposited crystals. Less differentiated monocytes will trigger the production of interleukin-1,6, and 8, tumor necrosis factor, and cause endothelial activation. Mast cells will induce gouty attacks by producing interleukin-1 and histamine (Towiwat et al., 2019). This results in enhanced vascular permeability and vasodilation that causes swelling and redness in the affected area.

Local vasodilation and monocyte and mast cell productions trigger neutrophilic chemotaxis. Other chemotactic factors produced by mast cells and monocytes, such as leukotrienes, platelet-activating factors, and interleukins, will further aggravate the inflammatory response and neutrophilic migrations. The interleukin-1 produced triggers the recruitment of other monocytes, thereby amplifying the inflammatory response. It can also result in cartilage breakdown. These changes further result in the production of other inflammatory mediators such as bradykinin, prostaglandins, and other products of the lipoxygenase pathway. These inflammatory mediators activate the TRPV1 nociceptors. These stimuli are conducted to the spinal cord and transmitted to the dorsal horn before being relayed to the supraspinal structures. This signal is detected as pain (Towiwat et al., 2019). The fever and chills seen in gout attacks result from the production of inflammatory mediators.

Racial/Ethnic Variables and How They Interact to Affect the Patient

Traditionally, gout has been considered a disease of white men who indulge in overconsumption of gamey meat. However, epidemiologic findings have revealed that the disease also affects other racial/ethnic groups. Potential racial differences in the epidemiology of gout may be due to nongenetic social determinants of health. These include lifestyle, diet, health-seeking behavior, and others (McCormick et al., 2022). Environmental risk factors for the disease, such as obesity/overweight, alcohol consumption, and health-seeking behavior, make blacks more predisposed to the disease than other ethnic groups. Factors within this group that make them more vulnerable to the disease compared to their white counterparts include their culturally informed efforts to lower current gout-related disparities, diet, and lifestyle.

Conclusion

The case presented reveals the manifestation of gouty attacks. It also demonstrates individual manifestations and findings that help in diagnosing the disease. Gout is a musculoskeletal disorder. It manifests with pain and swelling. Systemic manifestations of the disease include fever and chills. The disease has a multi-factorial cause. Aspects of race and ethnicity, such as lifestyle and diet, have been shown to interplay in the pathophysiologic development of the disease.

References

Evans, P. L., Prior, J. A., Belcher, J., Mallen, C. D., Hay, C. A., & Roddy, E. (2019). Obesity, hypertension, and diuretic use as risk factors for incident gout: A systematic review and meta-analysis of Cohort studies. Arthritis Research & Therapy, 20(1). https://doi.org/10.1186/s13075-018-1612-1

McCormick, N., Lu, N., Yokose, C., Joshi, A. D., Sheehy, S., Rosenberg, L., Warner, E. T., Dalbeth, N., Merriman, T. R., Saag, K. G., Zhang, Y., & Choi, H. K. (2022). Racial and sex disparities in gout prevalence among us adults. JAMA Network Open, 5(8). https://doi.org/10.1001/jamanetworkopen.2022.26804

Towiwat, P., Chhana, A., & Dalbeth, N. (2019). The anatomical pathology of gout: A systematic literature review. BMC Musculoskeletal Disorders, 20(1). https://doi.org/10.1186/s12891-019-2519-y

Yip, K., & Berman, J. (2021). What is gout? JAMA, 326(24), 2541. https://doi.org/10.1001/

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CASE STUDY

A 58-year-old obese white male presents to ED with a 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 is positive for hypertension and Type II diabetes mellitus. Current medications include hydrochlorothiazide 50 mg po q am, and metformin 500 mg po bid. CBC is normal except for an elevated sedimentation rate (ESR) of 33 mm/hr and C-reactive protein (CRP) of 24 mg/L. The metabolic panel is normal. Uric acid level 6.7 mg/dl.

The Assignment (1- to 2-page case study analysis)

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

Both the neurological and musculoskeletal pathophysiologic processes 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.

Please provide the Introduction, body, and reference pages.
Thank You!!!