Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Abstract
Background context
The past three decades have witnessed increasing interest in strategies to improve neurologic function after spinal cord injury. As progress is made in our understanding of the pathophysiologic events that occur after acute spinal cord injury, neuroprotective agents are being developed.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Purpose
Clinicians who treat acute spinal cord injuries should have a basic understanding of the pathophysiologic processes that are initiated after the spinal cord has been injured. A familiarity with the literature on which the current use of methylprednisolone is based is also essential.
Study design/setting
Literature review.
Methods
Literature review of animal data on pathophysiologic mechanisms, and of both animal and human trials of neuroprotective agents.
Results
The mechanical forces imparted to the spinal cord cause primary damage to the neural tissue, but a complex cascade of pathophysiologic processes that imperil adjacent, initially spared tissue to secondary damage rapidly follows this.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes . Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. Many researchers are investigating the role of such processes as ischemia, inflammation, ionic homeostasis and apoptotic cell death in the secondary injury cascade, with hopes of developing specific therapies to diminish their injurious effects. Beyond methylprednisolone, a number of other pharmacologic treatments have been investigated for the acute treatment of spinal cord injury, and even more are on the horizon as potential therapies.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Conclusions
This review summarizes some of the important pathophysiologic processes involved in secondary damage after spinal cord injury and discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
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.
Neurologic and Musculoskeletal Pathophysiologic Processes
Concerning the patient’s presenting symptoms, it is highly likely that he has gouty arthritis. Inflammatory reaction due to the deposition of monosodium urate (MSU) crystals into the joints causes this diagnosis type. Gouty arthritis commonly occurs in patients with hyperuricemia. Components of the innate immune system drive the inflammation induced by MSU (Wilson & Saseen, 2016). The innate immunity normally provides with the initial nonspecific immune response against the invading pathogens. The synovial phagocytic cells engulf the MSU crystals deposits, leading to an inflammatory process involving chemokines, lysosomal enzymes, and other mediators. The cytokines released within the joint produce signals to the brain. The brain then processes sickness-related symptoms such as fever.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
The key inflammatory mediators or players of the immune response involved in gouty arthritis’s pathophysiology include IL-1β. Interleukin 1 regulates cell proliferation, differentiation, and apoptosis. IL-1β is a pro-inflammatory cytokine, which signals other cell types to promote inflammation (Cleophas et al., 2017). IL-1β leads to the expression of a number of inflammatory mediators. Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .The inflammatory mediators are directly responsible for neutrophil influx into the patient’s first metatarsophalangeal (MTP) joint synovium. The entrance of neutrophils into the joint fluid is the hallmark of gouty arthritis. Over time, repeated flares of gouty arthritis are accompanied by inflammation can cause pathologic joint damage. Tophi emerge from the inflammation and repeated deposition of the MSU crystals (Cleophas et al., 2017). Accumulation of MSU crystals occurs in the joints commonly in the small phalangeal joints and great toe.
Additionally, overproduction of uric acid involves neurological abnormalities such as cognitive dysfunction, dystonia, compulsive injurious behavior and articular manifestations. This pathogenesis explains the pathophysiologic processes that involve the neurologic and musculoskeletal systems of the patient as presented by the symptoms.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Racial and Ethnic Variables That May Impact Physiological Functioning
Development of gouty arthritis is common among black Americans men and women as compared to their white counterparts. According to Chen-Xu et al. 2018, some studies found that the African-Americans have genetic loci associated with hyperuricemia. Hyperuricemia increases the risk of developing MSU deposits among the African-Americans. The higher uric acid levels mediate the increased risk of developing MSU deposits within a joint. Due to the high acid levels and combination of conditions like hypertension, it is highly likely for the African-Americans to develop gouty arthritis.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Some studies found out that racial or ethnic variables shared a higher burden of gout. Ethical and racial variables determine one predisposition because of different aspects of their race. The prevalence of comorbidities such as obesity, hypertension, and renal failure, among others determines the risk of a person belonging to certain race or ethnic group (Chen-Xu et al., 2018).Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
Additionally, the use of predisposing medications such as diuretics could affect the pathophysiology of gout. The delay in diagnosis and or treatment affect the pathophysiological process of the disease. With these said, from the patient’s scenario, his comorbidity with hypertension and diabetes mellitus and his taking up with diuretics (hydrochlorothiazide) could potentially affect the prognosis of his gouty arthritis The risk of developing gout is even higher since African Americans have a higher prevalence of comorbidities, such as obesity, hypertension, renal failure, etc.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
These processes interact to cause the patient’s presenting symptoms. Swelling and inflammation in the right great toe lead tissue injury, subsequently activating the peripheral pain receptors. The inflammatory mediators stimulate the release of additional agents, which induce pain (Cleophas et al., 2017). The pain makes the patient unable to bear any weight by the foot.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
