NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Walden University NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 – Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
The introduction for the Walden University NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
After the introduction, move into the main part of the NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
The case study of the NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 assignment is gout, which is caused by disorders of purine metabolism, increased uric acid production, and reduced uric acid excretion, causing increased serum uric acid (sUA) levels. This forms monosodium urate (MSU) crystals deposited in the joints, kidneys, and other tissues. Gout occurs following the precipitation of monosodium urate crystals in a joint space (Clebak et al., 2020). The deposition of the urate crystals elicits activation of the immune system, causing the release of various inflammatory cytokines and the recruitment of neutrophils. Over time, the joint space becomes irreversibly damaged, causing chronic pain and disability with grossly deformed joints. Tophi may also form at the joint space. These are subcutaneous nodules containing monosodium urate crystals in a matrix of lipids, proteins, and mucopolysaccharides (Clebak et al., 2020). The first metatarsophalangeal joint is mostly affected.
Reference
Clebak, K. T., Morrison, A., & Croad, J. R. (2020). Gout: Rapid evidence review. American family physician, 102(9), 533-538.
Sample Answer 2 for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Gout patients commonly present with nephrolithiasis. The development of renal calculi in patients with gout is primarily related to high levels of uric acid. The ionized forms of uric acid form salts like monosodium urate, disodium urate, or potassium urate (Bardin et al., 2021). Sodium is the main cation in the extracellular fluid. Urine acidifies along the renal tubules, causing a portion of urate to convert to uric acid. The solubility of uric acid in an aqueous solution is lesser than that of urate, but the saturation increases markedly with the increase in the pH value of urine (Bardin et al., 2021). Gout patients with long-term high uric acid levels have increased urinary uric acid concentration and form crystals after surpassing the solubility, which gradually enlarges to shape calculus.
References
Bardin, T., Nguyen, Q. D., Tran, K. M., Le, N. H., Do, M. D., Richette, P., Letavernier, E., Correas, J. M., & Resche-Rigon, M. (2021). A cross-sectional study of 502 patients found a diffuse hyperechoic kidney medulla pattern in patients with severe gout. Kidney international, 99(1), 218–226. https://doi.org/10.1016/j.kint.2020.08.024
Jia, E., Zhu, H., Geng, H., Wang, Y., Zhong, L., Liu, S., Lin, F., & Zhang, J. (2021). Effect of alkalized urine on renal calculi in patients with gout: a protocol for a placebo-controlled, double-blinded randomized controlled trial. Trials, 22(1), 743. https://doi.org/10.1186/s13063-021-05721-8
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Sample Answer 3 for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Osteoporosis is a chronic metabolic disorder that presents with bone loss, causing a decreased bone density and increasing the risk of fracture. The commonly affected bones are the spine, hip, and wrist. Osteoporosis is diagnosed in a patient with a T-score at or below −2.5 (Akkawi & Zmerly, 2018). Common osteoporosis manifestations are loss of height, back pain with bending, lifting, or stooping, and fractures. Osteoporosis develops when bone resorption exceeds bone building, resulting in decreased bone mineral density (BMD). BMD decreases more rapidly in postmenopausal females due to decreased serum estrogen levels. Estrogen helps in preventing bone loss.
Reference
Akkawi, I., & Zmerly, H. (2018). Osteoporosis: Current Concepts. Joints, 6(2), 122–127. https://doi.org/10.1055/s-0038-1660790
Sample Answer 4 for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Scenario 3: Rheumatoid Arthritis
A 48-year-old woman presents with a five-month history of generalized joint pain, stiffness, and swelling, especially in her hands. She states that these symptoms have made it difficult to grasp objects and has made caring for her grandchildren problematic. She admits to increased fatigue, but she thought it was due to her stressful job.
FH: Grandmothers had “crippling” arthritis.
PE: remarkable for bilateral ulnar deviation of her hands as well as soft, boggy proximal interphalangeal joints. The metatarsals of both of her feet also exhibited swelling and warmth.
Diagnosis: rheumatoid arthritis.
Question:
The pt. had various symptoms, explain how these factors are associated with RA and what is the difference between RA and OA?
Your Answer:
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by inflammation of the synovial joints, which can lead to joint destruction and functional disability.
The patient’s symptoms are quite characteristic of RA. The generalized joint pain, stiffness, and swelling, particularly in the hands, are common early symptoms. The stiffness tends to be worst in the morning and after periods of inactivity, improving with physical activity. RA often affects joints symmetrically, meaning the same joints are affected on both sides of the body, as seen in this patient’s bilateral hand involvement.
The observed ulnar deviation of the hands and swollen, boggy proximal interphalangeal joints are also characteristic signs of RA, indicating ongoing joint inflammation and damage. Additionally, RA can cause systemic symptoms, such as fatigue, which the patient attributed to her stressful job. This is because RA is a systemic inflammatory condition that can affect more than just the joints.
Now, to compare Rheumatoid Arthritis (RA) with Osteoarthritis (OA):
OA is a degenerative joint disease characterized by the breakdown of the joint’s cartilage. The primary risk factors for OA include age, obesity, joint injury, overuse of the joint, and genetics. The main symptoms of OA are pain and stiffness in the affected joint, typically worsening with activity and improving with rest. OA often affects a single joint or is asymmetrical, affecting one side of the body more than the other. OA is most common in weight-bearing joints like the knees, hips, and spine, but it can also affect the fingers.
In contrast, RA is an autoimmune disease where the body’s immune system mistakenly attacks its tissues, including the joints, causing inflammation. RA typically affects multiple joints symmetrically and causes more systemic symptoms, like fatigue and occasional fever. Unlike OA, RA can occur at any age, though it is most common in middle age.
In summary, the key differences are that RA is an inflammatory, autoimmune disease, often causing symmetrical joint involvement and systemic symptoms, while OA is a degenerative disease that primarily affects high-use or weight-bearing joints, with symptoms typically worsening with activity.
Sample Answer 5 for NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4
Gout refers to chronic inflammatory arthritis characterized by the deposition of monosodium urate monohydrate crystals in tissues. Gout is relatively common with an estimated global prevalence of 1 to 4% (Dehlin et al., 2020). In the United States, gout affects more than 2 million adults (Dehlin et al., 2020). The incidence of gout increases with age as well as a family history of gout. Additionally, gout is slightly male preponderance with up to 2 to 6 times higher in males than females. The pathophysiology of gout is considered complex and multifactorial. Factors implicated in the development of gout include alcohol, medications, hypertension, hyperlipidemia, obesity, diabetes mellitus, cardiovascular disease, diet, chronic kidney disease, advanced age, ethnicity, family history, and male gender (Dehlin et al., 2020). Gout is contemplated as a disorder of metabolism resulting in the accumulation of urate and uric acid in blood and tissues. Consequently, tissues become supersaturated leading to the precipitation of urate salts forming monosodium urate crystals. The deposition of these crystals occurs in an array of tissues although the synovium, kidney, bone, ligament, skin, tendon, and cartilage are among the most common sites. Uric acid is less soluble under low temperatures and acidic conditions. Finally, microcrystals may be shed from preexisting tophi initiating an inflammatory response.
Explain why a patient with gout is more likely to develop renal calculi
Individuals with gout have high levels of urate and uric acid in their plasma. Uric acid is a weak organic acid. It exists in a less soluble non-ionized form in acid conditions such as in urine. Physiologically, uric acid production is from purine metabolism in the liver with a slight contribution from the small intestines. Similarly, the glomerulus filters almost all the urate. As a result, the entire pool of urate is managed by renal excretion in steady-state conditions. Hyperuricemia increases the urate pool which causes supersaturation and precipitation of uric acid and the formation of uric acid calculi. According to Cicerello (2018), hyperuricemia, diminished fractional excretion of uric acid, and constantly low urinary pH levels are common in patients with gout which leads to uric acid nephrolithiasis. For instance, a reduction in pH induces alterations in uric acid dissolution and acid-base status while a reduction in urine output leads to highly concentrated urinary solutes resulting in precipitation (Cicerello, 2018). Finally, individuals with gout may also develop renal calculi due to hyperuricosuria and a decrease in crystallization inhibitors such as urinary glycosaminoglycans.
Discuss what is osteoporosis and how it develops pathologically
Osteoporosis refers to low bone mineral density as a result of altered bone microstructure. Osteoporosis predisposes patients to fragility and low-impact fractures. Globally, osteoporosis affects over 200 million individuals with its incidence increasing with age. Generally, women are more affected. Osteoporosis can be primary or secondary. According to Pouresmaeili et al. (2018), primary osteoporosis is a consequence of aging and a reduction in sex hormones while other disease processes cause secondary osteoporosis. Osteoporosis develops from an imbalance between bone formation and resorption. An interplay of several factors including genetic, lifestyle, intrinsic and exogenous factors interact to cause an imbalance between bone resorption and formation leading to decreased skeletal mass (Pouresmaeili et al., 2018). For instance, with aging, bone resorption exceeds bone formation. Physiologically, bone mass peaks in the third decade. Consequently, factors that cause osteoporosis result in failure to achieve a normal peak bone mass as well as an acceleration of bone loss.
The pt. had various symptoms, explain how these factors are associated with RA and what is the difference between RA and OA
The patient had articular manifestations of rheumatoid arthritis such as polyarthralgia, morning stiffness, swelling of joints, ulnar deviation of her hands, and boggy proximal interphalangeal joints. According to Bullock et al. (2018), rheumatoid arthritis mostly affects metacarpophalangeal joints and proximal interphalangeal joints but rarely distal interphalangeal joints. Additionally, rheumatoid arthritis is a systemic disorder and hence commonly presents with constitutional symptoms such as fatigue. Rheumatoid arthritis refers to a chronic inflammatory autoimmune disorder that principally affects the joints but also causes extraarticular features (Bullock et al., 2018). On the other, osteoarthritis is a degenerative disease that results from the biochemical breakdown of articular cartilage. Osteoarthritis typically involves weight-bearing joints such as the hip, knee, and lower back while rheumatoid arthritis can affect any joint although common in hands, wrists, and feet. Similarly, osteoarthritis develops gradually over several years while rheumatoid arthritis develops acutely.
Describe what is MS and how did it cause the above patient’s symptoms
Multiple sclerosis is a chronic autoimmune disease of the central nervous system distinguished by demyelination, inflammation, neuronal loss, and gliosis (Lane & Yadav, 2020). The exact etiology of multiple sclerosis is unknown although environmental, immune, and genetic factors are involved in its pathogenesis. In multiple sclerosis, there is focal inflammation that is injurious to the blood-brain barrier and causes macroscopic plaques (Lane & Yadav, 2020). Similarly, there is microscopic injury as a result of the degeneration of various CNS components such as neurons, axons, and synapses. The aforementioned processes explain the multifocal nature of injury in multiple sclerosis and the neurological symptoms observed in this patient such as blurring of vision, tremors, difficulty concentrating, memory impairment, weakness, and difficulty voiding (Lane & Yadav, 2020). Finally, the course of multiple sclerosis varies considerably and can be remitting, relapsing, or progressive.
References
Bullock, J., Rizvi, S. A. A., Saleh, A. M., Ahmed, S. S., Do, D. P., Ansari, R. A., & Ahmed, J. (2018). Rheumatoid arthritis: A brief overview of the treatment. Medical Principles and Practice: International Journal of the Kuwait University, Health Science Centre, 27(6), 501–507. https://doi.org/10.1159/000493390
Cicerello, E. (2018). Uric acid nephrolithiasis: An update. Urologia, 85(3), 93–98. https://doi.org/10.1177/0391560318766823
Dehlin, M., Jacobsson, L., & Roddy, E. (2020). Global epidemiology of gout: prevalence, incidence, treatment patterns, and risk factors. Nature Reviews. Rheumatology, 16(7), 380–390. https://doi.org/10.1038/s41584-020-0441-1
Lane, M., & Yadav, V. (2020). Multiple Sclerosis. In Textbook of Natural Medicine (pp. 1587-1599.e3). Elsevier. https://doi.org/10.1016/b978-0-323-43044-9.00199-0
Pouresmaeili, F., Kamalidehghan, B., Kamarehei, M., & Goh, Y. M. (2018). A comprehensive overview of osteoporosis and its risk factors. Therapeutics and Clinical Risk Management, 14, 2029–2049. https://doi.org/10.2147/TCRM.S138000