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.
NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4 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.
NURS 6501 WEEK 4 Case Study Analysis
Case Study Analysis
The case study presents a 38-year-old female patient who arrives at the emergency room with symptoms of dyspnea and left leg pain. The patient has a medical history of systemic lupus erythematosus and has recently traveled by airplane. Additionally, she is using oral contraception. This paper elucidates the pulmonary pathophysiologic processes and explores the influence of racial/ethnic variables on these processes, highlighting their combined impact on the patient in question.
Pulmonary Pathophysiologic Processes
The patient exhibits dyspnea and left leg pain, which are typical symptoms of systemic lupus erythematosus (SLE). SLE can lead to various pulmonary conditions, including pleural effusion/pleuritis. This condition is characterized by chest pain, cough, dyspnea, and fluid accumulation in the pleural space (Dörner & Furie, 2019). Pleuritis, with or without pleural effusion, is a prevalent manifestation of acute pulmonary involvement in SLE. Immune complex deposits in different organs primarily cause the pathology in SLE. This activates complement and other inflammatory mediators, resulting in symptoms like leg pain and inflammation (Aringer, 2020).
Racial/Ethnic Variables
Compared to non-Hispanic Whites, Black and White Hispanics have a higher incidence and severity of SLE (Barber et al., 2021). SLE is three times more common in African-American women than in White women, and although the prevalence of SLE in Hispanic women is unknown, it is greater than in White women (Tsokos, 2020). A large percentage of Amerindian ancestry is correlated with an increased number of risk alleles for SLE, and there is abundant evidence that distinct susceptibility genes for SLE exist between Blacks and Whites or Hispanics (Fanouriakis et al., 2020).
Interaction of Processes
The patient’s medical history of systemic lupus erythematosus, recent airplane travel, and use of oral birth control may all contribute to her current clinical condition. Combined hormonal contraceptives, like the birth control pill, may be appropriate for certain lupus patients. However, caution should be exercised in individuals with highly active disease or heightened susceptibility to blood clots, such as those with positive antiphospholipid antibodies and previous instances of blood clots, among other risk factors (Basta et al., 2020). Extended periods of sitting can pose challenges for individuals with joint or muscle pain. Individuals with lupus may have an increased susceptibility to the formation of blood clots due to prolonged periods of sitting. It is advisable to take stretch breaks every hour while driving for extended periods, stand up, and frequently engage in movement during prolonged flights.
Conclusion
The patient has a history of systemic lupus erythematosus (SLE). However, she experiences flare-up symptoms due to risk factors, such as prolonged sitting during air travel. When managing this patient, it is essential to consider the genetic factors that contribute to the disease, particularly in patients from diverse racial backgrounds.
References
Aringer, M. (2020). Inflammatory markers in systemic lupus erythematosus. Journal of Autoimmunity, 110, 102374. https://doi.org/10.1016/j.jaut.2019.102374
Barber, M. R., Drenkard, C., Falasinnu, T., Hoi, A., Mak, A., Kow, N. Y., Svenungsson, E., Peterson, J., Clarke, A. E., & Ramsey‐Goldman, R. (2021). Global epidemiology of systemic lupus erythematosus. Nature Reviews Rheumatology, 17(9), 515–532. https://doi.org/10.1038/s41584-021-00668-1
Basta, F., Fasola, F., Triantafyllias, K., & Schwarting, A. (2020). Systemic Lupus erythematosus (SLE) therapy: the old and the new. Rheumatology and Therapy, 7(3), 433–446. https://doi.org/10.1007/s40744-020-00212-9
Dörner, T., & Furie, R. (2019). Novel paradigms in systemic lupus erythematosus. The Lancet, 393(10188), 2344–2358. https://doi.org/10.1016/s0140-6736(19)30546-x
Fanouriakis, A., Tziolos, N., Βertsias, G., & Boumpas, D. T. (2020). Update οn the diagnosis and management of systemic lupus erythematosus. Annals of the Rheumatic Diseases, 80(1), 14–25. https://doi.org/10.1136/annrheumdis-2020-218272
Tsokos, G. C. (2020). Autoimmunity and organ damage in systemic lupus erythematosus. Nature Immunology, 21(6), 605–614. https://doi.org/10.1038/s41590-020-0677-6