NUR-631 Topic 13 DQ 2

Grand Canyon University NUR-631 Topic 13 DQ 2– Step-By-Step Guide

This guide will demonstrate how to complete the Grand Canyon University NUR-631 Topic 13 DQ 2 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 NUR-631 Topic 13 DQ 2              

Whether one passes or fails an academic assignment such as the Grand Canyon University NUR-631 Topic 13 DQ 2  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 NUR-631 Topic 13 DQ 2              

The introduction for the Grand Canyon University NUR-631 Topic 13 DQ 2 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.

How to Write the Body for NUR-631 Topic 13 DQ 2              

After the introduction, move into the main part of the NUR-631 Topic 13 DQ 2 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 NUR-631 Topic 13 DQ 2              

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 NUR-631 Topic 13 DQ 2              

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 NUR-631 Topic 13 DQ 2

Both osteoarthritis and rheumatoid arthritis present with several of the same manifestations, such as joint pain and stiffness. How do the two disorders differ? 

Osteoarthritis is characterized by local areas of articular cartilage damage causing bone-to-bone connection by enzymatic destruction clinical evidence of OA is seen during the fifth or sixth decade of life. In addition, primary OA is idiopathic, progressive, not related to predisposing events of injury ie trauma, strains, dislocation, fractures, long-term mechanical stress overuse, chronic disease of DM, ochronosis, and hemochromatosis, and if certain medications are responsible for OA are colchicine, indomethacin, and steroids then it’s classified as secondary osteoarthritis. Moreover, the most affected joints include the hip, knees, lower lumbar and cervical vertebrae, proximal and distal interphalangeal joints of the fingers diagnose as Heberden nodes and Bouchard nodes (McCance et al., 2018). 

             Classic inflammatory joint disease, arthritis is characterized by damage or destruction in the synovial membrane or articular cartilage and by systemic signs of inflammation of fever, leukocytosis, malaise, anorexia, hyperfibrinogenemia, infectious or noninfectious, infection by bacteria, mycoplasmas, viruses, fungi, or protozoa, invasion of these pathogens causes a systemic reaction that invades bones, heart, and blood vessels. Furthermore, noninfectious inflammatory joint diseases like gout where deposits of crystals of monosodium urate inside and around a joint can lead to rheumatoid arthritis. Rheumatoid arthritis (RA) is chronic systemic inflammation and the primary joint tissue to be affected is the synovial membrane which is attacked by several inflammatory enzymes the combination of autoimmune genetic involvement ie HLA is most significant in these patients. In evidence of the clinical evaluation between OA and RA, there is many similarities but RA is an autoimmune systemic there is bilateral joint on the hands, feet, and does tend to affect at any age and therefore classification criteria is used for RA by using categories due to its complexity this can categories the principal of RA if the score is equal or > 6 of 10 for RA vs OA where clinical evaluation can subjective assessment usually in one side asymmetric involvement of the large joints and degenerative(McCance et al., 2018). 

A child born with osteogenesis imperfecta is at risk for pathological fractures. Explain the pathophysiology of this disorder and the associated risk factors. 

Osteogenesis imperfecta (OI) or brittle bone disease in collagen-related dysplasia; synthesis of collagen type I multiple genetic defects and characterized by fragile bones, skin, abnormal teeth, and weak tendons; mutation in genes encoding α1 and α2 collagen chains in single base substitutions used to convert glycine in Gly-X-Y repeat to bulk amino acid and hampering the folding of the collagen chains into the triple helix presentation. In addition, Type I collagen in bones defines the bones that are predominantly affected, and clinical variability characterized by bone fragility, osteopenia, variable degrees of stature, and progressive skeletal deformities are among the complexity of risk factors. Moreover, OI with osteoporosis increases the rate of bone fractures, bony deformation, triangular facies, and vascular weakness like aortic aneurysm, which are all associated risk factors according to the newer classifications based on the model of inheritance, identifying the defective genes, or mechanisms (McCance et al., 2018). 

McCance, K. L., & Huether, S. E. (2018). Pathophysiology – e-book (8th ed.). Elsevier Health Sciences. 

Sample Answer 2 for NUR-631 Topic 13 DQ 2

Both osteoarthritis and rheumatoid arthritis present with several of the same manifestations, such as joint pain and stiffness. How do the two disorders differ? 

Arthritis encompasses joint inflammation. RA and OA are two types of arthritis. RA and OA are distinct manifestations of the same illness that damage joints. OA is a degenerative joint disease, while RA is autoimmune. Autoimmune diseases like RA harm the body. In RA, your body assaults the soft lining around your joints like a virus or bacteria(Mohammed et al., 2020). This assault promotes joint fluid buildup. Fluid buildup causes swelling, joint discomfort, stiffness, and inflammation. 

 The most common form of arthritis, OA, is degenerative. OA damages joint cartilage. Bones rub due to cartilage wear. Exposing tiny nerves causes agony. Unlike RA, OA causes minimal inflammation. Women have greater arthritis than men(McCance et al., 2019). RA and OA are more common in elderly persons, but anybody can get them. RA is hereditary. If a parent, child, or sibling has it, your risk increases. Overweight, joint abnormalities, diabetes, gout, and joint trauma increase your risk of OA. Systemic diseases like RA can damage your lungs, heart, eyes, and joints. 

Low-grade fever, especially in youngsters, muscle aches, and weariness can indicate RA. Advanced RA patients may develop hard lumps near joints. Rheumatoid nodules can hurt. Small joints start RA. Finger joints may hurt, swell, and stiffen. RA can affect knees, shoulders, and ankles as it advances. OA patients rarely have symptoms. OA alone degenerates’ joints. Rheumatoid nodules are different from joint-area lumps. Bone spurs near joint margins are common in OA patients(Mohammed et al., 2020). 

Asymmetrical OA. One knee may hurt more than the other. Arthritis is incurable. Both methods of arthritis treatment aim to alleviate pain, symptoms, and joint damage. NSAIDs like ibuprofen reduce swelling and pain in both forms of arthritis(Mohammed et al., 2020). Because RA is an autoimmune condition, medications are administered to inhibit the immune system and limit antibody generation, reducing flare-ups and damage. Physical and occupational therapy increase mobility and everyday routines. Both conditions require exercise, weight management, and good living. 

A child born with osteogenesis imperfecta is at risk for pathological fractures. Explain the pathophysiology of this disorder and the associated risk factors. 

Mutations in the type I procollagen genes COL1A1 and COL1A2 cause osteogenesis imperfecta (OI), a bone fragility disorder. Ol is also called Lobstein disease, brittle-bone disease, blue-sclera syndrome, and fragile-bone disease. Skeletal dysplasia includes Ol (Deguchi et al., 2021). It is a connective tissue disorder that can cause blue sclerae, triangular facies, and macrocephaly. Hearing loss, Defective dentition, Barrel chest, Scoliosis, Limb abnormalities, Fractures, Joint laxity, Growth retardation. 

Ol is hereditary and incurable. The condition needs comprehensive treatment. Bone-building procedures are common. Orthotics fix loose joints and prevent increasing deformities and fractures (Deguchi et al., 2021). Walking aids, adapted wheelchairs, and home adaptation equipment are more critical for patient mobility and function. Surgery is still a key treatment, but only if it can improve function and the goals are clear. Bone, ligament, dentin, and sclera, which contain type 1 collagen, show pathologic alterations in Ol. Type 1 collagen is reduced. Mutations in type 1 collagen genes affect one of the two genes, causing 80% of Ol cases(McCance et al., 2019). 

Hereditary risk is greatest. If one parent has osteogenesis imperfecta, a child has a 50% chance. Most osteogenesis imperfecta cases are hereditary(McCance et al., 2019). Recessive inheritance passes rare forms. 35% of osteogenesis imperfecta children have no family history. Gene mutations cause this. Parents didn’t cause it. Brittle bone disease is treated to reduce its symptoms as there is no cure. Muscle and bone growth. Reduce fractures. Aligning bones. Musculoskeletal optimization. maximizing growth and health. 

References 

Deguchi, M., Tsuji, S., Katsura, D., Kasahara, K., Kimura, F., & Murakami, T. (2021). Current Overview of Osteogenesis Imperfecta. Medicina (Kaunas, Lithuania), 57(5), 464. https://doi.org/10.3390/medicina57050464 

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2019). Pathophysiology: The biologic basis for disease in adults and children. Elsevier. 

Mohammed, A., Alshamarri, T., Adeyeye, T., Lazariu, V., McNutt, L. A., & Carpenter, D. O. (2020). A comparison of risk factors for osteo- and rheumatoid arthritis using NHANES data. Preventive medicine reports, 20, 101242. https://doi.org/10.1016/j.pmedr.2020.101242 

Sample Answer 3 for NUR-631 Topic 13 DQ 2

Both osteoarthritis and rheumatoid arthritis present with several of the same manifestations, such as joint pain and stiffness. How do the two disorders differ? 

Rheumatoid arthritis and osteoarthritis are both diseases of the joint however, they have different etiologies. Osteoarthritis is a disease that is the result of wear and tear on the joints over time while rheumatoid arthritis is an autoimmune disease where joint tissues are attacked by the body’s immune system. Osteoarthritis is degenerative where the cartilage or cushion between the joints breakdown. This leads to pain, swelling, and stiffness. Osteoarthritis generally affects the weight-bearing joints, such as the knees and hips. Osteoarthritis is generally asymmetrical. Rheumatoid arthritis most often affects the small joints of the hands and feet and is usually symmetrical. Diagnosis of osteoarthritis is based on the patient’s history, physical examination, and radiographic evidence such as xray, MRI, or CT. Rheumatoid arthritis is also diagnosed based on the patient’s history and physical examination which will indicate synovitis in multiple joints (Mohammed, et al., 2020). 

A child born with osteogenesis imperfecta is at risk for pathological fractures. Explain the pathophysiology of this disorder and the associated risk factors. 

Osteogenesis imperfecta is also known as brittle bone disease. It is a disorder of collagen-related bone dysplasia. The manifestations of osteogenesis imperfecta are due to errors in the synthesis of collagen. The severity of the disease is based upon the genetic anomaly and the part of the triple helix of the collagen that is affected. (McCance & Heuther, 2019). 

Mohammed, A., Alshamarri, T., Adeyeye, T., Lazariu, V., McNutt, L., Carpenter, D. (2020). A comparison of risk factors for osteo- and rheumatoid arthritis using NHANES data. Preventive Medicine Reports, 20, 101242. https://doi.org/10.1016/j.pmedr.2020.101242 

McCance, K., Huether, S. (2019). Pathophysiology: The Biologic Basis for Disease in Adults and Children. (8th ed.) Elsevier.