NR 507 Week 6: Case Study
Chamberlain University NR 507 Week 6: Case Study– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 6: Case Study 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 NR 507 Week 6: Case Study
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 6: Case Study 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 NR 507 Week 6: Case Study
The introduction for the Chamberlain University NR 507 Week 6: Case Study 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 NR 507 Week 6: Case Study
After the introduction, move into the main part of the NR 507 Week 6: Case Study 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 NR 507 Week 6: Case Study
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 NR 507 Week 6: Case Study
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 NR 507 Week 6: Case Study
Pathophysiology and Clinical Findings of the Disease
The symptoms the 48-year-old male patient in the NR 507 Week 3: Case Study assignment reports relates to type 2 diabetes. The diagnosis has been derived from the patient’s description of his symptoms and past medical history. Besides, the condition entails the lack of adequate insulin being produced in the pancreas, leading to deficiency. The muscle and fat cells’ malfunction can prevent them from responding appropriately to insulin, causing them to absorb less sugar.
The pathophysiology of diabetes mellitus type 2 entails the failure of the B-cells to function correctly. B-cells produce insulin that helps maintain normal blood sugar levels (Galicia-Garcia et al., 2020; Mann et al., 2020). The insulin is synthesized as pre-proinsulin. Upon maturation, the pre-proinsulin undergoes modification with the help of specific proteins in the endoplasmic reticulum to become proinsulin (Galicia-Garcia et al., 2020). The proinsulin gets transported to the Golgi bodies from the endoplasmic reticulum and undergoes further modification to become insulin and C-peptide. Besides, the insulin is stored until it is ready to be released. Response to high glucose concentrations triggers the release of insulin (Galicia-Garcia et al., 2020). The B-cells take in the glucose and release it to the plasma membrane following a series of electrolyte actions in the B-cells. However, the B-cells could be impaired and fail to function as required. This patient’s case could be due to extreme nutritional conditions, including obesity and hyperlipidemia. These conditions lead to insulin resistance and chronic inflammation. Hence, the B-cells experience significant pressure, leading to their death.
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The diagnosis of type 2 diabetes in the NR 507 Week 3: Case Study patient results from subjective and objective findings. The subjective findings from this client include fatigue, extreme thirst, frequent urination at night, increased appetite, and unintended weight loss (Trikkalinou et al., 2017). The patient reports that these symptoms began around three weeks ago. He had been living normally until this period. Conversely, the objective findings leading to this diagnosis include a high fasting glucose level of 132 mg/dL, a high blood pressure of 136/80, and a BMI of 36.5 (Malone & Hansen, 2019). The objective and subjective patient information confirms that this patient has type 2 diabetes. The patient’s medical history, including obesity, hyperlipidemia, and hypertension, further support the diagnosis. Besides, the patient’s brother has the condition, indicating that genetics could have played a role in the patient developing diabetes.
Management of the Disease
Management of type 2 diabetes entails ensuring that the glucose level in the blood remains within the normal range. Medications and non-pharmacological treatments apply in this scenario. The two common medication classes for this condition are biguanides and sodium-glucose transporter (SGLT) 2 inhibitors. According to Grytsai et al. (2020), biguanides function by decreasing the amount of glucose produced by the liver. The medications also regulate the glucose absorbed in the intestines, causing the body to be more sensitive to insulin. Metformin is a common drug in this class. It is always the first drug patients are prescribed to manage the condition. The physician may combine the medication with others depending on the severity of the patient’s symptoms. The patient should take 500 mg to 2250 mg daily, depending on the physician’s observation of his symptoms. The patient can take the medication alongside or after meals.
The physician starts the dosage at low levels and increases it gradually. The patient can take the drug once to three times a day, depending on the form. The drug is suitable for this patient because it controls blood glucose levels throughout the day. By increasing the body’s sensitivity to insulin, the medication helps in weight management. However, the physician must evaluate the patient’s kidney function before administering the medication since people with advanced kidney disease may develop complications when they take this drug. Other side effects of the drug include nausea, stomach upsets, and diarrhea. The patient should also share with the physician whether he takes other drugs to avoid adverse drug interaction issues.
The other drug class for treating type 2 diabetes is sodium-glucose transporter (SGLT) 2 inhibitors. Joshi et al. (2021) indicate that the medications prevent the kidneys from holding onto glucose. Instead of maintaining glucose, the liver eliminates it through urine (Xu et al., 2022). Hence, these drugs are suitable for this patient’s condition because of his other underlying issues like obesity. The drugs also reduce the chances of cardiovascular problems, chronic kidney disease, and heart failure, possibly due to the patient’s underlying conditions. A typical drug under this medication category is dapagliflozin. The patient can take this drug with others, like metformin, based on the physician’s instructions. For instance, a physician may prescribe a dosage of 5 mg daily, which could increase to 10 mg based on the physician’s observation of the patient. The physician must monitor the patient’s kidney function before and during treatment to determine the drug’s effect on the organ.
Apart from the medications used to address type 2 diabetes mellitus, the patient can also undergo non-pharmacological treatment. The patient should strictly observe a healthy diet (Magkos et al., 2020). For example, this entails eating the healthiest foods in moderate amounts and having regular meal times. The diet should be rich in nutrients and low in calories and fats. Healthy food allows the client to control the glucose levels in the body. Foods with too much fat and calories often increase blood glucose levels. Failure to keep this level in check could lead to adverse outcomes like hyperglycemia and kidney and heart problems. Since this patient is already obese, he needs to see a dietician who would help him develop a healthy diet plan.
Another non-pharmacological treatment for type 2 diabetes entails regular physical activity. Physical activities help manage a person’s weight (Magkos et al., 2020). They help burn calories that would otherwise accumulate and increase blood sugar levels, increasing the risk of adverse effects. Being physically active improves the body’s sensitivity to insulin, helping to manage the client’s condition. Two common exercise categories suitable for this client are aerobic and resistance exercises. Aerobic exercise allows the patient to manage his blood pressure and triglyceride levels, lowering the chances of cardiovascular problems. Conversely, resistance exercise enables the client to build muscle strength and mass. Often, exercise allows the patient to manage his weight, considering that excess calories get burned up, preventing the chances of uncontrolled weight gain. Therefore, the patient must work with an exercise expert to develop a regular exercise plan.
Conclusion
The patient has type 2 diabetes mellitus. The diagnosis results from the patient’s symptoms, including fatigue, extreme thirst, frequent urination, weight loss, and increased appetite. The patient’s medical history also confirms that he is at risk of this condition, considering he has obesity and hyperlipidemia. Besides, the patient’s brother has type 2 diabetes. The most appropriate treatment for this client entails a combination of medication and non-pharmacotherapy. He can take metformin alongside dapagliflozin. He should also create a healthy diet plan and a regular exercise schedule with the assistance of relevant experts.
NR 507 Week 3: Case Study References
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., … & Martín, C. (2020). Pathophysiology of type 2 diabetes mellitus. International Journal of Molecular Sciences, 21(17), 6275.
Grytsai, O., Myrgorodska, I., Rocchi, S., Ronco, C., & Benhida, R. (2021). Biguanides drugs: Past success stories and promising future for drug discovery. European Journal of Medicinal Chemistry, 224, 113726.
Joshi, S. S., Singh, T., Newby, D. E., & Singh, J. (2021). Sodium-glucose co-transporter 2 inhibitor therapy: Mechanisms of action in heart failure. Heart, 107(13), 1032–1038.
Magkos, F., Hjorth, M. F., & Astrup, A. (2020). Diet and exercise in the prevention and treatment of type 2 diabetes mellitus. Nature Reviews Endocrinology, 16(10), 545-555. DOI: 10.1111/pedi.12787
Malone, J. I., & Hansen, B. C. (2019). Does obesity cause type 2 diabetes mellitus (T2DM)? Or is it the opposite? Pediatric diabetes, 20(1), 5–9.
Mann, E., Sunni, M., & Bellin, M. D. (2020). Secretion of insulin in response to diet and hormones. Pancreapedia: The Exocrine Pancreas Knowledge Base.
Trikkalinou, A., Papazafiropoulou, A. K., & Melidonis, A. (2017). Type 2 diabetes and quality of life. World Journal of Diabetes, 8(4), 120.
Xu, B., Li, S., Kang, B., & Zhou, J. (2022). The current role of sodium-glucose cotransporter 2 inhibitors in type 2 diabetes mellitus management. Cardiovascular Diabetology, 21(1), 83.
Sample Answer 2 for NR 507 Week 6: Case Study
Pathophysiology & Clinical Findings of the Disease
- Based on the review of the history, physical and lab findings what is the most likely diabetes diagnosis for this patient?
The patient has an elevated fasting plasma glucose (FPG) 132mg/dL, oral glucose tolerance test (OGTT) 220mg/dL, A1C is high at 7.2%, and urinalysis indicates glucose has spilled into urine since it was positive for glucose. According the American Diabetes Associations 2023 TABLE 2.2/2.5, A1C >6.5%, FPG >126,mg/dL, and OGTT >200mg/dL put him in the diabetes category DM II. He has fatigue, weight loss, and extreme thirst which are symptoms of hyperglycemia, though he is also finding himself eating more. He has hyperlipidemia. Based on the patients physical he is morbidly obese according to his BMI 36.5, weighs 240lbs and he is only 5’8, has familial history of his brother being DM II. According to the ADA’s Diabetes Risk Test, J.T. has Type II DM.
- Explain the pathophysiology associated with the chosen diabetes diagnosis.
Type II DM is because there is a decline in insulin secretion from β-cells , often with insulin resistance (American Diabetes Association, 2023). Obesity is a major contributor to insulin resistance and the development of Type 2 diabetes mellitus (McCance & Huether, 2019). With obesity there’s increased leptin production, elevated serum of free fatty acid, triglycerides and cholesterol, inflammatory cytokines, and alterations in oxidative phosphorylation in cells mitochondria that collectively contribute to the development of insulin resistance (McCance & Huether, 2019). The pancreas doesn’t secrete enough insulin and or the body is insulin resistant.
- Identify at least three subjective findings from the case which support the chosen diagnosis.
Fatigue
Polyphagia
Polydipsia
- Identify at least three objective findings from the case which support the chosen diagnosis
Obesity 240lb BMI 36.5
A1C 7.2%
FPG 132mg/dL
Management of the Disease
*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.
- Utilizes the required Clinical Practice Guideline (CPG) to support the chosen treatment recommendations.
The Clinical Practice Guideline (CPG) of the American Diabetes Association, numerous treatments exist that are both pharmacological and non-pharmacological.
- Identify two (2) “Evidence A” recommended medication classes for the treatment of this condition and provide an example (drug name) for each.
Biguanides
Metformin
GLP-1 RA
Semaglutide
- Describe the mechanism of action for each of the medication classes identified above.
Metformin functions as an antihyperglycemic agent, enhancing glucose tolerance by reducing both basal and postprandial plasma glucose levels through mechanisms distinct from other oral antidiabetic agents (Prescribers Drug Summary, n.d.). It diminishes hepatic gluconeogenesis, reduces intestinal glucose absorption, and enhances insulin sensitivity by promoting peripheral glucose uptake and utilization (Prescribers Drug Summary, n.d.).
GLP-1 RA serves as a crucial regulator of glucose homeostasis, originating from the gut, and is released following the oral consumption of carbohydrates or fats (Prescribers Drug Summary,n.d.). It inhibits the release of glucagon, delays the emptying of the stomach, diminishes food consumption, and stimulates the proliferation of beta cells (Prescribers Drug Summary, n.d.). It increases insulin production in response to increased glucose, along with gastric emptying delay (Prescribers Drug Summary, n.d.).
- Identify two (2) “Evidence A” recommended non-pharmacological treatment options for this patient.
Energy Deficit – high frequency of counseling (≥16 sessions in 6 months) and focus on nutrition changes, physical activity, and behavioral strategies to achieve a 500–750 kcal/day energy deficit (American Diabetes Association, 2023).
Weight Maintenance Program – Monthly contact and support, recommend ongoing monitoring of body weight (weekly or more frequently) and other self-monitoring strategies, and encourage regular physical activity (200–300 minutes/week (American Diabetes Association, 2023).
References
American Diabetes Association. (2023). Standards of Care in Diabetes—2023 abridged for primary care providers. Clinical Diabetes: A Publication of the American Diabetes Association, 41(1), 4–31. https://doi.org/10.2337/cd23-as01
Hartanto, D. (n.d.). Take the risk test today. Diabetes.org. https://donations.diabetes.org/site/SPageServer/?pagename=Diabetes_Risk_Test&source=ADA&cate=DgtlSOC&loca=VA&adas=90200
McCance, K., & Huether, S. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences
Prescribers Drug summary. (n.d.). https://www.pdr.net/drug-summary/?drugLabelId=892
NR 507 Case Study Week 7 Discussion Questions
Compare and Contrast the Pathophysiology between Alzheimer’s Disease and Frontotemporal Dementia
Alzheimer’s disease is a neurodegenerative disorder characterized by mild to severe impairments in one or more cognitive domains (McCance & Huether, 2019). Cells and neurons in the brain become damaged and die off over time, causing permanent changes in the brain. Two proteins in the brain are the primary subjects for the changes in the brain. The first plaque consists of sticky brain protein fragments called beta-amyloid that accumulate in nerve cell spaces as the brain ages (Alzheimer’s Association, n.d.). The second type of tangle is tau tangle, a buildup of twisted fibers within the cells (Alzheimer’s Association, n.d.).
Everyone develops plaques and tangles with age, but Alzheimer’s patients have more because of brain atrophy (Alzheimer’s Association, n.d.). These changes in the brain cause issues with thinking, memory, and behavior (Alzheimer’s Association, n.d.). Alzheimer’s disease is usually diagnosed after the age of 65; there is no cure, and symptoms vary depending on stage. Frontotemporal dementia occurs when the frontal and temporal lobes of the brain shrink; on imaging, the onset is usually less than 60 years of age. This results in the accumulation of substances in the brain (McCance & Huether, 2019). Clinical manifestations differ depending on the affected brain area and can vary from person to person. Because of the changes in personalities, impulsivity, emotional changes, and loss of speech and language, it is frequently misdiagnosed as a psychiatric disorder or Alzheimer’s disease (Alzheimer’s Association, n.d.).
Identify the Clinical Findings from the case that support a Diagnosis of Alzheimer’s Disease.
The clinical findings from the case support a diagnosis of Alzheimer’s disease, including worsening memory, getting lost in the neighborhood he has lived in for the past 35 years, being found wandering and brought home by neighbors, being angry and defensive when addressed, purchasing a security system that he already had in his home, challenges dressing and even balancing the checkbook. The patient is 76 years old, and his father died at the age of 78 due to Alzheimer’s disease deterioration.
The patient also underwent a Mini-Mental State Examination (MMSE), with a baseline score of 12 out of 30, indicating moderate dementia. With his clinical and diagnostic findings, the patient was diagnosed with Alzheimer’s type dementia.
Explain one Hypothesis that Explains the Development of Alzheimer’s Disease. The “amyloid hypothesis” is one Explanation for the Emergence of Alzheimer’s Disease
According to Stakos et al. (2020), the amyloid hypothesis is that sticky brain protein fragments known as beta-amyloid build up in the brain, disrupting cell-to-cell communication and killing brain cells (Alzheimer’s Association, 2021). The beta-amyloid protein is a factor in the development of Alzheimer’s disease. Recent studies have found a direct correlation between beta-amyloid buildup and cardiovascular disease (Stakos et al., 2020).
Discuss the Patient’s Likely Stage of Alzheimer’s Disease
According to the Alzheimer’s Association (N.D.), there are three stages of Alzheimer’s disease: Early, Middle, and Late. The patient is wandering and getting lost in a neighborhood he has lived in for 35 years, forgetfulness and confusion, moodiness, needing help getting dressed, and acting in unexpected ways, all of which indicate that he may be in the middle stage of the disease. The middle stage of Alzheimer’s disease is the longest, but the patient is still functional with assistance and supervision of daily needs (Alzheimer’s Association, N.D).
References
Alzheimer’s Association. (N.D). Stages of Alzheimer’s Disease. alz.org
https://www.alz.org/Links to an external site..
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8 ed.). Elsevier Health Sciences
Stakos, D. A., Stamatelopoulos, K., Bampatsias, D., Sachse, M., Zormpas, E., Vlachogiannis, N. I., Tual-Chalot, S., & Stellos, K. (2020). The Alzheimer’s Disease Amyloid-Beta Hypothesis in Cardiovascular Aging and Disease: JACC Focus Seminar. Journal of the American College of Cardiology, 75(8), 952–967. https://doi.org/10.1016/j.jacc.2019.12.033