NURS 6501 ENDOCRINE DISORDERS MODULE 4
Walden University NURS 6501 ENDOCRINE DISORDERS MODULE 4– Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 ENDOCRINE DISORDERS MODULE 4assignment 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 ENDOCRINE DISORDERS MODULE 4
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 ENDOCRINE 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 ENDOCRINE DISORDERS MODULE 4
The introduction for the Walden University NURS 6501 ENDOCRINE 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 ENDOCRINE DISORDERS MODULE 4
After the introduction, move into the main part of the NURS 6501 ENDOCRINE 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 ENDOCRINE 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 ENDOCRINE 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 ENDOCRINE DISORDERS MODULE 4
The NURS 6501 ENDOCRINE DISORDERS MODULE 4 discussion question is about a 77-year-old female patient brought to the hospital by her daughter with complains that have led her being diagnosed with syndrome of inappropriate antidiuretic hormone. Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder characterized by the increased release of antidiuretic hormones. There is the inability to suppress the secretion of the ADH hormone leading to water toxicity. The kidneys cannot excrete excess water due to too much reabsorption, hence, hyponatremia. Patient factors contribute to the development of SIADH. One of them as seen in this case study is medications use. Some medications increase the patient’s risk of developing SIADH when used for a long time. They include drugs such as antidepressants, seizure medications, diabetes, cancer, and hypertension treatment drugs(Kim, 2022). The patient in the case study is currently using drugs such as metformin and escitalopram, which have an elevated risk of SIADH.
Predisposing Conditions
Respiratory conditions such as acute respiratory failure, tuberculosis, and pneumonia also predispose patients to developing the disorder. The patient in the case study has a history of emphysema, which could precipitate other respiratory complications associated with SIADH. Disorders of the nervous system have also been linked with the development of SIADH in some patients. Accordingly, conditions such as head injury, tumors, stroke, and meningitis carry an increased risk of SIADH because of the involvement of the brain. The patient in the case study has neuropathy due to diabetes mellitus. In addition, she is at a risk of developing diabetes-related complication such as stroke. The fact that she experienced slight confusion and stumbling at home could indicate stroke (Mentrasti et al., 2020). Therefore, additional investigations should be conducted to rule out SIADH secondary to neurological conditions such as stroke.
References
Kim, G.-H. (2022). Pathophysiology of Drug-Induced Hyponatremia. Journal of Clinical Medicine, 11(19), Article 19. https://doi.org/10.3390/jcm11195810
Mentrasti, G., Scortichini, L., Torniai, M., Giampieri, R., Morgese, F., Rinaldi, S., & Berardi, R. (2020). Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Optimal Management. Therapeutics and Clinical Risk Management, 16, 663–672. https://doi.org/10.2147/TCRM.S206066
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Sample Answer 2 for NURS 6501 ENDOCRINE DISORDERS MODULE 4
This discussion question is about a 14-year-old girl that has been brought to the pediatrician’s office with complains of weight loss despite eating more, frequent urination, fatigue, and unquenchable thirst that has interfered with her school activities. The patient has been diagnosed with type 1 diabetes mellitus. Type 1 diabetes mellitus is a disorder characterized by the lack of insulin needed for the regulation of the normal blood glucose levels(Acharya et al., 2021). The patients present with symptoms that include polyuria, polydipsia, and polyphagia.
Polydipsia is an increase in thirst. Patients with type 1 diabetes mellitus often complain of an insatiable thirst. Patients with this disorder develop polydipsia because of the elevated blood glucose levels. The elevation results in the stimulation of the kidneys to excrete the excess glucose via the urine leading to glycosuria. On the other hand, the loss of fluids via the kidneys stimulates the brain to raise thirst level for the patient to take fluids to replace the loss (Del Chierico et al., 2022). Diabetes also causes osmotic diuresis, which is associated with dehydration and the increased need for body fluids.
Polyuria is the passage of urine more than normal. It is mostly more than 1-2 liters daily. As noted above an elevated blood glucose level results in the brain stimulating the kidneys to pass more urine, as a way of losing the excess glucose in it. The kidneys are stimulated to filter out more water, which increases the frequency, urgency, and volume of urine being passed. Polyphagia refers to excessive hunger. Patients with diabetes mellitus type I experience hunger because of glucose resistance. The glucose in the blood stream cannot enter the cells for metabolism due to the lack of insulin (Acharya et al., 2021). As a result, the cells continue being starved despite the high level of glucose, hence polyphagia.
References
Acharya, S., Shukla, S., & Vaswani, R. (2021). Pathophysiology of Complication in Diabetes Mellitus. Journal of Pharmaceutical Research International, 89–95. https://doi.org/10.9734/jpri/2021/v33i60A34459
Del Chierico, F., Rapini, N., Deodati, A., Matteoli, M. C., Cianfarani, S., &Putignani, L. (2022). Pathophysiology of Type 1 Diabetes and Gut Microbiota Role. International Journal of Molecular Sciences, 23(23), Article 23. https://doi.org/10.3390/ijms232314650
Sample Answer 3 for NURS 6501 ENDOCRINE DISORDERS MODULE 4
Scenario 3: Type II DM
A 55-year-old male presents with complaints of polyuria, polydipsia, polyphagia, and weight loss. He also noted that his feet on the bottom are feeling “strange” “like ants crawling on them” and noted his vision is blurry sometimes. He has increased an increased appetite, but still losing weight. He also complains of “swelling” and enlargement of his abdomen.
PMH: HTN – well controlled with medications. He has mixed hyperlipidemia, and central abdominal obesity. Physical exam unremarkable except for decreased filament test both feet. Random glucose in office 333 mg/dl.
Diagnosis: Type II DM and prescribes oral medication to control the glucose level and also referred the patient to a dietician for dietary teaching.
Question:
- How would you describe the pathophysiology of Type II DM?
Your Answer:
Type II diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by resistance to the effects of insulin, impaired insulin secretion, and excessive or inappropriate glucagon secretion.
Insulin Resistance
In the early stages of T2DM, the body’s cells become resistant to the effects of insulin, a hormone produced by the pancreas that facilitates the entry of glucose into cells for energy production. The exact mechanisms of insulin resistance are complex and multifactorial, involving genetic factors, obesity (especially central abdominal obesity, as seen in this patient), physical inactivity, poor diet, and other lifestyle factors.
When the body’s cells are insulin resistant, more insulin is required to keep blood glucose levels within the normal range. The pancreas responds by increasing the production of insulin, leading to a state of hyperinsulinemia.
Beta-cell Dysfunction
Over time, the pancreatic beta cells, which produce insulin, cannot keep up with the body’s increased demand for insulin. This insulin deficiency leads to elevated levels of blood glucose, or hyperglycemia, a hallmark sign of diabetes. The persistent high blood glucose levels can lead to glucotoxicity, which further deteriorates beta-cell function and insulin secretion.
Inappropriate Glucagon Secretion
In T2DM, the alpha cells of the pancreas, which secrete the hormone glucagon, are not suppressed by high glucose levels as they should be. This leads to an excessive release of glucagon, which promotes the conversion of stored glycogen in the liver into glucose, further exacerbating hyperglycemia.
In the patient’s case, the symptoms of polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), and unexplained weight loss, along with his history of central obesity and high blood pressure, are typical manifestations of T2DM.
NURS 6501 WEEK 5 Gastrointestinal Disorders
Concept Map Template
Primary Diagnosis: Acute diverticulitis
- Describe the pathophysiology of the primary diagnosis in your own words. What are the patient’s risk factors for this diagnosis?
Pathophysiology of Primary Diagnosis | |
Diverticulitis occurs due to perforations in the wall of the diverticula, which can be either microscopic or macroscopic. Earlier, practitioners believed that the blockage of the colonic diverticulum by fecaliths resulted in elevated pressure within the diverticulum, leading to perforation (Piccioni et al., 2021). It is currently theorized that high luminal pressure is caused by food particles, which subsequently result in erosion of the diverticular wall. This results in localized inflammation and tissue death, leading to perforation. The mesenteric fat can potentially have micro-perforations. These complications may include the formation of local abscesses, the development of fistulas in nearby organs, or intestinal obstruction. Untreated frank bowel wall perforations can result in peritonitis and mortality if not promptly diagnosed and treated. | |
Causes | Risk Factors (genetic/ethnic/physical) |
Diverticular disease arises from the inflammation of the diverticula, which are small bulges that form in the large intestine. Infection of diverticula results in symptoms of diverticulitis. The etiology of diverticula formation remains uncertain; however, a notable association has been observed between insufficient dietary fiber intake and their development (Turner et al., 2021). | Turner et al. (2021) suggest a hereditary nature of diverticulitis, with a potential gene association, particularly prevalent among families. Insufficient presence of beneficial bacteria in the colon can lead to the development of this condition. Obesity is a significant risk factor for the development of diverticulitis. Cigarette smokers have a higher likelihood of developing diverticulitis compared to individuals who do not smoke—physical inactivity. |
- 2. What are the patient’s signs and symptoms for this diagnosis? How does the diagnosis impact other body systems, and what are the possible complications?
Signs and Symptoms – Common presentation | How does the diagnosis impact each body system? Complications? |
The clinical presentation of acute diverticulitis exhibits variability by the disease’s severity. Due to the tendency of diverticulitis to occur on the left side of the body in Western countries, patients with simple cases usually have lower quadrant stomach discomfort. Patients of Asian descent commonly exhibit right-sided abdominal pain. The pain may indicate either a continuous or sporadic pattern. Sugi et al. (2020) found that abdominal pain can be associated with changes in bowel habits, such as diarrhea (35%) or constipation (50%). Patients may experience vomiting and nausea, potentially due to bowel obstruction. Fever frequently occurs in patients who have abscesses and perforation. When the inflammatory part of the intestine comes into direct touch with the bladder wall, patients may have dysuria, frequency, and urgency. This condition is known as sympathetic cystitis. | Approximately 25% of individuals experiencing acute diverticulitis may encounter complications such as abscess formation, bowel obstruction due to scarring, the development of abnormal connections (fistulas) between different sections of the bowel or between the bowel and other organs, and peritonitis resulting from the rupture of an infected or inflamed pouch, leading to the release of intestinal contents into the gut (Sugi et al., 2020). |
- 3. What is another potential diagnosis that presents similarly to this diagnosis (differentials)?
According to Qaseem et al. (2022), other conditions might be considered in the differential diagnosis of acute diverticulitis, such as Crohn’s disease, acute appendicitis, colitis, and colon cancer.
- 4. What diagnostic tests or labs would you order to rule out the differentials for this patient or confirm the primary diagnosis?
Clinical diagnosis of acute diverticulitis may be established only by evaluating the patient’s medical history and physical examination. Leukocytosis and increased levels of acute phase reactants, such as ESR and CRP, may be detected using laboratory testing (Sugi et al., 2020). The preferred radiographic examination for diagnosing acute diverticulitis is a computed tomography (CT) scan of the abdomen and pelvis. It is recommended to use water-soluble oral or rectal contrast, along with intravenous contrast, unless there are any reasons to avoid it. It is advisable to schedule a colonoscopy around six to eight weeks after the symptoms have subsided to exclude the possibility of cancer, inflammatory bowel disease, or colitis, especially if the patient has not had a colonoscopy recently (Rottier et al., 2019).
- 5. What treatment options would you consider? Include possible referrals and medications.
The conventional approach of treating diverticulitis in an outpatient setting involves abstaining from food intake, increasing fluid consumption, and administering oral antibiotics that target gram-negative rods and anaerobic bacteria. In the United States, the most often prescribed treatment involves the use of quinolones or sulfa medications together with metronidazole or amoxicillin-clavulanate as a single agent. This treatment regimen typically lasts for a duration of 7 to 10 days (Sagar, 2019). Nurses must aid in instructing the patient on adherence to dietary limitations. An infectious disease specialist and a gastroenterologist must ascertain the optimal period of antibiotic treatment, while a general surgeon must establish a care regimen for any pelvic abscess.
References
Piccioni, A., Franza, L., Brigida, M., Zanza, C., Torelli, E., Petrucci, M., Nicolò, R., Covino, M., Candelli, M., Saviano, A., Ojetti, V., & Franceschi, F. (2021). Gut microbiota and acute diverticulitis: Role of probiotics in managing this delicate pathophysiological balance. Journal of Personalized Medicine, 11(4), 298. https://doi.org/10.3390/jpm11040298
Qaseem, A., Etxeandia-Ikobaltzeta, I., Lin, J. S., Fitterman, N., Shamliyan, T. A., & Wilt, T. J. (2022). Diagnosis and Management of Acute Left-Sided Colonic Diverticulitis: A clinical guideline from the American College of Physicians. Annals of Internal Medicine, 175(3), 399–415. https://doi.org/10.7326/m21-2710
Rottier, S. J., Van Dijk, S. T., Van Geloven, A. a. W., Schreurs, W. H., Draaisma, W. A., Van Enst, W. A., Puylaert, J. B. C. M., De Boer, M., Klarenbeek, B., Otte, J. A., Felt, R. J. F., & Boermeester, M. A. (2019). Meta-analysis of the role of colonoscopy after an episode of left-sided acute diverticulitis. British Journal of Surgery, 106(8), 988–997. https://doi.org/10.1002/bjs.11191
Sagar, A. (2019). Management of acute diverticulitis. British Journal of Hospital Medicine, 80(3), 146–150. https://doi.org/10.12968/hmed.2019.80.3.146
Sugi, M., Sun, D., Menias, C. O., Prabhu, V., & Choi, H. H. (2020). Acute diverticulitis: Key features for guiding clinical management. European Journal of Radiology, 128, 109026. https://doi.org/10.1016/j.ejrad.2020.109026
Turner, G. A., O’Grady, M. J., Purcell, R., & Frizelle, F. (2021). Acute diverticulitis in Young Patients: A review of the changing Epidemiology and etiology. Digestive Diseases and Sciences, 67(4), 1156–1162. https://doi.org/10.1007/s10620-021-06956-w