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.
Sample Answer 4 for NURS 6501 ENDOCRINE DISORDERS MODULE 4
Scenario 1
Syndrome of inappropriate antidiuretic hormone release (SIADH) is a disorder that is characterized by the unregulated release of antidiuretic hormone (ADH). ADH is a hormone that is involved in the regulation of water reabsorption in the kidney tubules. The pituitary gland produces it. The 77-year-old female has been diagnosed with SIADH. Several patient characteristics may have contributed to her developing the disorder. One of them is the use of medications. Medications such as those utilized in the treatment of depression and diabetes increase the risk of SIAD. The patient in the case study is diabetic and currently uses metformin to manage her blood sugar levels(Bal et al., 2022). She also has depression and uses escitalopram, which is among the risk factors associated with SIADH.
The other patient characteristic that may have contributed to the development of SIADH in the patient is neurological deficits. The patient currently suffers from peripheral neuropathy because of diabetes. Neurological disorders increase the risk of SIADH. The patient also has symptoms similar to those seen in patients suffering from stroke. Stroke is among the neurological disorders that increase the risk of patients developing SIADH. The signs and symptoms of stroke include unilateral paralysis, losing balance, and slurred or difficulty speaking. The patient in the case study demonstrates these symptoms. She may be suffering from early stages of stroke, which is a risk factor for SIADH. The patient may also have unknown hereditary SIADH. Hereditary SIADH also known as nephrogenic SIADH arises from vasopressin 2 mutations and may be transmitted from one family member to another (Harrois& Anstey, 2019). Therefore, history about the disease in the family should be obtained to rule out hereditary SIADH.
References
Bal, C., Gompelmann, D., Krebs, M., Antoniewicz, L., Guttmann-Ducke, C., Lehmann, A., Milacek, C. O., Gysan, M. R., Wolf, P., Jentus, M.-M., Steiner, I., &Idzko, M. (2022). Associations of hyponatremia and SIADH with increased mortality, young age and infection parameters in patients with tuberculosis. PLOS ONE, 17(10), e0275827. https://doi.org/10.1371/journal.pone.0275827
Harrois, A., & Anstey, J. R. (2019). Diabetes Insipidus and Syndrome of Inappropriate Antidiuretic Hormone in Critically Ill Patients. Critical Care Clinics, 35(2), 187–200. https://doi.org/10.1016/j.ccc.2018.11.001
Scenario 2
Patients suffering from type 1 diabetes mellitus often experience symptoms that include polydipsia, polyphagia, and polyuria. Polydipsia refers to excessive thirst. Patients with type 1 diabetes mellitus develop excessive thirst due to several reasons. One of them is the excessive loss of fluids via the kidneys. Patients with this disorder have hyperglycemia. Under normal circumstances, the kidneys excrete negligible amounts of glucose. In diabetes mellitus type 1, the high level of glucose in the blood must be excreted in the urine, which causes fluid imbalances, hence, unsatiable thirst (Donath et al., 2019). Patients may also develop symptoms such as diarrhea and vomiting, which causes fluid and electrolyte imbalances, hence, polydipsia.
Polyuria refers to the passage of large amounts of dilute urine. As noted above, patients with type 1 diabetes mellitus have elevated blood glucose levels. The brain senses the elevated levels and stimulate glucose excretion through the kidneys with urine. As a result, patients report passing large amounts of urine frequently as part of the symptoms of type 1 diabetes mellitus. Polyphagia refers to increased appetite. Patients with type 1 diabetes mellitus lack insulin in their bodies. This means that the glucose in the blood cannot be moved into the cells for use for metabolism and undertaking cellular activities. The lack of glucose movement into the cells and tissues lowers energy production, with cells demanding more energy for optimum functioning, hence, the increased appetite. The brain stimulates the hunger centers to increase the need for food intake to meet the demands of the cells and tissues(Roep et al., 2019). Therefore, despite the high glucose levels in the blood, the cells do not get enough supplies for their functioning, leading to polyphagia.
References
Donath, M. Y., Dinarello, C. A., & Mandrup-Poulsen, T. (2019). Targeting innate immune mediators in type 1 and type 2 diabetes. Nature Reviews Immunology, 19(12), Article 12. https://doi.org/10.1038/s41577-019-0213-9
Roep, B. O., Wheeler, D. C. S., &Peakman, M. (2019). Antigen-based immune modulation therapy for type 1 diabetes: The era of precision medicine. The Lancet Diabetes & Endocrinology, 7(1), 65–74. https://doi.org/10.1016/S2213-8587(18)30109-8
Scenario 3
The patient in the case study has been diagnosed with type 1 diabetes mellitus. A correlation exists between genetics, environmental exposures, and type 1 diabetes mellitus. Genetic and environmental exposure interaction affect the development of the disease as well as response to treatment. The influence of genetics is evidence in individuals born to families with a history of diabetes mellitus. The susceptibility is estimated to be at least 80% in twin and family studies. Several genetic mutations have been shown to raise the risk of an individual developing type 1 diabetes mellitus. For example, the RAB38 gene mutation has been shown to increase the risk of type 1 diabetes and kidney disease in the affected populations. The major histocompatibility complex is also noted to contribute to about 4-50% of the familiar aggregation of type 1 diabetes mellitus (Blanter et al., 2019). Alles such as the human leukocyte antigen cause polymorphisms of class II human leukocyte antigen, a determinant of type 1 diabetes mellitus.
Environmental factors also contribute to the development of type 1 diabetes mellitus. For example, studies conducted in regions such as China shows that the risk of type 1 diabetes increases as one resides further aware from the equator. Environmental factors also cause changes in the autoantibody profiles of the populations, raising their susceptibility to type 1 diabetes mellitus. Additional aspects such as infant nutrition have also been identified as the risk factors for type 1 diabetes mellitus. The use of supplements for maternal breastmilk have been associated with the disease. Seasonal variations have also been shown to raise the risk of the disease among children (Cerna, 2020). Therefore, a strong correlation exists between type 1 diabetes mellitus, genetics, and environmental influences.
References
Blanter, M., Sork, H., Tuomela, S., & Flodström-Tullberg, M. (2019). Genetic and Environmental Interaction in Type 1 Diabetes: A Relationship Between Genetic Risk Alleles and Molecular Traits of Enterovirus Infection? Current Diabetes Reports, 19(9), 82. https://doi.org/10.1007/s11892-019-1192-8
Cerna, M. (2020). Epigenetic Regulation in Etiology of Type 1 Diabetes Mellitus. International Journal of Molecular Sciences, 21(1), Article 1. https://doi.org/10.3390/ijms21010036
Scenario 4
Type 2 diabetes mellitus is a type of diabetes that is characterized by the inadequate production of insulin by the pancreas. The insulin is essential for moving glucose into the cells for use in cell and tissue metabolism. The lack of adequate insulin results in the increase in the blood glucose level, leading to hyperglycemia. Patients with type 2 diabetes mellitus present the hospital with complaints such as polyuria, polydipsia, and polyphagia. Polyuria develops due to the brain stimulation of the kidneys to excrete excess glucose through urine. Patients also develop polydipsia. This refers to the increased thirst that patients report. The thirst arises from the excessive fluid loss from the body through the kidneys, as it tries to eliminate the excess glucose. Patients may also develop vomiting, which causes dehydration, fluid and electrolyte imbalances, and increased need for fluid intake. Polyphagia refers to the patients complaining of frequent hunger. The hunger arises from the decreased glucose supply to the cells(Galicia-Garcia et al., 2020). The inadequate production of insulin results in lowered movement of glucose to the cells, hence, low energy production. The body must meet its energy needs by stimulating increased food intake, which results in polyphagia.
Individuals develop type 2 diabetes mellitus because of several risk factors. One of them is genetics. Individuals that are born to families with individuals affected by type 2 diabetes mellitus are highly at a risk of developing the disease because of the inheritance of gene mutations. The other risk factor is sedentary lifestyle. Minimal engagement in active physical activity increases the risk of the disease due to obesity and overweight problems(Padhi et al., 2020). Unhealthy lifestyle such as poor diet also increases the risk.
References
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020). Pathophysiology of Type 2 Diabetes Mellitus. International Journal of Molecular Sciences, 21(17), Article 17. https://doi.org/10.3390/ijms21176275
Padhi, S., Nayak, A. K., & Behera, A. (2020). Type II diabetes mellitus: A review on recent drug based therapeutics. Biomedicine & Pharmacotherapy, 131, 110708. https://doi.org/10.1016/j.biopha.2020.110708
Scenario 5
Hypothyroidism is a thyroid disorder that is characterized by low levels of thyroid hormones. Thyroid hormones play essential roles such as regulating body’s metabolism rate. Several factors cause hypothyroidism. One of them is the excessive use of medications used to treat hyperthyroidism. Overdose of thyroid medications may cause severely low levels of thyroid hormones, leading to the disorder. The other cause is thyroid surgery. Total or partial removal of thyroid gland due to causes such as cancer may result in hypothyroidism(Gosi& Garla, 2022). The surgery may alter the normal functioning of the thyroid gland, leading to hypothyroidism.
The other cause of hypothyroidism is iodine deficiency. Iodine is a crucial ingredient needed for the development of thyroid hormones. Dietary sources such as salt are good sources of iodine. Inadequate dietary supplementation of iodine may result in hypothyroidism. Hypothyroidism may also develop from autoimmune disorders. Autoimmune diseases of the thyroid gland cause destruction of thyroid cells, causing reduced production of thyroid hormones. Treatments such as thyroid radioactive iodine therapy also cause hypothyroidism. Accordingly, it lowers the functioning ability of the thyroid gland, resulting in the reduced production of thyroid hormones.
The pituitary gland regulates the secretion of thyroid hormones. Any problems that affect the gland may also alter the production of the thyroid hormones, hence, hypothyroidism. Cancer treatments with medications such as anti-PD-L1/PD-1 therapy also cause hypothyroidism(Patil et al., 2022). They cause immunosuppression, which lowers the thyroid ability to produce thyroid hormones for use in body’s metabolism.
References
Gosi, S. K. Y., & Garla, V. V. (2022). Subclinical Hypothyroidism. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK536970/
Patil, N., Rehman, A., & Jialal, I. (2022). Hypothyroidism. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK519536/