Knowledge Check: Endocrine Disorders NURS 6501

Knowledge Check: Endocrine Disorders NURS 6501

Walden University Knowledge Check: Endocrine Disorders NURS 6501-Step-By-Step Guide

 

This guide will demonstrate how to complete the Walden University  Knowledge Check: Endocrine Disorders NURS 6501 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 Knowledge Check: Endocrine Disorders NURS 6501

 

Whether one passes or fails an academic assignment such as the Walden University  Knowledge Check: Endocrine Disorders NURS 6501 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  Knowledge Check: Endocrine Disorders NURS 6501 

 

The introduction for the Walden University  Knowledge Check: Endocrine Disorders NURS 6501 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  Knowledge Check: Endocrine Disorders NURS 6501 

 

After the introduction, move into the main part of the  Knowledge Check: Endocrine Disorders NURS 6501 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  Knowledge Check: Endocrine Disorders NURS 6501 

 

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  Knowledge Check: Endocrine Disorders NURS 6501

 

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  Knowledge Check: Endocrine Disorders NURS 6501

The endocrine system is composed of glands that produce hormones, which control and regulate important body functions. One of the endocrine glands is the Parathyroid, which secretes the Parathyroid hormone (PTH). The purpose of this guide is to educate nurses on the differences between hyperparathyroidism and hypoparathyroidism.

Causes and Diagnostic Tests

Hyperparathyroidism is a parathyroid condition caused by increased secretion of PTH. PTH acts on receptors in the intestines, kidneys, and bones. Elevated PTH levels act directly on the kidneys, resulting in increased reabsorption of calcium and excretion of phosphate in the kidneys. The outcome is hypercalcemia and hypophosphatemia. Elevated PTH levels in the bones cause increased bone resorption and calcium (Kochman, 2023). On the other hand, hypoparathyroidism occurs following a decreased parathyroid function (Pasieka et al., 2022). It results from Iatrogenic and Idiopathic causes and Hypomagnesaemia. Iatrogenic hypoparathyroidism occurs following the removal of the parathyroid tissue or surgical removal of the parathyroid glands. Idiopathic hypoparathyroidism is caused by autoimmune disorders.

The diagnostic tests for Hyperparathyroidism include measurement of serum calcium, phosphate, and PTH levels and urine cyclic adenosine monophosphate (cAMP) (Kochman, 2023). Diagnostic tests for hypoparathyroidism include blood tests, electroencephalography (EEG), and CT scans. Serum phosphate, calcium, magnesium, vitamin D, and cAMP levels are used to diagnose hypoparathyroidism.

Signs and Symptoms

The signs and symptoms of hyperparathyroidism include anorexia, nausea, vomiting, epigastric pain, weight loss, constipation, bone fractures, arthritis, and psychological distress (Kochman, 2023). Clinical manifestations of hypoparathyroidism are linked to the lack of PTH secretion or diminished efficiency of PTH on target tissue leading to hypocalcemia (Pasieka et al., 2022). Mild to moderate hypocalcemia causes mild tingling and numbness in the mouth, hands, and feet. Severe hypocalcemia causes spasms of hands and feet, muscle cramps, and seizures.

Nurse’s Role in Providing Multidimensional Care

Nurses have a primary role in the care of patients with hyperparathyroidism and hypoparathyroidism. The nurse’s role in caring for a patient with hyperparathyroidism includes monitoring the patient’s cardiac function and fluid intake and output every 2 to 4 hours during hydration therapy (Bandeira et al., 2022). Besides, the nurse has a role in preventing injury caused by pathologic bone fractures. The nurse should be aware that a patient with chronic hyperparathyroidism usually has marked bone density loss and is at high risk for pathologic fractures. Thus, the nurse should take appropriate interventions to prevent falls in the patient, like ensuring they are always escorted when ambulating. The nurse’s role when caring for a patient with hypoparathyroidism includes providing patient education on the medication (Clarke, 2022). Besides, patients are often anxious, and the nurse should teach them measures to alleviate anxiety. The nurse also has a role in providing dietary education like consuming high calcium and low phosphorus foods.

Response to the Interventions

A patient’s response to interventions for hyperparathyroidism can be evaluated by measuring serum calcium, phosphate, and PTH levels (Pavlidis & Pavlidis, 2023). The success of interventions for hypoparathyroidism can be evaluated through EEG. EEG changes get back to normal when hypocalcemia is corrected (Khan et al., 2022).

Conclusion

Hyperparathyroidism is caused by increased secretion of PTH, while hypoparathyroidism is caused by decreased parathyroid function. The signs of Hyperparathyroidism are linked to the effects of elevated PTH or the effects of hypercalcemia. Signs of hypoparathyroidism are due to hypocalcemia.

References

Bandeira, F., de Moura Nóbrega, J., de Oliveira, L. B., & Bilezikian, J. (2022). Medical management of primary hyperparathyroidism. Archives of endocrinology and metabolism, 66(5), 689–693. https://doi.org/10.20945/2359-3997000000558

Clarke, B. L. (2022). Hypoparathyroidism: update of guidelines from the 2022 International Task Force. Archives of endocrinology and metabolism, 66(5), 604–610. https://doi.org/10.20945/2359-3997000000549

Khan, A. A., Bilezikian, J. P., Brandi, M. L., Clarke, B. L., Gittoes, N. J., Pasieka, J. L., Rejnmark, L., Shoback, D. M., Potts, J. T., Guyatt, G. H., & Mannstadt, M. (2022). Evaluation and Management of Hypoparathyroidism Summary Statement and Guidelines from the Second International Workshop. Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research, 37(12), 2568–2585. https://doi.org/10.1002/jbmr.4691

Kochman, M. (2023). Primary hyperparathyroidism: clinical manifestations, diagnosis and evaluation according to the Fifth International Workshop guidelines. Reumatologia, 61(4), 256–263. https://doi.org/10.5114/reum/170705

Pasieka, J. L., Wentworth, K., Yeo, C. T., Cremers, S., Dempster, D., Fukumoto, S., Goswami, R., Houillier, P., Levine, M. A., Pasternak, J. D., Perrier, N. D., Sitges-Serra, A., & Shoback, D. M. (2022). Etiology and Pathophysiology of Hypoparathyroidism: A Narrative Review. Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research, 37(12), 2586–2601. https://doi.org/10.1002/jbmr.4714

Pavlidis, E. T., & Pavlidis, T. E. (2023). Update on the current management of persistent and recurrent primary hyperparathyroidism after parathyroidectomy. World journal of clinical cases, 11(10), 2213–2225. https://doi.org/10.12998/wjcc.v11.i10.2213

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Sample Answer 2 for  Knowledge Check: Endocrine Disorders NURS 6501

• Question 1

  4 out of 4 points

  	Scenario 1: Syndrome of Antidiuretic Hormone (SIADH) A 77-year-old female was brought to the clinic by her daughter who stated that her mother had become slightly confused over the past several days. She had been stumbling at home and had fallen twice but was able to walk with some difficulty. She had no other obvious problems and had been eating and drinking. The daughter became concerned when she forgot he r daughter’s name, so she thought she better bring her to the clinic. HPI: Type II diabetes mellitus (DM) with peripheral neuropathy x 30 years. Emphysema. Situational depression after death of spouse 6-months ago SHFH: – non contributary except for 40 pack/year history tobacco use. Meds: Metformin 1000 mg po BID, ASA 81 mg po qam, escitalopram (Lexapro) 5 mg po q am started 2 months ago Labs-CBC WNL; Chem 7- Glucose-102 mg/dl, BUN 16 mg/dl, Creatinine 1.1 mg/dl, Na+116 mmol/L, K+4.2 mmol/L, CO237 m mol/L, Cl–97 mmol/L. The APRN refers the patient to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH). Question: 1.     Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
  	Selected Answer: SIADH happens when increased ADH is produced in the body, causing water retention and electrolyte imbalance. Hypothalamus produces ADH, and the posterior pituitary secretes and stores ADH. ADH regulates water in the body through water retention, and it constricts blood vessels. It accomplishes this with kidneys. ADH causes renal tubules to retain water. An increased level of ADH causes extra water retention in the body, resulting in hyponatremia with hypo-osmolality and high urine osmolality. Causes of SIADH can be damage to the hypothalamus or posterior pituitary gland or ADH being produced somewhere else. The symptoms continue to become more severe if the SIADH goes untreated, including confusion, hallucinations, seizures, and even coma. Based on the patient history, this patient has emphysema and currently smokes 40 packs of tobacco a year. The current lab work shows that patient’s carbon dioxide level is elevated at 37. The normal range for serum carbon dioxide is 23-29. Also, their sodium level is abnormal at 116. The normal range of serum sodium ranges between 135-and 145. When the serum sodium level is too low, the syndrome of inappropriate antidiuretic hormone secretion (SIADH) diagnosis is possible Correct Answer:   SIADH is a group of symptoms that occurs when antidiuretic hormone (ADH, arginine vasopressin) is secreted in the absence of osmotic or physiologic stimuli. These stimuli include: Increased serum osmolality, decreased plasma volume, and hypotension. A decrease in plasma osmolality normally inhibits ADH production and secretion. SIADH is characterized by fluid retention, dilutional hyponatremia, hypochloremia, concentrated urine, and lack of intravascular volume depletion. SIADH is characterized by normal to increased blood volume in normoproteinemia, nonedematous, and hyponatremic patients with normal renal and endocrine function. Response Feedback: [None Given]

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• Question 2

  4 out of 4 points

  	Scenario 2: Type 1 Diabetes A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily. PMH: noncontributory. Allergies-NKDA FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process SH: denies alcohol, tobacco or illicit drug use. Not sexually active. Labs: random glucose 244 mg/dl. DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan. Question 1.     Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM.
  	Selected Answer: Diabetes type 1 is also known as juvenile diabetes and is dependent on insulin injections. Type 1 diabetes happens when the pancreas does not produce enough or any of the insulin hormones in the body, which are necessary to help regulate the glucose in the body. Common signs and symptoms of type 1 DM can appear relatively suddenly. These symptoms include; increased thirst(polydipsia), frequent urination (polyuria), bed-wetting in children who previously did not wet the bed during the night, extreme hunger (polyphagia), and unintended weight loss, irritability and other mood changes, fatigue, weakness, and blurred vision. Pathophysiology of Polyuria Polyuria is one of the diabetes symptoms which means urine excretion is more than usual. High amounts of solutes within the renal tubules cause a passive osmotic diuresis and increased urine volume. In Diabetic patients, high urinary glucose levels exceed tubular reabsorption capacity, leading to increased glucose levels in the renal tubules; water follows passively, resulting in glucosuria and increased urine volume. Pathophysiology of Polydipsia Polydipsia can be the first sign that blood glucose levels are too high. A high blood glucose level in diabetic patients causes the kidney to produce more urine in order to remove excess glucose from the body. Furthermore, high blood glucose levels cause intracellular dehydration, and hypothalamus activation sends the thirst signal (Christ-Crain et al., 2019, pp. 2-3). Because more urine is being produced to reduce the amount of glucose circulating in the bloodstream, the brain instructs the body to increase the amount of fluid consumed. According to Seladi-Schulman (2020), persistent thirst can be caused by dehydration, osmotic diuresis (an increase in urination caused by excess glucose entering the kidney tubules that cannot be reabsorbed, resulting in increased water in the tubules), and mental health issues such as psychogenic polydipsia. Pathophysiology of Polyphagia Polyphagia is an excessive hunger feeling. This hunger usually dissipates once the person satisfies the craving by eating. In diabetics, the sense of hunger does not dissipate following consuming food. in diabetes, glucose can’t enter cells to be used for energy due to either low insulin levels or insulin resistance. The issue occurs when the conversion from glucose to energy is impaired, leading to continued hunger. With this being said, when the person consumes food, the glucose from that food then leads to increased blood glucose levels. Correct Answer:   (polyuria) Hyperglycemia acts as an osmotic diuretic. The amount of glucose filtered by the glomeruli of the kidneys exceeds the amount that can be reabsorbed by the renal tubules. Glycosuria results accompanied by large amounts of water lost in the urine. (polydipsia) Because elevated blood glucose levels, water is osmotically attracted from body cells which results in intracellular dehydration and hypothalamic stimulation of thirst. (polyphagia) Depletion of cellular stores of carbohydrates, fats, and proteins results in cellular starvation and a corresponding increase in hunger. Response Feedback: [None Given]

• Question 3

  4 out of 4 points

  	Scenario 2: Type 1 Diabetes A 14-year-old girl is brought to the pediatrician’s office by his parents who are concerned about their daughter’s weight loss despite eating more, frequent urination, unquenchable thirst, and fatigue that is interfering with her school activities. She had been seemingly healthy until about 4 months ago when her parents started noticing these symptoms. She admits to sleeping more and gets tired very easily. PMH: noncontributory. Allergies-NKDA FH:- maternal uncle with “some kind of sugar diabetes problem” but parents unclear on the exact disease process SH: denies alcohol, tobacco or illicit drug use. Not sexually active. Labs: random glucose 244 mg/dl. DIAGNOSIS: Diabetes Mellitus type 1 and refers to an endocrinologist for further work up and management plan. Question 1.    Explain the genetics relationship and how this and the environment can contribute to Type I DM.
  	Selected Answer:  Type 1 diabetes can occur due to genetics, environmental, and or lifestyle influences. Type 1 diabetes (T1D) is a chronic autoimmune disorder that leads to progressive pancreatic ß-cell destruction and culminates in absolute insulin deficiency and stable hyperglycemia. Environmental factors likely play a role in triggering islet autoimmunity. Factors such as gluten, breastfeeding and cow’s milk, vitamin D intake, the composition of your gut microbiota, infections acquired, antibiotics, and other medications taken may all play a role and affect the patient, leading to type 1 diabetes. Genetic factors include: Islet autoantibodies found in serum – Interferon (IFN)-stimulated genes – Excess IFIH1 (MDA5) levels may contribute to inflammation and autoimmunity. – PTPN22 contains risk polymorphisms that almost double the risk for T1D – High expression of CTLA-4 leads to inhibition of T cell activation – IL10 has an anti-inflammatory effect and has been identified as a risk factor for T1D – TNFAIP3 exerts anti-inflammatory function by inhibiting NF-κB activation and is associated with T1D. – Interleukin-21 and IL-2. Correct Answer:   Islet cell autoantibodies (ICAs) were detected in serum from patients with autoimmune polyendocrine deficiency. They have subsequently been identified in 85 percent of patients with newly diagnosed type 1 diabetes and in prediabetic people. Autoantigens form on insulin producing beta cells and circulate in the blood and lymphatics. This leads to processing and presentation of autoantigen by antigen presenting cells Response Feedback: [None Given]

• Question 4

  4 out of 4 points

  	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: 1.     How would you describe the pathophysiology of Type II DM?
  	Selected Answer: Type 2 diabetes is a chronic medical condition regarding how the body metabolizes glucose in the body. Two situations cause type 2 diabetes: the body develops insulin resistance, or the pancreas does not produce enough insulin. The cause of type 2 diabetes is unknown, although genetics and environmental factors, such as being overweight and inactive, seem to be contributing factors. Type 2 diabetes can be managed with diet and exercise in some cases. Once this therapy is unsuccessful, medications are added, changed, or increased. factors that put one at a higher risk for type ll DM include being overweight, high-fat content in the trunk, inactivity, family history, ethnicity/race, age, prediabetic, gestational diabetes, and polycystic ovarian syndrome. Correct Answer:   There are very complex interactions that result in the development of Type II diabetes. The pathophysiology of type 2 diabetes mellitus is characterized by peripheral insulin resistance, impaired regulation of hepatic glucose production, and declining β-cell function, eventually leading toβ -cell failure. Type 2 diabetes mellitus consists of a constellation of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. It is often associated with obesity. Response Feedback: [None Given]