NURS 6501 Knowledge Check Endocrine Disorders
NURS 6501 Knowledge Check Endocrine Disorders
NURS 6501 Knowledge Check Endocrine Disorders
In this exercise, you will complete a 10- to 20-essay type question Knowledge Check to gauge your understanding of this module’s content.
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Possible topics covered in this Knowledge Check include:
-
- Diabetes
- Hyper- and hypothyroidism
- Adrenal disorders
- Parathyroidism (hyper and hypo)
- Checks & balances / negative feedback
- Syndrome of Inappropriate Antidiuretic Hormone
- Pheochromocytosis
- Diabetes insipidus
- Diabetic ketoacidosis
Photo Credit: Getty Images/Science Photo Library RF
(Note: It is strongly recommended that you take the Knowledge Check at least 48 hours before taking the Midterm Exam.)
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Complete the Knowledge Check By Day 5 of Week 6
To complete this Knowledge Check:
Module 4 Knowledge Check
Midterm Exam
This 101-question exam is a test of your knowledge in preparation for your certification exam. No outside resources, including books, notes, websites, or any other type of resource, are to be used to complete this exam. You are expected to comply with Walden University’s Code of Conduct.
This exam will be on topics covered in Weeks 1, 2, 3, 4, 5, and 6. Prior to starting the exam, you should review all of your materials. This exam is timed with a limit of 2 hours for completion. When time is up, your exam will automatically submit.
(Note: It is strongly recommended that you take the Knowledge Check at least 48 hours before taking the Midterm exam.)
Photo Credit: Getty Images
To prepare:
To help you review for your midterm exam, access the Midterm Exam Review document found in this week’s Learning Resources as well as any Knowledge Check feedback you might have received. (Note: You will also need to review all of your materials from each of these weeks to also help you better prepare for your midterm.)
By Day 7 of Week 6
Submit your Midterm Exam.
To complete your exam:
Midterm Exam
What’s Coming Up in Module 5?
Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images
In Module 5, you will analyze processes related to neurological and musculoskeletal disorders through case study analysis. To do this, you will analyze alterations in the relevant systems and the resultant disease processes. You will also consider patient characteristics, including racial and ethnic variables, which may impact physiological functioning and altered physiology.
Week 7 Knowledge Check: Neurological and Musculoskeletal Disorders
In the Week 7 Knowledge Check, you will demonstrate your understanding of the topics covered during Module 5. This Knowledge Check will be composed of a series of questions related to specific scenarios provided. It is highly recommended that you review the Learning Resources in their entirety prior to taking the Knowledge Check, since the resources cover the topics addressed. Plan your time accordingly.
Next Module
Week 6: Concepts of Endocrine Disorders
Endocrine disorders are complex matters, and there is not always a one-size-fits-all treatment. Particularly in matters requiring the adjustment of hormone levels, treatment may require a custom approach tailored to individual patients. An understanding of these complications is essential to supporting these individual treatment plans.
This week, you examine alterations in the endocrine system and the resultant disease processes. You also consider patient characteristics, including racial and ethnic variables, and the impact they have on altered physiology.
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Learning Objectives
Students will:
- Analyze concepts and principles of pathophysiology across the lifespan
Learning Resources
Required Readings (click to expand/reduce)
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
- Chapter 21: Mechanisms of Hormonal Regulation, including Summary Review
- Chapter 22: Alterations of Hormonal Regulation, including Summary Review
- Chapter 23: Obesity and Disorders of Nutrition, including Summary Review
Document: NURS 6501 Midterm Exam Review (PDF document)
Note: Use this document to help you as you review for your Midterm Exam in Week 6.
Required Media (click to expand/reduce)
Module 4 Overview with Dr. Tara Harris
Dr. Tara Harris reviews the structure of Module 4 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check and your Midterm. (3m)
Concepts of Endocrine Disorders – Week 6 (24m)
Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children
In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 21 through 23 related to the endocrine system and disorders. Refer to the Learning Resources in Week 1 for registration instructions. If you have already registered, you may access the resources at https://evolve.elsevier.com/
Optional Resources (click to expand/reduce)
The following source provides various tutorials related to maximizing your time management and managing stress. Feel free to access this resource to support you as you move through this course.
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
- Explain the genetics relationship and how this and the environment can contribute to Type I DM.
Your Answer:
Type 1 DM is a chronic metabolic condition characterized by autoimmune destruction of insulin-producing pancreatic islet beta cells in genetically predisposed persons. Yahaya & Salisu (2020) found more than 73 genes which were suspected in the pathogenesis of T1DM. The genes that accounted for most of the T1DM cases include the insulin gene, human leukocyte antigen (HLA), and cytotoxic T lymphocyte-associated antigen 4. The mutations in these genes, in addition to environmental factors, can result in a defective immune response in the pancreas, causing insulin deficiency, β-cell autoimmunity, and hyperglycemia. The mechanisms causing the cellular reactions are usually gene-specific and, if targeted in diabetic patients can result in improved treatment.
what are the environmental factors?
Question 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 2 diabetes is a heterogeneous disorder where insulin resistance occurs, and the beta cells lack the ability to overcome this resistance. Galicia-Garcia et al. (2020)explain that Type 2 DM is caused by a combination of two factors: impaired insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond to insulin secretion. In the case of impaired β-cell function, the body experiences decreased insulin secretion, which limits its ability to maintain physiological glucose levels (Galicia-Garcia et al., 2020). On the other hand, an impairment of the feedback loops between insulin secretion and action causes abnormally elevated glucose levels in blood, resulting in hyperglycemia and eventually Type II DM.
Question 5
Scenario 4: Hypothyroidism
A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue, cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful. She does have blurry vision.
PMH: Non-contributory.
Vitals: Temp 96.4˚F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted.
Diagnosis: hypothyroidism.
Question:
What causes hypothyroidism?
Your Answer:
Hypothyroidism is caused by various factors including deficient hormone synthesis,
Congenital thyroid defects, Prenatal and postnatal iodine deficiency, and Autoimmune diseases like Hashimoto disease and sarcoidosis (Hegedüs et al. 2022). It is characterized by decreased levels of thyroid hormones (T3 and T4), which causes a slow basal metabolic rate (BMR). The decreased BMR affects lipid metabolism resulting in increased cholesterol and triglyceride levels.
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
- Explain the genetics relationship and how this and the environment can contribute to Type I DM.
Your Answer:
Type 1 DM is a chronic metabolic condition characterized by autoimmune destruction of insulin-producing pancreatic islet beta cells in genetically predisposed persons. Yahaya & Salisu (2020) found more than 73 genes which were suspected in the pathogenesis of T1DM. The genes that accounted for most of the T1DM cases include the insulin gene, human leukocyte antigen (HLA), and cytotoxic T lymphocyte-associated antigen 4. The mutations in these genes, in addition to environmental factors, can result in a defective immune response in the pancreas, causing insulin deficiency, β-cell autoimmunity, and hyperglycemia. The mechanisms causing the cellular reactions are usually gene-specific and, if targeted in diabetic patients can result in improved treatment.
what are the environmental factors?
Question 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 2 diabetes is a heterogeneous disorder where insulin resistance occurs, and the beta cells lack the ability to overcome this resistance. Galicia-Garcia et al. (2020)explain that Type 2 DM is caused by a combination of two factors: impaired insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond to insulin secretion. In the case of impaired β-cell function, the body experiences decreased insulin secretion, which limits its ability to maintain physiological glucose levels (Galicia-Garcia et al., 2020). On the other hand, an impairment of the feedback loops between insulin secretion and action causes abnormally elevated glucose levels in blood, resulting in hyperglycemia and eventually Type II DM.
Question 5
Scenario 4: Hypothyroidism
A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue, cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful. She does have blurry vision.
PMH: Non-contributory.
Vitals: Temp 96.4˚F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted.
Diagnosis: hypothyroidism.
Question:
What causes hypothyroidism?
Your Answer:
Hypothyroidism is caused by various factors including deficient hormone synthesis,
Congenital thyroid defects, Prenatal and postnatal iodine deficiency, and Autoimmune diseases like Hashimoto disease and sarcoidosis (Hegedüs et al. 2022). It is characterized by decreased levels of thyroid hormones (T3 and T4), which causes a slow basal metabolic rate (BMR). The decreased BMR affects lipid metabolism resulting in increased cholesterol and triglyceride levels.
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 4: Hypothyroidism
A patient walked into your clinic today with the following complaints: Weight gain (15 pounds), however has a decreased appetite with extreme fatigue, cold intolerance, dry skin, hair loss, and falls asleep watching television. The patient also tearfulness with depression, and with an unknown cause and has noted she is more forgetful. She does have blurry vision.
PMH: Non-contributory.
Vitals: Temp 96.4˚F, pulse 58 and regular, BP 106/92, 12 respirations. Dull facial expression with coarse facial features. Periorbital puffiness noted.
Diagnosis: hypothyroidism.
Question:
What causes hypothyroidism?
Your Answer:
Hypothyroidism can stem from various causes, each with its own implications for management. The most common cause is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, wherein the body’s immune system mistakenly attacks and damages the thyroid gland, leading to reduced hormone production. Other causes include thyroid surgery or radioactive iodine treatment, which can diminish thyroid hormone output. Congenital hypothyroidism occurs when an infant is born with an underactive or absent thyroid gland, necessitating lifelong hormone replacement therapy.
Certain medications like lithium or amiodarone, as well as radiation therapy to the neck area, can also disrupt thyroid function. Dysfunction in the pituitary or hypothalamus, which regulate thyroid-stimulating hormone production, may result in hypothyroidism. Lastly, iodine deficiency, although rare in many countries due to the widespread use of iodized salt, can contribute to insufficient thyroid hormone production. Identifying the specific cause of hypothyroidism is crucial for tailoring treatment plans and ensuring effective long-term management.