Assignment: Week 6 Concepts of Endocrine Disorders/ NURS 6501

Assignment: Week 6 Concepts of Endocrine Disorders/ NURS 6501

Assignment: Week 6 Concepts of Endocrine Disorders/ NURS 6501

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

American Diabetes Association (2020). Standards of medical care of patients with diabetes mellitus. Diabetes Care, 26(suppl 1), pp. s33-s50. https://care.diabetesjournals.org/content/26/suppl_1/s33

Orlander, P. R. (2018). Hypothyroidism. Retrieved from https://emedicine.medscape.com/article/122393-overview

Hoorn, E. J., & Zietse, R. (2017). Diagnosis and treatment of hyponatremia: Compilation of the guidelines. Journal of the American Society of Nephrology, 28(5), 1340–1349

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)

Accessible player

Concepts of Endocrine Disorders – Week 6 (24m)

Accessible player

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.

Walden University. (2019). ASC success strategies interactive tutorials. Retrieved from https://academicguides.waldenu.edu/academic-skills-center/skills/tutorials/success-strategies

Knowledge Check: Endocrine Disorders

In this exercise, you will complete a 5-essay type question Knowledge Check to gauge your understanding of this module’s content.

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.)

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

To go to the next Module:

Module 5

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QUESTION 1

1. 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 her 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

      SIADH is characterized by less than maximally dilute urine with serum hypo-osmolality in patients with normal thyroid, adrenal, renal, hepatic, and cardiac function and who do not have volume depletion, hypotension, or other physiologic causes affecting ADH secretion. Low plasma osmolality impedes ADH secretion, causing the kidneys to produce dilute urine (Mentrasti et al., 2020). Inappropriate vasopressin secretion is associated with central nervous system disorders, pulmonary disorders, and certain malignancies. Some drugs also trigger ADH secretion, particularly analgesics (opioids and NSAIDs), antiseizure drugs (carbamazepine), hypoglycemic (metformin) Prostaglandin synthetase inhibitors, antidepressants (SSRIs and venlafaxine), antipsychotics, and cytotoxics (Mentrasti et al., 2020). Therefore, patient factors contributing to SIADH are emphysema (pulmonary disorder) and medications like escitalopram (SSRI), aspirin, and Metformin.

QUESTION 2

1. 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.

      Insulin deficiency in the body results in blood glucose build-up and, eventually, hyperglycemia. Hyperglycemia causes an imbalance in fluid and electrolytes that contribute to the classic features of diabetes: polyuria, polydipsia, and polyphagia. Increased glucose levels in the urine create an osmotic dieresis that results in increased and excessive urination (polyuria) (DiMeglio et al., 2018). The osmotic dieresis contributes to the excretion of electrolytes, particularly potassium, sodium, and chloride, through the urine, causing severe water loss and eventually dehydration that results in acute thirst (polydipsia) (DiMeglio et al., 2018). Lack of glucose in body cells causes them to starve, which causes increased hunger (polyphagia) even when one consumes large amounts of food since there is deficient insulin to facilitate the movement of glucose into body cells.

QUESTION 3

1. 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.

The overall risk of developing Type 1 diabetes (T1DM) is higher in individuals with close relatives having the disease. Redondo et al. (2018) explain that siblings of diabetic patients have an average of 6-7% lifetime risk. Besides, the offspring of a female patient with T1DM have a 1.3-4% risk, while that of a male patient is 6-9%. Genetic factors directly involved in controlling beta cell function and immune response are attributed to the development of T1DM. In addition, some environmental factors damage the beta cells, including cytotoxins, toxic chemicals, and viruses like enterovirus, mumps, and rubella (Redondo et al., 2018). Therefore, the client’s family history of diabetes and environmental factors could have contributed to T1DM.

QUESTION 4

1. 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?  

Type 2 diabetes mellitus (T2DM) occurs due to the resistance of body cells to insulin. It is caused by inadequate insulin secretion when a person develops insulin resistance, primarily due to obesity. Hepatic insulin resistance causes an inability to curb hepatic glucose production (Banday et al., 2020). Besides, peripheral insulin resistance hinders peripheral glucose uptake. The combination results in fasting and postprandial hyperglycemia. Hyperglycemia impairs insulin secretion in persons with T2DM since elevated glucose levels desensitize beta cells, causing beta-cell dysfunction. As a result, insulin secretion reduces later in the disease, worsening hyperglycemia.

QUESTION 5

1. 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?

Hypothyroidism is characterized by thyroid hormone deficiency. It occurs when thyroid cells fail to produce adequate amounts of thyroid hormone. This is usually due to abnormal functioning of thyroid cells, destruction of thyroid cells, or limited dietary intake of iodine and tyrosine, which play a major role in the synthesis of thyroid hormones (Chiovato et al., 2019). The consumption of lithium can also cause hypothyroidism since it hinders the release of thyroid hormone by the thyroid. It can also occur in persons taking medications, including amiodarone, iodine-containing drugs, interferon-alfa, and tyrosine kinase inhibitors for cancer.                                                            

References

Banday, M. Z., Sameer, A. S., & Nissar, S. (2020). Pathophysiology of diabetes: An overview. Avicenna Journal of Medicine, 10(4), 174–188. https://doi.org/10.4103/ajm.ajm_53_20

Chiovato, L., Magri, F., & Carlé, A. (2019). Hypothyroidism in Context: Where We’ve Been and Where We’re Going. Advances in Therapy, 36(Suppl 2), 47–58. https://doi.org/10.1007/s12325-019-01080-8

DiMeglio, L. A., Evans-Molina, C., & Oram, R. A. (2018). Type 1 diabetes. Lancet (London, England), 391(10138), 2449–2462. https://doi.org/10.1016/S0140-6736(18)31320-5

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

Redondo, M. J., Steck, A. K., & Pugliese, A. (2018). Genetics of type 1 diabetes. Pediatric Diabetes, 19(3), 346–353. https://doi.org/10.1111/pedi.12597