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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KNOWLEDGE CHECK: ENDOCRINE DISORDERS NURS 6501

KNOWLEDGE CHECK: ENDOCRINE DISORDERS NURS 6501

Scenario 1: Syndrome of Antidiuretic Hormone (SIADH)

Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH 

SIADH is an endocrine disorder characterized by excessive production of antidiuretic hormone, leading to retention of water in the body and reduction in the levels of certain electrolytes in the blood such as sodium (Jones, 2018). This condition is common among heart failure patients or those with defects in the hypothalamus. Other causes include substance use, brain disorders like trauma or infection, substance abuse, and certain medications such as seizure drugs and antidepressants. The 77-year-old female patient provided in the case study displays signs of SIADH. The development of this condition might have resulted from hyponatremia in diabetic peripheral neuropathy as seen in the patient’s history of presenting illness. The patient’s smoking habits, emphysema, and use of metformin and escitalopram also contributed to the development of SIADH.

Scenario 2: Type 1 Diabetes

Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM.

Diabetes type 1 is an autoimmune disorder characterized by elevated blood glucose levels. The immune system attacks and destroys pancreatic beta cells, which are responsible for insulin production (Saberzadeh-Ardestani et al., 2018). This leads to complete insulin deficiency, hence unable to convert glucose to glycogen for storage. The patient will present with the 3P’s (polyuria, polydipsia, polyphagia) as the early signs and symptoms. Elevated blood glucose levels lead to increased blood osmolarity, as it makes it more concentrated, hence promoting excessive thirst (polydipsia) as a compensation mechanism. Excessive fluid intake, from thirst, in addition to glucose-induced urination, is responsible for increased urine frequency (Polyuria). Lastly, polyphagia/ increased hunger occurs because of excessive loss of glucose in the urine, which makes the body crave for more.

Explain the genetic relationship and how this and the environment can contribute to Type I DM.

Even though it’s still unclear on the actual triggers of β cell destruction in the development of type 1 DM, most studies have revealed the factors which regulate the risk of developing the disease. Previously reported evidence to suggest that T1DM is heritable with the HLA class II genes such as HLA-DR, DQ, DP strongly associated with the development of the disease (DiMeglio et al., 2018). While the genetic factors determine the likelihood of an individual to develop T1DM, environmental factors expose the individual to triggers that lead to the onset of the disease such as viruses.

Scenario 3: Type II DM

How would you describe the pathophysiology of Type II DM?

T2DM is a metabolic disorder characterized by elevated blood glucose levels because of a

combination of two main primary factors, such as decreased sensitivity of insulin receptors to the ligand, and defective secretion of insulin by the pancreatic β cells (Padhi et al., 2020). Insulin is involved in maintaining the physiological levels of glucose in the blood. A defect in this mechanism can lead to increased production of glucose and decreased uptake of glucose both in the liver, muscles, and adipose tissue, leading to T2DM.

Scenario 4: Hypothyroidism

What causes hypothyroidism?

Hypothyroidism is an endocrine disorder characterized by the failure of the thyroid gland to produce enough amount of thyroid hormone to satisfy the body’s needs. Several factors have been associated with the cause of hypothyroidism, such as autoimmune disorders, radiation therapy, certain medications, and hyperthyroidism treatment (Chiovato et al., 2019). Some of the less common causes of hypothyroidism include pregnancy, iodine deficiency, pituitary disorder, and congenital disease.

 

References

Chiovato, L., Magri, F., & Carlé, A. (2019). Hypothyroidism in context: where we’ve been and where we’re going. Advances in therapy, 36(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. The Lancet, 391(10138), 2449-2462. https://doi.org/10.1016/S0140-6736(18)31320-5

Jones, D. P. (2018). Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia. Pediatrics in Review, 39(1), 27-35. https://doi.org/10.1542/pir.2016-0165

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

Saberzadeh-Ardestani, B., Karamzadeh, R., Basiri, M., Hajizadeh-Saffar, E., Farhadi, A., Shapiro, A. J., … & Baharvand, H. (2018). Type 1 diabetes mellitus: cellular and molecular pathophysiology at a glance. Cell Journal (Yakhteh), 20(3), 294. https://doi.org/10.22074/cellj.2018.5513

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 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
	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]

Question 2

4 out of 4 points

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	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 primary indication that blood glucose levels may be high. In diabetic patients, a high blood glucose level causes the kidney to produce more urine to remove excess glucose from the body. Moreover, intracellular dehydration occurs due to high blood glucose levels, and the hypothalamus activation sends the signal for thirst (Christ-Crain et al., 2019, pp. 2-3). The brain tells the body to increase the amount of fluid ingested because more urine is being produced to decrease the glucose circulating in the bloodstream. Seladi-Schulman (2020) states that Persistent feelings of thirst can also be caused by dehydration, osmotic diuresis, an increase in urination due to excess glucose entering the kidney tubules which can’t be reabsorbed, leading to 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] Knowledge Check: Endocrine Disorders Scenario 1: Syndrome of Antidiuretic Hormone (SIADH) Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH  SIADH is an endocrine disorder characterized by excessive production of antidiuretic hormone, leading to retention of water in the body and reduction in the levels of certain electrolytes in the blood such as sodium (Jones, 2018). This condition is common among heart failure patients or those with defects in the hypothalamus. Other causes include substance use, brain disorders like trauma or infection, substance abuse, and certain medications such as seizure drugs and antidepressants. The 77-year-old female patient provided in the case study displays signs of SIADH. The development of this condition might have resulted from hyponatremia in diabetic peripheral neuropathy as seen in the patient’s history of presenting illness. The patient’s smoking habits, emphysema, and use of metformin and escitalopram also contributed to the development of SIADH. Scenario 2: Type 1 Diabetes Explain the pathophysiology of the three P’s for (polyuria, polydipsia, polyphagia)” with the given diagnosis of Type I DM. Diabetes type 1 is an autoimmune disorder characterized by elevated blood glucose levels. The immune system attacks and destroys pancreatic beta cells, which are responsible for insulin production (Saberzadeh-Ardestani et al., 2018). This leads to complete insulin deficiency, hence unable to convert glucose to glycogen for storage. The patient will present with the 3P’s (polyuria, polydipsia, polyphagia) as the early signs and symptoms. Elevated blood glucose levels lead to increased blood osmolarity, as it makes it more concentrated, hence promoting excessive thirst (polydipsia) as a compensation mechanism. Excessive fluid intake, from thirst, in addition to glucose-induced urination, is responsible for increased urine frequency (Polyuria). Lastly, polyphagia/ increased hunger occurs because of excessive loss of glucose in the urine, which makes the body crave for more. Explain the genetic relationship and how this and the environment can contribute to Type I DM. Even though it’s still unclear on the actual triggers of β cell destruction in the development of type 1 DM, most studies have revealed the factors which regulate the risk of developing the disease. Previously reported evidence to suggest that T1DM is heritable with the HLA class II genes such as HLA-DR, DQ, DP strongly associated with the development of the disease (DiMeglio et al., 2018). While the genetic factors determine the likelihood of an individual to develop T1DM, environmental factors expose the individual to triggers that lead to the onset of the disease such as viruses. Scenario 3: Type II DM How would you describe the pathophysiology of Type II DM? T2DM is a metabolic disorder characterized by elevated blood glucose levels because of a combination of two main primary factors, such as decreased sensitivity of insulin receptors to the ligand, and defective secretion of insulin by the pancreatic β cells (Padhi et al., 2020). Insulin is involved in maintaining the physiological levels of glucose in the blood. A defect in this mechanism can lead to increased production of glucose and decreased uptake of glucose both in the liver, muscles, and adipose tissue, leading to T2DM. Scenario 4: Hypothyroidism What causes hypothyroidism? Hypothyroidism is an endocrine disorder characterized by the failure of the thyroid gland to produce enough amount of thyroid hormone to satisfy the body’s needs. Several factors have been associated with the cause of hypothyroidism, such as autoimmune disorders, radiation therapy, certain medications, and hyperthyroidism treatment (Chiovato et al., 2019). Some of the less common causes of hypothyroidism include pregnancy, iodine deficiency, pituitary disorder, and congenital disease. References Chiovato, L., Magri, F., & Carlé, A. (2019). Hypothyroidism in context: where we’ve been and where we’re going. Advances in therapy, 36(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. The Lancet, 391(10138), 2449-2462. https://doi.org/10.1016/S0140-6736(18)31320-5 Jones, D. P. (2018). Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia. Pediatrics in Review, 39(1), 27-35. https://doi.org/10.1542/pir.2016-0165 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 Saberzadeh-Ardestani, B., Karamzadeh, R., Basiri, M., Hajizadeh-Saffar, E., Farhadi, A., Shapiro, A. J., … & Baharvand, H. (2018). Type 1 diabetes mellitus: cellular and molecular pathophysiology at a glance. Cell Journal (Yakhteh), 20(3), 294. https://doi.org/10.22074/cellj.2018.5513

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.

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

4 / 4 pts

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?  

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

4 / 4 pts

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