NURS 6501 / NURS6501: Advanced Pathophysiology - Module 4 Knowledge Check (Latest 2021 / 2022) Walden University

NURS 6501 / NURS6501: Advanced Pathophysiology - Module 4 Knowledge Check (Latest 2021 / 2022) Walden University

NURS 6501 - Advanced Pathophysiology Review Test Submission: Module 4 Knowledge Check • Question 1 Needs Grading A 67-year-old Caucasian woman was brought to the clinic by her son who stated that his mother had become slightly confused over the past several days. She had been stumbling at home and had fallen once but was able to ambulate with some difficulty. She had no other obvious problems and had been eating and drinking. The son became concerned when she forgot her son’s name, so he thought he better bring her to the clinic. PMH-Type II diabetes mellitus (DM) with peripheral neuropathy x 20 years. COPD. Depression after death of spouse several months ago Social/family hx - non contributary except for 30 pack/year history tobacco use. Meds: Metformin 500 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-92 mg/dl, BUN 18 mg/dl, Creatinine 1.1 mg/dl, Na+120 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: Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH. Selected SIADH is a condition in which the release of ADH from the Answer: posterior pituitary is elevated relative to serum sodium levels, resulting in increased water reabsorption by the kidneys and fluid overload. Elderly patients on medications such as metformin, NSAIDs, and antidepressants, cause SIADH. These drugs either stimulate ADH release, enhance the physiologic effects of ADH, or have a biologic action similar to that of ADH. 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. ADH regulates the body's water balance. It is synthesized in the hypothalamus and stored in the posterior pituitary gland. When released into the circulation, it acts on the kidney's distal tubules and collecting ducts, increasing their permeability to water. This decreases urine volume because more water is being reabsorbed and returned to the circulation. It also serves to produce more concentrated urine. Response Feedback: [None Given] • Question 2 Needs Grading A 43-year-old female presents to the clinic with a chief complaint of fever, chills, nausea and vomiting and weakness. She has been unable to keep any food, liquids or medications down. The symptoms began 3 days ago and have not responded to ibuprofen, acetaminophen, or Nyquil when she tried to take them. The temperature has reached as high as 102˚F. Allergies: none known to drugs or food or environmental Medications-20 mg prednisone po qd, omeprazole 10 po qam PMH-significant for 20-year history of steroid dependent rheumatoid arthritis (RA). GERD. No other significant illnesses or surgeries. Social-denies alcohol, illicit drugs, vaping, tobacco use Physical exam Thin, ill appearing woman who is sitting in exam room chair as she said she was too weak to climb on the exam table. VS Temp 101.2˚F, BP 98/64, pulse 110, Resp 16, PaO2 96% on room air. ROS negative other than GI symptoms. Based on the patient’s clinical presentation, the APRN diagnoses the patient as having secondary hypocortisolism due to the lack of prednisone the patie nt was taking for her RA secondary to vomiting. Question: Explain why the patient exhibited these symptoms? Selected Answer: High levels of glucocorticoids decrease hypothalamic corticotropin-releasing hormone synthesis and secretion and also block the trophic and ACTH-secretagogue actions of CRH on anterior pituitary cells, resulting in loss of ACTH and its actions on the adrenal gland. The patient exhibited these symptoms as a result of abrupt withdrawal of exogenous glucocorticoids. Correct Answer: An adrenal insufficiency requires some type of trigger or stressor such as surgery, trauma, infection or acute withdrawal of glucocorticoids. The patient had several factors contributing to her present situation. She had RA x 20 years that necessitated oral prednisone. Increased levels of both glucocorticoids (primarily cortisol) and mineralocorticoids (primarily aldosterone) are needed for the body to adapt to the stress Corticotropin-releasing hormone (CRH) from the hypothalamus eventually prompts release of ACTH from the anterior pituitary gland. ACTH then stimulates release and 3 synthesis of cortisol from the adrenal cortex. Cortisol mobilizes amino acids from skeletal muscle and generally enhances the liver's capacity for gluconeogenesis as well as enhances normal immune activity and maintenance of cardiovascular integrity. It also influences fat, carbohydrate and protein. Catecholamines cause vasoconstriction, which in the kidney, probably initiates release of renin, stimulating the renninangiotensionaldosterone-system (RAAS). Antidiuretic hormone (ADH, also called vasopressin), is released from the hypothalamus and posterior pituitary during periods of stress. Both aldosterone and ADH attempt to conserve water and electrolytes to sustain a sufficient vascular volume. Response Feedback: [None Given] • Question 3 Needs Grading A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had about of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved. The APRN examining the patient orders a Chem 7 which revealed a serum Ca++ of 13.1 mg/dl. The APN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist who does a complete work up and concurs with the APRN’s diagnosis. Question: What is the role of parathyroid hormone in the development of primary hyperparathyroidism? Selected Answer: Role of parathyroid hormone in the development of primary hyperparathyroidism includes the inappropriate excess secretion of PTH by one or more of the parathyroid glands. PTH secretion is increased and is not under the usual feedback control mechanisms. Correct Answer: Primary hyperparathyroidism is the unregulated overproduction of parathyroid hormone (PTH) resulting in abnormal calcium balance. PTH secretion is increased and is not under the usual feedback control mechanisms. The Ca++ level in the blood increase because of increased resorption and GI absorption of calcium but fails to inhibit PTH secretion at normal levels of calcium because the feedback threshold for calcium is set at a higher level in the abnormal parathyroid tissues. Hypercalcemia and hypophosphatemia are the clinical hallmarks of hyperparathyroidism. Response Feedback: 

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Version 2021
Category Exam (elaborations)
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Language English
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