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Case Study in Endocrine in preparation for Discussion A 51-year old unemployed salesman is brought to...

Case Study in Endocrine in preparation for Discussion

A 51-year old unemployed salesman is brought to the emergency department by EMS at 0800, accompanied by his wife. His wife tells the emergency department nurse that her husband has not been feeling well for the last week, but that when he got up this morning, he was so weak he couldn’t dress himself and didn’t know where he was. She also tells the nurse her husband has been taking a cortisone drug for treatment of his rheumatoid arthritis for the past 2 years, but notes, “We didn’t have the money to buy it this month.” Assessment data includes: The patient is dehydrated with dry oral mucous membranes and tongue, poor skin turgor, and sunken eyeballs. His blood pressure is 94/44, and his pulse is rapid and thread. He is weak, dizzy, and disoriented about time and place. Diagnostic tests done at 0830 reveal the following abnormal findings: o EKG: widening QRS complex and increased PR interval (had peaked T-waves in the ambulance) o Sodium: 129 mEg/L (normal range: 135-145 mEq/L) o Glucose: 54 mg/ dL (normal range: 70-110 mg/dL) o Potassium: 6.2 mEq/L (normal range: 3.5-5 mEq/L) o Cortisol: 2 mg/dL (normal for morning draw: 5-23 mg/dL) The physician determines that the patient is probably suffering from adrenal insufficiency. The physician orders 5% Dextrose in 0.9 % sodium chloride in water (D5NS) to run at 250 mL/hr intravenously and Hydrocortisone 200 mg IV. After initiation of the IV fluids and medication, the patient is admitted to an inpatient bed with continuous heart monitoring. ------------------------------------------------------------------------------------------------------------------------------------------

1. Briefly explain what adrenal insufficiency is. Is there one kind or multiple—if so, what are the differences—this should be a discussion of the pathophysiology and presentation of adrenal insufficiency (you can use your patho, med-surg, and pharm texts for this (4 points) 2. What are the data that support this diagnosis in this patient? Which of the above does the patient have? (3 points) 3. What contributed to the patient developing this condition? (this is worth 2 points, so don’t just give a 1 sentence answer) 4. Give a brief explanation of each of the above lab/diagnostic test results, with the pathophysiology behind each. (10 points) 5. Identify at least 2 methods that could be used to lower the potassium level if the patient has symptomatic hyperkalemia. (2 points) 6. Name 1 priority nursing diagnosis and 1 educational nursing diagnosis. This condition is potentially deadly for the patient, so the priority diagnosis must reflect a serious response to adrenal insufficiency that the nurse can address (4 points) 7. Name a goal statement for each nursing diagnosis. (2 points) 8. List 3 nursing interventions for each nursing diagnosis and please be specific about what is essential to teach this patient and his wife (6 points) Citations and References are required.

Solutions

Expert Solution

1. Adrenal insufficiency, including Addison’s disease, is a disorder that occurs when the adrenal glands don’t make enough of certain hormones. These include cortisol, sometimes called the “stress hormone,” which is essential for life.

Addison's disease symptoms usually develop slowly, often over several months. Often, the disease progresses so slowly that symptoms are ignored until a stress, such as illness or injury, occurs and makes symptoms worse. Signs and symptoms may include:

  • Extreme fatigue
  • Weight loss and decreased appetite
  • Darkening of your skin (hyperpigmentation)
  • Low blood pressure, even fainting
  • Salt craving
  • Low blood sugar (hypoglycemia)
  • Nausea, diarrhea or vomiting (gastrointestinal symptoms)
  • Abdominal pain
  • Muscle or joint pains
  • Irritability
  • Depression or other behavioral symptoms
  • Body hair loss or sexual dysfunction in women

2 and 4 .

. dehydrated with dry oral mucous membranes and tongue,

poor skin turgor,

sunken eyeballs.

blood pressure is 94/44,

pulse is rapid and thread.

weak, dizzy, and disoriented about time and place.

EKG: widening QRS complex and increased PR interval (had peaked T-waves in the ambulance) o

Sodium: 129 mEg/L (normal range: 135-145 mEq/L) o

Glucose: 54 mg/ dL (normal range: 70-110 mg/dL) o

Potassium: 6.2 mEq/L (normal range: 3.5-5 mEq/L) o

Cortisol: 2 mg/ all points towards addisons disease.

3. Patient was on cortisol. sudden stoppage of cortisol resulted in adrenal crisis and the adrenal crisis resulted in above symptoms

4.

Mineralocorticoid deficiency

Because mineralocorticoids stimulate sodium reabsorption and potassium excretion, deficiency results in increased excretion of sodium and decreased excretion of potassium, chiefly in urine but also in sweat, saliva, and the gastrointestinal tract. A low serum concentration of sodium (hyponatremia) and a high concentration of potassium (hyperkalemia) result.

Urinary salt and water loss cause severe dehydration, plasma hypertonicity, acidosis, decreased circulatory volume, hypotension, and, eventually, circulatory collapse. However, when adrenal insufficiency is caused by inadequate adrenocorticotropic hormone (ACTH) production (secondary adrenal insufficiency), electrolyte levels are often normal or only mildly deranged, and the circulatory problems are less severe.

Glucocorticoid deficiency

Glucocorticoid deficiency contributes to hypotension and causes severe insulin sensitivity and disturbances in carbohydrate, fat, and protein metabolism. In the absence of cortisol, insufficient carbohydrate is formed from protein; hypoglycemia and decreased liver glycogen result. Weakness follows, due in part to deficient neuromuscular function. Resistance to infection, trauma, and other stress is decreased. Myocardial weakness and dehydration reduce cardiac output, and circulatory failure can occur.

Decreased blood cortisol results in increased pituitary ACTH production and increased blood beta-lipotropin, which has melanocyte-stimulating activity and, together with ACTH, causes the hyperpigmentation of skin and mucous membranes characteristic of Addison disease. Thus, adrenal insufficiency secondary to pituitary failure does not cause hyperpigmentation.


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