1. Focus on Addison’s Disease
(Relates to Chapter 50, “Nursing Management: Endocrine Problems,” in the textbook)
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2. Addison’s Disease Etiology and Pathophysiology
Adrenocortical insufficiency may
Be Addison’s disease
Primary
Result from lack of pituitary ACTH
Secondary
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3. Addison’s Disease Etiology and Pathophysiology
All three classes of adrenal corticosteroids are ↓ in Addison’s disease.
Glucocorticoids
Mineralocorticoids
Androgens
In secondary adrenocortical insufficiency, corticosteroids and androgens are deficient, but mineralocorticoids rarely are. ACTH deficiency may be caused by pituitary disease or suppression of the hypothalamic-pituitary axis as a result of administration of exogenous corticosteroids.
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4. Addison’s Disease Etiology and Pathophysiology
Common cause is autoimmune response to adrenal tissue.
Susceptibility genes beginning to be identified
Other endocrine conditions often found
When other endocrine conditions are present, Addison’s disease is considered a component of polyendocrine deficiency syndrome.
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5. Addison’s Disease Etiology and Pathophysiology
Other causes of Addison’s disease
Tuberculosis (rare in North America)
Infarction
Fungal infection
AIDS
Metastatic cancer
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6. Addison’s Disease Etiology and Pathophysiology
Iatrogenic Addison’s disease may be due to adrenal hemorrhage.
Anticoagulant therapy
Antineoplastic chemotherapy
Nizoral therapy for AIDS
Bilateral adrenalectomy
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7. Addison’s Disease Etiology and Pathophysiology
Most often occurs in adults <60 years old
Affects both genders equally
More common in white females if from autoimmune response
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8. Addison’s Disease Clinical Manifestations
Does not become evident until 90% of adrenal cortex is destroyed
Disease usually advanced before diagnosis
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9. Addison’s Disease Clinical Manifestations
Primary features
Progressive weakness
Fatigue
Weight loss
Anorexia
Skin hyperpigmentation
The manifestations have a very slow (insidious) onset.
Skin hyperpigmentation, a striking feature, is seen primarily in sun-exposed areas of the body, at pressure points, over joints, and in the creases, especially palmar creases.
{See next slide for figure.}
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10. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Hyperpigmentation
It most likely is due to increased secretion of β-lipotropin (which contains melanocyte-stimulating hormone [MSH]) or ACTH. These tropic hormones are increased because of decreased negative feedback and subsequent low corticosteroid levels.
Fig Hyperpigmentation typically seen in Addison’s disease.
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11. Addison’s Disease Clinical Manifestations
Orthostatic hypotension
Hyponatremia
Hyperkalemia
Nausea and vomiting
Diarrhea
Irritability, depression
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12. Addison’s Disease Clinical Manifestations
Secondary adrenocortical hypofunction
Signs and symptoms common with Addison’s disease
Patients characteristically lack hyperpigmentation.
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13. Addison’s Disease Complications
Risk for life-threatening addisonian crisis caused by
Insufficient adrenocortical hormones
Sudden, sharp decrease in these hormones
Triggered by
Stress
Withdrawal of hormone replacement
After adrenal surgery
Following sudden pituitary gland destruction
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14. Addison’s Disease Complications
Severe manifestations of glucocorticosteroid and mineralocorticoid deficiencies
Hypotension
Tachycardia
Dehydration
Hyponatremia
Hypotension is particularly postural.
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15. Addison’s Disease Complications
Manifestations (cont’d)
Hyperkalemia
Hypoglycemia
Fever
Weakness
Confusion
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16. Addison’s Disease Complications
Hypotension can lead to shock.
Circulatory collapse is often unresponsive to usual treatment.
GI manifestations include severe vomiting, diarrhea, and abdominal pain.
Pain in lower back or legs
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17. Addison’s Disease Diagnostic Studies
Subnormal levels of cortisol
Levels fail to rise over basal levels with ACTH stimulation test.
Latter indicates primary adrenal disease.
Positive response to ACTH stimulation indicates functioning adrenal gland.
A positive response to ACTH stimulation points to a probable diagnosis of pituitary disease.
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18. Addison’s Disease Diagnostic Studies
Abnormal laboratory findings
Hyperkalemia
Hypochloremia
Hyponatremia
Hypoglycemia
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19. Addison’s Disease Diagnostic Studies
Abnormal laboratory findings (cont’d)
Anemia
↑ BUN
Low urine cortisol levels
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20. Addison’s Disease Diagnostic Studies
Other abnormal findings
ECG
Low voltage, vertical QRS axis, peaked T waves from hyperkalemia
CT and MRI used to
Localize tumors
Identify adrenal calcifications or enlargement
See Table for more information.
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21. Addison’s Disease Collaborative Care
Hydrocortisone
Most commonly used as replacement therapy
Glucocorticoid dosage must be ↑ during times of stress to prevent addisonian crisis.
Hydrocortisone has both glucocorticoid and mineralocorticoid properties.
Mineralocorticoid replacement with fludrocortisone (Florinef) is administered daily with increased salt in the diet.
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22. Addison’s Disease Collaborative Care
Addisonian crisis
Treatment directed at
Shock management
High-dose hydrocortisone replacement
Large volumes of 0.9% saline solution and 5% dextrose are administered to reverse hypotension and electrolyte imbalances until BP returns to normal.
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23. Addison’s Disease Nursing Implementation
Acute intervention
Frequent assessment necessary
Assess vital signs and signs of fluid and electrolyte imbalance every 30 minutes to 4 hours for first 24 hours.
Take daily weights.
Administer corticosteroid therapy diligently.
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24. Addison’s Disease Nursing Implementation
Acute intervention (cont’d)
Protect against infection.
Assist with daily hygiene.
Protect from extremes.
Light
Noise
Temperature
The patient cannot cope with these extremes because of the inability to produce corticosteroids.
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25. Addison’s Disease Nursing Implementation
Ambulatory and home care
Glucocorticoids usually given in divided doses
Mineralocorticoids given once in the morning
Reflects normal circadian rhythm
Decreases side effects of corticosteroids
The serious nature of the disease and the need for lifelong replacement therapy necessitate a well-organized and carefully presented teaching plan. Table outlines the major areas that must be included in the teaching plan.
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26. Addison’s Disease Nursing Implementation
Ambulatory and home care (cont’d)
Long-term care includes need for
Extra medication
Stress management
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27. Addison’s Disease Nursing Implementation
Ambulatory and home care (cont’d)
Situations requiring corticosteroid dose adjustment include
Fever
Influenza
Tooth extraction
Physical exertion
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28. Addison’s Disease Nursing Implementation
Ambulatory and home care (cont’d)
Doses are doubled for minor stressors and tripled for major stressors.
It is better to err on the side of overreplacement.
Minor stressor examples: Respiratory infection, dental work
Major stressor examples: Divorce, loss of a parent
If vomiting or diarrhea occurs, as may happen with influenza, the health care provider must be notified immediately because electrolyte replacement may be necessary. In addition, these manifestations may be early indicators of crisis.
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29. Addison’s Disease Nursing Implementation
Instruct on how to take BP and report findings.
Carry emergency kit with IM hydrocortisone, syringes, and instructions for use.
Teach patient and significant others how to give IM injection.
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30. Corticosteroid Therapy Effects of Corticosteroid Therapy
Long-term use of corticosteroids can lead to complications and side effects.
Reserved for cases with risk of death or loss of function
Potential benefits must be weighed against risks.
See Table for more information.
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31. Corticosteroid Therapy Effects of Corticosteroid Therapy
Expected effects of corticosteroid therapy
Antiinflammatory action
Immunosuppression
Maintenance of normal BP
Carbohydrate and protein metabolism
A beneficial effect in one situation may be a harmful one in another. For example, the vasopressive effect of the hormone is critical in enabling the organism to function in stressful situations but can produce hypertension when used for drug therapy.
Specific side effects related to corticosteroid therapy are listed in Table
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32. Corticosteroid Therapy Management
Should be taken in the morning with food to reduce gastric irritation
Must not be stopped abruptly
Assess for corticosteroid-induced osteoporosis.
Corticosteroids taken for >1 week will suppress adrenal production, and oral steroids should be tapered.
Therapies to reduce the resorption of bone may include increased calcium intake, vitamin D supplementation, bisphosphonates (e.g., alendronate [Fosamax]), and institution of a low-impact exercise program.
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33. Hyperaldosteronism Etiology and Pathophysiology
Excessive aldosterone secretion
Sodium retention
Potassium
Hydrogen ion excretion
Hallmark of hyperaldosteronism
Hypertension with hypokalemic alkalosis
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34. Hyperaldosteronism Etiology and Pathophysiology
Primary hyperaldosteronism
Usually caused by solitary adrenocortical adenoma
Secondary hyperaldosteronism
Due to renal artery stenosis, renin-secreting tumors, and chronic kidney disease
Occasionally, multiple lesions are involved and are associated with bilateral adrenal hyperplasia.
PA affects both genders equally and occurs most frequently between 30 and 50 years of age. It is estimated that approximately 1% of cases of hypertension are caused by PA.
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35. Hyperaldosteronism Clinical Manifestations
Elevated levels of aldosterone
Sodium retention
Elimination of potassium
Sodium retention leads to
Hypernatremia
Hypertension
Headache
Edema does not usually occur because the rate of sodium excretion increases, which prevents more severe sodium retention.
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36. Hyperaldosteronism Clinical Manifestations
Eliminating potassium leads to
Hypokalemia
Muscle weakness
Fatigue
Cardiac dysrhythmias
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37. Hyperaldosteronism Clinical Manifestations
Eliminating potassium (cont’d)
Glucose intolerance
Metabolic alkalosis
May lead to tetany
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38. Hyperaldosteronism Diagnostic Studies
Primary aldosteronism
↑ plasma aldosterone levels
↑ sodium levels
↓ potassium levels
↓ renin activity
Adenomas are localized by CT or MRI.
The diagnosis of hyperaldosteronism should be suspected in all hypertensive patients with hypokalemia who are not being treated with diuretics.
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39. Hyperaldosteronism Treatment
Preferred treatment for primary hyperaldosteronism is surgical removal of the adenoma.
Although this surgery can be done as an open procedure, laparoscopic adrenalectomy is most frequently performed because of the benefits that this minimally invasive surgery offers.
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40. Hyperaldosteronism Treatment
Before surgery, patients need
Low-sodium diet
Potassium-sparing diuretics
Antihypertensive agents
Assess BP
Fluid/electrolyte balance
Potassium-sparing diuretics include spironolactone (Aldactone) and eplerenone (Inspra).
Oral potassium supplements and sodium restrictions may also be necessary.
BP must be monitored because unilateral adrenalectomy is successful in controlling hypertension in only 80% of patients with adenoma.
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41. Pheochromocytoma Etiology and Pathophysiology
Caused by a tumor of the adrenal medulla
Produces excessive catecholamines
Most often in young to middle-aged adults
The most dangerous immediate effect of the disease is severe hypertension.
If left untreated, it may lead to hypertensive encephalopathy, diabetes mellitus, cardiomyopathy, and death.
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42. Pheochromocytoma Clinical Manifestations
Clinical features include
Severe, episodic hypertension
Severe, pounding headache
Tachycardia with palpitations
Profuse sweating
Abdominal or chest pain
Diagnosis is often missed.
Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants. The duration of the attacks may vary from a few minutes to several hours.
Pheochromocytoma is an uncommon cause of hypertension, accounting for only 0.1% of all cases of hypertension. Consider this condition in patients who do not respond to traditional hypertensive treatments.
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43. Pheochromocytoma Diagnostic Studies
Best test is measurement of urinary fractionated metanephrines and catecholamines in 24-hour collection.
Serum catecholamines are elevated.
CT and MRI are used for tumor localization.
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44. Pheochromocytoma Treatment
Surgical removal of tumor
Calcium channel blockers control BP.
Sympathetic blocking agents may
↓ BP
↓ symptoms of catecholamine excess
Beta blockers to ↓ dysrhythmias
Treatment with α-adrenergic and β-blockers is required preoperatively to control blood pressure and prevent intraoperative hypertensive crises.
After adequate α-adrenergic blockade, β-blockers (e.g., propranolol [Inderal]) are used to decrease tachycardia and other dysrhythmias.
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45. Pheochromocytoma Treatment
Monitor BP closely.
Make patient as comfortable as possible.
Monitor glucose.
Preoperative and postoperative care is similar to that for any patient undergoing adrenalectomy, except that BP fluctuations from catecholamine excesses tend to be severe and must be carefully monitored.
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46. Pheochromocytoma Treatment
Patient needs
Rest
Nourishment
Emotional support
Stress importance of
Follow-up care
Routine BP monitoring
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Audience Response Question
The nurse determines that the patient in acute adrenal insufficiency is responding favorably to treatment when:
1. The patient appears alert and oriented.
2. The patient’s urinary output has increased.
3. Pulmonary edema is reduced as evidenced by clear lung sounds.
4. Laboratory tests reveal elevations of potassium and glucose serum levels and a decrease in the sodium level.
Answer: 1
Rationale: The patient in acute adrenal insufficiency will have the following clinical manifestations: Hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion. Collaborative care will include administration of corticosteroids. An outcome that would indicate patient improvement would be improved level of consciousness (i.e., alert and oriented).
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48. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study
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Case Study
30-year-old woman arrives to the ED with syncope after standing up.
Her skin is hyperpigmented over her joints and on her palms.
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50. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
Case Study
Lab values reveal
↓ ACTH
↓ plasma cortisol
↓ Na
↓ glucose
↑ K
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51. Case Study Discussion Questions
Based on the findings, what are her possible diagnoses?
What is her primary acute nursing management?
Addison’s disease.
Frequent nursing assessment and protection from extremes.
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52. Case Study Discussion Questions
What critical patient teaching should you do with her about her home care?
What lifestyle modifications should she make?
3. Discuss the serious nature of the disease and the need for lifelong replacement therapy (see Table for major areas that must be included in the teaching plan).
4. Always carry an emergency kit.
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