Focus on Addison’s Disease (Relates to Chapter 50, “Nursing Management: Endocrine Problems,”...

Focus on Addison’s Disease

(Relates to Chapter 50, “Nursing Management: Endocrine Problems,”

in the textbook)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

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Addison’s DiseaseEtiology and Pathophysiology Adrenocortical insufficiency

may Be Addison’s disease

Primary Result from lack of pituitary

ACTH Secondary


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Addison’s DiseaseEtiology and Pathophysiology All three classes of adrenal

corticosteroids are ↓ in Addison’s disease. Glucocorticoids Mineralocorticoids Androgens


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Addison’s DiseaseEtiology and Pathophysiology Common cause is

autoimmune response to adrenal tissue.

Susceptibility genes beginning to be identified

Other endocrine conditions often found


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Addison’s DiseaseEtiology and Pathophysiology Other causes of Addison’s

disease Tuberculosis (rare in North

America) Infarction Fungal infection AIDS Metastatic cancer


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Addison’s DiseaseEtiology 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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Addison’s DiseaseEtiology 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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Addison’s DiseaseClinical Manifestations Does not become evident

until 90% of adrenal cortex is destroyed

Disease usually advanced before diagnosis


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Addison’s DiseaseClinical Manifestations Primary features

Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation


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Hyperpigmentation


Fig. 50-14. Hyperpigmentation typically seen in Addison’s disease.

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Addison’s DiseaseClinical Manifestations Orthostatic hypotension Hyponatremia Hyperkalemia Nausea and vomiting Diarrhea Irritability, depression


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Addison’s DiseaseClinical Manifestations Secondary adrenocortical

hypofunction Signs and symptoms common

with Addison’s disease Patients characteristically

lack hyperpigmentation.


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Addison’s DiseaseComplications 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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Addison’s DiseaseComplications Severe manifestations of

glucocorticosteroid and mineralocorticoid deficiencies Hypotension Tachycardia Dehydration Hyponatremia


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Addison’s DiseaseComplications Manifestations (cont’d)

Hyperkalemia Hypoglycemia Fever Weakness Confusion


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Addison’s DiseaseComplications 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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Addison’s DiseaseDiagnostic 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.


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Addison’s DiseaseDiagnostic Studies Abnormal laboratory

findings Hyperkalemia Hypochloremia Hyponatremia Hypoglycemia


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Addison’s DiseaseDiagnostic Studies Abnormal laboratory

findings (cont’d) Anemia ↑ BUN Low urine cortisol levels


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Addison’s DiseaseDiagnostic 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


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Addison’s DiseaseCollaborative Care Hydrocortisone

Most commonly used as replacement therapy

Glucocorticoid dosage must be ↑ during times of stress to prevent addisonian crisis.


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Addison’s DiseaseCollaborative Care Addisonian crisis

Treatment directed at Shock management High-dose hydrocortisone replacement


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Addison’s DiseaseNursing 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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Addison’s DiseaseNursing Implementation Acute intervention (cont’d)

Protect against infection. Assist with daily hygiene. Protect from extremes.

Light Noise Temperature


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Addison’s DiseaseNursing 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


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(cont’d) Long-term care includes need

for Extra medication Stress management


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(cont’d) Situations requiring

corticosteroid dose adjustment include

Fever Influenza Tooth extraction Physical exertion


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(cont’d) Doses are doubled for minor

stressors and tripled for major stressors.

It is better to err on the side of overreplacement.


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Addison’s DiseaseNursing 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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Corticosteroid TherapyEffects 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.


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Corticosteroid TherapyEffects of Corticosteroid Therapy Expected effects of

corticosteroid therapy Antiinflammatory action Immunosuppression Maintenance of normal BP Carbohydrate and protein

metabolism


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Corticosteroid TherapyManagement Should be taken in the

morning with food to reduce gastric irritation

Must not be stopped abruptly

Assess for corticosteroid-induced osteoporosis.


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Hyperaldosteronism Etiology and Pathophysiology Excessive aldosterone

secretion Sodium retention Potassium Hydrogen ion excretion

Hallmark of hyperaldosteronism Hypertension with

hypokalemic alkalosis


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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


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Hyperaldosteronism Clinical Manifestations Elevated levels of

aldosterone Sodium retention Elimination of potassium

Sodium retention leads to Hypernatremia Hypertension Headache


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Hyperaldosteronism Clinical Manifestations Eliminating potassium

leads to Hypokalemia Muscle weakness Fatigue Cardiac dysrhythmias


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Hyperaldosteronism Clinical Manifestations Eliminating potassium

(cont’d) Glucose intolerance Metabolic alkalosis May lead to tetany


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Hyperaldosteronism Diagnostic Studies Primary aldosteronism

↑ plasma aldosterone levels ↑ sodium levels ↓ potassium levels ↓ renin activity

Adenomas are localized by CT or MRI.


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Hyperaldosteronism Treatment Preferred treatment for

primary hyperaldosteronism is surgical removal of the adenoma.


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Hyperaldosteronism Treatment Before surgery, patients

need Low-sodium diet Potassium-sparing diuretics Antihypertensive agents

Assess BP Fluid/electrolyte balance


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Pheochromocytoma Etiology and Pathophysiology Caused by a tumor of the

adrenal medulla Produces excessive

catecholamines Most often in young to

middle-aged adults


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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.


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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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Pheochromocytoma Treatment Surgical removal of tumor Calcium channel blockers

control BP. Sympathetic blocking agents

may ↓ BP ↓ symptoms of catecholamine

excess Beta blockers to ↓

dysrhythmiasCopyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

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Pheochromocytoma Treatment Monitor BP closely. Make patient as

comfortable as possible. Monitor glucose.


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Pheochromocytoma Treatment Patient needs

Rest Nourishment Emotional support

Stress importance of Follow-up care Routine BP monitoring


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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.

Audience Response Question


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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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Case Study

Lab values reveal ↓ ACTH ↓ plasma cortisol ↓ Na ↓ glucose ↑ K


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Case Study Discussion Questions

1.Based on the findings, what are her possible diagnoses?

2.What is her primary acute nursing management?


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Case Study Discussion Questions

3. What critical patient teaching should you do with her about her home care?

4. What lifestyle modifications should she make?


Focus on Addison’s Disease (Relates to Chapter 50, “Nursing Management: Endocrine Problems,”...

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