focus on addison’s disease (relates to chapter 50, “nursing management: endocrine problems,”...
TRANSCRIPT
Focus on Addison’s Disease
(Relates to Chapter 50, “Nursing Management: Endocrine Problems,”
in the textbook)
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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
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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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Addison’s DiseaseNursing Implementation Ambulatory and home care
(cont’d) Long-term care includes need
for Extra medication Stress management
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Addison’s DiseaseNursing Implementation Ambulatory and home care
(cont’d) Situations requiring
corticosteroid dose adjustment include
Fever Influenza Tooth extraction Physical exertion
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Addison’s DiseaseNursing 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.
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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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