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DISORDERS OF THE ADRENAL GLANDS

DISORDERS OF THE ADRENAL GLANDS. ADRENAL HYPERFUNCTION (Cushing’s Syndrome). ETIOLOGY/PATHOPHYSIOLOGY May be caused by: 1. Hyperplasia of adrenal tissue resulting from overstimulation by the pituitary hormone – ACTH 2. Tumor of the adrenal cortex

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DISORDERS OF THE ADRENAL GLANDS

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  1. DISORDERS OF THE ADRENAL GLANDS

  2. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • ETIOLOGY/PATHOPHYSIOLOGY • May be caused by: • 1. Hyperplasia of adrenal tissue resulting from overstimulation by the pituitary hormone – ACTH • 2. Tumor of the adrenal cortex • 3. ACTH-secreting tumor outside the pituitary –e.g. oat cell cancer of lung • 4. Prolonged or overuse of corticosteroid drugs

  3. CUSHINGS SYNDROME IN TWIN GIRL

  4. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • CLINICAL MANIFESTATIONS • The overabundance of glucocorticoids, mineralocorticoids, and sex hormones  • Moonface • Buffalo hump • Thin arms and legs due to muscle wasting • Weight gain

  5. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • CLINICAL MANIFESTATIONS cont. • Hypokalemia; proteinuria; hyperglycemia • Increased urinary calcium excretion & renal calculi • Susceptible to infections • Loss of libido • Osteoporosis and kyphosis (due to abnormal Ca++ absorption)

  6. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • SUBJECTIVE DATA • Depression • Inability to concentrate • Mood disturbances • ↑ risk for self-harm • Back pain • Concern re: altered body image

  7. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • OBJECTIVE DATA: • Ecchymoses and petechiae, fragile skin, slow wound healing • Weight gain, abdominal enlargement (striae) • Back pain • Hirsutism in women • Menstrual irregularities • Deepening of the voice • HTN

  8. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • DIAGNOSTIC TESTS • Diagnosis usually based on clinical appearance and lab results • Plasma Cortisol - ↑ • Plasma ACTH - ↑ or ↓ • 24 hr urine for: 17-ketosteroids and 17-hydroxysteroids - ↑ • Blood and urine glucose

  9. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • DIAGNOSTIC TESTS cont. • Skull xray – visualize the sellaturcicca • Adrenal angiography • Abdominal CT, US, MRI

  10. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • MEDICAL MANAGEMENT • Treat the causative factor • Adrenalectomy for adrenal tumor • Radiation or surgical removal for pituitary tumors • Medication: • Lysodren (Mitodane therapy) – alters the peripheral metabolism of cortisol decreases plasma and corticosteroid level; supressescortisol production • Also known as a “medical adrenalectomy”

  11. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • MEDICAL MANAGEMENT cont. • Low Na+, high K+ diet • Low sodium  reduces edema • High potassium  correct hypocalemia and stabilize cardiac status • ↓ calorie, ↓CHO • If Cushing’s is due to prolonged corticosteroid use: • 1. gradually reduce and discontinue steroid therapy • 2. reduce dose of steroids • 3. convert to alternate-day regimen • *KEY NURSING INTERVENTION: gradualreduction of dose

  12. NURSING DIAGNOSIS/INTERVENTIONS • Deficit knowledge, r/t therapeutic regime • Activity Intolerance, r/t weakness and immobility • NURSING INTERVENTIONS: • Skin Care – gentle handling; frequent assessment • Encourage ambulation as tolerated • Paticipation in ADL’s • Encourage verbalization of concerns • Skilled observation of s/sx depression/ suicidal-thoughts

  13. ADRENAL HYPERFUNCTION(Cushing’s Syndrome) • NURSING INTERVENTIONS cont. • Pt. understanding of importance of complying with medication regimen • Medic-Alert bracelet • Avoid exposure to infections • Instruct s/sx Addison’s disease for post-op care • PROGNOSIS • If not resolved with tumor removal – major lifestyle changes are needed; ↑risk for complications, probable shortened lifespan

  14. ADRENAL HYPOFUNCTION(Addison’s Disease) • Etiology/pathophysiology – Adrenocortical Insufficiency • Adrenal glands do not secrete adequate amounts of glucocorticoids and mineralocorticoids, and androgens • May result from • Primary Addison’s (rare) • Adrenalectomy • Pituitary hypofunction • Long-standing steroid therapy

  15. ADRENAL HYPOFUNCTION(Addison’s Disease) • ETIOLOGY/PATHOPHYSIOLOGY cont. • Most common cause: • Antibodies destroy adrenal cortex (tissue outside) Common cause is autoimmune response • Deficiencies in aldosterone and cortisol disturbance in CHO, Fat, and Protein metabolism  fluid and electrolyte imbalance, dehydration, water loss, and hypovolemia

  16. ADRENAL HYPOFUNCTION(Addison’s Disease) • CLINICAL MANIFESTATIONS • Related to imbalances of adrenal hormones, nutrients, and electrolytes (not enough glucocorticoids and mineralocorticoids) • Progressive weakness and fatigue • Nausea; anorexia; craving for salt • Postural hypotension: vertigo, weakness, syncope • Headache • Disorientation • Abdominal pain; lower back pain • Anxiety, apprehension; increase reaction to stress

  17. ADRENAL HYPOFUNCTION(Addison’s Disease) • Clinical manifestations cont. • Darkly pigmented skin and mucous membranes • Weight loss • Vomiting/Diarrhea • Hypoglycemia and fatigue • Abnormally low or high body temperature • Hyponatremia, Hyperkalemia when these are present, you must assess for adrenal crisis

  18. ADRENAL HYPOFUNCTION(Addison’s Disease) • SUBJECTIVE ASSESSMENT • Patient may c/o: severe headache, disorientation, abdominal pain or lower back pain • c/o anxiety, apprehension; poor tolerance to stress • Assess overall understanding of disease

  19. ADRENAL HYPOFUNCTION(Addison’s Disease) • OBJECTIVE ASSESSMENT • Observation of skin and mucous membrane color; skin hyperpigmentation • Weight loss • Vomiting , diarrhea • Hypoglycemia, fatigue • ↑ or ↓ body temp • s/sx hypotension • Lab - hyperkalemia

  20. ADRENAL HYPOFUNCTION(Addison’s Disease) • MEDICAL MANAGEMENT • Treatment • Restore fluid and electrolyte balance • Replacement of deficient adrenal hormones • Diet high in sodium and low in potassium • Adrenal crisis • IV corticosteroids in a solution of saline and glucose • Medications: Oral Hydrocortisone (has mineralo- and gluco- corticoid properties) • Florinef – mineralocorticoid medication

  21. ADRENAL HYPOFUNCTION(Addison’s Disease) • DIAGNOSTIC TESTS • Serum: Na+, K+, glucose, and Fasting Plasma cortisol and aldosterone levels with ACTH stimulation test • Urine: 24hr collection • RESULTS: If + for adrenal hypofunction: • ↓ Na+, glucose, 17-ketosteroids & 17-hydroxysteroids, aldosterone and cortisol levels • ↑ K+ • GTT - abnormal

  22. ADRENAL HYPOFUNCTION(Addison’s Disease) • NURSING DIAGNOSES • Ineffective tissue perfusion, peripheral r/t electrolyte imbalance • Risk for infection r/t altered metabolic process • NURSING INTERVENTIONS • Monitor circulatory status/VS, particularly Temp, BP • I&O, daily weight • s/sx dehydration

  23. ADRENAL HYPOFUNCTION(Addison’s Disease) • NURSING INTERVENTIONS cont. • Safe administration IV meds; oral meds • s/sx adrenal crisis and note triggers (sl. 23) • Pt. Teaching • Use and carry IM hydrocortisone (solucortef, solumedrol, etc.) • Adherence to medication regimen • Reporting ALL illnesses to MD

  24. ADRENAL HYPOFUNCTION(Addison’s Disease) • PROGNOSIS: with long-term steroid treatment, good medical care and follow up - fair

  25. Development of AddisonianCrisis • Sudden, severe drop in BP; syncope • Nausea and vomiting • Extremely high temperature • Cyanosis progressing to vasomotor collapse and death • Treatment: • IV corticosteroids in saline and glucose; IM corticosteroid which patient should carry with them

  26. PHEOCHROMOCYTOMA • Etiology/pathophysiology • Rare tumor of the adrenal medulla  Causes excessive secretion of epinephrine and norepinephrine (catecholamines)  severe HTN • Clinical Manifestations • Hypertension (300/175) fluctuates  stroke, kidney damage, and retinopathy • Severe h/a, tachycardia, abdominal or chest pain • Cardiac damage  heart failure

  27. PHEOCHROMOCYTOMA • SUBJECTIVE DATA: During hypertensive crisis – pt. c/o or may feel: • Severe h.a. • Nervous • Palpitations, dizzy, dyspneic • Nausea, anxiety, heat intolerance • Interview pt. re: stressors or overexertion • Identify coping methods

  28. PHEOCHROMOCYTOMA • OBJECTIVE DATA: • VS – BP, pulse, resp. rate ↑ • Presence of: tremors, diaphoresis, dilated pupils, glycosuria, hyperglycemia • Response to medications

  29. PHEOCHROMOCYTOMA • DIAGNOSTIC TESTS • 24 hr urine for catecholamine metabolites • + for disease = ↑ values • CT/MRI of adrenal glands • Plasma catecholamine – lab draw, and measured during an ‘attack’.

  30. PHEOCHROMOCYTOMA • MEDICAL MANAGEMENT • Surgical removal of tumor • Pre-op administration of Ca++ channel blockers (eg. Cardene) or alpha-adrenergic blockers (eg. Regitine) to control HTN • Beta-blockers (e.g. Inderal) given to reduce tachycardia and dysrhythmias

  31. PHEOCHROMOCYTOMA • NURSING INTERVENTIONS • Same as for any major surgery • Post-op Adrenalectomy (due to large amounts of hydrocortisone administration) – Monitor for: • BP changes; s/sx cardiovascular collapse • IV fluid and med administration • Administration of vasopressors and corticosteroids • Adequate rest and avoidance of stress • I & O • Diet: avoid stimulants

  32. PHEOCHROMOCYTOMA • NURSINGDIAGNOSIS • Ineffective tissue perfusion, cp, renal, r/t hypertension • Activity Intolerance, r/t hypertension • PROGNOSIS: • If undiagnosed and untreated  DM, cardiomyopathy, and death • After tumor removal - good • Inoperative tumor – depends on adequate medical management of HTN

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