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ENDO MW2.pptx

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  1. 1. Adrenal Disorders Prof.Dr .RS Mehta 1 Insufficiency (Addison’ s disease) Excess (Cushing’s Syndrome)
  2. 2. ADDISON’S DISEASE Prof.Dr .RS Mehta 2
  3. 3. Introduction 3 • Also called chronic adrenal insufficiency, hypocortisolism,hypoadren alism) • is a rare, chronic endocrine system disorder in which the adrenalglandsdo not produce sufficientsteroid hormones.
  4. 4. Introduction 4 • Thomas Addison (1793-1860) first described the syndrome in 1855. • Age- can affect people of any age, most common between the ages of 30 and 50. • Sex- morecommon in women than men.
  5. 5. Etiology 5 • Anatomic destruction of gland (chronic or acute) • Autoimmune or idiopathic atrophy • Surgical removal of both adrenal glands • Infections (tuberculosis,fungal,viral— especially in AIDS) • Invasion:metastatic • Congenital adrenal hyperplasia • Inadequate secretion ofACTH from pitutary gland.
  6. 6. Types of Addison’s disease Prof.Dr .RS Mehta 6 Primary • associated with primary inability of the adrenal to secrete sufficient quantities of hormone Secondary • associated with a secondary failure due to inadequateACTH formation or release
  7. 7. Clinical Manifestations 7
  8. 8. Hyperpigmentation 8
  9. 9. Diagnostic Measures Specific LAB test • Serum cortisol • PlasmaACTH – IftheACTH level is high,the person probably has primary adrenal insufficiency . – If theACTH level is low,the person probably has secondary or tertiary adrenal insufficiency .
  10. 10. Diagnostic measures. • Serum glucose • Serum electrolytes level • Complete blood count • CT ,MRI:T o rule out pituitary and adrenal mass
  11. 11. Complications • Adrenal crisis(addisonian crisis): sudden pain in back, abdomen, legs, cyanosis and the classic signs of circulatory shock: pallor , apprehension, rapid and weak pulse, rapid respirations,and low blood pressure. • Osteoporosis
  12. 12. Management • 1. Correct fluid and electrolyte imbalances: Directed primarily toward repletion of circulating glucocorticoids and replacement of the sodium and water deficits. • 2. Correct Hypoglycemia: An IV infusion of 5% glucose in normal saline solution(DNS) or 25% dextrose bolus.
  13. 13. Management 3.Replace Steroids:a bolus iv infusion of 100 mg hydrocortisone. – Maintenance100-mg bolus of hydrocortisone IV every 6 h. • Lifelong replacement of corticosteroids and mineralocorticoids • Mineralocorticoid supplementation - 0.05–0.1 mg fludrocortisone per day PO.
  14. 14. NURSING MANAGEMENT Prof.Dr .RS Mehta 14
  15. 15. Nursing assessment • Patient’ s level of stress. • Vital signs • Assesses the skin color and turgor • Weight changes,muscle weakness,and fatigue
  16. 16. Nursing Diagnosis • Activity intolerance related to fatigue • Risk for Deficient FluidVolume • Risk for Imbalanced Nutrition:LessThan Body Requirements
  17. 17. Monitoring and managing addisonian crisis • Physical and psychological stressors must be avoided like exposure to cold, overexertion, infection,and emotional distress. • Intravenous administration of fluid, glucose, and electrolytes, especially sodium; replacement of missing steroid hormones; and vasopressors.
  18. 18. Restoring fluid balance • Assesses the patient’s skin turgor , mucous membranes,weight. • Encourages the patient to consume foods and fluids and select foods high in sodium • Administer hormone replacement as prescribed and to modify the dosage during illness and other stressful occasions.
  19. 19. Others 19 • Reliving fatigue • Maintaining optimal nutrition
  20. 20. Prognosis • T reatment ofAddison's disease is lifelong. • The prognosis depend on the underlying cause.
  21. 21. CUSHING’S SYNDROME
  22. 22. Introduction • Cushing’s syndrome (Hypercortisolism, Adrenal Hyperfunction) : is a cluster of clinical abnormalities caused by excessive levels of adrenocortical hormones (particularly cortisol) • 1st described by Harvey Cushing in 1932.
  23. 23. Incidence • Cushing’ s syndrome affects 13 of every 1 million people. • It is more common in women than in men and occurs primarily between ages 25 and 40.
  24. 24. Etiology • Excess. In approximately 70% of patients, Cushing’s syndrome results from excessive production of corticotropin and consequent hyperplasia of the adrenal cortex. • Pituitary hypersecretion and pituitary tumors
  25. 25. Clinical manifestation • Central-type obesity , • Fatty“buffalo hump” relatively A heavy trunk,and thin extremities. • “Moon-faced” appearance • Increased oiliness of the skin and acne. Prof.Dr .RS Mehta 25
  26. 26. Prof.Dr .RS Mehta 26
  27. 27. Contd… • Abnormal distribution results in fa t which a moon shaped face
  28. 28. Manifestations Due to: Prof.Dr .RS Mehta 29 Excess Glucocorticoids • Weight gain • Deposition of adipose tissue • Oily complexion. • Muscle weakness • osteoporosis • Mental disturbances Excess Mineralocorticoids • Hypertension • Hypernatremia • Hypokalemia • Expanded blood volume • Edema Excess androgens • Hirsutism • Breasts – Atrophy. • Amenorrhoea • Voice – masculine.
  29. 29. Diagnosis Prof.Dr .RS Mehta 30 • Low-dose dexamethasone suppression test • Imaging studies. Ultrasound,CT scan,or angiography localizes adrenal tumors and may identify pituitary tumors. • Serum Electrolyte levels • Increased blood glucose
  30. 30. Diagnosis Prof.Dr .RS Mehta 31 • Measurement of a 24-h urine free cortisol can also be used as a screening test. A level >140 nmol/d (50 μg/d) is suggestive of cushing’s syndrome.
  31. 31. Management Prof.Dr .RS Mehta 32 • Pituitary irradiation. with pituitary-dependent Patients Cushing’ s syndrome with adrenal hyperplasia may require pituitary irradiation.
  32. 32. Drug therapy Prof.Dr .RS Mehta 33 • Adrenal enzyme inhibitors: Metyrapone, aminoglutethimide, mitota ne, and ketoconazole may be used to reduce hyperadrenalism therapy is • Cortisol therapy Cortisol essential during and after surgery .
  33. 33. Management Prof.Dr .RS Mehta 34 • Diabetes mellitus and peptic ulcer common in the patient with Cushing’s syndrome. Therefore, insulin therapy and medication to treat peptic ulcer may be initiated if needed.
  34. 34. Surgical Management Prof.Dr .RS Mehta 35 • Transsphenoidal hypophysectomy: Surgical removal of the tumor by transsphenoidal hypophysectomy . • Adrenalectomy
  35. 35. NURSING MANAGEMENT Prof.Dr .RS Mehta 36
  36. 36. Nursing assessment Prof.Dr .RS Mehta 37 • Health history. The history includes information about the patient’s level of activity and ability to carry out routine and self-care activities. • Physical exam. The skin is observed and assessed for trauma,infection,breakdown,bruising,and edema. • Mental function. The nurse assesses the patient’s mental function including mood, responses to questions,awareness of environment,and level of
  37. 37. Nursing diagnosis Prof.Dr .RS Mehta 38 • Self-care deficit related to weakness, fatigue, muscle wasting,and altered sleep patterns • Impaired skin integrity related to edema, impaired healing,and thin and fragile skin • Disturbed body image related to physical appearance, impaired altere d sexual functioning,and decreased activity level
  38. 38. Nursing Diagnosis Prof.Dr .RS Mehta 39 • Disturbed thought processes related to mood swings,irritability,and depression. • Risk for injury related to weakness • Risk for infection related to suppression of inflammatory response
  39. 39. Nursing Interventions Prof.Dr .RS Mehta 40 • Decreasing Risk for injury • Decreasing risk for infection • Preparing patient for surgery • Encouraging rest and activity • Promoting Skin integrity • Improving Body image • Improving thought process
  40. 40. Prognosis Prof.Dr .RS Mehta 41 • Without treatment, hypercortisolism persists and in many patients worsens. • Untreated disease carries a dismal survival rate of 50% at 5 years. • Despite improvement of complications in most patients, cardiovascular risk, hypertension, obesity, and decreased quality of life may persist in some patients.

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