ADDISONS DISEASE

Introduction
In 1855, Thomas Addison, an English physician, provided the first detailed description of primary adrenal insufficiency, now called Addisons disease. The use of this term is reserved for primary adrenal insufficiency in which adrenal cortical hormones are deficient and ACTH levels are elevated because of lack of feedback inhibition.

Addisons disease is a relatively rare disorder in which all the layers of the adrenal cortex are destroyed. Addisons disease, like type 1 DM, is a chronic metabolic disorder that requires lifetime hormone replacement therapy. The adrenal cortex has a large reserve capacity, and the manifestations of adrenal insufficiency usually do not become apparent until approximately 90% of the gland has been destroyed.

Anatomy and Physiology The endocrine system is considered as one of the bodys most complex systems. It affects functions of the different organs or organ system. It is greatly interrelated with the function of the nervous system, to coordinate body processes. Alterations in function of the endocrine system result in a variety of physiologic changes, which may be very serious and fatal, but at times may require minimal hospital care. The end result of most pathologic processes affecting the endocrine system

Anatomy and Physiology

The endocrine system is composed of an interrelated complex of glands (pituitary, adrenals, thyroid, parathyroids, islets of Langerhans of the pancreas, thymus, pineal gland, ovaries, and testes) that secrete a variety of hormones directly into the bloodstream.

Although the nervous and endocrine systems act together to coordinate functions of all body systems, their means of control are different. Exocrine glands (exo- outside) secrete their products into ducts that carry the secretions into body cavities, into lumen of an organ, or to the outer surface of the body. Endocrine glands, by contrast, secrete their products (hormones) into the interstitial fluid surrounding

Functions: Maintenance and regulation of vital functions Response to stress and injury Growth and development Energy metabolism Reproduction Fluid, electrolyte, and acid-base balance

Adrenal Gland
Two small glands, one above each kidney Regulates sodium and electrolyte balance Affects carbohydrate, fat, and protein metabolism Influences the development of sexual characteristics Sustains the flight or fight response

Consist of two sections: Adrenal cortex (outer portion)

o The outer shell of the adrenal gland o Produces mineralocorticoids Aldosterone: regulates electrolyte balance by promoting sodium retention and potassium excretion. o Produces Glucocorticoids Cortisol, Cortisone, and Corticosterone

o Produces sex hormones govern development of certain secondary sex characteristics. Secretion of adrenal androgens is controlled by ACTH.

Adrenal medulla (inner portion)

o The inner core of the adrenal gland o Works as part of the sympathetic nervous system o Produces two catecholamines: epinephrine (also called as adrenalin), norepinephrine (sometimes called noradrenalin).

-Autoimmune disease -Idiopathic atrophy of adrenal glands (sudden cessation of glucocorticoids) -Endocrine disorders -Pituitary hypofunction Mineralocorticoid Glucocorticoid Hyperpigmentation deficiency deficiency

ADDISONS DISEASE

Clinical Manifestations: Subjective: muscle weakness and lethargy, fatigue; anorexia, nausea, abdominal pain, depression, thirst Objective: Increased bronzelike pigmentation of skin and nipples, scars, and buccal mucousa Personality changes Menstrual changes in women; impotence in men Vomiting; diarrhea (GI disturbance), weight loss, dehydration Hypotension, weak pulse Decreased pubic hair and axillary hair Decrease capacity to deal with stress

Diagnostic Test: Physical examination pariticularly for hyperpigmentation of the skin Cortisol level blood test X-ray adrenal glands detect calcium deposits from TB-related Addisons ACTH level blood test

Medications: Celestone (Bethamethasone) Cortone, Cortistan (Cortisone) Decadron (Dexamethasone) Florinef (Fludrocortisone) Cortef (Hydrocortisone) Medrol, Depo-Medrol, Solu-Medrol (Methylprednisolone) Delta-Cortef, Prelone, Orapred, Pediapred (Prednisone)

Surgery Patients with Addison's disease who need surgery with general anesthesia are treated with injections of hydrocortisone and saline. Injections begin on the evening before surgery and continue until the patient is fully awake and able to take medication by mouth. The dosage is adjusted until the maintenance dosage given before surgery is reached.

Nursing Diagnosis: Deficient fluid volume related to excess sodium loss Decrease cardiac output related to electrolyte imbalances

Implementati on
Monitor vital signs four times a day; be alert for the elevation in temperature (infection, dehydration), alterations in pulse rate and rhythm (hyperkalemia), and alterations in blood pressure. Observe for signs of sodium and potassium imbalance Monitor intake and output and weigh daily to assess for deficient fluid volume and nutritional status Administer hormone replacement therapy as ordered to maintain or improve the clients condition Glucocoticoids (cortisone, hydrocortisone): to stimulate diurnal rhythm of cortisol release,

 Mineralocorticoid: fludrocortisone acetate (Florinef) Give with milk or an antacid to limit ulcerogenic factor of the drug Put the client in a private room to prevent contact with clients having infectious diseases Limit the number of visitors; decrease stress in the environment Dont allow client to sit up or stand quickly to avoid orthostatic hypotension Prevent exposure to infection

 Assess fluid balance (and tell the client to increase fluid intake in hot weather) to prevent Addisonian crisis, which may be precipitated by salt or fluid loss in hot weather and during exercise Provide rest periods; prevent fatigue; advise the client to avoid physical and emotional stress Review signs of adrenal hypofunction or hyperfunction so client can recognize need for adjustment of steroid dose Instruct client to wear medical alert band Encourage the consistent goals with emphasis on diet high in nutriten-dense foods (high in carbohydrates and proteins) and adequate sodium to prevent hypoglycemia and hyponatremia Administer antiemetics to prevent fluid and electrolyte loss by vomiting

Nursing interventions for Steroid Therapy (Hormonal Replacement Therapy HRT)

Adrenocorticotropic Hormones Corticosteroids/Glucocorticoids Mineralocorticoids

a.Monitor VS. Retention of sodium and water may cause elevation of BP b.Monitor weight, I and O for edema. c. Avoid exposure to infection. Steroids may mask signs of infection and immunosuppresants.

d. Monitor potassium and calcium levels. Steroids may cause hyperkalemia and hypocalcemia. e. Administer steroids after meals or with milk. Steroids stimulate gastric acid secretions and may cause gastric irritation and peptic ulcer disease. f. Diet of the client should be high protein, high carbohydrate, high potassium, and low sodium diet.

Provide client teaching and discharge planning concerning: Disease process; signs of adrenal insufficiency Use prescribed medications for lifelong replacement therapy; never omit medications Need to avoid stress, trauma, and infections, and to notify physician if these occurr ad medications dosage may need to be adjusted Stress management techniques Diet modification (high in protein, carbohydrates, and sodium) to promote nutritional balance Use of table salt tablets (if prescribed) or ingestions of salty foods (potato chips) if experiencing increased sweating Importance of alternating regular exercise with rest periods

Prognosis With proper medication, patients can expect to live a healthy and normal life.

Adrenal Function After Living Kidney Donation

Due the lack of suitable donor organs a large proportion of kidney transplantations is now performed from living donors. In the year 2002 the number of living donors surpassed the number of cadaveric donors in Switzerland (Swisstransplant, Swiss Transplant Society 2005). Kidney grafts from living donors have superior long-term outcome (Hariharan S, N Engl J Med 2000). At the University Hospital Zurich 28 of the 84 kidney transplantations performed in the year 2004 were from living donors. During living donor nephrectomy the renal artery and renal vein are transected as far away from the kidney as possible, to ensure an

The arterial supply of the adrenal glands is accomplished by several small vessels (ca. 5-15), while the venous drainage is usually dependent on a single vein. While the right-sided adrenal vein drains directly into the inferior vena cava (IVC), the left-sided adrenal vein drains into the renal vein. Variants are relatively rare and occur in 5% of cases (Sebe P, Surg Radiol Anat 2002). Therefore, during donor nephrectomy of the left kidney the adrenal vein is transected, while this is not necessary on the right side.