Addison's Disease

ADDISONS DISEASE
Definition: Hyposecretion of the adrenal cortex hormones 90% of the gland is destroyed Originates within the adrenal gland and is characterized by the decreased secretion of mineralocorticoids, glucocorticoids and androgens. Usually caused by an auto immune process Uncommon; At any age and in both sexes
Causes: - Bilateral adrenelectomy - Hemorrhage into adrenal glands - TB, histoplasmosis, cytomegalovirus - Family history
ADDISONS CRISIS
"Addisonian crisis" or "adrenal crisis - is a constellation of symptoms that indicate severe adrenal insufficiency. This may be the result of either previously undiagnosed Addison's disease, a disease process suddenly affecting adrenal, or an intercurrent problem in someone known to have Addison's disease. It is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment.
CHARACTERISTIC SIGNS AND SYMPTOMS

Addisons Crisis
hyperkalemia due to reduced aldosterone secretion. BUN increase, as the GFR is reduced. Hyponatremia is caused by reduced aldosterone secretion. Reduced cortisol secretion leads to impaired glycogenesis and a reduction of glycogen in the liver and muscle, causing hypoglycemia.
Sudden penetrating pain in the legs, lower back or abdomen Severe vomiting and diarrhea dehydration Low blood pressure loss of consciousness and ability to stand Confusion, psychosis, slurred speech Severe lethargy
PATHOPHYSIOLOGY
ADDISONS DISEASE
ETIOLOGY (Autoimmune: e.g. TB, Fungal Infections, AIDS) Destruction of own tissue Affects functioning of Adrenal Cortex Decrease production of Mineralocorticoid and glucocorticoids Cortisol deficiency causes altered metabolism, decreased stress tolerance, and emotional ability. Aldosterone deficiency causes urinary loss of sodium, chloride, and water, resulting in dehydration and electrolyte imbalances. Androgen deficiency leads to the loss of secondary sex characteristics. ADDISONS DISEASE
ETIOLOGY (Defects, surgically removed)
Depressed Anterior Pituitary gland function
Decreased ACTH production
Depressed adrenal stimulation
Affects functioning of Adrenal Cortex
Decrease production of Mineralocorticoid and glucocorticoids
ADDISONS DISEASE
DIAGNOSTIC TESTS
Addisons Disease/Crisis
ACTH STIMULATION TEST

This test involves measuring the level of cortisol in a patients blood before and after an injection of synthetic ACTH. If the adrenal glands are functional, cortisol levels will rise in response to the ACTH stimulation. If they are damaged or non-functional, then their response to ACTH will be minimal. Normal: double from a baseline of 20-30 ug/dl within 60 minutes
Serum Sodium levels: low (hyponatremia) Serum Potassium levels: high (hyperkalemia) ABGs: metabolic acidosis FBS: low (hypoglycemia) X-rays: presence of granuloma (TB infection) Serum cortisol levels: low Serum ACTH levels: high Serum Aldosterone: decreased
MEDICAL MANAGEMENT
Addisons Disease/Crisis
HORMONE REPLACEMENT THERAPY

Treatment of Addison's disease involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced orally with hydrocortisone tablets, a synthetic glucocorticoid, taken once or twice a day. If aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid called fludrocortisone acetate (Florinef), which is taken once a day.
An ample intake of sodium is recommended, especially during heavy exercise, when the weather is hot, or if you have gastrointestinal upsets, such as diarrhea. Your doctor will also suggest a temporary increase in your dosage if you're facing a stressful situation, such as an operation, an infection or a minor illness.
Treatment must usually be continued for life.
ADDISONS CRISIS
Standard therapy involves intravenous injections of hydrocortisone, saline (salt water), and dextrose (sugar). This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the amount of hydrocortisone is decreased until a maintenance dose is achieved. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.
NURSING DIAGNOSIS
Fluid volume deficit, related to hypovolemia and vomiting secondary to adrenal insufficiency Decreased cardiac output, related to hypovolemia Risk for imbalanced nutrition: less than body requirements Risk for injury related to weakness
NURSING DIAGNOSIS
Disturbed body image related to change in skin pigmentation Activity intolerance related to weakness, fatigue, and/or muscle aches Disturbed thought process related to depression and irritability
NURSING INTERVENTIONS
Monitor vital signs, especially BP Monitor intake and output closely. Take and record weight at the same time daily. Monitor electrolytes, and report abnormal results. Provide small, frequent feedings.
Decrease stress in the environment. Prevent exposure to infection. Provide rest periods to prevent fatigue. Provide diet high in protein, Na and carbohydrates; low K Administer steroids after meals or with milk. Provide written and verbal instructions on administering steroids
Monitor neurological status, noting irritability and confusion. Administer IV fluids (5% dextrose in saline, plasma) as ordered to treat vascular collapse Administer IV glucocorticoids as ordered

Addison's Disease

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ADDISONS DISEASE

CHARACTERISTIC SIGNS AND SYMPTOMS

ETIOLOGY (Defects, surgically removed)

Depressed Anterior Pituitary gland function

Decreased ACTH production

Depressed adrenal stimulation

Affects functioning of Adrenal Cortex

Decrease production of Mineralocorticoid and glucocorticoids

ACTH STIMULATION TEST

HORMONE REPLACEMENT THERAPY

Treatment must usually be continued for life.

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