ADDISON’S DISEASE

(also called Addison disease, chronic adrenal insufficiency, adrenocortical insufficiency , hypocortisolism, and
hypoadrenalism)

DEFINITION
Addison’s disease is a rare, chronic endocrine disorder in which the adrenal glands do not produce sufficient
steroid hormones (glucocorticoids and often mineralocorticoids).

Addison’s disease results when adrenal cortex function is inadequate to meet the patient’s need for cortical
hormones.

CAUSES and RISK FACTORS

 Autoimmune or idiopathic atrophy of the adrenal glands is responsible for 80% of cases.
 Surgical removal of both adrenal glands
 Infection of the adrenal glands. Tuberculosisand histoplasmosis are the most common infections that destroy
adrenal gland tissue.
 Inadequate secretion of ACTH from the pituitary gland also results in adrenal insufficiency because of
decreased stimulation of the adrenal cortex.
 Therapeutic use of corticosteroids : Treatment with daily administration of corticosteroids for 2 to 4 weeks
may suppress function of the adrenal cortex
Risk factors include other autoimmune disease conditions such as
 Chronic thyroiditis
 Graves' disease
 Hypoparathyroidism
 Hypopituitarism
 Myasthenia gravis
 Pernicious anemia
 Testicular dysfunction
 Type I diabetes

PATHOPHYSIOLOGY

Cortisol plays many vital roles and is essential to many body functions because it:

 Works with adrenaline to help the body manage physical and emotional stress
 Converts protein into glucose to boost flagging blood sugar levels
 Works in tandem with the hormone insulin to maintain constant blood sugar levels
 Reduces inflammation
 Helps the body maintain a constant blood pressure
 Helps the workings of the immune system.
 Damage to the adrenal cortex

Progressive atrophy of gland

Deficiency in cortisone and aldosterone

Imbalance of these hormones causes deregulation of important body functions that are potentially life-
threatening.

CLINICAL MANIFESTATIONS
 Muscle weakness
 Anorexia
 Gastrointestinal symptoms
 Fatigue,
 Emaciation,
 Dark pigmentation of the skin, knees, elbows, and mucous membranes
 Hypotension
 Low blood glucose levels
 Low serum sodium levels, and high serum potassium levels.
 Mental status changes such as depression, emotional lability, apathy, and confusion
 In severe cases, the disturbance of sodium and potassium metabolism may be marked by depletion of
sodium and water and severe, chronic dehydration.
 With disease progression and acute hypotension, the patient develops addisonian crisis, which is
characterized by
 Cyanosis and the classic signs of circulatory shock: pallor, apprehension, rapid and weak
pulse, rapid respirations, and low blood pressure.
 Headache, nausea, abdominal pain, and diarrhea
 Signs of confusion and restlessness.
 Even slight overexertion, exposure to cold, acute infections, or a decrease in salt intake may
lead to circulatory collapse, shock, and death if untreated.

DIAGNOSTIC FINDINGS

 Laboratory findings include decreased blood glucose (hypoglycemia) and sodium (hyponatremia) levels, an
increased serum potassium (hyperkalemia) level, and an increased white blood cell count (leukocytosis).
 The diagnosis is confirmed by low levels of adrenocortical hormones in the blood or urine and decreased
serum cortisol levels
 Other tests may include:
 Abdominal x-ray
 Abdominal CT scan
MANAGEMENT

 Immediate treatment of circulatory shock:

 Restoring blood circulation
 Administering fluids and corticosteroids,
 Monitoring vital signs
 Placing the patient in a recumbent position with the legs elevated.
 Hydrocortisone is administered intravenously, followed with 5% dextrose in normal saline.
 Vasopressors may be required if hypotension persists.
 Antibiotics may be administered if infection has precipitated adrenal crisis in a patient with chronic
adrenal insufficiency.
 Oral intake may be initiated as soon as tolerated.
 Gradually, intravenous fluids are decreased when oral fluid intake is adequate to prevent hypovolemia.
 If the adrenal gland does not regain function, the patient needs lifelong replacement of corticosteroids
and mineralocorticoids to prevent recurrence of adrenal insufficiency.
 Additionally, the patient may need to supplement dietary intake with added salt during times of
gastrointestinal losses of fluids through vomiting and diarrhea.
 If patient have an illness such as an infection, or an accident, or anything else causing major stress,
such as an operation, need extra hydrocortisone. 

NURSING MANAGEMENT
1. Nursing Assessment
•Complete health history
•Baseline weight
•Muscle weakness/ fatigue
•History of illness
•Stress response
•Assess glucose levels
•Baseline vitals
•Skin pigmentation
•Skin turger
•Assess mood
•Assess knowledge of disease
2. NURSING DIAGNOSIS

• Fluid Volume Deficit related to hypovolemia or nausea and vomiting.

•Risk for injury related to weakness
•Self-Care deficit related to weakness, fatigue, muscle aches.
•Disturbed body image related to change in pigment
•Activity intolerance related to weakness, fatigue, and/or muscle aches.
•Risk for suicide related to depression
•Disturbed thought process related to depression and irritability.
3. PATIENT EDUCATION
•Adherence to prescribed cortisol dosage and schedule
•Increased cortisol dose in times of stress
•Never abruptly stop cortisol replacement therapy
•Always where a medical bracelet
•Carry an Emergency cortisol Kit
•Avoid periods of fasting
•Follow up
•Fever or nausea and vomiting notify MD.