Addison's disease

Addison's disease Addison's disease is an endocrine

disorder characterized by a severe deficiency of hormones produced in the adrenal cortex.

The disease tends to become clinically apparent during periods of metabolic stress or trauma.

Cortisol is a glucocorticoid hormone that plays a vital role in the body.

Addison's disease It mobilizes nutrients, regulates the

metabolism of proteins, fats and carbohydrates, stimulates the liver to raise blood sugar levels, acts as an anti- inflammatory agent and helps the body respond to stress.

Addison's Disease can have a severe effect on all of these bodily systems .

Addison's diseaseApproximately 70% of cases of Addison’s

disease are as a result of an auto-immune process (primary).

The body’s immune system produces antibodies against the cells of the adrenal cortex, and slowly destroys the healthy cells.

This is a slow process evolving over a long period and can take months, even years, to become clinically apparent

ETIOLOGYSecondary adrenocortical insufficiency – ACTH deficiency from pituitary disease suppression of hypothalamic-pituitary axis by

corticosteroid treatment for nonendocrine disorders causes atrophy of adrenal cortex

Treatment with daily administration of corticosteroids for 2 to 4 weeks may suppress function of the adrenal cortex; therefore, adrenal insufficiency should be considered in any patient who has been treated with corticosteroids.

surgical removal of both adrenal glands infection of the adrenal glands - TB

ETIOLOGYInadequate aldosterone produces

disturbances of sodium,potassium, and water metabolism

Cortisol deficiency produces abnormal fat, protein, and carbohydrate

metabolismno cortisol during a period of stress can

precipitate addisonian crisis, an exaggerated state of adrenal cortical insufficiency, and can lead to death.

ETIOLOGYCauses of adrenal insufficiency can be grouped by

the way they cause the adrenals to produce insufficient cortisol.

These are adrenal dysgenesis (the gland has not formed adequately during development),

impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol)

adrenal destruction (disease processes leading to the gland being damaged).

SIGNS AND SYMPTOMSwater loss, dehydration and hypovolemiamuscular weakness, fatigue, weight lossGI Problems-- anorexia, nausea, vomiting,

diarrhea, constipation, abdominal pain.hypotension, hypoglycemia, low basal

metabolic rate, increased insulin sensitivity.Mental Changes-- depression, irritability,

anxiety, apprehension caused by hypoglycemia and hypovolemia.

hyperpigmentation (darkening of an area of skin or nails caused by increased melanin.)

Addisonian crisisWith 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.

The patient may complain of headache, nausea, abdominal pain, and diarrhea and show 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.

The stress of surgery or dehydration resulting from preparation for diagnostic tests or surgery may precipitate an addisonian or hypotensive crisis.

DIAGNOSISBlood test

HypoglycemiaHyponatremiaHyperkalemialeukocytosis

The diagnosis is confirmed by low levels of adrenocortical hormones in the blood or urine and decreased serum cortisol levels

ACTH stimulation test. Imaging tests. 

MEDICAL MANAGEMENTRestoration of normal fluid and electrolyte balance:

high sodium, low-potassium diet and fluids.Treatment of glucocorticoids deficiency with such

agent as hydrocortisone (Cortef) or prednisone (Orasone).

Mineralocorticoid deficiency is treated with fludrocortisone (Florinef)

Immediate treatment if addisonian crisis or circulatory collapse:

a. I.V. sodium chloride solution to replace sodium ions.

b. Hydrocortisone (Cortef)c. Injection of circulatory stimulants, such as

atropine sulfate, calcium chloride, epinephrine.d. Vasopressor amines may be required if

hypotension persists

Protecting well-beingMinimize stressful situationProtect patient from infection

a. Control patient's contacts so that infectious organisms

b. Protect patients from drafts, dampness, exposure to cold.

c. Prevent overexertion.d. Use meticulous hand washing and asepsis

Assess comfort and emotional status of the patient Control the temperature of the room to avoid sharp

deviations in patients temperature.Maintain a quiet, peaceful environment, avoid loud talking

and noisy radios.Observe and report early signs of addisonians crisis

(sudden drop in BP, nausea and vomiting, fever)