Addison's disease

Addison's disease
Addison's diseaseis an endocrine

disordercharacterized 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 thatplays
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 antiinflammatory agent and helps the body
respond to stress.
Addison's Diseasecan have asevere effect on
all of these bodily systems.

Addison's disease
Approximately 70% of cases of Addisons

disease are as aresult of an auto-immune

process (primary).
The bodys 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

ETIOLOGY
Secondary 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

ETIOLOGY
Inadequate aldosterone produces
disturbances of sodium,potassium, and water
metabolism
Cortisol deficiency produces
abnormal fat, protein, and carbohydrate
metabolism
no cortisol during a period of stress can
precipitate addisonian crisis, an exaggerated
state of adrenal cortical insufficiency, and can
lead to death.

ETIOLOGY
Causes 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
SYMPTOMS
water loss, dehydration and hypovolemia
muscular weakness, fatigue, weight loss
GI 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 crisis
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.
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.

DIAGNOSIS
Blood test
Hypoglycemia
Hyponatremia
Hyperkalemia
leukocytosis

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 MANAGEMENT
Restoration 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 wellbeing
Minimize stressful situation
Protect 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)