Addison's Disease Flashcards
2 types of pathophysiology
Primary
Secondary
Primary
Addison's disease Lack of - glucocorticoids - mineralocorticoids - androgens
Secondary
Lack of pituitary ACTH
Lack of glucocorticoids and androgens
Etiology and pathophysiology
Autoimmune response against adrenal cortex (body is attacking itself)
Causes of Addison’s
TB infarction fungal infections AIDS metastatic cancer latrogenic (drugs, adrenalectomy)
Clinical manifestations
It is an insidious onset with
- progressive weakness
- fatigue
- weight loss
- anorexia
- orthostatic hypotension
- hyponatremia and salt craving
- hyperkalemia
- N/V
- diarrhea
- hypoglycemia
- irritability, depression
When is Addison’s evident?
When 90% of the adrenal cortex is destroyed
Cannot reverse it at this point
Addisonian Crisis
Complication Acute adrenal insufficiency Insufficient or sudden, sharp decrease in hormones LIFE-THREATENING Various triggers
Addisonian Crisis can be caused by…
rapid stress onset or rapid ending of steroids
Manifestations of glucocorticosteroid and mineralocorticoid defiicencies
Hypotention Tachycardia Decrease sodium Increase potassium Decrease glucose Fever Weakness Confusion Severe vomiting, diarrhea, pain Shock = circulatory collapse
Diagnostic Studies
Decreased serum and urinary cortisol ACTH levels - increase in primary adrenal insufficiency - decrease in secondary adrenal insufficiency ACTH stimulation test Decreased urinary cortisol and aldosterone Increased potassium Decrease chloride, sodium, glucose Anemia Increase BUN ECG changes CT scan, MRI
ACTH stimulation test
Distinguishes between primary and secondary disease
- primary: no change
- secondary: increased cortisol
How do we fix it?
Correct underlying cause
Hormone therapy
-hydrocortisone (increase during periods of stress)
-fludrocortisone (if aldosterone deficient)
Increase dietary salt intake
Addisonian Crisis Care
Shock management High-dose hydrocortisone replacement H2 histamine blocker for ulcer prevention 0.9% saline solution and 5% dextrose Treatment for hyperkalemia Hypoglycemia management
Why do we have sodium wasting?
Because of lack of aldosterone
What do we watch for when treating Addison’s?
Cushing’s crisis
Acute interventions
Frequent assessment necessary Ass VS and signs of fluid/electrolyte imbalance Monitor trends in lab values Monitor mental status and weight Obtain complete medication history Watch for signs of Cushing Syndrome Protect against infection Assist with daily hygiene
Protect from extremes like…
Light
Noise
Temperature
Patient teaching for dosing
Glucocorticoids: in divided doses
Mineralocorticoids: once in the morning
Reflects normal circadian rhythm
Decreases side effects of corticosteroids
What do you do during times of stress?
Notify physician and have your corticosteroids increased during that time
Patient teaching
Signs and symptoms of corticosteroid deficiency and excess
Wear medical ID bracelet
Patient teaching for those with fludrocortisone (mineralocorticoids)
Check BP
Know what to report to health care provider
Emergency kits
Patient teaching
Written instructions
How to adminster IM hydrocortisone
Expected effects of corticosteroid therapy
Anti-inflammatory action
Immunosuppression
Maintenance of normal BP
Side effects of corticosteroid therapy
Decreased potassium and calcium Increase glucose and BP Delayed healing Susceptibility to infection Suppressed immune response Peptic ulcer disease Muscle atrophy/weakness Mood and behavior changes Moon faces, truncal obesity Protein depletion Risk for acute adrenal crisis if therapy is stopped abruptly
Patient teaching with corticosteroid therapy
Dietary needs Rest and exercise needs Sodium restrictions of edema occurs Need to monitor for hyperglycemia Notify HCP if epigastric pain develops Need to prevent injury/infection Inform all HCP
