Chapter 49 Addison's Disease

etiology and pathophysiology

autoimmune polyglandular syndrome -co-occurring endocrine conditions >>type 1 diabetes >>autoimmune thyroid disease >>pernicious anemia -most common in white females

glucocorticoid/mineralocorticoid deficiencies

*clinical manifestations of complication* -hypotension, tachycardia -dehydration -decreased sodium, increased potassium, decreased glucose -fever, weakness, confusion -severe vomiting, diarrhea -pain >>lower back and legs -shock -> circulatory collapse

secondary adrenocortical hypofunction

*clinical manifestations* -abdominal pain -diarrhea -h/a -orthostatic hypotension -salt craving -joint pain -irritability and depression -do not have hyperpigmentation >>ACTH levels are low

addisonian crisis

*complications* -acute adrenal insufficiency -insufficient or sudden, sharp decrease in hormones -life-threatening >>hypoglycemia >>hypercalemia >>hyponatremia ++n/v, weakness, tremors/twitching, abdominal cramps, apathy >>hyperkalemia ++EKG changes >>Hypotension >>abnormally high temp >>sudden decrease in BP >>cyanosis >>death -various triggers >>sepsis, trauma, stress, adrenal hemorrhage, steroid withdrawal

CRH stimulation test

*diagnostic studies* -abnormal ACTH test response -IV injection of synthetic CRH -blood drawn after 30-60 minutes >>high ACTH levels with no cortisol indicates Addison's disease >>absence of ACTH or delayed response ++common in secondary adrenal insufficiency

ACTH stimulation test

*diagnostic studies* -baseline levels of cortisol and ACTH -IV injection of synthetic ACTH -levels rechecked after 30-60 minutes >>increased blood cortisol levels is normal >>little or no increased cortisol levels in Addison's disease -high ACTH level >>primary adrenal insufficiency (AI)

iatrogenic Addison's disease

*etiology and pathophysiology* -adrenal hemorrhage -chemotherapy -ketoconazole therapy for AIDS -bilateral adrenalectomy

corticosteroid therapy

*patient teaching* -dietary needs >>high in protein, calcium *at least 1500 mg/day), and potassium >>low in fat and concentrated simple carbohydrates -rest and exercise needs >>daily naps >>avoid caffeine late in the day -sodium restriction if edema occurs >>2 grams/day -need to monitor for hyperglycemia >>report 120 mg/dL -notify HCP if epigastric pain develops >>if not relieved by antacids -risk of cataracts >>see eye specialist yearly -need to prevent injury/infection -inform all health care providers

corticosteroid therapy

*patient teaching* -should be taken in morning with food >>reduce gastric irritation -must not be stopped abruptly >>corticosteroids taken for longer than 1 week ++suppresses adrenal production -needs to increase in times of stress -measures to reduce occurrence of osteoporosis *therapies to reduce bone resorption* -increased calcium intake -vitamin D supplementation -bisphosphonates (e.g. alendronate (fosomax)) -institution of a low-impact exercise program

corticosteroid therapy

*side effects* -decreased potassium and calcium >>anti-vitamin B effect may occur -increased glucose and BP -delayed healing -susceptibility to infection -suppressed immune response -PUD -muscle atrophy/weakness -mood and behavior changes -moon facies, truncal obesity -protein depletion -risk for acute adrenal crisis if therapy is stopped abruptly

etiology and pathophysiology

-TB (not a common cause in United States) -amyloidosis -fungal infections >>histoplasmosis -AIDS -metastatic cancer

corticosteroid therapy

-effecting in treating many diseases and disorders -complications and side effects with long-term use -potential benefits must be weighted against risk -expected effects of corticosteroid therapy >>antiinflammatory action >>immunosuppression >>maintenance of normal BP

acute care

-frequent assessment necessary -correct fluid and electrolyte imbalance >>assess vital signs and neurologic status >>daily weight >>accurate I and O -obtain complete medication history >>meds that interact with corticosteroids ++oral hypoglycemics, cardiac glycosides, oral contraceptives, anticoagulants, and NSAIDs -watch for signs of cushing syndrome >>changes in BP, weight gain, weakness

acute care

-guard against infection -assist with daily hygiene -protect from extremes >>light >>noise >>temperature ++cannot cope with these stresses; inability to produce corticosteroids

other diagnostic studies

-increased potassium -decreased chloride, sodium, glucose -anemia -increased BUN -ECG changes -CT scan -MRI >>to locate other causes ++tumors, fungal infections, tuberculosis, or adrenal calcification

patient teaching

-lifelong hormone therapy -dosing >>glucocorticoids in divided doses ++2/3 in morning ++1/3 in the afternoon >>mineralocorticoids once in the morning ++monitor BP, increase salt intake, report changes >>reflects normal circadian rhythm >>decreases side effects of corticosteroids -need to increase corticosteroids during times of stress >>illness, surgery, vigorous exercise >>report vomiting/diarrhea ++additional replacement may be necessary

interprofessional care

-manage underlying cause -hormone therapy >>hydrocortisone ++increase during periods of stress >>fludrocortisone (florinef) ++replaces mineralocorticoids >>women need androgen replacement ++dehydroepiandrosterone (DHEA) -increase dietary salt intake -low potassium diet

etiology and pathophysiology

-primary >>addison's disease >>lack of glucocorticoids, mineralocorticoids, and androgens -secondary >>lack of pituitary ACTH >>lack of glucocorticoids and androgens

patient teaching

-report s/s of corticosteroid deficiency and excess to HCP -carry identification and wear medical ID bracelet -emergency kit >>100 mg of IM hydrocortisone >>syringes -how to administer IM hydrocortisone -written instructions

addisonian crisis

-shock management -high-dose hydrocortisone replacement -0.9% saline solution and 5% dextrose -treat hyperkalemia >>kayexelate, insulin, glucose, calcium, sodium bicarbonate -treat hypoglycemia >>glucose

etiology and pathophysiology

80% of cases caused by an autoimmune response -autoimmune adrenalitis -antibodies destroy adrenal cortex -loss of >>glucocorticoid >>mineralocorticoid >>adrenal androgen hormones

C (Rationale: Hydrocortisone is administered IV during and after a bilateral adrenalectomy to ensure adequate responses to the stress of the procedure.)

An IV hydrocortisone infusion is started before a patient is taken to surgery for a bilateral adrenalectomy. Which explanation, if given by the nurse, is most appropriate? a. "The medication prevents sodium and water retention after surgery." b. "The drug prevent clots from forming in the legs during your recovery from surgery." c. "This medicine is given to help your body respond to stress after removal of the adrenal glands." d. "This drug stimulates your immune system and promotes wound healing."

A (Rationale: The patient in acute adrenal insufficiency will have the following clinical manifestations: hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion. Collaborative care will include administration of corticosteroids. An outcome that would indicate patient improvement would be improved level of consciousness (i.e., alert and oriented).)

The nurse administers corticosteroids to a patient with acute adrenal insufficiency. The nurse determines that treatment is effective if what is observed? a. The patient is alert and oriented. b. The patient's lung sounds are clear. c. The patient's urinary output decreases. d. The patient's potassium level is 5.7 mEq/L.

addison vs cushing

causes

addison vs cushing

clinical manifestations

clinical manifestations

insidious onset -not evident until 90% of the adrenal cortex is destroyed -anorexia -nausea -fluid loss -hypotension -progressive weakness -fatigue -anxiety -weight loss -hyperpigmentation -adrenal crisis disease often advanced before diagnosed

addison vs cushing

pathophysiology