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T3: Addison's
Chapter 50: Addison's disease
Question | Answer |
---|---|
Hypofunction of the adrenal cortex | adrenocortical insufficiency |
What causes adrenocortical insufficiency? | Prinary: Addison's disease, lack of glucocorticoids, mineralocorticoids, & androgens; Secondary: lack of pituitary ACTH secretion, lack of glucocorticoids & androgens |
What are the 3 classes of adrenal corticosteroids? | glucocorticoids, mineralocorticoids, & androgens |
In this disease, amounts of all 3 classes of adrenal corticosteroids are reduced. | Addison's disease |
What occurs in secondary adrenocortical insufficiency? | The corticosteroid and androgen levels are deficient. |
What can cause ACTH deficiency? | Pituitary disease or suppression of the hypothalamic-pituitary axis because of the administration of exogenous corticosteroids. |
What is the most common cause of Addison's in the U.S.? | an autoimmune response against adrenal cortex: adrenal tissue is destroyed by antibodies against the patient's own adrenal cortex |
Addison's disease is considered a component of? | autoimmune polyglandular syndrome |
What is autoimmune polyglandular syndrome? | A rare syndrome caused by a mutation in a gene that helps to regulate the immune system. It is inherited as an autosomal recessive trait. |
What are some other causes of Addison's disease? | TB (uncommon), infarction, fungal infections (histoplasmosis), AIDS, and metastatic cancer. |
Iatrogenic Addison's disease may be due to what? | Adrenal hemorrhage, often in relation to anticoagulant therapy, chemotherapy, ketoconazole (Nizoral) therapy for AIDS, or bilateral adrenalectomy. |
Manifestations of Addison's do not tend to become evident until what? | Until 90% of the adrenal cortex is destroyed, the disease is often advanced before it is diagnosed. |
CM of Addison's disease | Have a very slow (insidious) onset and include progressive weakness, fatigue, weight loss, and anorexia as primary features. |
In Addison's increased ACTH causes this striking feature. | bronze-colored skin hyperpigmentation |
In Addison's, where is the bronze-colored hyperpigmentation primarily seen? | Sun-exposed areas of the body, at pressure points, over joints, and in the creases, especially palmar creases. |
What causes the changes in the skin in Addison's? | Due to increased secretion of B-lipotropin (which contains melanocyte stimulating hormone). This tropic hormone is increased b/c of decreased negative feedback & subsequent low corticosteroid levels. |
Patients with secondary adrenocortical hypofunction usually do not have hyperpigmented skin because why? | ACTH levels are low |
CM of adrenal insufficiency | orthostatic hypotension, hyponatremia, salt craving, hyperkalemia, N/V/D, irritability, depression |
Patients with adrenocortical insufficiency are at risk for what? | acute adrenal insufficiency (Addisonian crisis) |
What is Addisonian crisis? | A life-threatening emergency caused by insufficient adrenocortical hormones or a sudden sharp decrease in these hormones. |
What can trigger an Addisonian crisis? | stress (from infection, surgery, psychologic distress); sudden withdrawal of corticosteroid hormone therapy (often done by pt lacking knowledge of importance of therapy); adrenal surgery; sudden pituitary gland destruction |
CM of glucocorticosteroid and mineralocorticoid deficiencies (Addisonian crisis) | hypotension, tachycardia, dehydration, dec. Na, inc. K, dec. glucose, fever, weakness, confusion, severe vomiting, diarrhea, pain in lower back or legs, hypotension may lead to shock which can lead to circulatory collapse |
Circulatory collapse associated with adrenal insufficiency is often unresponsive to the usual treatment which is? | vasopressors and fluid replacement |
Adrenal insufficiency is characterized by what? | depressed serum and urinary cortisol levels |
ACTH levels will be _____ in primary adrenal insufficiency and ____ in secondary disease. | increased; decreased |
How is primary adrenal insufficiency confirmed? | When cortisol levels fail to rise over basal levels with an ACTH stimulation test. |
What are some abnormal lab findings with Addison's? | dec. urinary cortisol and aldosterone; hyperkalemia; hypochloremia; hyponatremia; hypoglycemia; anemia; and inc. BUN levels |
What diagnostics would be done for Addison's? | ECG may show low voltage and peaked T waves caused by hyperkalemia. CT scans and MRI may be used to identify causes other than autoimmune including tumors, fungal infections, tuberculosis, or adrenal calcification. |
What is the treatment of adrenocortical insufficiency? | Focuses on management of the underlying cause when possible. Main tx is hormone therapy. |
What is the most commonly used form of hormone therapy for Addison;s? | hydrocortisone b/c it has both glucocorticoid and mineralocorticoid properties |
During situations associated with stress, the glucocorticoid dosage must be increased to prevent what? | addisonian crisis |
Mineralocorticoid replacement with this is administered daily. | fludrocortisone (Florinef) |
Should salt in the diet be increased or decreased in Addison's? | increased |
This is a life threatening emergency necessitating aggressive management. | Addisonian crisis |
How is Addisonian crisis treated? | Tx is directed toward shock mgmt & high dose hydrocortisone replacement. Lge volumes of 0.9% NS & 5% dextrose are administered to reverse hypotension & electrolyte imbalances until BP returns to normal. |
When a pt with Addison's disease is hospitalized, nursing management is focused on what? | Monitoring the patient while correcting fluid & electrolyte imbalance. |
What are basic nursing interventions for a patient with Addison's disease? | Vitals & s/s of FVD & electrolyte imbalance. Monitor trends of glucose, Na, & K. Baseline data of mental status, vitals, & weight. Complete med hx for interactions w/corticosteroids. Note changes in BP, wt gain, weakness, or s/s of Cushings syndrome. |
What drugs interact with corticosteroids? | oral hypoglycemics, cardiac glycosides, oral contraceptives, anticoagulants, and NSAIDS |
What are some other important interventions when caring for a patient with Addison's? | Protect against exposure to infection, & assist w/daily hygiene. Protect pt from noise, light, & environmental temp. extremes. The pt can't cope w/these stresses b/c of the inability to produce corticosteroids. |
What should you teach the patient when it comes to glucocorticoid dosing? | Should be given in divided doses: 2/3 in the morning & 1/3 in the afternoon |
What should you teach the patient about mineralocorticoid dosing? | Should be given once daily preferably in the morning. |
What is the importance of this dosage schedule with the glucocorticoids & the mineralocorticoids? | It reflects normal circadian rhythm in endogenous hormone secretion & decreases the side effects associated with corticosteroid therapy. |
Patients w/Addison's disease are unable to tolerate physical or emotional stress w/o additional what? | exogenous corticosteroids |
Long term care for Addison's revolves around what? | Recognizing the need for extra medication & techniques for stress management. |
What are some examples of situations necessitating corticosteroid adjustment? | fever, flu, teeth extraction, & rigorous physical activity (playing tennis on a hot day or running a marathon). If V/D occur (w/flu), notify doc immediately b/c electrolyte replacement & parenteral admix of cortisol may be necessary. |
It is critical that the patient with Addison's wears what or carries this? | Wear an identification bracelet (MedicAlert) & carry a wallet card stating the pt has Addison's so that appropriate therapy can be initiated in case of an emergency. |
Patient teaching for Addison's | Teach pt s/s of corticosteroid deficiency & excess (Cushings), how to take their BP, to increase salt intake, & report any significant changes to their HCP. |
An Addison's patient should carry an emergency kit at all times. What should this kit consist of? | 100 mg of IM hydrocortisone, syrines, & instructions for use. Teach pt & SO how to give an IM injection in case hormone therapy can't be taken orally. |
Corticosteroid therapy is used to relieve s/s associated with many diseases and disorders but what can occur with long-term administration of corticosteroids in therapeutic doses? | Serious comps & side effects occur. This therapy isnt rec. for minor chronic cond. Therapy reserved for diseases that carry a risk of death or permanent loss of function & for conditions which short term therapy is likely to produce remission or recovery. |
What are the expected effects of corticosteroid therapy? | antiinflammatory action, immunosuppression, and maintenance of normal BP |
Examples of how a beneficial effect of corticosteroids in one situation may be a harmful one in another. | Decreasing inflammation in arthritis can increase the risk for infection. Suppression of inflammation & the immune response can save a person w/anaphylaxis or an organ transplant but cause reactivation of latent TB & reduce resistance to other infections. |
The vasopressive effect of corticosteroids is critical in enabling a person to function in stressful situation, but this effect can produce what when used for drug therapy? | HTN |
What are some side effects of corticosteroid therapy? | Dec. K; dec. Ca r/t anti-vitamin D; BP inc b/c of excess blood vol, HTN lead to HF; Inc glucose lead to DM; delayed healing leads to inc risk for wound dehiscence; risk for infection inc.; s/s of inflammation (red, tender, heat, swell, edema) suppressed |
What can happen to the skeletal muscles due to corticosteroid therapy? | atrophy and weakness occur |
What can happen to the fat from extremities due to corticosteroid therapy? | redistributed to trunk and face |
Protein depletion is a side effect of corticosteroid therapy which can cause what to happen? | Decreases bone formation, density, & strength, leading to predisposition to pathologic fractures, especially compression fractures of the vertebrae (osteoporosis). |
If corticosteroid therapy is stopped abruptly what is the patient at risk for? | acute adrenal crisis |
Side effects of corticosteroid therapy. | PUD, muscle atrophy/weakness, mood & behavior changes, moon facies, truncal obesity, protein depletion, risk for acute adrenal crisis, dec. K & Ca, inc. glucose & BP, delayed healing, risk for infection, suppressed immune response |
When corticosteroids are used as nonreplacement therapies, when should they be taken? | Once daily or once every other day. Taken early in the morning w/food to decrease gastric irritation. |
Exogenous corticosteroid administration may suppress what? | endogenous ACTH and therefore endogenous cortisol (suppression is time and dose dependent) |
Because exogenous corticosteroid administration may suppress endogenous ACTH (therefore endogenous cortisol) what should you emphasize to the patient? | The danger of abrupt cessation of corticosteroid therapy. |
Corticosteroids taken for longer than 1 week will suppress what? | adrenal production |
Ensure that increased doses of corticosteroids are prescribed in acute care or home care settings in situations of what kind? | physical or emotional stress |
Corticosteroids-induced osteoporosis is an important concern for patients who receive corticosteroid treatment for prolonged periods of time, longer than what? | 3 months |
What therapies are used to reduce the resorption of bone? | Increased Ca intake, vitamin D supplementation; bisphosphonates (alendronate-Fosamax), and institution of a low impact exercise program. |
What kind of diet would you plan for a patient undergoing corticosteroid therapy? | Plan a diet high in protein, Ca (at least 1500mg/day), and K but low in fat and concentrated simple carbs such as sugar, honey, syrups, and candy. |
What are some measures to ensure adequate rest and sleep for patients undergoing corticosteroid therapy? | Daily naps and avoidance of caffeine late in the day. |
What should you teach the patient to do to maintain bone integrity while on corticosteroid therapy? | develop and maintain an exercise program |
Patients on corticosteroid therapy should be taught to recognize edema and restrict Na to how much a day? | <2000 mg/day |
Patients on corticosteroid therapy should be taught to monitor glucose levels and recognize symptoms of hyperglycemia such as? | polydipsia, polyura, blurred vision; report symptoms or glucose levels exceeding 120 mg/dL |
Patients on corticosteroid therapy should see an eye specialist yearly to assess for what? | development of cataracts |
What are some safety measures for patients on corticosteroid therapy? | Get up slowly from bed or chair, use good lighting to avoid accidental injury. |
Patients on corticosteroid therapy should do what to prevent infections? | Maintain good hygiene practices and avoid contact with persons with colds or other contagious illnesses. |