MSN Client with Cushing’s Disease Quiz 1

Oral steroids can cause gastric irritation and ulcers and should be administered with meals, if possible, or otherwise with an antacid. Only instructing the client to take the medication with a full glass of water will not help prevent gastric complications from steroids. Steroids should never be taken on an empty stomach. Glucocorticoids should be taken in the morning, not at bedtime.

Measuring daily weight is a reliable, objective way to monitor fluid balance. Rapid variations in weight reflect changes in fluid volume, which suggests insufficient control of the disease and the need for more glucocorticoids in the client with Addison’s disease. Nurses should instruct clients taking oral steroids to weigh themselves daily and to report any unusual weight loss or gain. Skin turgor testing does supply information about fluid status, but daily weight monitoring is more reliable. Temperature is not a direct measurement of fluid balance. Thirst is a nonspecific and very late sign of weight loss.

Rapid weight gain, because it reflects excess fluids, is a warning sign that the client is receiving too much hormone replacement. It may be difficult to individualize the correct dosage for a client taking glucocorticoids, and the therapeutic range between underdosage and overdosage is narrow. Maintaining the client on the lowest dose that provides satisfactory clinical response is always the goal of pharmacotherapeutics. Fluid balance is an important indicator of the adequacy of hormone replacement. Anorexia is not present with glucocorticoid therapy because these drugs increase the

appetite. Dizziness is not specific to the effects of glucocorticoid therapy. Poor skin turgor is a late sign of fluid volume deficit.

Medication compliance is an essential part of the self-care required to manage Addison’s disease.

The client must learn to adjust the glucocorticoid dose in response to the normal and unexpected

stresses of daily living. The nurse should instruct the client never to stop taking the drug without consulting the health care provider to avoid an addisonian crisis. Regularity in daily habits makes adjustment easier, but the client should not be encouraged to withdraw from normal activities to avoid stress. The client does not need to restrict sodium. The client is at risk for hyponatremia. Hypotension, not hypertension, is more common with Addison’s disease.

Illness or surgery places tremendous stress on the body, necessitating increased glucocorticoid

dosage. Extreme emotional or psychological stress also necessitates dosage adjustment. Increased dosages are needed in times of stress to prevent drug induced adrenal insufficiency. Returning to work

after the weekend, going on a vacation, or having a routine checkup usually will not alter glucocorticoid dosage needs.

Bronzing, or general deepening of skin pigmentation, is a classic sign of Addison’s disease and

is caused by melanocyte-stimulating hormone produced in response to increased ACTH secretion. The

hyperpigmentation is typically found in the distal portion of extremities and in areas exposed to sun.

Additionally, areas that may not be exposed to sun, such as the nipples, genitalia, tongue, and knuckles,

become bronze-colored. Treatment of Addison’s disease usually reverses the hyperpigmentation. Bilirubin level is not related to the pathophysiology of Addison’s disease. Hyperpigmentation is not

related to the effects of the glucocorticoid therapy.

Skin bruising from increased skin and blood vessel fragility is a classic sign of Cushing’s disease. Hyperpigmentation and bruising are caused by the hypersecretion of glucocorticoids. Fluid retention causes hypertension, not hypotension. Muscle wasting occurs in the extremities. Hair on the head thins, while body hair increases.

In Cushing’s disease, excessive cortisol secretion causes rapid protein catabolism, depleting the collagen support of the skin. The skin becomes thin and fragile and susceptible to easy bruising.

The typical “cushingoid” appearance of the client includes a moon face, buffalo hump, central obesity, and thin musculature. Weight gain, mood swings, and slow wound healing are other signs and symptoms of Cushing’s disease. Hypertension, not hypotension, is a sign of Cushing’s disease. Abdominal pain is not a symptom of Cushing’s disease.

Excessive levels of glucocorticoids, aldosterone, and androgens secreted from the adrenal cortex

result in the constellation of symptoms known as Cushing’s disease. Cushing’s disease can be caused by a tumor, overstimulation from the pituitary, or the use of prescription steroid drugs. Androgens are also secreted in excess. ACTH is only one hormone that is abnormal in Cushing’s disease. Excessive secretion of catecholamines accompanies pheochromocytoma, a disease of the adrenal medulla.

Sodium retention is typically accompanied by potassium depletion. Hypertension, hypokalemia,

edema, and heart failure may result from the hypersecretion of aldosterone. The client with Cushing’s disease exhibits postprandial or persistent hyperglycemia. Clients with Cushing’s disease have hypernatremia, not hyponatremia. Bone resorption of calcium increases the urine calcium level.

Cushing’s disease is commonly caused by loss of the diurnal cortisol secretion pattern. The client’s random morning cortisol level may be within normal limits, but secretion continues at that level throughout the entire day. Cortisol levels should normally decrease after the morning peak. Analysis of a 24-hour urine specimen is often useful in identifying the cumulative excess. Clients will not have

symptoms with normal cortisol levels. Hormones are present in the blood.

A primary dietary intervention is to restrict sodium, thereby reducing fluid retention. Increased protein catabolism results in loss of muscle mass and necessitates supplemental protein intake. The client may be asked to restrict total calories to reduce weight. The client should be encouraged to eat potassium-rich foods because serum levels are typically depleted. Although reducing fat intake as

part of an overall plan to restrict calories is appropriate, fat intake of less than 20% of total calories is not recommended.

Osteoporosis is a serious outcome of prolonged cortisol excess because calcium is resorbed out of the bone. Regular daily weight-bearing exercise (e.g., brisk walking) is an effective way to drive calcium back into the bones. The client should also be instructed to have a dietary or supplemental intake of calcium of 1,500 mg daily. Potassium levels are not relevant to prevention of bone resorption. Vitamin D is needed to aid in the absorption of calcium. Isometric exercises condition muscle tone but do not build bones.

Effective splinting for a high incision reduces stress on the incision line, decreases pain, and increases the client’s ability to deep-breathe effectively. Deep breathing should be done hourly by the client after surgery. Sitting upright ignores the need to splint the incision to prevent pain. Tightening the stomach muscles is not an effective strategy for promoting deep breathing. Raising the shoulders is not a feature of deep-breathing

exercises.

The priority in the first 24 hours after adrenalectomy is to identify and prevent adrenal crisis. Monitoring of vital signs is the most important evaluation measure. Hypotension, tachycardia, orthostatic hypotension, and arrhythmias can be indicators of pending vascular collapse and hypovolemic shock that can occur with adrenal crisis. Beginning oral nutrition is important, but not necessarily in the first 24 hours after surgery, and

it is not more important than preventing adrenal crisis. Promoting self-care activities is not as important as preventing adrenal crisis. Ambulating in the hallway is not a priority in the first 24 hours after adrenalectomy.