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This chapter is from the book

Adrenal Gland

The adrenal gland is a vascular gland located at the top of the kidney. It comprises the cortex (outer portion) and the medulla (inner portion), as illustrated in Figure 4.4. The action of the adrenal gland consists of production of mineralocorticoids that help control the body’s levels of minerals such as sodium and potassium. Glucocorticoids, androgens, and estrogens are made in the zona fasciculata and zona reticularis. The cortex produces the adrenal steroids and corticosteroids. The major mineralocorticoid produced in the cortex is aldosterone. As previously discussed, this mineralcorticoid helps to control reabsorption of sodium and potassium that the kidneys excrete. Other regulatory mechanisms controlled by the cortex are renin and adrenocorticotropic hormone (ACTH). The most prominent glucocorticoid secreted by the adrenal cortex is cortisol. This hormone helps to regulate the body’s stress response, metabolism of food, emotional stability, and the immune response. Small amounts of androgens and estrogen are secreted by the adrenal cortex.


FIGURE 4.4 Adrenal gland.

The adrenal medulla is a sympathetic nerve ganglion that stimulates the sympathetic nervous system. This stimulation results in elevations in catecholamines such as norepinephrine and epinephrine. These chemicals help to control response to stress. The “fight or flight” response results in changes in pulse rate, blood pressure, and central nervous system response.

Adrenal Gland Disorders

Adrenal disorders result in many problems. Some of these include fatigue, weakness, suppression of the immune response, muscle and bone loss, and many others. This section covers some of the most common types of adrenal disorders along with their causes and treatments.

Primary Aldosteronism (Conn’s Syndrome)

Conn’s syndrome is a disease of the adrenal glands that involves an excessive production of aldosterone. The most common reasons for development of Conn’s syndrome are a tumor of the adrenal gland or benign hyperplasia of the adrenal gland, but the syndrome can also be related to use of thiazide diuretics or high levels of angiotensin II caused by poor renal perfusion. Signs and symptoms of Conn’s syndrome include an elevated serum sodium level, decreased potassium serum levels, and hypertension with a related headache. Positive Trousseau’s and Chvostek’s signs might be present. Diagnosis of Conn’s is made by checking the serum levels for sodium and potassium and aldosterone levels. X-rays, CT scans, and an MRI confirm the presence of tumors. Treatment includes a low-sodium diet, potassium supplementation, and control of hypertension. Spironolactone (Aldactone)—a potassium-sparing diuretic—is prescribed to lower aldosterone levels and lower blood pressure. Surgical intervention is done when tumors are identified. Prognosis is good if the client is accurately diagnosed. If the client fails to receive an accurate diagnosis, the disease can lead to a stroke, heart attack, or renal disease.

Pheochromocytoma is a catecholamine-producing adrenal tumor that leads to a marked elevated blood pressure. Treatment includes treatment of malignant hypertension with drugs such as sodium nitroprusside (Nipride) or clonidine (Catapres). Removal of the tumor primarily corrects the hypertension. The client’s blood pressure must be stabilized prior to surgery. This is usually done by administration of an alpha-adrenergic–blocking agent such as phenoxybenzamine hydrochloride (Dibenzyline).

Adrenocortical Insuffiency (Addison’s Disease)

Addison’s disease can occur as a result of long-term use of steroids or the rapid cessation of corticosteroids. It can also be caused by sepsis, surgical stress, or hemorrhage of the adrenal glands (Waterhouse-Friderichsen syndrome).

Signs and symptoms associated with Addison’s disease include

  • Weakness.
  • Bronze-like pigmentation of the skin.
  • Decreased glucose levels.
  • Decreased blood pressure.
  • Anorexia.
  • Sparse axillary hair.
  • Urinary frequency.
  • Depression.
  • Addisonian crises. The symptoms of Addisonian crises are severe hypotension, cyanosis, and shock. This constitutes an emergency situation. The nurse should call the doctor immediately to obtain orders for medications to treat shock.

Diagnosis of Addison’s disease involves an evaluation of serum sodium and chloride levels. Evaluation of ketosteroids and 17-hydroxycorticoids is also done. Adrenal function is evaluated by administering adrenocorticoid-stimulating hormone (ACTH) and checking for changes in cortisol levels.

Management of the client with Addison’s disease includes the use of intravenous cortisone and plasma expanders to achieve and maintain the blood pressure. When stable, the client can be given intramuscular cortisol in the form of dexamethasone (Decadron) or orally in the form of prednisolone (Prednisone). The client with Addison’s disease requires lifelong maintenance with cortisone. The client should be instructed to take the medication exactly as prescribed and to avoid sudden cessation of the drug.

Adrenocortical Hypersecretion (Cushing’s Disease)

The terms Cushing’s disease and Cushing’s syndrome are often used interchangeably although they are not the same. Cushing’s syndrome or primary Cushing’s syndrome can be caused by tumors of the adrenal cortex. Secondary Cushing’s syndrome (Cushing’s disease) often is caused by pituitary hypothalamus or adrenal cortex problems that result in an increased ACTH (adrenocorticotropic hormone). Long-term administration of glucocortidoids or iatrogenic Cushing’s syndrome will also produce elevated levels of cortisole and symptoms associated with hypersecretion.

Diagnosis is made by checking serum cortisole, calcium, potassium, sodium, and glucose levels. Altered ACTH and 17 ketosteroid levels are also seen with Cushing’s. A positive ACTH suppression test can be performed to check for changes in cortisole levels when ACTH is administrated.

Signs and symptoms associated with Cushing’s disease include

  • Pendulous abdomen
  • Buffalo hump
  • Moon faces
  • Hirsutism (facial hair)
  • Ruddy complexion (dark red)
  • Increased BP
  • Hyperglycemia
  • Osteoporosis
  • Decreased serum potassium and decreased serum chloride
  • Increased 17-hydroxycorticoids
  • Decreased eosinophils and decreased lymphocytes

Management of the client with Cushing’s is accomplished by removing the cause—hyperplasia of the gland. Surgery can be required. A low-sodium diet, regulation of fluid and electrolytes, and administration of a potassium-sparing diuretic such as aldactone (Spironalactone) help to decrease the symptoms. Because elevated glucose levels are common in the client with Cushing’s syndrome, the client often requires frequent checks of glucose levels and administration of insulin or oral antidiabetic medications.

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