Chapter 50: Nursing Management: Endocrine Problems

ACROMEGALY • Acromegaly results from excess secretion of growth hormone (GH). • • • It is a rare condition of bone and soft tissue overgrowth. Bones increase in thickness and width but not length. Manifestations include enlargement of hands and feet, thickening and enlargement of face and head bony and soft tissue, sleep apnea, signs of diabetes mellitus, cardiomegaly, and hypertension. Treatment focuses on returning GH levels to normal through surgery, radiation, and drug therapy. The prognosis depends on age at onset, age when treatment is initiated, and tumor size. Nursing care for surgical patients postoperatively includes avoidance of vigorous coughing, sneezing, and straining at stool to prevent cerebrospinal fluid leakage from where the sella turcica was entered. After surgery with a transsphenoidal approach, the head of the bed is elevated to a 30-degree angle at all times, and neurologic status is monitored. Mild analgesia is used for headaches, and toothbrushing is avoided for at least 10 days. If hypophysectomy is done or the pituitary is damaged, antidiuretic hormone (ADH), cortisol, and thyroid hormone replacement must be taken for life. Patient teaching is essential with hormone replacement therapy.

HYPOPITUITARISM • Hypopituitarism is rare, and involves a decrease in one or more of the pituitary hormones: o The anterior pituitary gland secretes adrenocorticotrophic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), GH, and prolactin. o The posterior pituitary gland secretes ADH and oxytocin. • Most deficiencies associated with hypopituitarism involve GH and gonadotropins (e.g., LH, FSH) due to a pituitary tumor. SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE • Syndrome of inappropriate antidiuretic hormone (SIADH) results from an overproduction or oversecretion of ADH. • SIADH results from abnormal production or sustained secretion of ADH and is characterized by fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine in presence of normal or increased intravascular volume, and normal renal function. The most common cause is lung cancer.

Treatment is directed at underlying cause, with a goal to restore normal fluid volume and osmolality. Fluid restriction results in gradual, daily weight reductions, progressive rise in serum sodium concentration and osmolality, and symptomatic improvement. With chronic SIADH, the patient must learn self-management.

DIABETES INSIPIDUS • Diabetes insipidus (DI) is associated with deficiency of production or secretion of ADH or decreased renal response to ADH. • Decreases in ADH cause fluid and electrolyte imbalances due to increased urinary output and increased plasma osmolality. • •

Depending on the cause, DI may be transient or chronic lifelong condition. Types of DI include: Central DI (or neurogenic DI) occurs when an organic lesion of the hypothalamus, infundibular stem, or posterior pituitary interferes with ADH synthesis, transport, or release. Nephrogenic DI occurs when there is adequate ADH, but a decreased kidney response to ADH. Lithium is a common cause of drug-induced nephrogenic DI. Hypokalemia and hypercalcemia may also lead to nephrogenic DI. Psychogenic DI is associated with excessive water intake, caused by lesion in thirst center or by psychosis.



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DI is characterized by polydipsia and polyuria. If oral fluid intake cannot keep up with urinary losses, severe fluid volume deficit results as manifested by weight loss, constipation, poor tissue turgor, hypotension, and shock. Severe dehydration and hypovolemic shock may occur. Treating the primary cause is central to management. Therapeutic goal is maintenance of fluid and electrolyte balance. Nursing care includes early detection, maintenance of adequate hydration, and patient teaching for long-term management.

GOITER • Goiter is thyroid gland hypertrophy and enlargement caused by excess TSH stimulation, which can be caused by inadequate circulating thyroid hormones. • • • • • Goiter is also found in Graves’ disease. TSH and T4 levels are measured to determine if goiter is associated with hyperthyroidism, hypothyroidism, or normal thyroid function. Thyroid antibodies are measured to assess for thyroiditis. Treatment with thyroid hormone may prevent further thyroid enlargement. Surgery to remove large goiters may be done.

THYROID NODULES • A thyroid nodule, a palpable deformity of the thyroid gland, may be benign or malignant. • • • • • • • Benign nodules are usually not dangerous, but can cause tracheal compression if they become too large. Malignant tumors of thyroid gland are rare. A major sign of thyroid cancer is presence of hard, painless nodule or nodules on enlarged thyroid gland. Surgical tumor removal is usually indicated with cancer. Procedures include unilateral total lobectomy with removal of isthmus to total thyroidectomy with bilateral lobectomy. Radiation therapy may also be indicated. Nursing care for thyroid tumors is similar to care for patient who has undergone thyroidectomy.

THYROIDITIS • Thyroiditis is an inflammatory process in the thyroid gland. •
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Subacute and acute forms of thyroiditis have abrupt onset, and the thyroid gland is painful. Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) can lead to hypothyroidism. Hashimoto’s thyroiditis is a chronic autoimmune disease in which thyroid tissue is replaced by lymphocytes and fibrous tissue. It is most common cause of goiterous hypothyroidism. Recovery may be complete in weeks or months without treatment.

HYPERTHYROIDISM • Hyperthyroidism is thyroid gland hyperactivity with sustained increase in synthesis and release of thyroid hormones.

Thyrotoxicosis refers to physiologic effects or clinical syndrome of hypermetabolism resulting from excess circulating levels of T4, T3, or both. Hyperthyroidism and thyrotoxicosis usually occur together as in Graves’ disease. The most common form of hyperthyroidism is Graves’ disease. Other causes include toxic nodular goiter, thyroiditis, exogenous iodine excess, pituitary tumors, and thyroid cancer.

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Graves’ Disease • Graves’ disease is an autoimmune disease marked by diffuse thyroid enlargement and excessive thyroid hormone secretion.

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Factors such as insufficient iodine supply, infection, and stressful life events may interact with genetic factors to cause Graves’ disease. Manifestations relate to the effect of thyroid hormone excess. When thyroid gland is large, a goiter may be noted, and auscultation of thyroid gland may reveal bruits. A classic finding is exophthalmos, a protrusion of eyeballs from the orbits. Treatment options are antithyroid medications, radioactive iodine therapy, and subtotal thyroidectomy.

Thyrotoxic Crisis • Thyrotoxic crisis, also known as thyroid storm, is an acute, rare condition in which all hyperthyroid manifestations are heightened. • • • Although it is a life-threatening emergency, death is rare when treatment is vigorous and initiated early. Manifestations include severe tachycardia, shock, hyperthermia, seizures, abdominal pain, diarrhea, delirium, and coma. Treatment focuses on reducing circulating thyroid hormone levels by drug therapy.

HYPOTHYROIDISM • Hypothyroidism is one of most common medical disorders. • • It results from insufficient circulating thyroid hormone. This condition may be primary (related to destruction of thyroid tissue or defective hormone synthesis), or secondary (related to pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone [TRH] secretion). Hypothyroidism also can be transient and related to thyroiditis or from a discontinuation of thyroid hormone therapy. Iodine deficiency is the most common cause worldwide. In areas with adequate iodine intake, the most common cause is thyroid gland atrophy (end result of Hashimoto’s thyroiditis and Graves’ disease). Manifestations include fatigue, lethargy, personality and mental changes, decreased cardiac output, anemia, and constipation. Patients with severe long-standing hypothyroidism may display myxedema, an accumulation of hydrophilic mucopolysaccharides in dermis and other tissues. This mucinous edema causes characteristic facies of hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect).

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A myxedema coma can be precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates), exposure to cold, and trauma. This condition is characterized by subnormal temperature, hypotension, and hypoventilation. To survive, vital functions are supported and IV thyroid hormone replacement administered. The overall treatment in hypothyroidism is restoration of euthyroid state as safely and rapidly as possible with hormone replacement therapy. Levothyroxine (Synthroid) is the drug of choice. Patient teaching is imperative, and the need for lifelong drug therapy is stressed.

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HYPERPARATHYROIDISM • Hyperparathyroidism involves increased secretion of parathyroid hormone (PTH). • • • •

Excess PTH leads to hypercalcemia and hypophosphatemia. Manifestations include weakness, loss of appetite, constipation, emotional disorders, and shortened attention span. Major signs include osteoporosis, fractures, and kidney stones. Neuromuscular abnormalities are muscle weakness in proximal muscles of lower extremities. Parathyroidectomy leads to a reduction in chronically high calcium levels. Continued ambulation, avoidance of immobility, a high fluid intake and moderate calcium intake are important. Several drugs are helpful in lowering calcium levels: bisphosphonates (e.g., alendronate [Fosamax]) estrogen or progestin therapy, oral phosphate, diuretics, and calcimimetic agents (e.g., cinacalcet [Sensipar]).

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HYPOPARATHYROIDISM • Hypoparathyroidism is rare, and results from inadequate circulating PTH. • • • • • It is characterized by hypocalcemia resulting from a lack of PTH to maintain serum calcium levels. The most common cause is iatrogenic, due to accidental removal of parathyroid glands or damage to these glands during neck surgery. Sudden decreases in serum calcium cause tetany, which is characterized by tingling of lips, fingertips, and increased muscle tension with paresthesias and stiffness. Painful tonic spasms of smooth and skeletal muscles (extremities and face), and laryngospasms and a positive Chvostek sign and Trousseau sign are usually present. Focus of patient care is to treat tetany, maintain normal serum calcium levels, and prevent long-term complications. Emergency treatment of tetany requires IV calcium.

Instruction about lifelong treatment and follow-up care includes monitoring of calcium levels.

CUSHING SYNDROME • Cushing syndrome is a spectrum of clinical abnormalities caused by excessive corticosteroids, particularly glucocorticoids. • • • The most common cause is iatrogenic administration of exogenous corticosteroids (e.g., prednisone). Most cases of endogenous Cushing syndrome are due to adrenocorticotrophic hormone (ACTH) secreting pituitary tumor (Cushing’s disease). Key signs include centripedal or generalized obesity, “moon facies” (fullness of face), purplish red striae below the skin surface, hirsutism in women, hypertension, and unexplained hypokalemia. Treatment is dependent on the underlying cause, and includes surgery and drug therapy to normalize hormone levels. Discharge instructions are based on patient’s lack of endogenous corticosteroids and resulting inability to react to stressors physiologically. Lifetime replacement therapy is required by many patients.

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ADDISON’S DISEASE • In the patient with Addison’s disease, all three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) are reduced. • • • • The etiology is mostly autoimmune where adrenal cortex is destroyed by autoantibodies. Manifestations have a slow onset and include weakness, weight loss, and anorexia. Skin hyperpigmentation is seen in sun-exposed areas of body, at pressure points, over joints, and in palmar creases. The treatment is replacement therapy. Hydrocortisone, the most commonly used form of replacement therapy, has both glucocorticoid and mineralocorticoid properties. During times of stress, glucocorticoid dosage is increased to prevent addisonian crisis. Mineralocorticoid replacement with fludrocortisone acetate (Florinef) is given daily with increased dietary salt. Patient teaching covers medications, techniques for stress management, and that patient must always wear an identification bracelet (Medic Alert).

Addisonian Crisis • Patients with Addison’s disease are at risk for an acute adrenal insufficiency (addisonian crisis), a life-threatening emergency caused by insufficient or sudden decrease in adrenocortical hormones. • Addisonian crisis is triggered by stress (e.g., surgery, trauma, hemorrhage, or psychologic

distress); sudden withdrawal of corticosteroid hormone replacement therapy; and postadrenal surgery. • • Manifestations include postural hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion. Treatment is shock management and high-dose hydrocortisone replacement. Large volumes of 0.9% saline solution and 5% dextrose are given to reverse hypotension and electrolyte imbalances until blood pressure normalizes.

LONG-TERM ADMINISTRATION OF CORTICOSTEROIDS • The use of long-term corticosteroids in therapeutic doses often leads to serious complications and side effects. • Therapy is reserved for diseases in which there is a risk of death or permanent loss of function, and conditions in which short-term therapy is likely to produce remission or recovery. The potential treatment benefits must always be weighed against risks. The danger of abrupt cessation of corticosteroid therapy must be emphasized to patients and significant others. Corticosteroids taken longer than 1 week will suppress adrenal production and oral corticosteroids should be tapered. Nurses must ensure that increased doses of corticosteroids are prescribed in acute care or home care situations with increased physical or emotional stress.

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HYPERALDOSTERONISM • Hyperaldosteronism is characterized by excessive aldosterone secretion commonly caused by small solitary adrenocortical adenoma. • • • • • The main effects are sodium retention and potassium and hydrogen ion excretion. A key sign of this disease is hypertension with hypokalemic alkalosis. The preferred treatment is surgical removal of adenoma (adrenalectomy). Patients with bilateral adrenal hyperplasia are treated with drugs. Calcium channel blockers may be used to control BP. Patients are taught to monitor own BP and need for monitoring.

PHEOCHROMOCYTOMA • Pheochromocytoma is a rare condition characterized by an adrenal medulla tumor that produces excessive catecholamines (epinephrine, norepinephrine). • • The tumor is benign in most cases. The secretion of excessive catecholamines results in severe hypertension.

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If undiagnosed and untreated, pheochromocytoma may lead to diabetes mellitus, cardiomyopathy, and death. Manifestations include severe, episodic hypertension accompanied by classic triad of (1) severe, pounding headache, (2) tachycardia with palpitations and profuse sweating, and (3) unexplained abdominal or chest pain. Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants. The treatment consists of surgical removal of tumor.

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