Signs and Symptoms

Local symptoms of pituitary adenoma include headache from the pressure of the tumor, and visual disturbance—with possible blindness—from pressure within the optic chiasm. Systemic symptoms may be vague, and progress very slowly. Personality changes, weakness, fatigue, and vague abdominal pain can be present for years before the condition is diagnosed correctly.

Diagnosis

Diagnosis of a pituitary tumor begins with a complete history and physical examination. Magnetic resonance imaging (MRI) and high-resolution computed tomography (CT) with contrast media may be used to identify, localize, and determine the extent of the tumor. A thorough ophthalmologic examination will be performed to evaluate pressure on the optic chiasm or optic nerves.

Treatment

Nursing Management

After the surgery, the patient is kept in a semi-Fowler’s position. The nurse must closely monitor vital signs and the patient’s neurologic status. It is important to note and communicate promptly any change in vision, mental status, level of consciousness, or strength. The nurse must also monitor for any complications, such as diabetes insipidus (see p. 835). A nasal drip pad is in place and is changed as needed. Because nasal packing will be in place for 2 to 3 days, the patient must breathe through the mouth. After surgery it is important that the patient not brush his teeth, cough, sneeze, blow his nose, or bend forward, as these may interfere with the healing process. The nurse assists the patient with mouth rinses and encourages hourly deep-breathing exercises to prevent pulmonary problems.

Etiology and Pathophysiology

The most common cause of pituitary hypofunction is a tumor. Other causes include autoimmune disorders, infections, or destruction of the pituitary. A rare but serious postpartum complication, Sheehan syndrome, involves infarction of the gland secondary to postpartum hemorrhage.

The most common pituitary hormone deficiency involves a decrease in the amount of GH and gonadotropins. This decrease results in metabolic problems and sexual dysfunction. Decrease in GH will lead to short stature in children; in adults it leads to an increase in bone breakdown, resulting in increased bone fragility and risk for osteoporosis. The decrease in gonadotropins may lead to testicular failure in a man and, ultimately, sterility. Ovarian failure, amenorrhea, and infertility occur with decreased gonadotropins in women.

Signs and Symptoms

Diagnosis

Diagnosis of pituitary gland hypofunction is made by history, physical examination, and diagnostic studies. Laboratory blood tests are performed to measure levels of pituitary hormones. MRI and CT are used to determine the presence or absence of a pituitary tumor.

Treatment and Nursing Management

The mainstay of treatment for hypofunction of the pituitary gland is lifelong replacement of the hormone(s) affected. Somatropin, via subcutaneous injection, is used to replace GH. The patient experiences a feeling of increased energy and well-being, although there are side effects, such as edema, joint pain, and headache. Gonadal hormone therapy is usually offered, including testosterone for men and estrogen/progesterone for women, although associated risks may outweigh the benefits for some patients. If the disorder is caused by a tumor, surgery or radiation for tumor removal is usually performed, followed by hormone therapy.

Nursing management involves recognizing the signs and symptoms of hypofunction of the pituitary. Teach the patient about lifelong hormone replacement therapy, including method and frequency of hormone replacements, side effects, and follow-up.

Etiology and Pathophysiology

Diagnosis

To diagnose DI a complete history is obtained, and a physical examination and laboratory tests are performed, including urine and plasma osmolality, and urine specific gravity. A water deprivation test is done to confirm a suspected case of central DI.

Treatment and Nursing Management

Replacement of fluid and electrolytes, along with hormone therapy, represents the basis of treatment of DI. In central DI, the hormone of choice to replace insufficient ADH is desmopressin acetate (DDAVP), available orally, intravenously, or nasally. Other hormone medication choices exist, such as vasopressin (Pitressin) via nasal inhalation or by injection. For fluid replacement, hypertonic saline is used, titrated to match the patient’s urinary output.

Nursing management focuses on early detection, maintenance of fluid and electrolyte balance, and patient education. Baseline vital signs and weight are important to accurately document and monitor throughout therapy. Strict (hourly) intake and output are essential to correct fluid losses and to titrate hypertonic saline infusion.

Signs and Symptoms

Signs and symptoms of SIADH include confusion, seizure, and loss of consciousness accompanied by weight gain and edema. Hyponatremia from fluid excess is present with serum sodium often less than 120 mEq/L. As a result of the hyponatremia, the patient will experience muscle cramps and weakness. Urine output will be diminished.

Diagnosis

SIADH is diagnosed by performing urine and serum osmolality tests simultaneously. Results will demonstrate a decreased serum osmolality (less than 280 mOsm/kg) and elevated urine osmolality (more than 100 mmol/kg), which indicates the inappropriate excretion of concentrated urine in the presence of a dilute serum. Other laboratory tests to support the diagnosis include a decrease in blood urea nitrogen (BUN), hemoglobin, hematocrit, and creatinine clearance, and elevated urine sodium.

Treatment and Nursing Management

Treatment of SIADH is aimed at correcting the underlying cause, restricting fluids to 500 to 1000 mL/day, and administering sodium chloride, diuretics, and demeclocycline (a tetracycline) to increase excretion of water. In 2009 the U.S. Food and Drug Administration (FDA) approved tolvaptan (Samsca) for the treatment of hyponatremia in SIADH. Tolvaptan improves serum sodium levels within 8 hours; however, there is a danger of overcorrection and sodium levels need to be closely monitored. Hypertonic enemas may be prescribed to draw out excess water.

Thorough nursing assessment/data collection is essential to monitor treatment and prevent complications of SIADH. The nurse must closely focus on the cardiovascular and neurologic systems and remain alert to the possibility of fluid shifts. The nurse must promptly notify the physician of any change in level of consciousness. Electrolytes are monitored closely (as often as several times per day), and daily weights are measured.

Etiology and Pathophysiology

Signs, Symptoms, and Diagnosis

Because there may be no systemic symptoms or changes in the metabolic rate of a person with simple goiter, the first sign that is usually noticed is an enlargement in the front of the neck. Later, if the gland continues to grow bigger, it presses against the esophagus and causes some difficulty in swallowing. The goiter also can press against the trachea and interfere with normal breathing. The diagnosis of goiter is established by history and physical examination. Goiter can be associated with increased, normal, or decreased hormone production.

Treatment

If goiter resulting from iodine deficiency is treated early, the growth of the gland can be arrested, and in some cases the enlargement will eventually disappear. Medications prescribed include preparations containing elemental iodine (the iodide ion). A very large goiter that continues to grow and produces local symptoms of pressure—or one that presents the possibility of developing into a malignant growth or a toxic goiter—is surgically removed in a procedure similar to the one sometimes done for hyperthyroidism.

Nursing Management

Iodine preparations should be given well diluted and administered through a straw, as they can stain the teeth. Adverse effects of iodine preparations can include gastrointestinal upset, metallic taste, skin rashes, allergic reactions, and epigastric pain.

Etiology and Pathophysiology

Patients at greatest risk for hyperthyroidism are adult women between 30 and 50 years of age. Primary hyperthyroidism is the result of an abnormality of function involving the thyroid gland itself, and causes excessive circulation of thyroid T₄ and T₃ hormones. However, it is possible that only the T₃ level will be above normal if the patient has Graves’ disease, toxic adenoma of the thyroid, or toxic nodular goiter.

High serum levels of T₄ can be caused by either overactivity of the thyroid gland or by excessive doses of T₄ given in replacement therapy. Primary hyperthyroidism is more common in women 30 to 50 years of age. Secondary hyperthyroidism usually is the result of an abnormality in another gland, such as the pituitary gland, that could produce too much TSH and therefore overstimulate the thyroid gland.

Primary hyperthyroidism is also known as Graves’ disease or toxic goiter. Medications containing iodine, such as amiodarone (an antidysrhythmic heart medication) can predispose to hyperthyroidism. In addition, it has been discovered recently that women who smoke have nearly twice the risk of developing hyperthyroidism when compared with nonsmokers.

Signs and Symptoms

The earliest symptoms of hyperthyroidism may be weight loss (in spite of a good appetite) and nervousness. Symptoms can vary from mild to severe, and may include weakness, insomnia, tremulousness, agitation, tachycardia, palpitations, exertional dyspnea, ankle edema, difficulty concentrating, diarrhea, increased thirst and urination, decreased libido, scanty menstruation, and infertility. The condition sometimes is not diagnosed in its early stages because of the vagueness of the symptoms. In some cases hyperthyroidism is misdiagnosed as a cardiovascular disease, as symptoms are similar.

If hyperthyroidism is not diagnosed correctly and continues untreated for any length of time, the patient can develop true organic heart disease and may experience myocardial infarction.

Diagnosis

Medical diagnosis is based on clinical manifestations of hyperthyroidism and the results of laboratory tests for thyroid hormone levels. One indicator of hyperthyroidism is assessment of the heart rate while the patient is sleeping. A rate that is consistently above 80 could signify a toxic state resulting from excessive levels of thyroid hormone. The physician may also order an electrocardiogram (ECG) to evaluate cardiac dysrhthymias or a CT or MRI to rule out ocular complications.

Treatment and Nursing Management

Hyperthyroidism may be treated medically by administering radioactive iodine and antithyroid drugs, mild sedatives, and beta-adrenergic blocking agents to control tremor, temperature elevation, restlessness, and tachycardia. Radioactive iodine (¹³¹I), also known as ablation therapy, is the definitive treatment for hyperthyroidism. It is contraindicated in pregnant and nursing women, as it can disable the infant’s thyroid gland. The main disadvantage of ablation therapy is the possibility of hypothyroidism (deficient activity of the thyroid gland) caused by “overeffective” treatment. The hypothyroidism can occur immediately after treatment or long after it is completed; thus the patient must have ongoing follow-up.

Dosage depends on the size of the gland and the thyroid’s sensitivity to radiation. Patients receiving small doses can be given the drug orally for several doses on an outpatient basis. Larger doses require isolation of the patient for 8 days, which is the half-life (the time required for half the nuclei to undergo radioactive decay) of ¹³¹I.

Because the iodine circulates in the blood and is excreted by the kidneys, precautions must be taken when handling needles, syringes, and other equipment likely to be contaminated with blood, and bedpans, urinals, and specimen bottles likely to be contaminated by urine.

All patients receiving radioactive iodine must be observed for signs of thyroid crisis resulting from radiation-induced thyroiditis (discussed later). If hyperthyroidism is not controlled within several months of therapy with radioactive iodine alone, the patient will require adjunctive therapy in the form of potassium iodide and antithyroid drugs.

Antithyroid drugs are prescribed as the initial treatment of hyperthyroidism in children, young adults, and pregnant women. Methimazole (Tapazole) is the main drug used. The patient must take the antithyroid drug at the prescribed time and strictly according to schedule. Iodine preparations such as propylthiouracil (PTU) and potassium iodide (SSKI) have only a temporary effect.

Iodine preparations also may be given for a period of 10 to 14 days before surgery of the thyroid to reduce the vascularity of the gland, minimizing the danger of releasing large amounts of thyroid hormone into the bloodstream during surgery, and to decrease the risk of hemorrhage.