Chapter 52 Care of Patients with Pituitary, Thyroid, Parathyroid, and Adrenal Disorders Med-Surg II

Pituitary Tumors Etiology and pathophysiology Signs and symptoms Benign pituitary adenoma-Tumor secretes growth hormone (GH), leading to continued growth of bones & soft tissues. May cause optic nerve damage & acts against insulin, resulting in an increase in blood glucose & glucose intolerance. Signs and symptoms Local symptoms-HA, visual disturbances (possible blindness). Systemic symptoms-May be vague & progress slowly. Personality changes, weakness, fatigue, & abdominal pain may be present for years before diagnosis.

Pituitary Tumors (cont.) Excessive growth hormone may result in gigantism in children, leading to excessively tall stature, as the bone growth plates have not yet closed. In adults the result is acromegaly, and the adults facial features change: the lips thicken, the nose enlarges, and the forehead develops a bulge. Also, the adult’s hands & feet become enlarged; the 1st sign may be that the patient's shoes no longer fit. Muscle weakness may occur and osteoporosis & joint pain are common.

Progression of Acromegaly See Figure 37-1 on p. 834.

Pituitary Tumors Diagnosis Treatment Complete history and physical examination Magnetic resonance imaging (MRI) High-resolution computed tomography (CT) with contrast media Treatment Hormone therapy Irradiation Surgery—hypophysectomy (removal of pituitary gland). Usual route is transsphenoidal (through the nose)

Transsphenoidal Surgical Approach for Hypophysectomy See Figure 37-2 on p. 834.

Postoperative Nursing Care Semi-Fowler’s position Note any change in vision, mental status, level of consciousness, or strength Diabetes insipidus Nasal packing Patient teaching

Hypofunction of the Pituitary Gland Etiology and pathophysiology Autoimmune disorders, infections, or destruction of the pituitary gland Sheehan syndrome (a rare, but serious postpartum complication; involves infarction of the gland secondary to postpartum hemorrhage) Decrease in GH (in children, results in short stature; in adults, results in increased bone fragility) and gonadotropins (may lead to testicular failure in a man, and ovarian failure in women)

Diagnosis History and physical examination Levels of pituitary hormones MRI and CT

Treatment and Nursing Management Hormone replacement Surgery and radiation Patient teaching

Diabetes Insipidus Etiology and pathophysiology Central DI, associated with brain tumors, head injury, neurosurgery, or central nervous system (CNS) infections Nephrogenic DI, caused by drug therapy (lithium) or kidney disease Dispogenic DI, caused by excessive water intake (sometimes associated with schizophrenia)

Signs and Symptoms Diuresis Thirst, weakness, and fatigue, often from nocturia (urination at night) Deficient fluid volume Signs of shock and CNS manifestations

Diagnosis Complete history and physical examination Urine and plasma osmolality and urine specific gravity Water deprivation test

Treatment and Nursing Management Replacement of fluid and electrolytes Hormone therapy Early detection, maintenance of fluid and electrolyte balance, and patient education

Syndrome of Inappropriate Antidiuretic Hormone Signs and symptoms Confusion, seizure, loss of consciousness, weight gain, and edema Hyponatremia, muscle cramps, and weakness Diminished urine output

Pathophysiology See Concept Map 37-2 on p. 837.

Diagnosis Urine and serum osmolality tests Blood urea nitrogen (BUN), hemoglobin, hematocrit, and creatinine clearance

Treatment and Nursing Management Correct underlying cause Restrict fluids to 500 to 1000 mL/day Administer sodium chloride, diuretics, and demeclocycline

Regulation of Thyroid Hormone Secretion See Concept Map 37-3 on p. 838.

Goiter Etiology and pathophysiology: Greatly enlarged thyroid gland. One type is caused by iodine deficiency. Signs, symptoms, and diagnosis: First sign is usually enlargement in front of neck. Later, as it grows larger, it may press against the esophagus and cause difficulty swallowing. It may also press against the trachea, causing dyspnea. Treatment: Iodine will stop the growth, but will not cure it. If it becomes very large, may require surgical removal.

Goiter (cont.) See Figure 37-3 on p. 839.

Goiter (cont.) Nursing management: If giving iodine preparations, use a straw as iodine can stain the teeth. Also, be aware of side effects of iodine: stomach upset, metallic taste, skin rashes, allergic reactions, and epigastric pain.

Hyperthyroidism Etiology and pathophysiology Women 30-50 are at greatest risk. Primary hyperthyroidism—Graves’ disease or toxic goiter results from problem with gland itself. Secondary hyperthyroidism-Usually results from abnormality in another gland, such as pituitary. Signs and symptoms Earliest symptoms: Weight loss (in spite of a good appetite) and nervousness. Later symptoms include weakness, insomnia, agitation, tachycardia, diarrhea, ankle edema, exertional dyspnea, decreased libido, scanty menstruation, and infertility.

Hyperthyroidism (cont.) The condition is sometimes not diagnosed in early stages because of the vagueness of symptoms. In some cases, hyperthyroidism is misdiagnosed as a cardiovascular disease, as symptoms are similar. If not diagnosed correctly & continues to be untreated, may result in true heart disease & MI. Emotional upheaval may occur as a result of the action of thyroid hormones on the nervous system. Uncontrollable crying & depression followed by intense physical activity & euphoria are common.

Exophthalmos of Graves’ Disease See Figure 37-4 on p. 840.

Hyperthyroidism Diagnosis Treatment and nursing management Clinical manifestations Heart rate while sleeping (rate consistently >80) EKG, CT, or MRI Treatment and nursing management Radioactive iodine and antithyroid drugs Mild sedatives, and beta-adrenergic blocking agents

Treatment of Hyperthyroidism Thyroid crisis (thyroid storm) Antithyroid drugs Thyroidectomy Preoperative nursing care including thyroid crisis Postoperative nursing care Thyroid storm (also known as thyroid crisis or thyrotoxicosis) is caused by a sudden increase in the output of thyroxine caused by manipulation of the thyroid as it is being removed. Another cause of TS may be improper reduction of thyroid secretions before surgery. In a patient with hyperthyroidism, TS also can be triggered by other factors unrelated to surgery; TS can also be caused by a patient with hypothyroidism who consumes an overdose of levothyroxine. The symptoms of TS are produced by a sudden and extreme elevation of all body processes. The temperature may rise to 106° F (41.1° C) or more, the pulse increases to as much as 200 beats per minute, respirations become rapid, and the patient exhibits marked apprehension and restlessness. Unless the condition is relieved, the patient quickly passes from delirium to coma to death from heart failure.

Thyroid Storm Thyroid storm (also known as thyroid crisis or thyrotoxicosis) is caused by a sudden increase in the output of thyroxine caused by manipulation of the thyroid as it is being removed. Another cause of TS may be improper reduction of thyroid secretions before surgery. In a patient with hyperthyroidism, TS also can be triggered by other factors unrelated to surgery; TS can also be caused by a patient with hypothyroidism who consumes an overdose of levothyroxine. The symptoms of TS are produced by a sudden and extreme elevation of all body processes. The temperature may rise to 106° F (41.1° C) or more, the pulse increases to as much as 200 beats per minute, respirations become rapid, and the patient exhibits marked apprehension and restlessness. Unless the condition is relieved, the patient quickly passes from delirium to coma to death from heart failure.

Common Causes of Thyroid Storm Administration of drugs or dyes containing iodine Childbirth (immediately postpartum) Congestive heart failure Diabetic ketoacidosis Inadequate hormone replacement Infection Pulmonary embolism Severe emotional distress Stroke Trauma or surgery See Box 37-1 on p. 843.

Treatment of Thyroid Storm Reduce the temperature Cardiac drugs to slow the heart rate Sedatives such as a barbiturates to reduce restlessness and anxiety

Hypothyroidism Etiology and pathophysiology: Can be caused by inflammation of thyroid, decreased TSH secretion hypothalamus dysfunction, atrophy of thyroid gland, or by treatment of hyperthyroidism which may destroy thyroid cells. Congenital hypothyroidism—cretinism Signs and symptoms Myxedema (very low thyroid production) is characterized by a decrease in appetite but increase in weight due to very slow metabolism

Hypothyroidism (cont.) Other s/s are tiredness, low energy, lethargy, facial swelling, bags under eyes, slurred speech, cold intolerance, constipation, flatulence, impaired memory, depression, husky voice, hair loss, brittle nails, easy bruising, muscle cramps, dry skin, and non- pitting edema. Diagnosis and treatment: Clinical s/s and lab tests Clinical signs and symptoms Serum levels of thyroid hormones and TSH

Nursing Management Managing hypothyroidism Nurses should increase awareness of look-alike, sound-alike products and help patients to recognize the exact name and purpose of their medications Myxedema coma—cause, signs and symptoms, and treatment Myxedema coma is life-threatening. It can be precipitated by abrupt withdrawal of thyroid therapy, acute illness, anesthesia, use of sedatives or narcotics, surgery, or hypothermia in the hypothyroid patient. Signs and symptoms are loss of consciousness along with hypotension, hypothermia, respiratory failure, hyponatremia, and hypoglycemia. Treatment is administration of levothyroxine sodium IV, fluid replacement, maintenance of an airway and respiration, IV glucose administration, corticosteroids, and provision of warmth.

Myxedema Coma Myxedema coma is life-threatening. It can be precipitated by abrupt withdrawal of thyroid therapy, acute illness, anesthesia, use of sedatives or narcotics, surgery, or hypothermia in the hypothyroid patient. Signs and symptoms are loss of consciousness along with hypotension, hypothermia, respiratory failure, hyponatremia, and hypoglycemia. Treatment is administration of levothyroxine sodium IV, fluid replacement, maintenance of an airway and respiration, IV glucose administration, corticosteroids, and provision of warmth.

Thyroiditis Etiology and pathophysiology Inflammation of the thyroid gland Acute (infection related), subacute (related to upper respiratory viral infection, for example), or chronic (most common type) Autoimmune thyroiditis (Hashimoto’s thyroiditis) is a chronic form usually affecting women age 30-50. The body produces antibodies against the thyroid, which destroys the gland. Cause is unknown, but seems to be genetic as people who have this disease usually have other autoimmune disorders, such as RA.

Thyroiditis (cont.) Signs and symptoms: Painless enlargement of thyroid gland which may cause dysphagia. Diagnosis: Lab tests, including thyroid hormone levels, TSH levels and radioactive iodine uptake. Needle biopsy may be performed. Treatment: Thyroid hormone to prevent hypothyroidism and decrease the size of the thyroid (sometimes with surgery). Nursing management: Patient teaching; providing comfort.

Thyroid Cancer Etiology and pathophysiology: More common in recent years. Most common form is papillary carcinoma, which occurs most often in younger women. Slow growing tumor can be present for years before diagnosis. Cause is unknown. Signs and symptoms: First sign is a nodule found on routine physical examination. Only 5%-10% of nodules are found to be cancerous. Fatigue, weight changes, or depression may also be present.

Thyroid Cancer (cont.) Diagnosis: US used to assess thyroid size and locate nodules; Iodine uptake studies may also be used. The definitive test is fine-needle aspiration, in which a specimen of tissue is taken & analyzed. Treatment & Nursing Management: TX is thyroidectomy. In some cases, radioactive iodine (ablation) therapy may be used in lieu of surgery to disable the gland. A new drug, vandetanib, has been approved in 2011 which inhibits tumor growth in symptomatic thyroid cancer.

Hypoparathyroidism Etiology and pathophysiology: Most often caused by atrophy or traumatic injury to the parathyroid glands. This can occur as a result of accidental removal or destruction of parathyroid tissue during a thyroidectomy. Hypoparathyroidism will result in a drop in serum calcium levels and an increase in phosphorus levels.

Hypoparathyroidism (cont.) Signs and symptoms of low calcium include mild tingling, numbness, muscle cramps, and mental changes, such as irritability. Chvostek sign manifests as muscle irritability when the facial nerve is gently tapped. Trousseau sign manifests as a carpal spasm, elicited by inflating a BP cuff above the systolic blood pressure. Tetany is a serious sign resulting from low calcium. Muscular twitching & spasms occur because of extreme irritability of neuromuscular tissue. Convulsions, cardiac dysrhythmias, and spasms of the larynx will occur if calcium levels continue to fall.

Hypoparathyroidism (cont.) Diagnosis is established by clinical signs & lab tests. ECG may show abnormalities which return to normal when calcium level is corrected. CT scan may show calcifications in the brain if hypocalcemia is chronic. Treatment and nursing management: Acute hypoparathyroidism with tetany is treated with IV calcium gluconate. Oral calcium salts may be used simultaneously. In chronic hypoparathyroidism, treatment is aimed at restoring & maintaining blood calcium levels. This is accomplished by hormone replacement therapy, vitamin D in massive doses, & oral administration of calcium salts. Nursing care revolves around education & electrolyte replacement. Remind Pt. it is lifelong therapy & to wear a medical alert bracelet.

Hyperparathyroidism (Von Recklinghausen’s Disease) Etiology and pathophysiology: Common endocrine disorder that most often occurs in postmenopausal women. Hypercalcemia occurs with this disease. Signs and symptoms: More than 50% are asymptomatic. S/S may be mild or severe and include: dehydration, confusion, lethargy, arrhythmias, anorexia, n/v, weight loss, constipation, thirst, frequent urination, & HTN. May be skeletal changes, including thinning of the bone & bone cysts. A bone fracture may cause the pt. To seek medical attention.

Hyperparathyroidism (Von Recklinghausen’s Disease) Diagnosis: Labs Serum calcium elevated and phosphate levels low Serum parathyroid hormone is the best test for initial confirmation Serum albumin is also measured because serum calcium needs to be corrected for low albumin levels Treatment: Depends on the severity. Infusions of isotonic sodium chloride and administration of diuretic agents promotes excretion of excess calcium in the urine. Phosphate therapy is given to correct the deficit; mithramycin binds calcium & enhances secretion from body; calcitonin decreases the rate of skeletal calcium release. Surgical removal of portion of gland may be necessary. Nursing management: I&O; daily weight; electrolytes; cardiac monitoring.

Causes of Hyperparathyroidism Parathyroid tumor (benign or malignant) Congenital enlargement Neck trauma or irradiation Vitamin D deficiency Chronic renal failure with hypocalcemia Lung, kidney, or GI tract cancers See Box 37-2 on p. 846.

Comparison of Hyperparathyroidism and Hypoparathyroidism Serum calcium levels Serum phosphate levels Bone resorption Calcium and phosphate in urine Neuromuscular irritability SEE TABLE 37-2 ON P. 846! See Table 37-2 on p. 846.

Pheochromocytoma Etiology and pathophysiology: Rare tumor of the adrenal medulla that secretes catecholamines (epinephrine & norepinephrine). It often causes severe HTN and if left untreated it can lead to death. Signs, symptoms, and diagnosis: Tachycardia, severe HTN, profuse sweating, severe HA, and palpitations. Diagnosis is made by measuring serum catecholamines and 24-hour urine measurement. CT & MRI may be used to locate tumor.

Pheochromocytoma Treatment Surgical removal Nursing management Hypertensive crisis

Adrenocortical Insufficiency (Addison’s Disease) Etiology and pathophysiology: Characterized by decreased function of adrenal cortex resulting in a deficit of all three hormones secreted by the adrenal cortex. Major problems related to insufficiencies of mineralcorticoids & glucocorticoids. Insufficiency of androgenic hormones can be compensated for by the ovaries & testes. Primary insufficiency: Disorder in the cortex itself. Secondary insufficiency: Disorder in pituitary gland which stimulates adrenal secretion.

Adrenocortical Insufficiency (Addison’s Disease) (cont.) Signs and symptoms: Early symptoms are so vague, most patients don’t seek tx. Later, severe symptoms associated with fluid & electrolyte imbalance & hypoglycemia. A major problem is depletion of sodium (hyponatremia) which in turn causes depletion of extracellular fluid & potassium retention (hyperkalemia). Generalized malaise, muscle weakness, muscle pain, orthostatic hypotension, and cardiac dysrhythmias may also be present. GI symptoms, such as flatulence, N/V, and diarrhea may also be present.

Adrenocortical Insufficiency (Addison’s Disease) (cont.) Diagnosis of Addison’s is made by examining blood and urine electrolytes. ACTH stimulation test may determine if the problem lies in the adrenal gland or the pituitary. CT & MRI may be used to locate tumor. Abnormal serum electrolytes (hyponatremia & hyperkalemia), decreased glucose tolerance, elevated WBC’s and abnormally low levels of free cortisol are among the criteria used to diagnose Addison’s disease. Treatment: Replacement therapy providing the missing hormones usually brings about a rapid recovery, but lifelong therapy is required.

Adrenocortical Insufficiency (Addison’s Disease) (cont.) Intensive care and support and Addisonian crisis Prevent problems related to fatigue and orthostatic hypotension Alleviate gastrointestinal problems Patient teaching

Acute Adrenal Insufficiency or Addisonian Crisis Etiology: Physical stress from the flu or other infection, or from surgery, can send the patient with Addison’s disease into addisonian crisis. Treatment and nursing management Monitor vital signs, glucose, and potassium Fluid replacement Kayexalate, diuretics, insulin, and glucagon Hormone replacement

Excess Adrenocortical Hormone (Cushing Syndrome) Causes Excessive secretion of ACTH by the pituitary, which may result from faulty release of corticotropin- releasing factor (CRF) from the hypothalamus A secreting tumor of the adrenal cortex Ectopic production of ACTH by tumors outside the pituitary, such as lung cancer Iatrogenic Cushing syndrome from prolonged use of steroid therapy

Excess Adrenocortical Hormone (Cushing Syndrome) (cont.) Signs and symptoms: Buffalo hump, moon face, enlarged abdomen with thin extremities, bruising following even minor traumas, impotence, amenorrhea, HTN, and weakness. Diagnosis Plasma cortisol 24-hour urine test Dexamethasone suppression test Treatment: Surgery, using steroids cautiously. Nursing management: Assist w/psychosocial concerns.

Common Characteristics of Cushing Syndrome See Figure 37-5 on p. 852.