endocrine

adrenal crisis

Acute adrenal insufficiency, or addisonian crisis, is a life-threatening event in which the need for cortisol and aldosterone is greater than the available supply. Often, it occurs in response to a stressful event (e.g., surgery, trauma, severe infection), especially when the adrenal hormone output is already reduced. The problems of acute adrenal insufficiency are the same as those of chronic insufficiency but are more severe. Unless intervention is initiated promptly, however, sodium levels fall and potassium levels rise rapidly. Severe hypotension results from the blood volume depletion that occurs with the loss of aldosterone.

hyper function clinical manifestations Adrenocorticotropic Hormone (ACTH)

Adrenocorticotropic Hormone (ACTH) Cushing's Disease (Pituitary) • Elevated plasma cortisol levels • Weight gain • Truncal obesity • "Moon face" • Extremity muscle wasting • Loss of bone density • Hypertension • Hyperglycemia • Purple striae • Acne • Thin, easily damaged skin • Hyperpigmentation

assays

An assay measures the level of a specific hormone in blood or other body fluid. Some assays are indirect, such as the radioimmunoassay. Other hormone assay methods include immunometric assays, chromatographic assays, and mass spectrometry. On a graph, these separate hormones each shows as a unique "spike" pattern. Many different hormone concen� trations can be analyzed at the same time by this method

Imaging Assessment

Anterior, posterior, and lateral skull x-rays may be used to view the sella turcica. Erosion of the sella turcica indicates invasion of the wall from an abnormal growth. Magnetic resonance imaging (MRI) with contrast is the most sensitive method of imaging the pituitary gland, although computed tomography (CT) scans can also be used to evaluate it. The thyroid, parathyroid glands, ovaries, and testes are evaluated by ultrasound. In addition, CT scans are used to evaluate the adrenal glands, ovaries, and pancreas.

Venous Sampling.

Blood samples are taken directly from veins that drain a specific endocrine gland and hormone levels are measured. This test is used when a biopsy fails to identify a suspected mass. Unexpected blood hormone levels may indicate the location of a mass, a dysfunctional gland, or a dysfunctional part of a gland.

CHART 66-8 NURSING FOCUS ON THE OLDER ADULT

CHART 66-8 NURSING FOCUS ON THE OLDER ADULT Thyroid Problems Teach the patient these facts about changes in the thyroid gland related to aging: • The thyroid gland decreases in size with increasing age. • Thyroid hormone secretion decreases with age, but the horÂ� mone level remains stable because storage site clearance of the hormone also decreases with age. • The basal metabolic rate decreases with age, usually as a result of decreased activity. This decrease changes the body composition from predominantly muscular to predominantly fatty. • Older patients require lower doses of replacement thyroid hormone. Too large a dose may adversely affect the heart muscle.

calcitonin

Calcitonin lowers serum calcium and serum phosphorus levels by reducing bone resorption Its actions are opposite of parathyroid hormone.

CHART 65-5 KEY FEATURES Diabetes Insipidus

Cardiovascular Manifestations • Hypotension • Decreased pulse pressure • Tachycardia • Peripheral pulses weak, easily blocked • Hemoconcentration: • Increased hemoglobin • Increased hematocrit • Increased BUN Skin Manifestations • Poor turgor • Dry mucous membranes Neurologic Manifestations • Increased sensation of thirst • Irritability* • Decreased cognition* • Hyperthermia* • Lethargy to coma* • Ataxia* Kidney/Urinary Manifestations • Increased urine output: • Dilute, low specific gravity • Hypo-osmolar

TABLE 66-3 CAUSES OF PARATHYROID DYSFUNCTION

Causes of Hyperparathyroidism • Parathyroid adenoma • Parathyroid carcinoma • Congenital hyperplasia • Neck trauma or radiation • Vitamin D deficiency • Chronic kidney disease with hypocalcemia • Parathyroid hormone- secreting carcinomas of the lung, kidney, or GI tracK Causes of Hypoparathyroidism • Surgical or radiationinduced thyroid ablation • Parathyroidectomy • Congenital dysgenesis • Idiopathic (autoimmune) hypoparathyroidism • Hypomagnesemia

Chlorpropamide (Diabinese, Insulase)

Chlorpropamide (Diabinese, Insulase) 250-500╯mg orally daily The drug is an antidiabetic agent that also has some antidiuretic activity through an unknown mechanism. It decreases urine output.

Changes in the Endocrine System Related to Aging

Decreased antidiuretic hormone (ADH) production Urine is more dilute and may not concentrate when fluid intake is low. The patient is at greater risk for dehydration as a result of urine loss. Assess the older patient more frequently for dehydration. If fluids are not restricted because of another health problem, teach unlicensed assistive personnel (UAP) to offer fluids at least every 2 hours while awake. Decreased ovarian production of estrogen Bone density decreases. Teach the patient to engage in regular exercise and weight-bearing activity to maintain bone density. Handle the patient carefully to avoid injury from pathologic fractures. Skin is thinner, drier, and at greater risk for injury. Avoid pulling or dragging the patient. Use minimal tape on the skin. Assist patients confined to bed or chairs to change positions at least every 2 hours. Teach patients to use moisturizers on the skin and to avoid agents that promote skin dryness. Perineal and vaginal tissues become drier, and the risk for cystitis increases. Perform or assist the patient to perform perineal care at least twice daily. Unless another health problem requires fluid restriction, encourage all women to drink at least 2 liters of fluids daily. Teach sexually active women to urinate immediately after sexual intercourse. Teach sexually active women that using vaginal lubricants with sexual activity can reduce discomfort and the risk for tissue damage. Decreased glucose tolerance Weight becomes greater than ideal along with: • Elevated fasting blood glucose level • Elevated random blood glucose level • Slow wound healing • Frequent yeast infections • Polydipsia • Polyuria Obtain a family history of obesity and type 2 diabetes. Encourage the patient to engage in regular exercise and to keep body weight within 10 lbs of ideal. Teach patients the clinical manifestations of diabetes, and instruct them to report any of these manifestations to the health care provider. Suggest diabetes testing for any patient with: • Persistent vaginal candidiasis • Failure of a foot or leg skin wound to heal in 2 weeks or less • Increased hunger and thirst • Noticeable decrease in energy level Decreased general metabolism Less tolerant of cold. Decreased appetite. Decreased heart rate & blood pressure (BP). Can be difficult to distinguish from hypothyroidism. Check for additional manifestations of: • Lethargy • Constipation (as a change from usual bowel habits) • Decreased cognition • Slowed speech • Body temperature consistently below 97° F (36° C) • Heart rate below 60 beats/min Teach patients to dress warmly in cool or cold weather.

Adrenocorticotropic hormone (ACTH) deficiency clinical manifestations

Decreased serum cortisol levels Pale, sallow complexion Malaise and lethargy Anorexia Postural hypotension Headache Hypoglycemia Hyponatremia Decreased axillary and pubic hair (women)

Thyroid-stimulating hormone (thyrotropin) (TSH) deficiency clinical manifestations

Decreased thyroid hormone levels Weight gain Intolerance to cold Scalp alopecia Hirsutism Menstrual abnormalities Decreased libido Slowed cognition Lethargy

Desmopressin (DDAVP, Rhinal Tube, Minirin, Stimate)

Desmopressin (DDAVP, Rhinal Tube, Minirin, Stimate) Tablets: 0.1-0.2╯mg orally twice daily Nasal spray: 10-20╯mcg every 8-12╯hr Parenteral: 1-2╯mcg IV or subcutaneously every 12╯hr The drug is a synthetic type of ADH that serves as a replacement. It binds to kidney receptors and enhances the reabsorption of water, thus reducing urine output.

Posterior Pituitary Hormones Vasopressin (antidiuretic hormone [ADH]) deficiency clinical manifestations

Diabetes insipidus: • Greatly increased urine output • Low urine specific gravity (<1.005) • Hypovolemia: Hypotension Dehydration • Increased plasma osmolarity • Increased thirst • Output does not decrease when fluid intake decreases

HYPERPARATHYROIDISM

Diuretic and hydration therapies are used for reducing serum calcium levels in patients who are not candidates for surgery. Usually furosemide (Lasix, Uritol ), a diuretic that increases kidney excretion of calcium, is used together with IV saline in large volumes to promote calcium excretion. Calcitonin decreases the release of skeletal calcium and increases the kidney excretion of calcium. It is not effective when used alone because of its short duration of action. The therapeutic effects are greatly enhanced if calcitonin is given along with glucocorticoids. Some drugs known as calcium chelators lower calcium levels by binding (chelating) calcium, which reduces the levels of free calcium. Mithramycin, a cytotoxic agent, is the most effective and potent calcium chelator used to lower serum calcium levels. In most patients, a single IV dose of 10 to 15mg/kg of body weight by slow infusion can lower serum calcium levels within 48 hours. However, the toxic effects limit its use to two or three doses. Thrombocytopenia (decreased circulating platelets) and kidney and liver toxicity can result after only one dose. Liver function test, blood urea nitrogen and creatinine, complete blood count (CBC), and serum calcium levels are closely monitored in the patient receiving mithramycin. Another calcium chelator is penicillamine (Cuprimine, Pendramine). Monitor cardiac function and intake and output every 2 to 4 hours during hydration therapy. Continuous cardiac monitoring may be needed. Compare recent electrocardiogram (ECG) tracings with the patient's baseline tracings. Especially look for changes in the T waves and the QT interval, as well as changes in rate and rhythm. Closely monitor serum calcium levels, and immediately report any sudden drop to the health care provider. Sudden drops in calcium levels may cause tingling and numbness in the muscles.

Cushing's Drug therapy

Drug therapy involves the use of drugs that interfere with adrenocorticotropic hormone (ACTH) production or adrenal hormone synthesis for temporary relief. Aminoglutethimide (Elipten, Cytadren) and metyrapone (Metopirone) use different pathways to decrease cortisol production. For patients with hypercortisolism from increased ACTH production, cyproheptadine (Periactin) may be used because it interferes with ACTH production. Mitotane (Lysodren) is an adrenal cytotoxic agent used for inoperable tumors causing hypercortisolism. Nutrition therapy for the patient with hypercortisolism may involve restrictions of both fluid and sodium intake to control fluid volume. Each pound of weight gained (after the first half pound) equates to 500╯mL of retained water.

drugs for SIADH

Drug therapy with tolvaptan (Samsca) or conivaptan (Vaprisol) is used to treat SIADH when hyponatremia is present in hospitalized patients. These drugs are vasopressin antagonists that promote water excretion without causing sodium loss (Belavic, 2010). Tolvaptan is an oral drug, and conivaptan is given IV. Tolvaptan has a black box warning that rapid increases in serum sodium levels (those greater than a 12╯mEq/L increase in 24 hours) have been associated with central nervous system demyelination that can lead to serious complications and death. Diuretics may be used to manage SIADH when sodium levels are near normal and heart failure is present. Be aware of the diuretic effects on sodium loss. Sodium loss can be potentiated, further contributing to the problems caused by SIADH. For milder SIADH, demeclocycline (Declomycin), an oral antibiotic, may help correct the fluid imbalance, although the drug is not approved for this problem. Hypertonic saline (i.e., 3% sodium chloride [3% NaCl]) may be used to treat SIADH when the serum sodium level is very low. Give IV saline cautiously because it may add to existing fluid overload and promote heart failure. If the patient needs routine IV fluids, a saline solution rather than a water solution is prescribed.

TABLE 64-6 ANABOLIC EFFECTS OF INSULIN

Effects on Liver Effects • Promotes glycogen synthesis and storage • Inhibits glycogenolysis, gluconeogenesis, and ketogenesis • Increases triglyceride synthesis Effects on muscle . Promotes protein synthesis • Increases amino acid transport • Promotes glycogenesis Effects on Fat • Increases fatty acid synthesis • Promotes triglyceride storage • Decreases lipolysis

Thyroid Gland

Follicular cells produce the thyroid hormones thyroxine (T4) and triiodothyronine (T3). Parafollicular cells produce thyrocalcitonin (TCT, or calcitonin), which helps regulate serum calcium levels. Cold and stress are two factors that cause the hypothalamus to secrete TRH, which then stimulates the anterior pituitary to secrete TSH. T3 and T4. Both hormones increase metabolism, Thyroid hormone production involves a series of steps. Dietary intake of protein and iodine is needed to produce thyroid hormones. Iodine is absorbed from the intestinal tract as iodide. They enter many cells, bind to the nucleus, and turn on genes important in metabolism. Thus the presence of T4 and T3 directly regulates basal metabolic rate (BMR)

hypocalcemia drugs

For patients with acute and severe hypocalcemia, IV calcium is given as a 10% solution of calcium chloride or calcium gluconate over 10 to 15 minutes. Acute vitamin D deficiency is treated with calcitriol (Rocaltrol), 0.5 to 2╯mg daily. Acute hypomagnesemia is corrected with 50% magnesium sulfate in 2-mL doses (up to 4╯g daily) either IM or IV. Long-term oral therapy for hypocalcemia involves the intake of calcium, 0.5 to 2╯g daily, in divided doses. Long-term therapy for vitamin D deficiency is 50,000 to 400,000 units of ergocalciferol daily. Teach the patient to eat foods high in calcium but low in phosphorus. Milk, yogurt, and processed cheeses are avoided because of their high phosphorus content. Stress that therapy for hypocalcemia is lifelong.

CHART 65-11 KEY FEATURES Hypercortisolism (Cushing's Disease/Syndrome)

General Appearance • Fat redistribution: • Moon face • Buffalo hump • Truncal obesity • Weight gain Cardiovascular Manifestations • Hypertension • Increased risk for thromboembolic events Skin Manifestations • Frequent dependent edema • Capillary fragility: • Bruising • Petechiae • Thinning skin ("paper-like" appearance, especially on the back of the hands) • Striae • Increased pigmentation (with ectopic or pituitary production of ACTH) Immune System Manifestations • Increased risk for infection • Decreased immune function: • Decreased circulating lymphocytes • Decreased production of immunoglobulins (antibodies) • Decreased inflammatory responses: • Decreased eosinophil count • Slight increase in neutrophil count but activity is reduced • Decreased production of proinflammatory cytokines, histamine, and prostaglandins • Manifestations of infection/ inflammation may be masked Musculoskeletal Manifestations • Muscle atrophy (most apparent in extremities) • Osteoporosis (bone density loss) • Pathologic fractures • Decreased height with vertebral collapse • Aseptic necrosis of the femur head • Slow or poor healing of bone fractures Glucose metabolism is profoundly affected by hypercortisolism. Fasting blood glucose levels are high because the liver is stimulated to convert more glycogen to glucose and the insulin receptors are less sensitive, so blood glucose does not move as easily into the tissues. In addition, muscle mass loss reduces glucose uptake. Additional laboratory findings that accompany hypercortisolism include: • Increased blood glucose level • Decreased lymphocyte count • Increased sodium level • Decreased serum calcium level • Decreased serum potassium level

hyper function clinical manifestations Gonadotropins (Luteinizing Hormone [LH], Follicle- Stimulating Hormone [FSH])

Gonadotropins (Luteinizing Hormone [LH], Follicle- Stimulating Hormone [FSH]) Men: • Elevated LH and FSH levels • Hypogonadism or hypergonadism Women: • Normal LH and FSH levels (The most common clinical manifestations in men and women are related to the physical presence of a tumor rather than to excessive hormone secretion.)

Graves' disease

Graves' disease is an autoimmune disorder in which antibodies (thyroid-stimulating immunoglobulins [TSIs]) are made and attach to the thyroid-stimulating hormone (TSH) receptors on the thyroid tissue. The thyroid gland responds by increasing the number and size of glandular cells, which enlarges the gland, forming a goiter, and overproduces thyroid hormones (thyrotoxicosis).

hyper function clinical manifestations Growth Hormone (GH) Acromegaly

Growth Hormone (GH) Acromegaly • Folding of the scalp skin • Thickened lips • Coarse facial features • Increasing head size • Protrusion of the lower jaw • Deepening of the voice • Tufting of the fingertips • Enlarged hands and feet • Joint enlargement and pain • Kyphosis and backache • Barrel-shaped chest • Excessive sweating • Hyperglycemia • Airway narrowing, sleep apnea • Enlarged heart, lungs, and liver

Growth hormone (GH) deficiency clinical manifestations

Growth hormone (GH) Decreased bone density Pathologic fractures Decreased muscle strength Increased serum cholesterol levels

Emergency Care of the Patient with Acute Adrenal Insufficiency

Hormone Replacement • Start rapid infusion of normal saline or dextrose 5% in normal saline. • Initial dose of hydrocortisone sodium succinate (Solu-Cortef) is 100 to 300╯mg or dexamethasone 4 to 12╯mg as an IV bolus. • Infuse additional 100╯mg of hydrocortisone sodium succinate by continuous IV drip over the next 8 hours. • Give hydrocortisone 50╯mg IM concomitantly every 12 hours. • Initiate an H2 histamine blocker (e.g., ranitidine) IV for ulcer prevention. Hyperkalemia Management • Administer insulin (20 to 50 units) with dextrose (20 to 50╯mg) in normal saline to shift potassium into cells. • Administer potassium binding and excreting resin (e.g., Kayexalate). • Give loop or thiazide diuretics. • Avoid potassium-sparing diuretics, as prescribed. • Initiate potassium restriction. • Monitor intake and output. • Monitor heart rate, rhythm, and ECG for manifestations of hyperkalemia (slow heart rate; heart block; tall, peaked T waves; fibrillation; asystole). Hypoglycemia Management • Administer IV glucose, as prescribed. • Administer glucagon, as needed and prescribed. • Maintain IV access. • Monitor blood glucose level hourly

Urine Tests.

Hormone levels and their metabolites in the urine are often measured to determine endocrine function. Because many of the endocrine hormones are secreted in a pulsatile fashion, measurement of a specific hormone in a 24-hour urine collection, rather than as a single blood or urine sample, better reflects the overall function of certain glands, such as the adrenal gland. Teach the patient how to collect a 24-hour urine sample (see also Chart 64-3). Certain hormones require additives in the container at the beginning of the collection. Instruct the patient not to discard the preservative from the container and to use caution when handling it because some solutions are caustic. Remind him or her that this collection is timed for exactly 24 hours. Instruct the patient to avoid taking any unnecessary drugs during endocrine testing because some drugs can interfere with the laboratory assays.

Hypersecretion adrenal

Hypersecretion by the adrenal cortex results in hypercortisolism (e.g., Cushing's disease or Cushing's syndrome), hyperaldosteronism (excessive mineralocorticoid production), or excessive androgen production. Hyperstimulation of the adrenal medulla caused by a tumor (pheochromocytoma) results in excessive secretion of catecholamines (epinephrine and norepinephrine).

exogenous hyperthyroidism.

Hyperthyroidism also can be caused by excessive use of thyroid replacement hormones. This type of problem is called exogenous hyperthyroidism.

toxic multinodular goiter

Hyperthyroidism caused by multiple thyroid nodules is termed toxic multinodular goiter. The nodules may be enlarged thyroid tissues or benign tumors (adenomas). These patients usually have had a goiter for years. The overproduction of thyroid hormones is milder than that seen in Graves' disease, and the patient does not have exophthalmos or pretibial edema.

Hypoparathyroidism

Hypoparathyroidism is a rare endocrine disorder in which parathyroid function is decreased. Problems are directly related to a lack of parathyroid hormone (PTH) secretion or to decreased effectiveness of PTH on target tissue. Whether the problem is a lack of PTH secretion or an ineffectiveness of PTH on tissues, the result is the same: hypocalcemia. manifestations of hypoparathyroidism, which may range from mild tingling and numbness to muscle tetany Severe muscle cramps, spasms of the hands and feet, and seizures (with no loss of consciousness or incontinence) reflect a more severe hypocalcemia. The patient or family may notice mental changes ranging from irritability to psychosis. The physical assessment may show excessive or inappropriate muscle contractions that cause finger, hand, and elbow flexion. This can signal an impending attack of tetany. Check for Chvostek's sign and Trousseau's sign; positive responses indicate potential tetany (see Chapter 13). Bands or pits may encircle the crowns of the teeth, which indicates a loss of calcium from the teeth with enamel loss

SIADH

In SIADH, ADH continues to be released even when plasma is hypo-osmolar. Water is retained, which results in dilutional hyponatremia (a decreased serum sodium level) and fluid overload Medical interventions for SIADH focus on restricting fluid intake, promoting the excretion of water, replacing any lost sodium, and interfering with the action of ADH. Nursing interventions focus on monitoring response to therapy, preventing complications, teaching the patient and family about fluid restrictions and drug therapy, and preventing injury. Fluid restriction is essential because fluid intake further dilutes plasma sodium levels. In some cases, fluid intake may be kept as low as 500 to 600╯mL/24╯hr. Dilute tube feedings with saline rather than plain water, and use saline to irrigate GI tubes. Mix drugs to be given by GI tube with saline. Measure intake, output, and daily weights to assess the degree of fluid restriction needed. A weight gain of 2 pounds or more per day or a gradual increase over several days is cause for concern. A 1-kg weight increase is equal to a 1000-mL fluid retention (1kg = 1L). The patient may be uncomfortable during fluid restriction. Keep mucous membranes moist by offering frequent oral rinsing (remind the patient not to swallow the rinses).

Adrenal Insufficiency

Neuromuscular Manifestations • Muscle weakness • Fatigue • Joint/muscle pain Gastrointestinal Manifestations • Anorexia • Nausea, vomiting • Abdominal pain • Bowel changes (constipation/diarrhea) • Weight loss • Salt craving Skin Manifestations • Vitiligo • Hyperpigmentation Cardiovascular Manifestations • Anemia • Hypotension • Hyponatremia • Hyperkalemia • Hypercalcemia

adrenal gland hypofunction

Insufficiency of adrenocortical steroids causes problems through the loss of aldosterone and cortisol action. Impaired secretion of cortisol results in decreased gluconeogenesis (making glucose from proteins) along with depletion of liver and muscle glycogen, leading to hypoglycemia (low blood glucose levels). Glomerular filtration and gastric acid production decrease, leading to reduced urea nitrogen excretion, causing anorexia and weight loss. Reduced aldosterone secretion causes potassium, sodium, and water imbalances. Potassium excretion is decreased, causing hyperkalemia. Sodium and water excretion are increased, causing hyponatremia and hypovolemia. Potassium retention also promotes reabsorption of hydrogen ions, which can lead to acidosis. Low adrenal androgen levels decrease the body, axillary, and pubic hair, especially in women, because the adrenals produce most of the androgens in females. The severity of symptoms is related to the degree of hormone deficiency.

stimulation testing.

Measured amounts of selected hormones are given to stimulate the target gland to maximum production. Hormone levels are then measured and compared with expected normal values. Failure of the hormone level to rise with stimulation indicates hypofunction For example, insulin injection should stimulate increased release of growth hormone (GH) and adrenocorticotropic hormone (ACTH) from a normal anterior pituitary gland. When insulin injection does not result in increased release of these hormones, a problem with the anterior pituitary gland is likely, especially hypofunction.

CHART 66-1 KEY FEATURES Hyperthyroidism

Metabolic Manifestations • Increased basal metabolic rate • Heat intolerance • Low-grade fever • Fatigue Psychological/Emotional Manifestations • Decreased attention span • Restlessness • Irritability • Emotional lability • Manic behavior Reproductive Manifestations • Amenorrhea • Decreased menstrual flow • Increased libido Other Manifestations • Goiter • Wide-eyed or startled appearance (exophthalmos)* • Decreased total white blood cell count • Enlarged spleen Neurologic Manifestations • Blurred or double vision • Eye fatigue • Corneal ulcers or infections • Increased tears • Injected (red) conjunctiva • Photophobia • Eyelid retraction, eyelid lag* • Globe lag* • Hyperactive deep tendon reflexes • Tremors • Insomnia Skin Manifestations • Diaphoresis (excessive sweating) • Fine, soft, silky body hair • Smooth, warm, moist skin • Thinning of scalp hair Manifestations • Shortness of breath with or without exertion • Rapid, shallow respirations • Decreased vital capacity Cardiovascular Manifestations • Palpitations • Chest pain • Increased systolic blood pressure • Widened pulse pressure • Tachycardia • Dysrhythmias Gastrointestinal Manifestations • Weight loss • Increased appetite • Increased stools • Hypoproteinemia Musculoskeletal Manifestations • Muscle weakness • Muscle wasting

Myxedema coma hypo thyroid

Myxedema coma is a rare, serious complication of untreated or poorly treated hypothyroidism. The decreased metabolism causes the heart muscle to become flabby and the chamber size to increase. The result is decreased cardiac output and decreased perfusion to the brain and other vital organs. The decreased perfusion makes the already slowed cellular metabolism worse, resulting in tissue and organ failure. The mortality rate for myxedema coma is extremely high, and this condition is considered a life-threatening emergency. Myxedema coma can be caused by a variety of events, drugs, or conditions • Coma • Respiratory failure • Hypotension • Hyponatremia • Hypothermia • Hypoglycemia Emergency Care of the Patient During Myxedema Coma • Maintain a patent airway. • Replace fluids with IV normal or hypertonic saline, as prescribed. • Give levothyroxine sodium IV as prescribed. • Give glucose IV as prescribed. • Give corticosteroids as prescribed. • Check the patient's temperature hourly. • Monitor blood pressure hourly. • Cover the patient with warm blankets. • Monitor for changes in mental status. • Turn every 2 hours. • Institute Aspiration Precautions.

catecholamine receptors

NE acts mainly on alpha-adrenergic receptors, and epinephrine acts mainly on beta-adrenergic receptors.

treatment of adrenal insufficiency

Nursing interventions focus on promoting fluid balance, monitoring for fluid deficit, and preventing hypoglycemia. Cortisol and aldosterone deficiencies are corrected by replacement therapy. Hydrocortisone corrects glucocorticoid deficiency (Chart 65-10). Oral cortisol replacement regimens vary. The most common drug used for this purpose is prednisone. Generally, divided doses are given, with two-thirds given in the morning and one-third in the late afternoon to mimic the normal release of this hormone. Although most patients do well on this regimen, some may not tolerate the dosage or may need more. An additional mineralocorticoid hormone, such as fludrocortisone (Florinef), may be needed to maintain electrolyte balance (especially sodium and potassium). Dosage adjustment may be needed, especially in hot weather when more sodium is lost because of excessive perspiration. Salt restriction or diuretic therapy should not be started without considering whether it might lead to an adrenal crisis.

TABLE 64-4 CATECHOLAMINE RECEPTORS AND EFFECTS OF ADRENAL MEDULLARY HORMONE STIMULATION ON SELECTED ORGANS AND TISSUES

ORGAN OR TISSUE RECEPTORS EFFECTS Heart Beta1 Increased heart rate Increased contractility Blood vessels Alpha Vasoconstriction Beta2 Vasodilation Gastrointestinal tract Alpha Increased sphincter tone Beta Decreased motility Kidneys Beta2 Increased renin release Bronchioles Beta2 Relaxation; dilation Bladder Alpha Sphincter contractions Beta2 Relaxation of detrusor muscle Skin Alpha Increased sweating Fat cells Beta Increased lipolysis Liver Alpha Increased gluconeogenesis and glycogenolysis Pancreas Alpha Decreased glucagon and insulin release Beta Increased glucagon and insulin release Eyes Alpha Dilation of pupils

parathyroid hormone

PTH increases bone resorption thus increasing serum calcium. In the kidneys, PTH activates vitamin D, which then increases the absorption of calcium and phosphorus from the intestines. In the kidney tubules, PTH allows calcium to be reabsorbed and put back into the blood. Serum phosphorus levels also affect PTH secretion.

Pheochromocytoma

Pheochromocytoma is a catecholamine-producing tumor that arises in the adrenal medulla. These tumors usually occur as a single lesion in one adrenal gland, although they can be bilateral or in the abdomen. Pheochromocytomas are usually benign, but at least 10% are malignant (Young, 2008). The tumors produce, store, and release epinephrine and norepinephrine (NE). Excessive epinephrine and NE stimulate adrenergic receptors and can have wide-ranging adverse effects mimicking the action of the sympathetic division of the autonomic nervous system. The patient often has intermittent episodes of hypertension or attacks that range from a few minutes to several hours. During these episodes, the patient has severe headaches, palpitations, profuse diaphoresis, flushing, apprehension, or a sense of impending doom. Pain in the chest or abdomen, with nausea and vomiting, can also occur. Increased abdominal pressure, defecation, and vigorous abdominal palpation can provoke a hypertensive crisis. Drugs such as tricyclic antidepressants, droperidol, glucagon, metoclopramide, phenothiazines, and naloxone can induce a hypertensive crisis in the patient with pheochromocytoma. Foods or beverages high in tyramine (e.g., aged cheese, red wine) also induce hypertension. The patient may also report heat intolerance, weight loss, and tremors. don't palpate abdomen could cause crisis The most common diagnostic test is a 24-hour urine collection for vanillylmandelic acid (VMA) (a product of catecholamine metabolism), metanephrine, and catecholamines, all of which are elevated in the presence of a pheochromocytoma

TABLE 66-2 CAUSES OF HYPOTHYROIDISM

Primary Causes Decreased Thyroid Tissue • Surgical removal of the thyroid • Radiation-induced thyroid destruction • Autoimmune thyroid destruction • Congenital thyroid agenesis • Congenital thyroid hypoplasia • Congenital thyroid dysgenesis • Cancer (thyroidal or metastatic) Decreased Synthesis of Thyroid Hormone • Endemic iodine deficiency • Excessive exposure to iodine • Drugs • Lithium • Phenylbutazone • Propylthiouracil • Sodium or potassium perchlorate • Aminoglutethimide Secondary Causes Inadequate Production of Thyroid-Stimulating Hormone • Pituitary tumors, trauma, infections, or infarcts • Congenital pituitary defects • Hypothalamic tumors, trauma, infections, or infarcts

Prolactin (PRL) hyper function clinical manifestations

Prolactin (PRL) • Hypogonadism (loss of secondary sexual characteristics) • Decreased gonadotropin levels • Galactorrhea • Increased body fat • Increased serum prolactin levels

CHART 66-6 KEY FEATURES Hypothyroidism

Skin Manifestations Psychological/Emotional • Cool, pale or yellowish, dry, Manifestations coarse, scaly skin • Thick, brittle nails • Dry, coarse, brittle hair • Decreased hair growth, with loss of eyebrow hair • Poor wound healing Pulmonary Manifestations • Apathy • Depression • Paranoia • Withdrawal Gastrointestinal Manifestations • Anorexia • Weight gain • Constipation • Abdominal distention • Hypoventilation • Pleural effusion • Dyspnea Cardiovascular Manifestations • Bradycardia • Dysrhythmias • Enlarged heart • Decreased activity tolerance • Hypotension Metabolic Manifestations • Decreased basal metabolic rate • Decreased body temperature • Cold intolerance Musculoskeletal Manifestations • Muscle aches and pains • Delayed contraction and relaxation of muscles Neurologic Manifestations • Slowing of intellectual functions: • Slowness or slurring of speech • Impaired memory • Inattentiveness • Lethargy or somnolence • Confusion • Hearing loss • Paresthesia (numbness and tingling) of the extremities • Decreased tendon reflexes Reproductive Manifestations Women • Changes in menses (amenorrhea or prolonged menstrual periods) • Anovulation • Decreased libido Men • Decreased libido • Impotence Other Manifestations • Periorbital edema • Facial puffiness • Nonpitting edema of the hands and feet • Hoarseness • Goiter (enlarged thyroid gland) • Thick tongue • Increased sensitivity to opioids and tranquilizers • Weakness, fatigue • Decreased urine output • Anemia • Easy bruising • Iron deficiency • Folate deficiency • Vitamin B12 deficiency

Tests for Glucose.

Tests for functions of the islet cells of the pancreas are indirect. They measure the result of pancreatic islet cell function. Blood glucose values and the oral glucose tolerance test help diagnose diabetes mellitus. The glycosylated hemoglobin (HbA1C) value reveals the average blood glucose level over a period of 2 to 3 months. (See Chapter 67 for a full discussion of diabetes mellitus.)

dm

The American Diabetes Association (ADA) recommends that blood pressure be maintained below 130/80╯mm╯Hg and that low-density lipoprotein (LDL) cholesterol remain below 100╯mg/dL (2.60╯mmol/L) for patients without manifestations of CVD and to less than 70╯mg/dL (1.8╯mmol/L) for patients with manifestations of CVD (ADA, 2010b). Diets high in saturated fat raise total cholesterol and LDL cholesterol levels, which increase the risk for coronary artery disease. Lifestyle modifications that focus on reducing saturated fat, trans fat, and cholesterol intake; increasing intake of omega-3 fatty acids, fiber, and plant sterols; weight loss (if indicated); and increasing physical activity are recommended to improve the lipid profile for patients with DM

catecholamine

The adrenal medulla secretes about 15% norepinephrine (NE) and 85% epinephrine.

thyroid cancer

The four distinct types of thyroid cancer are papillary, follicular, medullary, and anaplastic (American Cancer Society, 2011). The initial manifestation of thyroid cancer is a single, painless lump or nodule in the thyroid gland.

levothyroxine

The most common is levothyroxine sodium (Synthroid, T4, Eltroxin ). Therapy is started with low doses and gradually increased over a period of weeks. The patient with more severe symptoms of hypothyroidism is started on the lowest dose of thyroid hormone replacement. This caution is especially important when the patient has known cardiac problems. Starting at too high a dose or increasing the dose too rapidly can cause severe hypertension, heart failure, and myocardial infarction

HYPERPARATHYROIDISM

The parathyroid glands maintain calcium and phosphate balance (Fig. 66-4). Serum calcium level is normally maintained within a narrow range. Phosphate levels vary more widely. Increased levels of parathyroid hormone (PTH) act directly on the kidney, causing increased kidney reabsorption of calcium and increased phosphate excretion. These processes cause hypercalcemia (excessive calcium) and hypophosphatemia (inadequate phosphate) in the patient with hyperparathyroidism. The patient with long-standing disease may have a waxy pallor of the skin and bone deformities in the extremities and back. High levels of PTH cause renal calculi (kidney stones) and deposits of calcium in the soft tissue of the kidney. Bone lesions are due to an increased rate of bone destruction and may result in pathologic fractures, bone cysts, and osteoporosis. GI problems (e.g., anorexia, nausea, vomiting, epigastric pain, constipation, weight loss) are common, particularly when serum calcium levels are high. Elevated serum gastrin levels are caused by hypercalcemia and lead to peptic ulcer disease. Fatigue and lethargy may be present and become more severe as the serum calcium levels increase. When serum calcium levels are greater than 12╯mg/dL, the patient may have psychosis with mental confusion, which leads to coma and death if left untreated.

hyperthyroid drugs

The preferred drugs are the thionamides, which include propylthiouracil (PTU) and methimazole (Tapazole). These drugs block thyroid hormone production by preventing iodide binding in the thyroid gland (see Chart 66-3). In addition, PTU also prevents T4 from being converted to the more powerful T3 in the tissues. Methimazole doses are lower than PTU doses. The response to these drugs is delayed because the patient may have large amounts of stored thyroid hormones that continue to be released. Iodine preparations may be used for short-term therapy before surgery. They decrease blood flow through the thyroid gland, reducing the production and release of thyroid hor� mone. Improvement usually occurs within 2 weeks, but it may be weeks before metabolism returns to normal. This treatment can result in hypothyroidism, and the patient is monitored closely for the need to adjust the drug regimen. Lithium also inhibits thyroid hormone release. However, its use is limited because of side effects such as depression, diabetes insipidus, tremors, nausea, and vomiting. Lithium may be used for a patient who cannot tolerate other antithyroid drugs. Beta-adrenergic blocking drugs, such as propranolol (Inderal, Detensol ) may be used as supportive therapy. These drugs relieve diaphoresis, anxiety, tachycardia, and palpitations but do not inhibit thyroid hormone production. See Chapters 36 and 40 for a discussion of the actions and nursing implications of these agents.

The priority problems for patients who have hypothyroidism are:

The priority problems for patients who have hypothyroidism are: 1. Decreased oxygenation related to decreased energy, obesity, muscle weakness, and fatigue 2. Hypotension related to altered heart rate and rhythm as a result of decreased myocardial metabolism 3. Altered cognitive functioning related to impaired brain metabolism and edema 4. Potential for myxedema coma • Maintenance of Spo2 of at least 90% • Absence of cyanosis • Maintenance of cognitive orientation • Maintains heart rate above 60 beats/min • Maintains blood pressure within normal limits for his or her age and general health • Has no dysrhythmias, peripheral edema, or neck vein distention

The priority problems for patients with Cushing's disease or Cushing's syndrome are:

The priority problems for patients with Cushing's disease or Cushing's syndrome are: 1. Fluid overload 2. Risk for Injury related to skin thinning, poor wound healing, and bone density loss 3. Potential for infection 4. Potential for acute adrenal insufficiency

Three glucose-related emergencies can occur in patients with

Three glucose-related emergencies can occur in patients with diabetes: • Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis • Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration • Hypoglycemia from too much insulin or too little glucose

Thyroid storm,

Thyroid storm, or thyroid crisis, is a life-threatening event that occurs in patients with uncontrolled hyper� thyroidism and occurs most often with Graves' disease (McAdams-Jones, 2008). Manifestations of crisis develop quickly. It is often triggered by stressors such as trauma, infection, diabetic ketoacidosis, and pregnancy. Other conditions that can lead to thyroid storm include vigorous palpation of the goiter, exposure to iodine, and radioactive iodine (RAI) therapy Key manifestations include fever, tachycardia, and systolic hypertension. The patient may have GI problems such as abdominal pain, nausea, vomiting, and diarrhea. Often he or she is very anxious and has tremors. As the crisis progresses, the patient may become restless, confused, or psychotic and may have seizures, leading to coma. Even with treatment, thyroid storm may lead to death.

Thyroiditis

Thyroiditis is an inflammation of the thyroid gland. There are three types: acute, subacute, and chronic. Chronic thyroiditis (Hashimoto's disease) is the most common type. Acute thyroiditis is caused by bacterial invasion of the thyroid gland. Manifestations include pain, neck tenderness, malaise, fever, and dysphagia (difficulty swallowing). It usually resolves with antibiotic therapy. Subacute or granulomatous thyroiditis results from a viral infection of the thyroid gland after a cold or other upper respiratory infection. Manifestations include fever, chills, dysphagia, and muscle and joint pain. Pain can radiate to the ears and the jaw. The thyroid gland feels hard and enlarged on palpation. Thyroid function can remain normal, although hyperthyroidism or hypothyroidism may develop. Chronic thyroiditis (Hashimoto's disease) is a common type of hypothyroidism that affects women more often than men, usually when patients are in their 30s to 50s (Brent et al., 2008). Hashimoto's disease is an autoimmune disorder that is usually triggered by a bacterial or viral infection. The thyroid is invaded by antithyroid antibodies and lymphocytes, causing thyroid tissue destruction. When large amounts of the gland are destroyed, serum thyroid hormone levels are low and secretion of thyroid-stimulating hormone (TSH) is increased.

hyper function clinical manifestations Thyrotropin (Thyroid- Stimulating Hormone [TSH])

Thyrotropin (Thyroid- Stimulating Hormone [TSH]) • Elevated plasma TSH levels • Elevated plasma thyroid hormone levels • Weight loss • Tachycardia and dysrhythmias • Heat intolerance • Increased GI motility • Fine tremors

Vasopressin (Pitressin)

Vasopressin (Pitressin) 5-10 units parenterally two to four times daily The drug is an exogenous form of ADH that serves as a replacement. It binds to kidney receptors and enhances the reabsorption of water, thus reducing urine output.

Gonadotropins (luteinizing hormone [LH], folliclestimulating hormone [FSH]) deficiency clinical manifestations

Women: • Amenorrhea • Anovulation • Low estrogen levels • Breast atrophy • Loss of bone density • Decreased axillary and pubic hair • Decreased libido Men: • Decreased facial hair • Decreased ejaculate volume • Reduced muscle mass • Loss of bone density • Decreased body hair • Decreased libido • Impotence

pancreas

alpha cells, which secrete glucagon; beta cells, which secrete insulin; and delta cells, which secrete somatostatin. Glucagon and insulin affect carbohydrate, protein, and fat metabolism. Somatostatin, which is secreted not only in the pancreas but also in the intestinal tract and the brain, inhibits the release of glucagon and insulin from the pancreas

Suppression tests

are used when hormone levels are high or in the upper range of normal. Failure of suppression of hormone production during testing indicates hyperfunction. For example, when a bolus of glucose is given orally or intravenously, the normal anterior pituitary responds by suppressing the release of GH. A hyperfunctioning anterior pituitary gland fails to suppress GH release when blood glucose levels are elevated rapidly.

Glucagon

is a hormone that increases blood glucose levels. It is triggered by decreased blood glucose levels and increased blood amino acid levels. Together with epinephrine, growth hormone (GH), and cortisol, glucagon prevents hypoglycemia.

dm voc

ketogenesis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose). Incretin hormones (e.g., GLP-1), secreted in response to the presence of food in the stomach, have several actions. They increase insulin secretion, inhibit glucagon secretion, and slow the rate of gastric emptying, thereby preventing hyperglycemia after meals. The dehydration that occurs with diabetes leads to hemoconcentration (an increased blood concentration), hypovolemia (a decreased blood volume), hyperviscosity (thick, concentrated blood), poor tissue perfusion, and hypoxia (poor tissue oxygenation), especially to the brain.cells do not metabolize glucose efficiently, the Krebs' cycle is blocked, and lactic acid increases, causing more acidosis.

known causative factors DI

known causative factors, such as recent surgery, head trauma, or drug use (e.g., lithium).

Insulin

promotes the movement and storage of carbohydrate (CHO), protein, and fat (Table 64-6). It lowers blood glucose levels by enhancing glucose movement across cell membranes and into the cells of many tissues

Primary hyperaldosteronism (Conn's syndrome)

sodium retention with potassium and hydrogen ion excretion. Hypernatremia, hypokalemia, and metabolic alkalosis result. Sodium retention increases blood volume, which raises blood pressure but usually does not cause peripheral edema. The elevated blood pressure may cause strokes, heart attacks, and kidney damage. Hypokalemia and elevated blood pressure are the most common problems of the patient with hyperaldosteronism. He or she may have headache, fatigue, muscle weakness, nocturia (excessive urination at night), and loss of stamina. Polydipsia (excessive fluid intake) and polyuria (excessive urine output) occur less frequently. Paresthesias (sensations of numbness and tingling) may occur if potassium depletion is severe Hydrogen ion loss leads to metabolic alkalemia Drugs used to increase potassium levels include spironolactone (Aldactone, Spirono, Sincomen ), a potassium-sparing diuretic and aldosterone antagonist. Potassium supplements may be prescribed to increase potassium levels before surgery

It is important to consider these factors when assessing the older adult with endocrine dysfunction.

• Acute and chronic illnesses • Alterations in diet, activity, and lean body mass-to-fat ratio • Disturbances in sleep patterns • Decreased metabolic clearance rate of hormones • Increased use of multiple drugs that may affect hormone function Encourage the older adult to participate in regular screening examinations, including fasting and random blood glucose checks, calcium level determinations, and thyroid function testing.

Glucocorticoids Cortisol affects:

• Carbohydrate, protein, and fat metabolism • The body's response to stress • Emotional stability • Immune function The release of CRH and ACTH is affected by the serum level of free cortisol, the normal sleep-wake cycle, and stress.

TABLE 64-5 FUNCTIONS OF THYROID HORMONES IN ADULTS

• Control metabolic rate of all cells • Promote sufficient pituitary secretion of growth hormone and gonadotropins • Regulate protein, carbohydrate, and fat metabolism • Exert effects on heart rate and contractility • Increase red blood cell production • Affect respiratory rate and drive • Increase bone formation and decrease bone resorption of calcium • Act as insulin antagonists

Emergency Care of the Patient During Thyroid Storm

• Maintain a patent airway and adequate ventilation. • Give antithyroid drugs as prescribed: methimazole (Tapazole), up to 60╯mg daily; propylthiouracil (PTU, Propyl-Thyracil ), 300 to 900╯mg daily. • Administer sodium iodide solution, 2╯g IV daily as prescribed. • Give propranolol (Inderal, Detensol ), 1 to 3╯mg IV as prescribed. Give slowly over 3 minutes. The patient should be connected to a cardiac monitor, and a central venous pressure catheter should be in place. • Give glucocorticoids as prescribed: hydrocortisone, 100 to 500╯mg IV daily; prednisone, 4 to 60╯mg IV daily; or dexamethasone, 2╯mg IM every 6 hours. • Monitor continually for cardiac dysrhythmias. • Monitor vital signs every 30 minutes. • Provide comfort measures, including a cooling blanket. • Give non-salicylate antipyretics as prescribed. • Correct dehydration with normal saline infusions. • Apply cooling blanket or ice packs to reduce fever.

The Patient After Hypophysectomy

• Monitor the patient's neurologic status hourly for the first 24 hours and then every 4 hours. • Monitor fluid balance, especially for output greater than intake, because transient diabetes insipidus can occur. • Encourage the patient to maintain pulmonary hygiene through deep-breathing exercises. • Instruct the patient to not cough, blow the nose, or sneeze. • Instruct the patient to use dental floss and oral mouth rinses, because brushing the teeth is not permitted until the incision heals sufficiently. • Instruct the patient to avoid bending at the waist for any reason, because this position increases intracranial pressure. • Monitor the nasal drip pad for the type and amount of drainage. The presence of the halo sign may indicate a CSF leak. • Monitor bowel movements to prevent constipation and subsequent "straining." • Teach the patient self-administration of the prescribed hormones.

TABLE 64-3 FUNCTIONS OF GLUCOCORTICOID HORMONES

• Prevent hypoglycemia by increasing liver gluconeogenesis and inhibiting peripheral glucose use • Maintain excitability and responsiveness of cardiac muscle • Increase lipolysis, releasing glycerol and free fatty acids • Increase protein catabolism • Degrade collagen and connective tissue • Increase the number of mature neutrophils released from bone marrow • Exert anti-inflammatory effects that decrease the migration of inflammatory cells to sites of injury • Maintain behavior and cognitive functions Glucocorticoid release peaks in the morning and reaches its lowest level 12 hours after each peak. Emotional, chemical, or physical stress increases the release of glucocorticoids.

conditions that occur with the development of SIADH.

• Recent head trauma • Cerebrovascular disease • Tuberculosis or other pulmonary disease • Cancer • All past and current drug use