- Hyperactivity of one or more of the parathyroid glands, which is manifested as hypercalcemia.

Causes and Incidence Primary hyperparathyroidism is caused by a parathyroid adenoma, multiple endocrine neoplasia, or a genetic defect. Secondary hyperparathyroidism is caused by underlying disease such as rickets, renal failure, or osteomalacia; pregnancy; vitamin D or calcium deficiency; or an excessive intake of laxatives. The disease most often occurs in adults 30 to 70 years of age. Women are more likely than men to be diagnosed (3:2 ratio).

Disease Process In primary hyperparathyroidism, one or more of the parathyroid glands hypertrophies, increasing secretion of parathyroid hormone (PTH) and elevating serum calcium levels. Increased PTH causes an increase in osteoblast formation, which increases bone turnover rate. Cysts and fibrous tissue invade the bone. Increased calcium causes renal calculi, a decrease in neuromuscular excitability, a delay in gastrointestinal motility, defects in cardiac conduction, and decreased neuronal permeability. In secondary disease the elevated PTH stems from a hypocalcemia-producing abnormality outside the gland that stimulates the gland to produce more calcium.

Symptoms Manifestations include bone pain, backache, pain on weight bearing, pathologic fractures, dilute urine and hematuria, fatigue, clumsiness, constipation, acute abdominal pain, mood swings, and paranoia.

Potential Complications Renal failure, cardiac arrhythmias, cardiac failure, central nervous system coma, and death are complications associated with untreated hyperparathyroidism.

Diagnostic Tests Increases in total serum calcium, ionized calcium, PTH, uric acid, and chloride are the usual diagnostic findings. A thyroid scan, ultrasound, computed tomography, or magnetic resonance imaging may be used to locate parathyroid lesions. X-ray studies reveal bone demineralization. Intact PTH is used to distinguish primary from secondary and malignant disease.

Treatments

Surgery
Parathyroidectomy to remove adenoma or other abnormal parathyroid tissue.

Drugs
Diuretics (no thiazides, since they can lead to hypercalcemia) to increase urinary secretion of calcium; phosphate as an antihypercalcemic.

General
Treatment of the underlying disease in secondary hyperparathyroidism; increased fluid intake; restriction of dietary intake of calcium; monitoring of daily serum calcium, blood urea nitrogen, and potassium and magnesium levels.

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- An intermittent or sustained elevation in systolic blood pressure (above 140 mm Hg) or diastolic blood pressure (above 90 mm Hg) or a systolic and diastolic pressure 20 mm Hg above the individual’s baseline pressure.

Causes and Incidence The cause of primary (essential) hypertension is unknown. However, known risk factors include a familial history of the disease, race, obesity, tobacco smoking, stress, and a high-fat or high-sodium diet in genetically susceptible individuals. Secondary hypertension is related to an underlying disease process such as renal parenchymal disorders, renal artery disease, endocrine and metabolic disorders, central nervous system disorders, and coarctation of the aorta. It is estimated that 60 to 85 million Americans have hypertension, which is a major factor in strokes and cardiac and renal disease.

Disease Process Hypertension is a disease of the vascular regulatory system in which the mechanisms that usually control arterial pressure within a certain (normal) range are altered. The central nervous system and renal pressor system, as well as extracellular volume, are the predominant mechanisms that control arterial pressure. Some combination of factors effects changes in one or more of these systems, ultimately leading to increased cardiac output and increased peripheral resistance. This elevates the arterial pressure, reducing cerebral perfusion and the cerebral oxygen supply, increasing the myocardial workload and oxygen consumption, and decreasing the blood flow to and oxygenation of the kidneys.

Symptoms Hypertension is generally asymptomatic until complications develop. It is usually discovered on routine examination.

Potential Complications Complications include atherosclerotic disease, left ventricular failure, cerebrovascular insufficiency with or without stroke, retinal hemorrhage, and renal failure. When the pathologic process is accelerated, malignant hypertension results, the blood pressure becomes extremely high, and nephrosclerosis, encephalopathy, and cardiac failure rapidly ensue.

Diagnostic Tests Elevated pressures on at least two occasions from measurements taken on three separate days are needed to label a person hypertensive. Secondary causes are then ruled out to make a determination of primary hypertension.

Treatments

Surgery
None.

Drugs
Diuretics, alphaor beta-adrenergic blocking agents, or antihypertensives to reduce blood pressure (prescribed according to the stepped-care approach outlined by the 1988 Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure).

General
Treatment of underlying disease in secondary hypertension; systematic exercise, moderate restriction of dietary sodium, decreased alcohol intake, quitting smoking, stress reduction, and weight loss, if indicated; regular monitoring of blood pressure; instruction in the importance of taking medications consistently and the potential long-term complications.

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(Graves’ Disease, Thyrotoxicosis, Toxic Diffuse Goiter, Toxic Nodular Goiter, Plummer’s Disease, Basedow’s Disease)

- A syndrome initiated by excessive production of thyroid hormones that results in multiple-system abnormalities ranging from mild to severe.

Causes and Incidence The cause of hyperthyroidism is unclear, but it is thought to be autoimmune in origin with a genetic component. The most common type of hyperthyroidism is Graves’ disease, which occurs about eight times more often in women than men and is seen in about 2% of the female population in the United States.

Disease Process Thyroid hormones are generally stimulatory, and excess production of these hormones produces a state of hypermetabolism in which the functions of various organ and tissue systems are increased. This is manifested by increased activity of the neuromuscular and sympathetic nervous systems. Compensatory mechanisms are called into play, and cardiac output, peripheral blood flow, body temperature, and respiratory rate increase. Other effects include increased cellular use of glucose and hyperinsulinemia, decreased supply of fats and carbohydrates, increased vitamin metabolism, increased bone mobilization and hypercalcemia, and increased secretion of adrenocorticotropic hormone and melanocyte-stimulating hormone. The organ systems eventually have trouble coping with the increased demand, and failure can result.

Symptoms The most common signs are goiter; warm, moist skin; erythema; sweating; tremor; weakness; restlessness; insomnia; emotional lability; increased food intake; lid lag; lid retraction; proptosis; tearing; and a startled look.

Potential Complications Cardiac insufficiency, generalized muscle wasting, corneal ulcers, decreased libido, osteoporosis, myasthenia gravis, and impaired fertility are among the complications. The elderly are the most likely to exhibit these complications. Thyroid storm is a severe, dramatic form of hyperthyroidism with an abrupt onset and rapid progression. It is a life-threatening emergency requiring immediate treatment to prevent shock, coma, cardiovascular collapse, and death.

Diagnostic Tests Diagnosis depends on the clinical history and examination coupled with a serum triiodothyronine and thyroxine assay and thyroid hormone binding ratio. All of the laboratory test results are elevated in hyperthyroidism.

Treatments

Surgery
Thyroidectomy in individuals who cannot receive radioactive iodine, have large goiters, or have toxic adenoma.

Drugs
Radioactive iodine to destroy thyroid tissue (treatment of choice); thiamides to inhibit hormone synthesis; beta-adrenergic blockers to diminish clinical manifestations; iodines to reduce the size of the thyroid before surgery; corticosteroids for palliation in Graves’ disease.

General
Monitoring for signs of hypothyroidism; planned rest and exercise cycles; long-term follow-up; counseling for lability; instruction about medications.

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- Decreased secretion of parathyroid hormone by the parathyroid glands, manifested as hypocalcemia.

Causes and Incidence The cause is usually unintentional damage to or removal of the parathyroid glands during thyroidectomy. There is a rare idiopathic form in which the parathyroids are absent or atrophied, as well as a genetic form that is part of a polyendocrine syndrome called HAM (hypoparathyroidism, Addison’s disease, and moniliasis). The idiopathic form generally occurs in childhood.

Disease Process A decrease in the secretion of parathyroid hormone (PTH) leads to a reduced resorption of calcium from the renal tubules, decreased absorption of calcium in the gastrointestinal (GI) tract, and decreased resorption of calcium from bone. The serum calcium level falls, increasing neuromuscular excitability and leading to spasms and tetany.

Symptoms Hypoparathyroidism is often asymptomatic in the early stages. The most characteristic sign is tetany with paresthesias of the lips, tongue, fingers, and feet; other signs are carpopedal and facial spasms, generalized muscle aches, and fatigue. Encephalopathy, depression, dementia, and papilledema may also be present.

Potential Complications Acute onset of hypocalcemia leads to laryngospasm, airway obstruction, and cardiac failure. Long-standing disease leads to bone deformities, cataract formation, reduced cardiac contractility, and heart failure. Childhood disease can lead to mental retardation and stunted growth.

Diagnostic Tests Parathyroid deficiency is characterized by a low serum calcium level, high serum phosphorus level, and normal alkaline phosphatase level. Serum intact PTH is decreased. Chvostek’s and Trousseau’s signs are positive.

Treatments

Surgery
None.

Drugs
Calcium supplements; vitamin D to increase calcium absorption in the GI tract.

General
Calcium-rich diet; monitoring of calcium levels.

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- A clinical state resulting from a deficiency of thyroid hormones.

Causes and Incidence The cause of some hypothyroidism is unknown but is thought to be autoimmune in origin. Other hypothyroidism is caused by destruction of thyroid or pituitary tissue by underlying disease, surgery, or radiation treatment. Hypothyroidism is a common disorder that affects all age groups. Women between 30 and 60 years of age are most often affected. It also occurs in approximately 1 of every 4,500 live births. The incidence is rising in the elderly population.

Disease Process When the supply of thyroid hormone is inadequate, a general depression of most cellular enzyme systems and oxidative processes results, reducing the metabolic activity of the cells. This in turn reduces oxygen consumption, decreases energy production, and lessens body heat. Tissues are infiltrated by mucopolysaccharides, carotene is deposited in epidermal layers, adrenergic stimulation is decreased, protein effusion collects in the pericardial and pleural sacs, and proteinaceous ground substances are deposited in tissues.

Symptoms Signs and symptoms are often insidious in onset. They include fatigue and lethargy; mild weight gain; cold, pale, dry, rough hands and feet; reduced attention span with memory impairment, slowed speech, and loss of initiative; swelling in extremities and around the eyes, eyelids, and face; menstrual irregularities; muscle aches and weakness; joint aches and stiffness; clumsiness; hyperstiff reflexes; decreased pulse; decreased blood pressure; agitation; depression; and paranoia.

Potential Complications Myxedema coma is a life-threatening complication of hypothyroidism that requires immediate treatment. Other complications include ischemic heart disease, congestive failure, pleural and pericardial effusion, deafness, psychosis, and anemia.

Diagnostic Tests Serum and serum-free triiodothyronine and thyroxine are decreased; serum thyroid-stimulating hormone is increased in primary hypothyroidism and decreased in secondary hypothyroidism.
Treatments

Surgery
None.

Drugs
Oral replacement thyroid hormone; IV form is used for myxedemic coma.

General
Lifelong monitoring; instruction about lifelong thyroid hormone replacement therapy and the importance of consistent and timely use.

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