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Hyperparathyroidism results from excessive secretion of parathyroid hormone (PTH) from one or more of the four parathyroid glands. PTH promotes bone resorption, and hypersecretion leads to hypercalcemia and hypophosphatemia. Overproduction of PTH by a tumor or hyperplastic tissue increases intestinal calcium absorption, reduces renal calcium clearance, and increases bone calcium release. Response to this excess varies for each patient for an unknown reason. It's three times more common in women than in men and the frequency increases with age.

What causes Hyperparathyroidism?

Hyperparathyroidism may be primary or secondary. Although the exact cause is unknown, it's thought that primary hyperparathyroidism may be caused by:

  • increased secretion of PTH (which can lead to increased serum calcium levels) by one or more enlarged parathyroid glands (most commonly caused by a single adenoma, but may be a component of multiple endocrine neoplasia, which usually involves all four glands)
  • parathyroid carcinoma
  • previous exposure to radiation in the face or neck
  • certain medications, such as thiazide diuretics and lithium
  • heredity.

Secondary hyperparathyroidism occurs when the parathyroid gland chronically releases excessive PTH. A hypocalcemic state (decrease in circulating calcium) causes this release. Causes include:

  • rickets
  • chronic renal failure
  • vitamin D deficiency
  • malabsorption syndrome
  • osteomalacia due to phenytoin (Dilantin).

Signs and symptoms of Hyperparathyroidism

Signs and symptoms of primary hyperparathyroidism result from hypercalcemia and are typically present in several body systems. They may include:

  • Tenal and urinary systems - polyuria, nephrocalcinosis, nocturia, polydipsia, dehydration, uremia symptoms, renal colic pain, nephrolithiasis, and renal insufficiency
  • musculoskeletal system - vague aches and pains; arthralgias; localized swellings; chronic lower back pain and easy fracturing due to bone degeneration; bone tenderness; chondrocalcinosis (decreased bone mass); osteopenia and osteoporosis, especially affecting the vertebrae; erosions of the juxta-articular (adjoining joint) surface; subchondral fractures; traumatic synovitis; pseudogout (skeletal and articular systems); and muscle weakness and atrophy, particularly in the legs
  • gastrointestinal system - pancreatitis causing constant, severe epigastric pain that radiates to the back; peptic ulcers causing abdominal pain, anorexia, nausea, and vomiting
  • central nervous system - psychomotor and personality disturbances, emotional lability, depression, slow mentation, poor memory, drowsiness, ataxia, overt psychosis, stupor and, possibly. coma
  • integumentary system - skin necrosis and pruritus caused by ectopic calcifications in the skin
  • other systems - calcium microthrombi to lungs and pancreas, cataracts, anemia, and subcutaneous calcification.

Secondary hyperparathyroidism may produce the same features of calcium imbalance with skeletal deformities of the long bones (such as rickets) as well as symptoms of the underlying disease.

Complications of hyperparathy roidism include:

  • pathologic fractures
  • renal damage
  • urinary tract infections
  • hypertension
  • arrhythmias
  • insulin hypersecretion, decreased insulin sensitivity
  • pseudogout.
Diagnosis information

Primary hyperparathyroidism is commonly diagnosed based on elevated calcium levels (more than 10.5 mg/dl) in asymptomatic patients. Findings differ in primary and secondary disease. In primary disease, diagnosis also may be based on:

  • hypercalcemia and high concentrations of serum PTR on radioimmunoassay, which confirms the diagnosis (Inununoradiometric assay [IRMA] is specific and sensitive in distinguishing primary hyperparathyroidism from other causes of hypercalcemia.)
  • X-rays showing diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles
  • microscopic bone examination by X-ray spectrophotometry typically showing increased bone turnover
  • elevated urine and serum calcium, chloride, and alkaline phosphatase levels; decreased serum phosphorus levels
  • elevated uric acid and creatinine levels, which may also increase basal gastric acid secretion and serum immunoreactive gastrin
  • increased serum amylase levels (may indicate acute pancreatitis).
  • Diagnosis of secondary disease is based on; normal or slightly decreased serum calcium level, variable serum phosphorus level. especially when the cause is rickets, osteomalacia, or kidney disease.
  • patient history possibly showing familial kidney disease, seizure disorders, or drug ingestion.

Treatment of Hyperparathyroidism

Effective treatment varies, depending on the cause of the disease. In primary hyperparathyroidism, surgery is the only definitive therapy. In mild hyperparathyroidism, the only effective long-term medical therapy is maintaining hydration.

Treatment of primary disease includes:

  • surgery to remove the adenoma or, depending on the extent of hyperplasia, all but one-half of one gland, to provide normal PTR levels (may relieve bone pain within 3 days, but renal damage may be irreversible)
  • decreasing calcium levels using such methods as forcing fluids,limiting dietary intake of calcium, and promoting sodium and calcium excretion through forced diuresis (causing as much as 6 qt [6 L] of urine output in life-threatening circumstances), and use of furosemide (Lasix) or ethacrynic acid (Edecrin) (preoperatively or if surgery isn't feasible or necessary)
  • oral sodium or potassium phosphate, subcutaneous calcitonin (Calcimar), IV. plicamycin
  • IV. magnesium and phosphate or sodium phosphate solution by mouth or retention enema (for potential postoperative magnesium and phosphate deficiencies), possibly supplemental calcium, vitamin D, or calcitriol (Calcijex) (serum calcium level decreases to low-normal range during the first 4 to 5 days after surgery).

Treatment of secondary disease includes:

  • vitamin D to correct the underlying cause of parathyroid hyperplasia; aluminum hydroxide preparation to correct hyperphosphatemia in the patient with kidney disease
  • dialysis in the patient with renal failure to decrease phosphorus levels (may be lifelong)
  • decreasing calcium levels, although enlarged glands may not revert to normal size and function even after calcium levels have been controlled in the patient with chronic secondary hyperparathyroidism
  • for severe hypercalcemia (serum calcium greater than 14 mg/ dl) or for the patient with severe symptoms, administration of calcitonin, a rapid-acting agent, along with hydration; possible initiation of pamidronate, a slower acting agent. to provide a longer lasting effect.

Special considerations or prevention

Care emphasizes prevention of complications from the underlying disease and its treatment:

  • Obtain pretreatment baseline serum potassium, calcium, phosphate, and magnesium levels because these values may change abruptly during treatment.
  • During hydration to reduce serum calcium level, record intake and output accurately. Strain urine to check for calculi. Provide at least 3 qt (3 L) of fluid per day, including cranberry or prune juice to increase urine acidity and help prevent calculus formation. As ordered, obtain blood samples and urine specimens to measure sodium, potassium, and magnesium levels, especially for the patient taking furosemide.
  • Watch for signs of peptic ulcer and administer antacids as appropriate. after parathyroidectomy:
  • Check frequently for respiratory distress, and keep a tracheotomy tray at the bedside. Watch for postoperative complications, such as laryngeal nerve damage or, rarely, hemorrhage. Monitor intake and output carefully.
  • Check for swelling at the operative site. Place the patient in semi-Fowler's position, and support the head and neck with sandbags to decrease edema, which may cause pressure on the trachea.
  • Watch for signs of mild tetany, such as complaints of tingling in the hands and around the mouth. These symptoms should subside quickly but may be prodromal signs of tetany, so keep calcium gluconate or calcium chloride LV. available for emergency administration. Watch for increased neuromuscular irritability and other signs of severe tetany, and report them immediately.
  • Ambulate the patient as soon as possible postoperatively, even though she may find this uncomfortable, because pressure on bones speeds up bone recalcification.
  • Check laboratory results for low serum calcium and magnesium levels. . Monitor for changes in mental status and watch for listlessness. In the patient with persistent hypercalcemia, check for muscle weakness and psychiatric symptoms. (Hypercalcemic states may cause anxiety, depression, psychosis, apathy, and fatigue.)
  • At discharge, provide thorough patient-teaching to help avoid complications. (See Patient teaching for hyperparathyroidism.

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