Hyperparathyroidism
Hyperparathyroidism: Excerpt from Professional Guide to Diseases (Eighth Edition)
Hyperparathyroidism is characterized by overactivity of one or more of the four parathyroid glands, resulting in excessive secretion of parathyroid hormone (PTH). Hypersecretion of PTH promotes bone resorption and leads to hypercalcemia and hypophosphatemia, which in turn results in increased renal and GI absorption of calcium.
Causes and incidence
Hyperparathyroidism may be primary or secondary. In primary hyperparathyroidism, one or more of the parathyroid glands enlarges, increasing PTH secretion and elevating serum calcium levels. The most common cause is a single adenoma. Other causes include a genetic disorder or multiple endocrine neoplasia. Primary hyperparathyroidism usually occurs between ages 30 and 50 but can also occur in children and the elderly. It affects two to three times more females than males. It’s a common disorder, affecting 1 in 1,000 people.
In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, which causes a resistance to the metabolic action of PTH. Some hypocalcemia-producing abnormalities are chronic renal failure, renal absorption disorders, vitamin D deficiency (especially in the housebound elderly), or osteomalacia due to phenytoin or laxative abuse.
Signs and symptoms
Clinical effects of primary hyperparathyroidism result from hypercalcemia and are typically present in several body systems:
❑ Renal system: nephrocalcinosis due to elevated levels of calcium and, possibly, recurring nephrolithiasis, which may lead to renal insufficiency. Renal manifestations, including polyuria, are the most common effects of hyperparathyroidism.
❑ Skeletal and articular system: chronic low back pain and easy fracturing due to bone degeneration, bone tenderness, chondrocalcinosis, occasional severe osteopenia, especially on the vertebrae, erosions of the juxta-articular surface, subchondral fractures, traumatic synovitis, and pseudogout
❑ GI system: pancreatitis, causing constant, severe epigastric pain radiating to the back; peptic ulcers, causing abdominal pain, anorexia, nausea, and vomiting
❑ Neuromuscular system: marked muscle weakness and atrophy, particularly in the legs
❑ Central nervous system: psychomotor and personality disturbances, depression, overt psychosis, stupor and, possibly, coma
❑ Other: skin necrosis, cataracts, calcium microthrombi to lungs and pancreas, polyuria, anemia, and subcutaneous calcification.
Similarly, in secondary hyperparathyroidism, decreased serum calcium levels may produce the same features of calcium imbalance, with skeletal deformities of the long bones (rickets, for example) as well as symptoms of the underlying disease.
Diagnosis
Confirming diagnosis In primary disease, a high concentration of serum PTH on radioimmunoassay with accompanying hypercalcemia confirms the diagnosis.
In addition, X-rays may show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles. (See Bone resorption in primary hyperparathyroidism.) Microscopic examination of the bone with tests such as X-ray spectrophotometry typically demonstrates increased bone turnover.Reduced bone mineral density, particularly of the forearm, is seen on bone densitometry.
Laboratory tests reveal elevated urine and serum calcium, chloride, and alkaline phosphatase levels and decreased serum phosphorus levels. Hyperparathyroidism may also raise uric acid and creatinine levels and increase basal acid secretion and serum immunoreactive gastrin. Increased serum amylase levels may indicate acute pancreatitis.
Laboratory findings in secondary hyperparathyroidism show normal or slightly decreased serum calcium levels and variable serum phosphorus levels. Phosphorus can be quite elevated, especially in osteomalacia or renal disease. Patient history may reveal familial renal disease, seizure disorders, or drug ingestion. Other laboratory values and physical examination findings identify the cause of secondary hyperparathyroidism.
Treatment
Treatment varies, depending on the cause of the disease. Treatment of primary hyperparathyroidism may include surgery to remove the adenoma or, depending on the extent of hyperplasia, all but half of one gland (the remaining part of the gland is necessary to maintain normal PTH levels). Surgery may relieve bone pain within 3 days. However, renal damage may be irreversible.
Preoperatively — or if surgery isn’t feasible or necessary — other treatments can decrease calcium levels. These include forcing fluids; limiting dietary intake of calcium; promoting sodium and calcium excretion through forced diuresis using normal saline solution (up to 6 L in life-threatening circumstances), furosemide, or ethacrynic acid; and administering oral sodium or potassium phosphate, subcutaneous calcitonin, I.V. plicamycin, or I.V. biphosphonates.
Therapy for potential postoperative magnesium and phosphate deficiencies includes I.V. administration of magnesium and phosphate, or sodium phosphate solution given orally or by retention enema. In addition, during the first 4 to 5 days after surgery, when serum calcium falls to low normal levels, supplemental calcium may be necessary; vitamin D or calcitriol may also be used to raise serum calcium levels.
Treatment of secondary hyperparathyroidism must correct the underlying cause of parathyroid hypertrophy. Vitamin D therapy or, in the patient with renal disease, administration of an oral calcium preparation (calcium acetate, if possible) for hyperphosphatemia, are typically used, although surgical excision may be necessary. In the patient with renal failure, dialysis is necessary to lower calcium levels and may have to continue for the remainder of the patient’s life. In the patient with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled.
Special considerations
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 a day, including cranberry or prune juice to increase urine acidity and help prevent calculus formation. As ordered, obtain blood and urine samples to measure sodium, potassium, and magnesium levels, especially for the patient taking furosemide.
❑ Auscultate for breath sounds often. Listen for signs of pulmonary edema in the patient receiving large amounts of saline solution I.V., especially if he has pulmonary or cardiac disease. Monitor the patient on digitalis glycosides carefully because elevated calcium levels can rapidly produce toxic effects.
❑ Because the patient is predisposed to pathologic fractures, take safety precautions to minimize the risk of injury. Assist him with walking, keep the bed at its lowest position, and raise the side rails. Lift the immobilized patient carefully to minimize bone stress. Schedule care to allow the patient with muscle weakness as much rest as possible.
❑ 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 his 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 I.V. 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 he may find this uncomfortable, because pressure on bones speeds up bone recalcification.
❑ Check laboratory results for low serum calcium and magnesium levels.
❑ Monitor mental status and watch for listlessness. In the patient with persistent hypercalcemia, check for muscle weakness and psychiatric symptoms.
❑ Before discharge, advise the patient of the possible adverse effects of drug therapy. Emphasize the need for periodic follow-up through laboratory blood tests. If hyperparathyroidism wasn’t corrected surgically, warn the patient to avoid calcium-containing antacids and thiazide diuretics.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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