Hyper-parathyroidism
Hyper-parathyroidism: Excerpt from Handbook of Diseases
Characterized by overactivity of one or more of the four parathyroid glands, hyperparathyroidism results from excessive secretion of parathyroid hormone (PTH). Such hypersecretion of PTH promotes bone resorption and leads to hypercalcemia and hypophosphatemia. (See Bone resorption in primary hyperparathyroidism.)
Increased renal and GI absorption of calcium occurs.
Primary hyperparathyroidism is commonly diagnosed by elevated calcium levels found on laboratory profiles in asymptomatic patients. It affects women two to three times more commonly than men.
Causes
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. Primary hyperparathyroidism is also a component of multiple endocrine neoplasia, in which all four glands are usually involved.
❑ In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, such as rickets, vitamin D deficiency, chronic renal failure, and osteomalacia due to phenytoin.
Signs and symptoms
The clinical effects of primary hyperparathyroidism result from hypercalcemia and are typically present in several body systems.
❑ Renal: 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: chronic lower back pain and easy fracturing due to bone degeneration; bone tenderness; chondrocalcinosis; osteopenia and osteoporosis, especially on the vertebrae; erosions of the juxta-articular surface; subchondral fractures; traumatic synovitis; and pseudogout
❑ GI: pancreatitis, causing constant, severe epigastric pain that radiates to the back; peptic ulcers, causing abdominal pain, anorexia, nausea, and vomiting
❑ Neuromuscular: 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
Findings differ in primary and secondary disease.
Primary disease
In primary disease, a high concentration of serum PTH on radioimmunoassay with accompanying hypercalcemia confirms the diagnosis. In addition, X-rays show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subper-iosteal erosion of the phalanges and distal clavicles.
Microscopic examination of the bone with such tests as X-ray spectrophotometry typically demonstrates increased bone turnover. 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.
Secondary disease
Laboratory findings in secondary hyperparathyroidism show normal or slightly decreased serum calcium levels and variable serum phosphorus levels, especially when hyperparathyroidism is due to rickets, osteomalacia, or kidney disease. The patient history may reveal familial kidney disease, seizure disorders, or drug ingestion.
Other laboratory values and physical examination findings identify the cause of secondary hyperparathyroidism.
Treatment
Effective treatment varies, depending on the cause of the disease.
Primary disease
Treatment for primary hyperparathyroidism may include surgery to remove the adenoma or, depending on the extent of hyperplasia, all but one-half of one gland (the remaining part of the gland is necessary to maintain normal PTH levels). Such surgery may relieve bone pain within 3 days. However, renal damage may be irreversible.
Clinical tip Patients with primary hyperparathyroidism should be considered for surgery when:
❑ calcium levels are greater than or equal to 1 mg/dl above normal
❑ osteoporosis is present
❑ recurrent peptic ulcer disease is present
❑ nephrolithiasis is present
❑ impaired kidney function is noted
❑ patient is young or consistent follow-up is unavailable.
Preoperatively — or if surgery isn’t feasible or necessary — other treatments can decrease calcium levels. They include forcing fluids, limiting dietary intake of calcium, and promoting sodium and calcium excretion through forced diuresis using normal saline solution (up to 6 L in life-threatening circumstances), furosemide, or ethacrynic acid.
Other treatments include administering oral sodium or potassium phosphate, subcutaneous calcitonin, I.V. plicamycin, or I.V. biphosphonates. In primary hyperparathyroidism, surgery is the only definitive therapy. There are no effective long-term medical therapies for hyperparathyroidism.
Therapy for potential postoperative magnesium and phosphate deficiencies includes I.V. administration of magnesium and phosphate or sodium phosphate solution given by mouth or 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 the serum calcium level.
Secondary disease
Treatment of secondary hyperparathyroidism must correct the underlying cause of parathyroid hyperplasia. It consists of vitamin D therapy or, in the patient with kidney disease, administration of an oral calcium preparation for hyperphosphatemia.
In the patient with renal failure, dialysis is necessary to lower phosphorus 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 the serum calcium level, record intake and output accurately. Strain the urine to check for calculi. Provide at least 3 L of fluid per day, including cranberry or prune juice to increase urine acidity and help prevent calculus formation.
❑ Obtain blood samples and urine specimens 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 lung or heart disease.
❑ Monitor the patient receiving cardiac 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 bedside. Watch for postoperative complications, such as laryngeal nerve damage and, 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 I.V. available for emergency administration. Watch for increased neuromuscular irritability and other signs of severe tetany.
❑ 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 the patient’s 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.
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Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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