Article Contents ::
- 1 Details Descriptions About :: Hyperparathyroidism
- 2 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. Renal and GI absorption of calcium increase. Primary hyperparathyroidism is commonly diagnosed when an asymptomatic patient has elevated calcium levels in routine laboratory tests. Age Alert Hyperparathyroidism affects women 2 to 3 times more frequently than it does men and is seen most frequently in women older than age 40.
- 3 Causes for Hyperparathyroidism
- 4 Pathophysiology Hyperparathyroidism
- 5 Signs and symptoms Hyperparathyroidism
- 6 Diagnostic Lab Test results
- 7 Treatment for Hyperparathyroidism
- 8 Disclaimer ::
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Details Descriptions About :: Hyperparathyroidism
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. Renal and GI absorption of calcium increase. Primary hyperparathyroidism is commonly diagnosed when an asymptomatic patient has elevated calcium levels in routine laboratory tests. Age Alert Hyperparathyroidism affects women 2 to 3 times more frequently than it does men and is seen most frequently in women older than age 40.
Causes for Hyperparathyroidism
Causes Primary hyperparathyroidism Most commonly a single adenoma Multiple endocrine neoplasia (all four glands usually involved) Secondary hyperparathyroidism Rickets, vitamin D deficiency, chronic renal failure, and osteomalacia due to phenytoin
Pathophysiology 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 unknown reasons. Hypophosphatemia results when excessive PTH inhibits renal tubular phosphate reabsorption. It aggravates hypercalcemia by increasing the sensitivity of the bone to PTH. Pathologic fractures may be a presenting symptom. A hypocalcemia-producing abnormality outside the parathyroids can cause excessive compensatory production of PTH, or secondary hyperparathyroidism.
Signs and symptoms Hyperparathyroidism
Signs and symptoms Primary hyperparathyroidism Polyuria, nephrocalcinosis, or recurring nephrolithiasis and consequent renal insufficiency Chronic low back pain and easy fracturing Bone tenderness, chondrocalcinosis Osteopenia and osteoporosis, especially of vertebrae Erosions of juxta-articular (adjoining joint) surface Subchondral fractures Traumatic synovitis Pseudogout Pancreatitis causing constant, severe epigastric pain that radiates to the back Peptic ulcers, causing abdominal pain, anorexia, nausea, and vomiting Muscle weakness and atrophy, particularly in the legs Psychomotor and personality disturbances, depression, overt psychosis Stupor, and possibly coma Skin necrosis, cataracts, calcium microthrombi to lungs and pancreas, anemia, and subcutaneous calcification Secondary hyperparathyroidism Same features of calcium imbalance as in primary hyperparathyroidism Skeletal deformities of the long bones (such as rickets) Symptoms of the underlying disease
Diagnostic Lab Test results
Diagnostic test results Primary hyperparathyroidism Hypercalcemia and high concentrations of serum PTH on radioimmunoassay (confirms the diagnosis). X-rays show 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 shows increased bone turnover. Laboratory studies detect elevated urine and serum calcium, chloride, and alkaline phosphatase levels; decreased serum phosphorus levels; elevated uric acid and creatinine levels; increased serum amylase levels. Secondary hyperparathyroidism Laboratory analysis reveals normal or slightly decreased serum calcium level, variable serum phosphorus level, especially when the cause is rickets, osteomalacia, or kidney disease.
Treatment for Hyperparathyroidism
Treatment Primary hyperparathyroidism Surgery to remove the adenoma or, depending on the extent of hyperplasia, all but half of one gland, to provide normal PTH levels Treatments to decrease calcium levels—forcing fluids, limiting dietary intake of calcium, promoting sodium and calcium excretion through forced diuresis Oral sodium or potassium phosphate; subcutaneous calcitonin; I.V. mithramycin or biphosphonate I.V. magnesium and phosphate; sodium phosphate solution by mouth or retention enema; possibly supplemental calcium, vitamin D, or calcitrol Secondary hyperparathyroidism Vitamin D to correct the underlying cause of parathyroid hyperplasia; oral calcium preparation to correct hyperphosphatemia in the patient with kidney disease Dialysis in patient with renal failure to decrease phosphorus levels Calcitonin Pamidronate Clinical Tip Bone resorption in primary hyperparathyroidism In hyperparathyroidism, body mechanisms sacrifice bone to preserve intracellular calcium levels. X-rays may show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles. Microscopic examination of the bone with tests—such as X-ray spectrophotometry—typically demonstrates increased bone turnover.