Page 42 Complete Your CE Test Online - Click Here ● ● Musculoskeletal system: Significant muscle weakness and atrophy, especially in the legs. Chronic low back pain and bones that easily fracture because of bone degeneration, bone pain, chondrocalcinosis, and occasional severe osteopena[5] . ● ● Renal system: Elevated calcium levels cause nephrocalcinosis, possible recurring nephrolithiasis that may lead to renal insufficiency. Various renal signs and symptoms such as polyuria, are among the most common effects of hyperthyroidism[5] . ● ● Miscellaneous effects: Skin necrosis, cataracts, anemia, and subcutaneous calcification[5] . Secondary hyperparathyroidism decreased serum calcium levels cause symptoms of hypocalcemia with skeletal deformities accompanied by signs and symptoms of the underlying disease[5] . Secondary hyperparathyroidism may be prevented by ensuring a diet that contains adequate amounts of calcium or by taking calcium and vitamin D supplements[5] . Diagnosis Diagnosis is based on history, clinical manifestations, identification of underlying disorders, and the results of diagnostic tests. Primary hyperparathyroidism diagnosis The following findings are indicative of primary hyperparathyroidism [5,6] : ● ● Radioimmunoassay shows high serum PTH accompanied by hypercalcemia. The hypercalcemia must be noted on at least two separate tests to validate consistency of results. ● ● Elevated chloride and alkaline phosphate levels and a decreased serum phosphorus level. ● ● Elevated uric acid and creatinine levels. ● ● Increased basal acid secretion. ● ● Skeletal changes are revealed on x-ray. Early diagnosis of hyperparathyroidism can be difficult and complications may be evident before diagnosis is confirmed. CT scan can identify parathyroid tumors more quickly than traditional X-rays. Sestamibi scan can help to assess tumor location[6] . Secondary hypoparathyroidism diagnosis Laboratory findings in the presence of secondary hypoparathyroidism show[5] : ● ● Normal or slightly decreased serum calcium levels. ● ● Significantly elevated phosphorus levels. Diagnostic work-up is performed to identify the underlying cause of the disease[5] . Treatment and nursing considerations Treatment of primary hyperparathyroidism may include surgical removal of abnormal parathyroid tissue and initial management of hypercalcemia[5,6] . Treatment of hypercalcemia includes[6] : ● ● Administration of intravenous normal saline solution and diuretics such as Lasix and Edecrin to increase urinary excretion of calcium for those patients who are not in renal failure. ● ● Administration of agents to inhibit bone resorption of calcium. These include Aredia, Cibacalcin, or Didronel. ● ● Administration of oral phosphate as an anti-hypercalcemia agent. ● ● Restriction of dietary calcium and discontinuation of drugs that might facilitate hypercalcemia such as thiazides, and vitamin D. ● ● Dialysis for patients in renal failure or for those whose hypercalcemia does not respond to other treatments. ● ● Reduced dosage of digoxin since hypercalcemic patients are more vulnerable to the toxic effects of this drug. ● ● Monitoring of calcium (daily), blood urea nitrogen (BUN), potassium, and magnesium levels. Surgical removal of parathyroid tissue may relieve bone pain within 3 days of the surgery. Unfortunately, renal damage may be irreversible [5] . Surgical alert! All but half of one remaining parathyroid gland is needed to maintain normal PTH levels[5] . Nursing consideration: Following surgery nursing interventions include[5,6] : ● ● Monitor intake and output. ● ● Provide adequate fluid and electrolyte replacement. ● ● Strain all urine for renal calculi. ● ● Limit dietary intake of calcium. ● ● Monitor for urinary tract infections, hematuria, and renal colic. ● ● Take safety precautions to prevent pathologic fractures, to which the patient is prone. ● ● Monitor for signs of tetany. ● ● Monitor fluid and electrolyte levels. Pathology of hyperparathyroidism involves significant effects of hypercalcemia. Now, postoperatively, the patient must be monitored for hypocalcemia. Such signs and symptoms include[6] : ● ● Paresthesia. ● ● Positive Chvostek’s sign: Tapping the check over the facial nerve causes a twitch of the lip or facial muscles. ● ● Positive Trousseau’s sign: Carpopedal spasm induced by applying a blood pressure cuff and occluding circulation in the arm. ● ● Take safety precautions if the patient is prone to seizures. Treatment of secondary hyperparathyroidism focuses on correction and treatment of the underlying cause. Remember that secondary hyperparathyroidism causes hypocalcemia as opposed to primary hypothyroidism, which causes hypercalcemia. Generalized treatment initiatives include[5] : ● ● Vitamin D therapy. ● ● Administration of oral calcium preparation in the presence of renal disease. ● ● Administration of a new classification of drugs (calcimimetics) approved for the treatment of secondary hyperparathyroidism. These drugs act by stopping the secretion of PTH. Patients with chronic secondary hyperparathyroidism may find that the parathyroid glands do not revert to normal function even after calcium levels have been returned to normal[5] . Adrenal insufficiency Jackie is 55-year-old account executive with a major industrial company in a small urban area. She complains of not being able to get over the “flu” that she has had for nearly a month. She feels week, tired, has lost weight, and has periods of nausea, vomiting, and diarrhea. Her colleagues tease her that she has not been taking sick time from work but has actually been vacationing at the beach. They make these comments because Jackie appears to be deeply suntanned, especially in the creases of her hands, elbows, and knees. She also notices that several scars over her knees appear to be darker. Jackie discusses her symptoms with the company’s nurse. The nurse is disturbed, believing that these symptoms may indicate an endocrine disorder. After consulting several reference books the nurse wonders if Jackie may be suffering from Addison’s disease.