Page 58 Complete Your CE Test Online - Click Here ● ● Chvostek’s Sign: Hyperirritability of the facial nerve manifested by a spasm of facial muscles, which occurs when muscles or branches of the facial nerve are tapped. ● ● Trousseau’s Sign: Carpopedal spasm (spasmodic contractions of the muscles of the hands and feet) triggered within three minutes after a blood pressure cuff is applied to the arm and inflated to 20 mm Hg above patient’s systolic pressure. ● ● Laryngeal spasm. Central nervous signs and symptoms of hypoparathyroidism are exaggerated during what conditions? Central nervous system signs and symptoms are exaggerated during pregnancy, infection, thyroid hormone withdrawal, before menstruation, hyperventilation, and right before menstruation[5] . What drug interferes with normal parathyroid function especially if renal failure is also a problem? Cimetidine (Tagamet) interferes with normal parathyroid function. Remember that any interference with parathyroid function increases the risk of hypocalcemia. In the event of acute, life-threatening tetany, what treatment measures must be initiated immediately? Intravenous calcium administration is needed in the presence of acute life-threatening tetany. The most effective calcium solution is ionized calcium chloride (10%). All intravenous calcium preparations are given slowly since it is a highly irritating solution that stings and causes thrombosis. The patient experiences burning flushing feelings of the skin and tongue. However, the intravenous calcium solution also seems to rapidly relieve feelings of anxiety[6] . Hyperparathyroidism is a fairly common disorder, affecting one in 1,000 people and is two to three times more common in females than in males[5] . It is defined as the unregulated, hypersecretion of parathyroid hormone (PTH)[6,24] . Differentiate between the two types of hyperparathyroidism. Explain the pathophysiology of hyperparathyroidism. Describe treatment initiatives for hyperparathyroidism. There are two types of hyperparathyroidism: primary and secondary. ● ● Primary hyperparathyroidism: In primary hyperparathyroidism one or more of the parathyroid glands enlarge, increasing PTH secretion and causing elevated serum calcium levels. The most common cause of primary hyperparathyroidism is a single parathyroid adenoma, a benign tumor. Parathyroid hyperplasia is responsible for the remainder of cases[5,6,24] . ● ● Secondary hyperparathyroidism: Secondary hyperparathyroidism is due to a chronic abnormal stimulus, usually chronic renal failure, vitamin D deficiency, or osteomalacia[5,6,24] . Chronic overproduction of PTH causes increased serum calcium levels. Normal negative feedback mechanisms do not function, and chronic excessive resorption of calcium can lead to osteopenia (loss of some bone density). In secondary hyperparathyroidism overproduction of parathyroid hormone in patients with renal failure add to the pathophysiology of bone disease found in patients on dialysis[24] . Clinical signs and symptoms of primary hyperparathyroidism are due to hypercalcemia and include arrhythmias, hypertension, emotional instability, fatigue, personality changes, severe epigastric pain, peptic ulcers, chronic low back pain, muscle weakness and atrophy, polyuria, cataracts, anemia, and calcifications[5,6] . Secondary hyperparathyroidism causes signs and symptoms of hypocalcemia as well as the underlying disorder. Secondary hyperparathyroidism may be prevented by ensuring a diet that contains adequate amounts of calcium or by taking calcium and vitamin D supplements[5] . 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 three days of the surgery. Unfortunately, renal damage may be irreversible[5] . 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 (the 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] . Andrea is a nurse practitioner. One of her patients has just been diagnosed with Addison’s disease. The patient, who is also a nurse, is distraught, and has many questions about the disease. Andrea needs to do a great deal of patient education. She begins by explaining what Addison’s disease is, what causes it, prognosis, and treatment options. What do you think Andrea will tell her patient? Addison’s disease is also known as adrenal hypofunction or adrenal insufficiency. It occurs in two forms: primary and secondary. Primary adrenal insufficiency is the form commonly referred to as Addison’s disease. It originates within the adrenal glands and is characterized by a decrease in mineralocorticoid, glucocorticoids, and androgen secretion [11,25] . Secondary adrenal insufficiency occurs secondary to a disorder outside of the adrenal glands such as a pituitary tumor[5,11] . Adrenal hypofunction affects about eight in 100,000 people[5] . Up to 80% of cases of Addison’s disease cases are caused by an autoimmune process in which circulating antibodies specifically “attack” adrenal tissue. This disease is found primarily in middle-aged females and gradually destroys the adrenal cortex[25] . All patients affected by Addison’s disease, in fact all patients affected by either primary or secondary adrenal hypofunction, need life- long corticosteroid replacement therapy in the form of cortisone or hydrocortisone[5,11] . Andrea should tell her patient that she must take corticosteroid replacement therapy for the rest of her life. The patient should be instructed to wear a medical alert bracelet as well. She should also tell her patient[5,25] : ● ● To keep her HCP informed of any medications she takes including prescription, OTC, herbal preparations, vitamins, minerals, and other supplements. ● ● To take steroid therapy in the morning since taking steroids in the late afternoon or evening may stimulate the central nervous system and cause insomnia. ● ● Caution her that steroid therapy can make it easier to bruise. Additional nursing concerns include advising patients who are diabetic that steroid replacement therapy may require insulin dose adjustments [5,25] . Patients must also be warned about the possibility of adrenal crisis. Adrenal crisis is a critical deficiency of mineralocorticoids and glucocorticoids. It is the most serious complication of adrenal hypofunction and can develop gradually or abruptly. It is most likely to occur in patients who fail to respond to hormone replacement therapy, who abruptly stop hormone therapy, who experience physiologic stress,