Page 28 Complete Your CE Test Online - Click Here preparations, minerals, OTC medications, and any other supplement such as weight loss products. ● ● Advise patients and families that patients should wear a medical alert bracelet at all times. ● ● Emphasize the importance of life-long follow-up examinations. Tumors may reoccur and life-long evaluation of hormone therapy is necessary. Nursing consideration: Teaching patients and families how to take medications is often the responsibility of nurses. Nurses must be sure to assess the patients’/families’ knowledge regarding the patient’s medications. Be sure not to ask questions that can be answered simply with either a “yes” or a “no.” For instance if the nurse asks, “Do you know what side effects your medicine might cause?” the patient/family may simply answer “yes” to avoid admitting they don’t understand or to just satisfy the nurse. Instead say something like, “Explain what side effects your medicine might cause and what you should do if they happen.” Diabetes insipidus Mark is a 35-year-old marketing executive. Since he sits at a desk for the majority of his working hours he enjoys biking and hiking during his leisure time. One afternoon he takes a nasty fall from his bicycle while cycling with his two young sons. He strikes his head on the sidewalk and sustains what his physician describes as a mild concussion. Several days later Mark experiences an abrupt onset of needing to void frequently. His urine is dilute, and he voids as much as 30 L/day. He experiences extreme thirst, and suffers from severe lack of sleep since he must get up to void several times a night. After several days he becomes weak and dizzy. Mark’s wife insists on taking him to the emergency department where he is diagnosed as having diabetes insipidus. Diabetes insipidus is a disorder of water metabolism as the result of a deficiency of antidiuretic hormone (ADH), also called vasopressin [5,11] . There are two primary forms of diabetes insipidus: central diabetes insipidus and nephrogenic diabetes insipidus[10] . ● ● Central diabetes insipidus: Also called neurogenic, pituitary, or neurohypophyseal, central diabetes insipidus is marked by a decreased secretion of ADH. ● ● Nephrogenic diabetes insipidus: Nephrogenic diabetes insipidus is characterized by a decreased ability to concentrate urine because of resistance to the action of ADH in the kidneys. Diabetes insipidus alert! Nephrogenic diabetes insipidus is a rare congenital disturbance of water metabolism due to renal tubular resistance to ADH (vasopressin)[5] . Incidence and etiology Diabetes insipidus may begin in childhood or early adulthood and is more common in males than in females. The disease is characterized by excessive urination and excessive thirst accompanied by significant fluid intake [5,11] . Incidence is slightly higher today than in the past, but it is still a rare disorder affecting one in 25,000 people[5] . Central diabetes insipidus is the result of[5,11] : ● ● Intracranial neoplastic tumors. ● ● Metastatic lesions. ● ● Surgical removal of the pituitary or other neurosurgery. ● ● Skull fracture. ● ● Head trauma. Nephrogenically, diabetes insipidus occurs due to[5,11] : ● ● Infection. ● ● Granulomatous disease. ● ● Vascular lesions. In some cases, the exact cause of the disease may not be able to be identified[5] . Nephrogenic diabetes insipidus is the result of a defect in the areas of the kidneys that reabsorb water back into the bloodstream. It is less common central diabetes insipidus[5,11] . Nephrogenic diabetes insipidus may also be due to[5,10] : ● ● An inherited disorder wherein boys inherit the abnormal gene on the X chromosome from their mothers. ● ● Renal disease. ● ● Effects of drugs such as lithium. ● ● Hypercalcemia. ● ● Hypokalemia. ● ● Hyperglycemia. ● ● Certain drugs such as Amphotericin B, Cidofovir, and Didanosine. Diabetes insipidus alert! Gestational diabetes insipidus occurs during pregnancy when an enzyme produced by the placenta destroys the mother’s ADH[5] . Pathophysiology Under normal conditions ADH is manufactured in the hypothalamus and stored in the posterior pituitary gland. When serum osmolality increases and circulating volume decreases, ADH is released into the general circulation. ADH increases water permeability of the distal and collecting tubules of the kidneys. This leads to reabsorption of water and decreased serum osmolality and increased circulating volume. These changes cause the release of ADH to stop[11] . In diabetes insipidus, interference with ADH synthesis, transport, or release causes decreased amounts of ADH to be released from the pituitary[5] . Thus, this lack of ADH causes[5,11] : ● ● Decreased renal tubular permeability to water. ● ● Decreased water reabsorption. ● ● Polyuria (excessive urinary output). ● ● Decreased urine osmolality. ● ● Decreased specific gravity. ● ● Increased serum osmolality. ● ● Increased thirst (polydipsia). Diagnosis Diagnosis is based on history, signs and symptoms, and various diagnostic tests. Characteristic signs and symptoms of diabetes insipidus include[5,11] : ● ● Abrupt onset of extreme polyuria generally between 4 to 6 L/day. However, urinary output may be as high as 30 L/day. ● ● Extreme thirst. ● ● Nocturia. ● ● Extreme fatigue as the result of lost sleep due to nocturia. ● ● Dehydration. ● ● Poor skin turgor. ● ● Muscle weakness. ● ● Constipation. ● ● Dizziness. ● ● Hypotension. Symptoms usually have an abrupt onset, starting within one to days after surgery, skull fracture, or stroke. As cerebral edema or increased intracranial pressure is relieved, symptoms stop as quickly as they began[5] . A number of complications are associated with prolonged polyuria. These include[5,11] : ● ● Hypovolemia. ● ● Hyperosmolality. ● ● Circulatory collapse. ● ● Loss of consciousness.