Nursing 212

Health Differences Across the Lifespan 2 Study Guide appropriate slippers or shoes. Medication therapy is hydrocortisone (Cortef) to replace cortisol and fludrocortisone (Florinef) to replace mineralcorticoids as needed. Have the patient avoid strenuous exercise, particularly in hot weather, increase fluid intake in hot weather, and carry injectable dexamethasone. The diet should be a high carbohydrate, high protein, high sodium, and low potassium in small, frequent feedings before steroid therapy. The diet should be high potassium and low sodium when on steroid replacement therapy. Diabetes Insipidus Diabetes insipidus is a deficiency of ADH (vasopressin) that is secreted by the posterior lobe of the pituitary gland. Decreased ADH reduces the ability of distal and collecting renal tubules to concentrate urine, resulting in copious, dilute urine and intense thirst. Polyuria can lead to severe dehydration if the patient does not replace lost water. Causes can be neurogenic (insufficient ADH secretion by posterior pituitary gland), nephrogenic (kidneys unable to respond to ADH), and medication (lithium carbonate and demeclocycline can cause kidneys to alter response to ADH). Primary DI results from inherited or idiopathic malfunction of the posterior pituitary gland. Secondary DI is caused by brain tumors from the lung or breast, cerebrovascular hemorrhage, granulomatous disease, or cerebral aneurysm. Signs and symptoms include a history of head injury, brain surgery, infection, or tumor. Polyuria (greater than 5 L/day), polydipsia (4-40 L/day), muscle weakness and pain, fatigue, dry skin, and mucous membranes. Decreased sodium and potassium levels are also seen. Polydipsia (excessive thirst), tenting or sagging of skin, and orthostatic blood pressure are additional symptoms. Diagnostics: urine chemistry specific gravity less than 1.004; urine osmolality less than 300mOsm/kg; positive water deprivation test; reduced serumADH level in primary DI; serum sodium greater than 145 mEq/L Treatment: Water replacement orally is preferred or IV D5W as needed to normalize lab values. For neurogenic DI, hormone replacement with desmopression (DDAVP), a synthetic vasopressin, and adjunctive medication, such as Chlorpropamide (Diabinese) or carbamazepine (Tegretol), may increase ADH release or enhance the effect of ADH on renal collecting duct. For nephrogenic DI, correct the underlying disease to stop causative medication; begin a low salt, low protein diet to decrease net excretion of solute. Monitor I&O hourly, report urine output over 200ml/hour for two consecutive hours or 500ml over two hours, monitor for continence, and provide easy access to bathroom appropriate. Weigh daily and report weight loss. Monitor urine specific gravity and report if it decreases; monitor serum osmolality and sodium for increases. Encourage fluid intake greater than urinary output and provide fluids within reach at all times. Provide IV fluid replacement as ordered. Use skin protective barriers with incontinence. Hypoparathyroidism Hypoparathyroidism is a decrease in PTH secretion. It involves decreased stimulation to osteoclasts, resulting in decreased release of calcium and phosphorus from bone. There is reduced GI absorption of calcium and increased absorption of phosphorus. Decreased blood calcium causes a rise in serum phosphates and decreased phosphate excretion by the kidney. Hypocalcemia raises the threshold for

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