Nursing 105

Essentials of Nursing Study Guide

©2018 Achieve Page 94 of 160 • Risk factors: increased intake of calcium; increased intestinal absorption hyperparathyroidism); increased release of calcium from bone (hyperparathyroidism and malignancies); increased urinary excretion (renal failure and thiazide diuretics); increased ionized calcium (acidosis) • Signs and symptoms: lethargy; anorexia; nausea; polyuria (hypercalcemia limits the kidneys ability to concentrate urine); bone pain; fractures; flank pain due to renal calculi; confusion; paresthesias; coma; shortening of QT interval; ventricular dysrhythmias • Treatment: treat the underlying cause; hemodilution with normal saline Hypophosphatemia may occur with shifts of phosphate between the intracellular and extracellular spaces, increased urinary losses, decreased intestinal absorption, or increased utilization. Acute alcohol withdrawal can precipitate decreased serum phosphate levels due to poor intake, vomiting, diarrhea, hyperventilation, and increased urinary losses. Patients in acute diabetic ketoacidosis may also experience significant hypophosphatemia. The normal serum phosphates level is 2.7-4.5 mg/dl. • Risk factors: intracellular shifts such as respiratory alkalosis; increased urinary losses such as hypomagnesemia; hyperparathyroidism; use of thiazide diuretics; reduced intestinal absorption or increased intestinal loss; use of phosphorous binding antacids (Amphojel); vomiting; diarrhea; alcoholism; DKA; severe burns; renal failure • Signs and symptoms: o Acute: confusion; seizures; coma; chest pain due to decreased availability of oxygen to the myocardial cells; increased risk of sepsis; numbness; tingling of fingers and lips; decreased muscle strength o Chronic: memory loss; lethargy; bone pain; bruising and bleeding; joint stiffness; cyanosis • Treatment: treat the cause; phosphate supplementation; do not administer phosphate rapidly as tetany could result (sudden drop in calcium levels); be aware of potential to develop soft tissue calcification if hyperphosphatemia develops; prevent patient from hyperventilating if at all possible as alkalosis causes a drop in serum phosphate levels; be alert for signs of infection as the patient’s white blood cells are impaired due to a decreased available ATP Hyperphosphatemia is most commonly associated with renal failure but may also be caused by extracellular shifts and cellular destruction with release of intracellular phosphorous. • Risk factors: renal failure; increased intake; excessive phosphorous supplements; vitamin D; phosphorous containing laxatives or enemas; extracellular shift; respiratory acidosis; DKA (before treatment); cellular destruction; neoplastic disease; increased tissue breakdown as in rhabdomyolysis; decreased urinary losses; hypoparathyroidism; volume depletion • Signs and symptoms: anorexia; nausea; vomiting; muscle weakness; hyperreflexia; tetany; tachycardia; the most serious symptoms occur when the patient develops metastatic calcifications due to elevated phosphorous and calcium levels • Treatment: treat the cause; use of aluminum, magnesium or calcium antacids (avoid magnesium antacids in renal failure); dialysis; slightly high phosphorous levels are tolerated