Nursing 105

Essentials of Nursing Study Guide

©2018 Achieve Page 95 of 160 is caused by decreased intake or increased urinary loss of magnesium. It often occurs in the setting of hypokalemia and hypocalcemia. Serum potassium levels may be decreased due to the inability of the sodium-potassium pump to actively restore intracellular potassium levels. Hypomagnesemia also contributes to hypocalcemia due to the decreased production of parathormone, which is responsible for maintaining adequate calcium levels. Magnesium plays an important role in the functioning of a cell; it activates enzymes involved in breaking down proteins and it helps to keep the sodium and potassium pump within cells functioning. This, in turn, helps to maintain potassium levels within the cell. The normal serum magnesium level is 1.8-2.6 mg/dl. • Risk factors: chronic alcoholism; malabsorption syndromes (cancer and colitis); vomiting; NGT suctioning; diarrhea; diabetic ketoacidosis due to the movement of magnesium out of the cell and loss in the urine because of osmotic diuresis; drug use such as diuretics, amphotericin, tobramycin, gentamycin, digoxin and laxatives • Signs and symptoms: agitation; leg cramps; confusion; anorexia; nausea; vomiting; increased reflexes; dysphasia (ensure swallowing is intact before giving anything P.O.) • Treatment: treatment of the cause, magnesium replacement Hypermagnesemia most often occurs during renal failure but may also occur with adrenocortical insufficiency (Addison’s disease). • Risk factors: decreased excretion with renal failure; increased intake with the excessive use of magnesium containing antacids; enemas or laxatives; excessive administration of magnesium (especially in renal failure) • Signs and symptoms: nausea; vomiting; flushing; diaphoresis; drowsiness; coma; muscular weakness or paralysis; bradycardia; depressed deep tendon knee reflex; hypotension • Treatment: removal of the cause; diuretics and 0.45% normal saline to enhance magnesium excretion in patients with normal renal function; IV calcium to antagonize neuromuscular effects; dialysis Diabetic ketoacidosis (DKA) may occur in patients who are newly diagnosed with diabetes or in the individual who either did not administer enough insulin or the body requirements exceeded the supply available. The body will demand more insulin whenever faced with increased physical activity or serious illness. Excessive glucose and ketones in the blood cause the serum osmolarity to rise. Water will exit the cells to dilute the blood and make it less hypertonic. The cells become dehydrated and the patient will develop neurological changes. Glucose and ketones spill over into the urine causing an osmotic diuresis to occur in the kidneys. This compounds the original problem as now the cells must release more water and become more dehydrated. This profound diuresis also causes significant electrolyte losses (potassium, phosphate, and magnesium). Acidosis promotes potassium moving out of cells to buffer the pH change (hydrogen moves in cells, potassium out). in renal failure to allow maximum production of 2, 3-DPG levels to minimize anemic state in chronic renal failure Hypomagnesemia