Nursing 212

Health Differences Across the Lifespan 2 Study Guide drugs to stimulate endogenous insulin production and increase insulin sensitivity at the cellular level. Oral antidiabetic medications include oral sulfonylureas, alpha glucosidase inhibitors, meglitinides, thiazolidinedione’s, Biguanides, and combination agents. The nurse should reinforce to cpatient taking oral sulfonylureas that concurrent use of alcohol can cause a disulfiram type reaction (hypoglycemia, flushing, headache, nausea, and abdominal cramps). Reinforce the risk of metabolic acidosis and to notify physician if severe diarrhea, infection, or dehydration occurs. Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is a life threatening metabolic acidosis resulting from persistent hyperglycemia and breakdown of fats into glucose, leading to the presence of ketones in blood. It may be triggered by emotional stress, uncompensated exercise, infection, trauma, or insufficient or delayed insulin administration. Hyperglycemia causes uncompensated polyuria, dehydration, Hemoconcentration, hyperosmolarity, and electrolyte imbalance; a significant accumulation of serum ketones leads to acidosis. Assessment: thirst, nausea and vomiting; malaise and lethargy; polyuria; warm, dry skin; flushed face; acene (fruit) odor to breath; Kussmaul’s respirations (deep, labored, and rapid respirations); serum glucose above 250 mEq/L; plasma pH under 7.35; plasma bicarbonate under 15 mEq/L; serum ketones present; urine positive for glucose and ketones; may have abnormal sodium and chloride levels and hyperkalemia Treatment: IV fluids, electrolytes, and regular insulin are used to correct hyperglycemia and dehydration; supportive care as indicated such as NPO status, vasopressors, and respiratory support. Insulin: A bolus of IV regular insulin is given followed by a continuous IV drip (0.1 unit/kg body weight) until BG level drops to 250 mg/dL or pH is 7.30. Once this occurs, insulin (regular) is given on a sliding scale per BG results. BG monitoring is done every 1-2 hours to evaluate effectiveness of therapy. Fluid therapy: As much as 1 to 2L of normal saline solution may be given during the first hour, then the IV rate is decreased to 500ml/hr as tolerated by cardiac and respiratory systems. When BG reaches 250-300 mg/dL, a 5% glucose solute (such as D5 1/2NS) is added to prevent hypoglycemia and cerebral edema. Central venous pressure or hemodynamic monitoring may be needed to evaluate effectiveness of therapy. Potassium replacement: Initial potassium is usually elevated. With the reversal of acidosis and the administration of insulin, the potassium shifts into the cells and the serum level can drop rapidly. Institute replacement therapy based on serum potassium level and urine output. Institute cardiac monitoring to detect cardiac changes due to hyper and hypokalemia, and to monitor the effects of therapy on serumpotassium level. Replace other electrolytes, such as phosphate, based on lab results; bicarbonate is not given routinely in DKA because rapid correction of acidosis can cause severe hypokalemia.

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