THERAPY OF DIABETES MELLITUS Posttest Instructions: To facilitate later discussion and review, please mark these posttest pages with your answers to the following questions. If your instructor has provided a separate answer form, mark your answers both on that form (being sure to fill in the identification section) and on these pages. Choose the one correct answer or most appropriate answer. A semicomatose insulin-dependent diabetic has been brought to the emergency department. Her plasma pH is 7.0 (normal, 7.35 to 7.45), with a serum bicarbonate of 2 mEq/L (normal = 22 to 29 mEq/L) and an elevated blood glucose of 500 mg/dL. She exhibits rapid deep (Kussmaul) breathing. Recognizing that the patient is at risk for cardiac arrest with any further reduction in plasma pH, the physician starts a 2-hour infusion of saline containing sodium bicarbonate. At the same time fluid therapy was initiated, 5 units of regular insulin were injected intravenously and followed by an intravenous infusion of 5 units/h of the same preparation. Blood glucose is to be monitored every hour, and the goal is to reduce plasma glucose by 100 mg/dL/h. 1. Why use regular insulin rather than NPH insulin for IV therapy? A. Regular insulin is a soluble preparation, whereas NPH insulin is a suspension B. Regular insulin has the most rapid onset of action C. Regular insulin has the shortest plasma half-life, and it is therefore possible to most effectively manipulate plasma hormone concentrations D. Protamine in the NPH insulin may induce an anaphylactic reaction2. Even though plasma potassium may be in the normal range in patients with diabetic ketoacidosis, intracellular and whole-body potassium concentrations are significantly reduced. Potassium should be infused early in the treatment of diabetic ketoacidosis to prevent hypokalemia and cardiac abnormalities, especially in the patient receiving bicarbonate. Why is the patient at risk for hypokalemia in response to therapy? A. Reduced potassium efflux from cells, secondary to reversal of the ketoacidosis with both insulin therapy and the infusion of alkali (bicarbonate) B. Insulin stimulation of Na+-K+ ATPase C. Volume expansion D. All of the above3. After 3 hours, the plasma glucose is 200 mg/dL, and it is suggested that the insulin infusion should now be stopped and the patient started on a regimen of subcutaneous NPH insulin (normal peak 5 to 7 h, duration 13 to 16 h) with glucose administration. Why is this plan not reasonable? A. Because of the short half-life of regular insulin and the delay in onset of therapeutic effects of NPH insulin, plasma insulin levels will fall rapidly and remain low for several hours B. Peak blood levels of insulin achieved with standard subcutaneous doses of NPH insulin are not sufficient to control ketoacidosis C. The protamine in the NPH will complex with circulating potassium D. Because of the poor peripheral perfusion, NPH insulin will be absorbed at a much slower rate than normal, and therapeutic levels will not be achieved4. The IV infusion of insulin must be maintained to reverse the ketoacidosis, a process that may take 24 hours or longer; glucose will now be infused to maintain normal blood glucose levels. After 8 to 12 hours of sustained insulin and glucose infusion, the ketonemia should substantially improve, due in part to A. Increased activity of endothelial lipoprotein lipase B. Increased fatty acid secretion in the proximal renal tubule C. Increased uptake of glucose by fat cells (leading to enhanced glycerol production and its subsequent esterification with fatty acids) and inhibition of hormone sensitive lipase D. Increased activity of adipose cell hormone sensitive lipase generating free fatty acids, which can be directly used by neural tissue as an energy source5. After stabilization of the metabolic problems associated with diabetic ketoacidosis, the patient was discharged from the hospital with an insulin treatment regimen of 20 units of NPH insulin (approximate peak of action 8 h) before breakfast and 10 units of NPH insulin before dinner. Regular insulin (5 units) was prescribed for one-half hour before breakfast, lunch, and dinner. She is now complaining of new onset frightening nightmares. Measured glucose levels are 200 mg/dL prior to breakfast, 150 mg/dL prior to lunch, 100 mg/dL prior to dinner, and 120 mg/dL prior to sleep. With the hope of maintaining premeal glucose values in the 80 to 120 mg/dL range and avoiding the hypoglycemia, the best therapeutic adjustment is: A Increase the morning NPH insulin by 5 units B. Decrease the evening NPH insulin by 5 units, and increase the breakfast regular by 5 units C. Increase the lunch regular by 5 units and dinner regular by 5 units D. As a first step, switch the timing of the PM-NPH insulin from prior to dinner to prior to sleep6. Elevated VLDL-triglycerides represent a significant risk factor for coronary artery disease in diabetics. Which of the following mechanisms is responsible for the insulin-induced reduction in plasma triglycerides. A. Activation of endothelial cell lipoprotein lipase B. Activation of hormone-sensitive lipase in fat cells C. Inhibition of adipose cell VLDL production D. Inhibition of fatty acid assimilation by hepatic mitochondria7. In the management of type II diabetic patients to reduce the risk of atherosclerosis, which is the most correct dietary recommendation? A. Increase complex carbohydrate intake B. Decrease complex carbohydrate intake C. Substitute polyunsaturated fats for saturated fats D. Substitute mono-unsaturated fats for saturated fats8. Sulfonylurea-induced hypoglycemia is much more common in elderly patients than in younger diabetics. Which reason is not consistent with this observation? A. Adult onset diabetes is more common in the elderly B. Elderly patients are more likely to stop eating with the onset of aches, pains, and various illnesses C. The plasma half-life of sulfonylureas can be prolonged in elderly patients relative to younger diabetic cohorts due to increased storage in body fat D. All of the above9. What following maneuvers may delay the chronic complications of diabetes–neuropathy, nephropathy, retinopathy, and coronary artery disease? A. Maintaining blood glucose within normal limits (tight control) B. Appropriate use of the angiotensin converting enzyme inhibitors C. Lowering LDL cholesterol by diet and/or appropriate use of
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