Category: Fundamentals
Metabolic acidosis, in DKA, with an anion gap is primarily the result of elevated plasma levels of acetoacetate and β-hydroxybutyrate, although lactate, FFAs, phosphates, volume depletion and several medications can also contribute.
Category: Fundamentals
Typical findings of DKA include tachypnea with Kussmaul’s breathing, tachycardia, frank hypotension or orthostatic blood pressure changes, odor of acetone on the breath and signs of dehydration.
Category: Fundamentals
DKA most commonly occurs in patients with type 1 diabetes and is associated with inadequate administration of insulin, infection or MI. DKA can also occur in type 2 diabetics and may be associated with types of stress, such as sepsis or GI bleeding.
Category: Fundamentals
Acidosis plays a prominent role in the clinical presentation of DKA. The acidotic patient attempts to increase lung ventilation to rid the body of excess acid with Kussmaul’s breathing. Bicarbonate is used up in the process.
Category: Fundamentals
Glucose in the renal tubules draws water, Na, K, Mg, Ca and Phos from the circulation into the urine. This diuresis, combined with poor intake, produces the profound dehydration and electrolyte imbalance associated with DKA.
Category: Fundamentals
DKA may be caused by cessation of insulin intake or by physical or emotional stress, despite insulin therapy. When the hyperglycemia becomes sufficiently marked, the renal threshold is surpassed and glucose is excreted in the urine
Category: Fundamentals
Diabetic ketoacidosis (DKA) is a syndrome in which insulin deficiency and glucagon excess combine to produce a hyperglycemic, dehydrated, acidotic patient, with profound electrolyte imbalance.
Category: Fundamentals
Type 2 diabetes is associated with a decline of beta cell function over time, and intensive insulin therapy has been advocated early to rest the beta cells and possibly preserve their function over time.
Category: Fundamentals
Long-acting insulin analogs are detemir (Levemir) and glargine (Lantus). Their onset of action is 3 to 4 hours and their duration of action approaches 24 hours, similar to that of NPH.
Category: Fundamentals
NPH insulin (Humulin, Novolin) is typically dosed 4 to 6 hours before a meal. It has a 12- to 24-hour duration of action. Regular and NPH insulin may be mixed together to lessen the number of daily injections.
Category: Fundamentals
Regular insulin, which is used in the treatment of DKA, has an onset of action within 30 to 60 minutes and is typically dosed 30 to 45 minutes before a meal. Its duration of action is approximately 4 to 12 hours.
Category: Fundamentals
Certain principles apply to all insulins, such as their ability to enhance gluconeogenesis and lipogenesis and suppress glycogenolysis. Human insulins are available today as regular insulin and neutral protamine hagedorn (NPH).
Category: Fundamentals
Meglitinides have a rapid onset of action and should be taken before a meal. Management of refractory hypoglycemia with these agents may be done in a manner similar to that for sulfonylureas, with the use of octreotide.
Category: Fundamentals
The nonsulfonylurea secretagogues, the meglitinides, are similar to the sulfonylureas in action and mechanism. They bind to adenosine triphosphate (ATP) sensitive potassium channels of beta cells to increase insulin secretion.
Category: Fundamentals
The α-glucosidase inhibitors delay intestinal monosaccharide absorption and prevent complex carbohydrate breakdown. They must be titrated to minimize GI side effects and should not be used in patients with certain GI disorders.
