Pharmacology Flashcards: Diabetes Medications, Insulin Types, Metformin, GLP-1 Agonists

Metformin is an oral antidiabetic drug in the biguanide class that lowers blood glucose by decreasing hepatic glucose production, improving insulin sensitivity in peripheral tissues, and reducing intestinal glucose absorption. It is first-line for type 2 diabetes because it effectively lowers hemoglobin A1C by 1 to 1.5 percent, does not cause weight gain and may promote modest weight loss, does not cause hypoglycemia when used alone, has cardiovascular benefits, and is inexpensive.

Insulin types are classified by speed of action. Rapid-acting insulins like lispro, aspart, and glulisine begin working within 15 minutes and peak in one to two hours, used for mealtime glucose control. Short-acting regular insulin begins in 30 minutes, peaks in two to four hours, and is the only insulin given intravenously. Intermediate-acting NPH insulin begins in one to two hours and peaks in four to twelve hours. Long-acting insulins like glargine and detemir begin in one to two hours with no pronounced peak and last 24 hours, providing basal coverage.

Hypoglycemia occurs when blood glucose falls below 70 milligrams per deciliter and presents with two categories of symptoms. Adrenergic symptoms from the sympathetic nervous system response include sweating, tremor, tachycardia, hunger, and anxiety. Neuroglycopenic symptoms from inadequate brain glucose include confusion, dizziness, difficulty speaking, seizures, and loss of consciousness. Conscious patients should consume 15 grams of fast-acting carbohydrates such as glucose tablets or fruit juice, wait 15 minutes, and recheck glucose, known as the "rule of 15.

Glucagon-like peptide-1 receptor agonists, or GLP-1 agonists, including semaglutide, liraglutide, and dulaglutide, mimic the incretin hormone GLP-1. They stimulate insulin secretion only when blood glucose is elevated, suppress glucagon, slow gastric emptying, and promote satiety, leading to significant weight loss in addition to glucose lowering. They reduce hemoglobin A1C by 1 to 1.8 percent. Major cardiovascular and renal benefits have been demonstrated in clinical trials. Common side effects are nausea, vomiting, and diarrhea.

Diabetic ketoacidosis, or DKA, is a life-threatening complication primarily of type 1 diabetes caused by absolute or relative insulin deficiency. Without insulin, cells cannot use glucose for energy and the body breaks down fat, producing ketone bodies that make the blood dangerously acidic. Symptoms include nausea, vomiting, abdominal pain, fruity breath odor from acetone, Kussmaul respirations meaning deep rapid breathing, and altered consciousness.

Sulfonylureas like glipizide, glyburide, and glimepiride lower blood glucose by stimulating pancreatic beta cells to secrete more insulin, regardless of blood glucose level. This insulin-independent stimulation makes hypoglycemia their most significant adverse effect, particularly in elderly patients, those with irregular eating patterns, and those with kidney impairment. Sulfonylureas also cause weight gain. They are inexpensive and effective, reducing hemoglobin A1C by 1 to 1.5 percent.

Sodium-glucose cotransporter 2 inhibitors, or SGLT2 inhibitors, including empagliflozin, dapagliflozin, and canagliflozin, lower blood glucose by blocking glucose reabsorption in the kidneys, causing excess glucose to be excreted in the urine. They reduce hemoglobin A1C, promote weight loss, and lower blood pressure. Major benefits include proven cardiovascular protection and slowing of chronic kidney disease progression.

Potassium must be checked before insulin administration in diabetic ketoacidosis because insulin drives potassium from the blood into cells. During DKA, serum potassium may appear normal or even elevated due to acidosis shifting potassium out of cells, but total body potassium is actually depleted from urinary losses. Giving insulin without correcting low potassium can cause life-threatening hypokalemia leading to cardiac arrhythmias and respiratory muscle paralysis.

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, so patients require exogenous insulin for survival. Treatment uses basal-bolus insulin regimens combining long-acting and rapid-acting insulin, or insulin pumps. Type 2 diabetes results from insulin resistance and progressive beta cell dysfunction. Treatment begins with lifestyle modifications and metformin, adding other oral agents like SGLT2 inhibitors, GLP-1 agonists, or sulfonylureas as needed. Many type 2 patients eventually require insulin as beta cell function declines.