MOA Notecards Flashcards
Inhibit Na and Cl resorption causing profound diuresis from the excretion or urinary Na, Cl and K
loop diuretics
Partial fatty acis oxidation inhibitor- alters myocardial energy metabolism decreasing cardiac workload
ranolazine (first drug in the class of antianginal agents that is not a nitrate)
Increases coronary artery blood flow by vasodilation, reduces myocardial oxygen demand by decreasing preload
nitrates
Reduces HR and contractility
BB
causes coronary and peripheral vasodilation, reducing contractility
CCB
Inhibits platelet aggregation
ASA
increases the pH of the gastric refluxate by neutralizing gastric acid, thereby decreasing its potential to cause damage to the esophageal mucosa. These agents also increase the LES tone through alkanization of gastric contents
Antacids
A mucosal coating agent that forms a protective barrier between esophageal tissue and gastric refluxate
sucralfate
Acid suppressive agents that inhibit the action of histamine at the H2 receptor of the parietal cell, decreasing basal acid secretion
H2 blockers
Irreversibly bind to the H+/K+ATPase pump of the parietal cell, thereby inhibiting the final step of acid secretion
PPIs
Inhibits the production and release of glucose from the liver and enhances insulin sensitivity in muscle and fat
biguanides (metformin)
biguanides bring out the insulin
insulin secretagoguges that promote pancreatic B-cell secretion of insulin and potentiate insulin action on extra-hepatic tissue.
sulfonylureas (glyburide, glipizide, glimepiride)
**glipizide preferred in renal disease
delay GI breakdown and absorption of carbohydrates
alpha-glucosidase inhibitors (acarbose, miglitol)
insulin sensitizers that reduce insulin resistance by decreasing hepatic glucose release and promoting skeletal muscle glucose absorption
Thiazolidinediones or TZDs (“zones”)
increased incretin levels, inhibiting glucagon secretion, decreasing blood glucose, increasing insulin secretion and decreasing gastric emptying
DPP-4 inhibitors (gliptins)
