Drug Classes and MOA Flashcards
Thiazides (diuretic)
Inhibits Na and Cl transporters in the ascending and distal convoluted tubules; increasing Na and Cl excretion; reduces blood volume
Loop diuretic
Inhibits Na-K-Cl co-transporter in the thick ascending loop of henle
ACE Inhibitors
Blocks conversion of angiotensin I to angiotensin II, decreasing peripheral vasoconstriction; also inhibits bradykinin degradation
Angiotensin II Receptor Blockers (ARBs)
Blocks the effects of angiotensin II resulting in significant decreases in peripheral vasoconstriction
Benzothiazepines (CCB)
Blocks Ca influx with resultant improved myocardial tone and decreased cardiac output; targets cardiac cells
Diphenyl alkamines (CCB)
Blocks Ca influx with resultant improved myocardial tone and decreased cardiac output; targets cardiac cells
Dihydropyridine class (CCB)
Blocks Ca influx with resultant peripheral vasodilation and improved myocardial tone; targets peripheral smooth muscle cells
Beta Blockers
All clinically available beta-blockers are competitive antagonists - antagonize effects of catecholamines (epinephrine [adrenaline], norepinephrine) on the heart
Non-selective act on both B1 and B2 receptors
Anti-arrhythmic - Class Ia
Moderate block of both open Na and K channels
Anti-arrhythmic - Class Ib
Mild blocking or inactivating Na channels
Anti-arrhythmic - Class Ic
Block open Na channels
Anti-arrhythmic - Class II
Block catecholamines; block at the AV node
Anti-arrhythmic - Class III
Blocking lKr; potassium channel blockade
Anti-arrhythmic - Class IV
Non-dihydropyridine CCBs
Block L-type calcium channels, decrease AV node conduction and increase refractory period
Nitrate
Relaxation of vascular smooth muscle and vasodilation
Anti-platelet
NSAIDS - COX inhibition
Others - block P2Y of ADP receptors on platelet surface
Anti-coagulants
Vitamin K Inhibitor
Factor Xa Inhibitors
Factor IIa Inhibitor
Statins:
High-intensity (>50%)
Moderate-intensity (30-49%)
Low-intensity (<30%)
Inhibit HMG-CoA reductase; inhibits cholesterol production; liver increases cholesterol uptake from the blood stream by increasing LDL receptors; PCSK9 up regulation
Bile Acid Sequestrants (BAS)
BAS are resins that bind bile acids in the intestine; reduces enterohepatic recycling; increases hepatic conversion of cholesterol to bile acid; upregulates LDL receptors on the liver
Prevents absorption of dietary biliary cholesterol; upregulates LDL receptors in the liver, lowering plasma LDL
Fibrates
Lower production and increased clearance of VLDL; increases HDL production; lowers TG and inc. HDL but has a variable effect on LDL
