Cardio Pharmacology Flashcards
Nifedipine
Calcium channel antagonist, DHP. Binds while L-type channel is resting, most peripheral smooth muscle (vasodilation) where channels are more frequently resting.
Amlodipine
Calcium channel antagonist, DHP. Binds while L-type channel is resting, most peripheral smooth muscle (vasodilation) where channels are more frequently resting.
Diltiazem
Calcium channel antagonist, Non-DHP. Binds to L-type channel when OPEN - most effective in cardiac myocytes (which frequently depolarize). Decrease cardiac contractility. Induce Coronary Vasodilation. Lowers automaticity in SA/AV nodes (Reduces HR).
Verapamil
Calcium channel antagonist, Non-DHP. Binds to L-type channel when OPEN - most effective in cardiac myocytes (which frequently depolarize). Decrease cardiac contractility. Induce Coronary Vasodilation. Lowers automaticity in SA/AV nodes (Reduces HR).
Furosemide
Loop diuretic. Binds Na/K/Cl transporter in Ascending tubule,
HCTZ (hydrochorthiazide)
Thiazide diuretic. Acutely Acts on distal tubule, fluid excretion, Na+ excretion, lower blood volume, less BP. Chronically - NO release, vasodilation, decreased PVR - so, volume recovers but BP stays low.
Losartan
ARB (angiotensin receptor blocker). Blocks AT1 receptor for A-II. Blocks TGF-B1 activation. Downside: DoesnÕt stop cleavage of bradykinin.
Enlalapril
ACEi. Blocks conversion of A-I to A-II, which prevents downstream actions of A-II. Also blocks cleavage of bradykinin, so it can go on to do great things (NO release).
Direct Renin Inhibitors
Éinhibits renin.
Phenoxybenzamine
Non-selective alpha blocker. Vasodilation, decreased PVR.
Prazosin
Selective alpha blocker. Alpha 1 and 2. Vasodilation, decreased PVR.
Doxazosin/Terazosin
Selective alpha blocker, Alpha 1 only. Vasodilation, decreased PVR.
Clonidine
Central alpha agonist, alpha 2. Stimulate pre-gang alpha-2 receptors in medulla, reduction of sympathetic outflow. Unopposed vagal tone. Decreased PVR, HR, CO, BP.
Spironolactone
Aldosterone antagonist/mineralocorticoid receptor antagonist. Potassium sparing diuretic.
Hydralazine
Arterial vasodilator. Mechanism unknown. Arteriolar dilation, doesn’t affect veins. Mostly renal, periph, splanchnic, and coronary arterties. Decrease BP.
Sodium nitroprusside
Arterial vasodilator. Metabolised by SMCs into NO –> vasodilation, decrease in PVR. Byproduct = cyanide, which is metabolized by RBCs by rhodanase with help of cofactor sodium thiosulfate. Sodium thiosulfate added to solution to prevent cyanide tox. Unstable in sunlight, they wrap it in foil.
Nitrates
Venodilator. Converts to NO in endothelium, gas diffuses to receptors. Activates guanylyl cyclase which forms c-GMP which inactives myosin light-chain kinase É causes SMC relaxation, esp in veins, decreased platelet aggregation. Also GI and bronchial relaxation. Decreases venous blood return, decreases LV cavity size and ejection force, decreases systolic wall stress, myocardial O2 demand. Increases endocardial perfusion. Decreases thrombs.
Propranolol
Non-selective beta blocker. Reduce heart rate and renin release by inhibiting sympathetic nervous signaling. Antagonize these systems: 1) Alpha1/2 - increase in vasoconstriction 2) Beta1 - acts on SA/AV nodes and causes increase in chronotropy and ionotropy 3) Beta2 - vasodilation of cardiac vessels and bronchodilator
Metoprolol
Selective beta blocker.
Carvedilol
Special (alpha 1 and non-selective beta blocker) . Blocks myocyte hypertrophy, myocyte injury, increased arrhythmias, vasoconstriction, RAS activation, etc.
Epinephrine
Inotrope Pressor Vasoactive Drug. Bends alpha 1/2, Beta 1/2/3. Increase in HR, CO and PVR
Norepinephrine
Inotrope Pressor Vasoactive Drug. Binds alpha 1/2, Beta 1. Decreased HR, CO. Increased PVR and BP. These effects are mediated by alpha1 (which overrides beta1)
Dopamine
Inotrope Pressor Vasoactive Drug. Low dose: Delta (renal vasodilation), Med: Delta, Beta 1 (increased CO, renal vasodilation), High: Delta, Beta 1, Alpha 1. (Decreased HR, CO and increased PVR)
Dobutamine
Inotrope Pressor Vasoactive Drug. Beta 1 and Alpha. Decreases afterload and increases inotropy. Chronic infusions can lead to densensitization. Short acting.
Isoproterenol
Sympathetic Adrenergic Agonist. Beta 1/2. Increases HR, CO, and decreases PVR.
Phenylephrine
Inotrope Pressor Vasoactive Drug, Alpha 1/2, increases SVR, decreases HR, CO.
Milrinone
Inotrope Pressor Vasoactive Drug, PDE3 Inhibitor. Inhibits the degradation of cAMP by PDE. This results in 1) an increase in cardiac conractility and 2) a decrease in PVR (venous dilation)
Digoxin
Digitalis - “cardiac glycoside”. Blocks Na+/K+ ATPase increases intracellular Na+. As a result, Na+/Ca++ brings more Ca++ into cell. *Competes with K+ to bind, extra-cell K+ prevents toxicity, low K+ can lead to toxicity. Increases inotropy without increase in HR. Also acts like a muscarinic agonist – slows SA/AV node conduction, increases ERP, risk of bradycardia. Can cause v-tach due to delayed afterdepolarizations.
Atropine
Antimuscarinic (Ach receptor antagonist). Blocks parasympathetic action. Increases HR, decreases refractory period, etc.
Acetylcholine
Muscarinic agonist. Parasympathetic. Very short half-life, not really used.
Edrophonium
Ach-esterase inhibitor. Strong parasympathetic discharge.
Physostigmine
Ach-esterase inhibitor. Strong parasympathetic discharge. Longer acting than edrophonium.
Neostigmine
Ach-esterase inhibitor. Strong parasympathetic discharge. Longer acting than edrophonium.
Anything-astatin
Statins - HMG CoA reductaste inhibitor. Increases LDL uptake instead of synthesizing endogenous cholesterol. LDL receptors are up-regulated, and clearance increases. (cholesterol level in liver may be almost normal, but elevated clearance reduces plasma LDLs).
Fibrates
Fibric acid derivative. Activate nuclear receptor PPAR alpha in liver and periph tissue .. Decreases LDL production, increases VLDL clearance, increases HDLs, decrease TGs.
Niacin
Vitamin B3 at high doses – reduces FFA release and flux to liver. Increases HDLs, decrease TG, decrease LDL, decrease Lp(a). Adverse: flushing, hepatotoxicityÉ lots of bad crap.
Cholesterol absorption inhibitor
Éinhibits cholesterol absorption. Acts at brush border, binds and inhibits NPC1L1 cholesterol transporter. Reduces hepatic cholesterol stores, LDL receptor up-regulates, increased clearance.
Bile acid sequestrant
Bile acid sequestrant. high MW, binds to bile acids and prevents re-absorption.
Aspirin
Binds Cox 1/2, inhibits. Inhibits platelet aggregation.
Clopidogrel
Binds P2Y12 receptor. Platelet ADP inhibitor, prevents platelet activation.
Glycoprotein Iib/IIIa inhibitor
Binds Glycoprotein Iib/IIIa, blocks fibrinogen mediated platelet binding and crosslinking.
t-PA, streptokinase, urokinase
Thrombolytic drugs. Binds plasminogen. Increase conversion of plasminogen to plasmin, accelerates clot breakdown.
Heparin
Anticoagulant. Blocks factor Xa and thrombin.
Procainamide/Quinidine
Class IA Na channel blocker, and inward rect. K+. Affects fast response tissues. Elongates AP. More potent in cells with depol RMP. Strongest.
Lidocaine
Class IB Na channel blocker, affects fast response tissue, elongates AP, more potent in cells with depol RMP. Weakest.
Flecainide
Class IC Na channel blocker, affects fast response tissue, elongates AP, more potent in cells with depol RMP. Stronger than IB, weaker than IC.
Amiodarone
Class III K+ channel blocker, has beta blocker effects too. Increase the refractory period. As heart rate or extracellular K decreases, the refractory period increases. Effective in controlling fast reponse tissues.
Sotalol
Class III K+ channel blocker, has beta blocker effects too. Increase the refractory period. As heart rate or extracellular K decreases, the refractory period increases. Effective in controlling fast reponse tissues.
Adenosine
Local metabolite. Binds A1 receptor. 1) Reduces cAMP in cardiac tissue, allowing K to hyperpolarize cells resulting in a greater ERP. 2) Vasodilation of VSMCs
