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41 Cards in this Set
- Front
- Back
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Quinidine
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-Class IA
-block open or activated state of Na+ channel -antiarrythmic: increase AP duration & effective refractory period -alpha blockade and muscarinic blockade -AE: cinchonism, displaces digoxin from tissue binding sites |
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Procainamide
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-Class IA
-block open or activated state of Na+ channel -antiarrythmic: increase AP duration & effective refractory period -metabolized by N-acetyltransferase AE: SLE-like syndrome!, thrombocytopenia, agranulocytosis |
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Lidocaine
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-Class IB
-block inactivated Na+ channels (prefer hypoxic tissue) -antiarrythmic: decrease AP duration, with increased diastole -Rx: post-MI, via IV -least cardiotoxic |
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Mexiletine
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-Class IB
-block inactivated Na+ channels (prefer hypoxic tissue) -antiarrythmic: decrease AP duration, with increased diastole -Oral |
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Flecainide
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-Class IC
-block fast Na+ channels -NO EFFECT on AP duration or ANS |
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Acebutolol, esmolol, propranolol
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-Class II
-beta blockers -decrease SA and AV nodal activity -Rx: supraventrical tachyarrythmias |
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Amiodarone
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-Class III
-blocks delayed rectified K+ current -increases AP duration and ERP -LONG half life: >80 days -large Vd -AE:(b/c IODinated): pulmonary fibrosis, "smurf skin", phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfunction |
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Sotalol
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-Class III
-blocks delayed rectified K+ current -increases AP duration and ERP -also B1 blockade --> decrease HR & AV conduction -Rx: life-threatening ventricular arrythmias |
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Verapamil, Diltiazem
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-Class IV
-block slow cardiac Ca2+ channels -decrease SA and AV nodal activity -Rx: supraventricular arrythmias -Verapamil: displaces digoxin! |
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Adenosine
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-Gi-coupled decrease of cAMP
-decrease SA and AV nodal activity -SHORT half-life -DOC paroxysmal supraventricular arrythmias |
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Clonidine, methyldopa
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-alpha2 agonists
-stimulate negative feedback --> decreased NE -decreased TPR and HR -TCAs decrease drug effects -Methyldopa: Rx of HTN in pregnancy |
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Reserpine
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-destroys vesicles
-decrease NE, DA, and 5HT -decrease CO & TPR -AE: depression |
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Guanethidine
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-accumulated into nerve endings via reuptake
-binds vesicles -inhibits NE release -TCAs block reuptake and action of guanethidine |
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Prazosin, doxazosin, terazosin
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-alpha1 blockers
-decrease arteriolar & venous resistance -potential reflex bradycardia -GOOD effect on lipid profile |
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Hydralazine
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-arteriolar dilation via NO
-decrease TPR -potential reflex tachycardia -AE: SLE-like syndrome |
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Nitroprusside
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-arteriolar & venule dilation via NO
-DOC hypertensive emergencies (IV) -AE: cyanide toxicity! |
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Minoxidil, diazoxide
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-open K+ channels
-hyperpolarization -arteriolar dilation Minoxidil: AE hypertrichosis Diazoxide: AE decrease insulin release |
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Diltiazem, verapimil, dihydropyridines (ie nifedipine)
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-block L-type Ca2+ channels
-decrease TPR -AE of dihydropyridines ("-dipines"): reflex tachycardia, gingival hyperplasia! |
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Captopril
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-ACE inhibitor
-decrease aldosterone, vasodilation -prevent bradykinin degradation --> dry cough |
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Losartan
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-ARB
-decrease aldosterone, vasodilation -NO dry cough |
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Aliskiren
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-Renin inhibitor
-blocks formation of Ang I -decrease aldosterone, vasodilation |
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Bosentan
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-Endothelin A antagonist
-AE due to vasodilation -Rx pulmonary HTN -Contraindicated: pregnancy! |
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Epoprostenol
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-Prostocyclin PGI2
-Rx pulm HTN |
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Sildenafil
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-Inhibits Type V PDE
-increases cGMP -Rx pulm HTN |
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Digoxin
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-inhibits cardiac Na+/K+ ATPase --> decreased Na+/Ca2+ exchange --> increased intracellular Ca2+
-inotrope -Long half life -does NOT increase survival! -Displaced from tissues by verapamil and quinidine |
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Inamrinone, milrinone
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-phosphodiesterase inhibitors
-can not break cAMP down to AMP --> increased cAMP -inotrope |
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Nesiritide
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-recombinant human B-type natriuretic peptide (rh BNP)
-increases cGMP -vasodilation -Rx acutely decompensated CHF |
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Nitroglycerine
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-venodilation --> decreased preload --> decreased oxygen requirement
-AE: orthostatic HTN, reflex tachycardia -Contraind: tachyphylaxis, cardiotoxic with sildenafil! |
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Ranolazine
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-blocks late inward Na+ current --> decreased Ca2+ accumulation
-decreased EDP -Contraind: pts with long QT syndrome |
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Mannitol
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-inhibits water reabsorption throughout the tubule
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Acetazolamide, dorzolamide
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-carbonic anhydrase inhibitor
-proximal convoluted tubule -decreased H+ formation in cell --> decreased Na+/H+ antiport) --> increased Na+ and HCO3- in lumen -diuresis AE: hypokalemia, renal stones, sulfonamide hypersensitivity |
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Ethacrynic acid, furosemide
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-loop diuretics
-thick ascending loop -Na+/K+/2Cl- inhibition -decreased intracellular K+ --> decreased positive potential --> decreased reabsorption of Mg2+ & Ca2+ -AE: hypokalemia (& alkalosis), hypocalcemia, hypomagnesemia; ototoxicity -Furosemide: AE sulfonamide hypersensitivity -with Lithium: decreased clearance |
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Hydrochlorothiazide, indapamide
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-thiazides
-inhibit Na+/Cl- transporter (symport) -increase Na+ and Cl- in lumen of DCT --> diuresis AE: sulfonamide hypersensitivity |
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Spirinolactone
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-K+ sparing diuretic
-aldosterone rec antagonist AE: hyperkalemia, acidosis, antiandrogen! |
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Amiloride, triamterene
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-K+ sparing diuretic
-Na+ channel blockers -Rx lithium-induced nephrogenic diabetes insipidus AE: hyperkalemia, acidoses |
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Lovastatins, all "-statin"s
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-HMG-CoA reductase inhibitor
-decreased liver cholesterol --> increased LDL rec --> decreased plasma LDL AE: rhabdomyolysis, hepatotoxicity |
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Cholestyramine, colestipol
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-bile acid sequestrant
-cannot reabsorb bile acid in gut --> cholesterol converted to bile acid --> decreased cholesterol --> increased LDL rec --> decreased plasma LDL AE: malabsorption of fat soluble vitamins Contraind: hypertriglyceridemia |
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Nicotinic acid (Niacin, Vit B3)
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-inhibit VDLD synthesis
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Gemfibrozil, Fenofibrate
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-bind to PPARalpha
-increase expression of lipoprotein lipases -Rx: hypertriglyceridemia -AE: gallstones, myositis |
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Ezetimibe
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-prevents intestinal absorption of cholesterol
-decreases LDL |
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Orlistat
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-inhibits pancreatic lipase
-decreases triglyceride breakdown in intestine -Rx: weight loss -AE: steatorrhea, decreased absorption of fat-soluble vits |
