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70 Cards in this Set
- Front
- Back
Quinidine class
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IA antiarrhythmic
|
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Procainamide class
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1A
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Disopyramide class
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IA
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lidocaine class
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IB
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mexiletine class
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IB
|
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Tocainamide class
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IB
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Flecainamide class
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IC
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Encainide class
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IC
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Propafenone class
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IC
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class IA antiarrhythmics?
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quinidine, procainamide, disopyramide
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class IB antiarrhythmics
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lidocaine, mexiletine, tocainide
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Class IC antiarrhythmics
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flecainide, Encainide, Propafenone
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four classes of antiarrhythmcs?
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I - Na blockers
II - beta blockers III - potassium blockers IV - calcium channel blockers |
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class IA effect on AP duration?
IB? IC? |
IA increases
IB decreases IC has NO EFFECT |
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class IA has what effects?
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increases AP duration, increases Effective refractory period, increases QT interval
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class IA for?
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affects atrial and ventricular arrhythmias - esp. reentrant and ectopic SVT and V-tach
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headache, tinnitus, thrombocytopenia?
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cinchonism from quinidne
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procainamide maj. SE
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SLE like syndrome
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all IA major SE?
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prolonged QT predisposes to torsades de pointes
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IB prefer..
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ischemic or depolarized purkinje and ventricular tissue
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IB useful for?
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acute ventricular arrhythmias post MI
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use of IC?
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V tachs progressing to Vgib and intractable SVT's but usually a last resort. doesn't work on structurally abnormal
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main toxicity of class IC?
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proarrhythmic - and contraindicated in post-MI
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MOA of HMG CoA reductase inhibitors
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inhibit cholesterol precursor, mevalonate
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SE of HMG CoA reductase inhibitors
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hepatotoxicity, rhabdomyolysis
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HMG CoA reductaes effects on lipids?
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super decrease in LDL, small increase of HDL, and small decrease of TG
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Niacin MOA?
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inhibits lipolysis in adipose tissue and reduces hepatic VLDL secretion into circulation
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SE of Niacin?
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red flushed fase, hyperglycemia, hyperuricemia
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effects of niacin on lipids
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moderate decrease of LDL
moderate increase of HDL small decrease of TG |
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bile acid resins MOA
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prevent intesinal reabsoroption of bile acids and liver has to use cholesterol to make more
|
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bile acid resins effect on lipids?
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moderate decrease of LDL
slight increase of HDL and TG's |
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main problems with bile acid resins?
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patients don't like it b/c of discomfort, decreases absorption of fat soluble vitamins and increases risk for gallstones
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ezetimibe MOA
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prevents cholesterol reabsorption at small intestine brush border
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ezetimibe effect on lipids
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ONLY a moderate decrease of LDL
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MOA of fibrates
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upregulate LPL which increases TG clearance
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SE of fibrates
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myositis
hepatotoxicity cholesterol stones |
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fibrates effects on lipids?
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small decrease of LDL
small increase of HDL large decrease in TG's |
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i want to decrease TG's
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fibrates
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i want to decrease LDL's
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HMB CoA reductase inhibitor
|
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I want to increase HDL and decrease LDL
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Niacin
|
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i want to decrease LDL and am willing to sacrifice a bit of TG increase
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bile acid resins
|
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class IV MOA?
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primarily affect AV nodal cells which decreases conduction velocity, increases ERP and PR interval
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class IV antiarrhythmics used for
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preventing nodal arrhythmias
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outside of the heart what are Ca channel blockers good for?
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reduce muscle contractility - so HTN, angina, Raynauds
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which calcium channel blockers better for the heart?
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V for Ventricle V for Verapamil
Verapamil > Diltiazem > Nifedipine |
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which of the calcium channel blckers better for vasc smooth muscle?
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nifedipine>diltiazem>verapamil
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main toxicity of digoxin?
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cholinergic - N/V/D blurry yellowed vision. tons of ECG changes
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class II antiarrhythmics
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propranolol, esmolol, metoprolol, atenolol, timolol
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i want to decrease LDL and am willing to sacrifice a bit of TG increase
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bile acid resins
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Class II antiarrhythmic MOA
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decreases cAMP shich decreases calcium currents.
suppress abnormal pacemakers by decreasing the slope of phase 4 |
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class IV MOA?
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primarily affect AV nodal cells which decreases conduction velocity, increases ERP and PR interval
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what part of the heart is particularly sensitive to beta blockers?
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AV node so increases PR interval
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class IV antiarrhythmics used for
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preventing nodal arrhythmias
|
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outside of the heart what are Ca channel blockers good for?
|
reduce muscle contractility - so HTN, angina, Raynauds
|
|
which calcium channel blockers better for the heart?
|
V for Ventricle V for Verapamil
Verapamil > Diltiazem > Nifedipine |
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which of the calcium channel blckers better for vasc smooth muscle?
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nifedipine>diltiazem>verapamil
|
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main toxicity of digoxin?
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cholinergic - N/V/D blurry yellowed vision. tons of ECG changes
|
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class II antiarrhythmics
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propranolol, esmolol, metoprolol, atenolol, timolol
|
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Class II antiarrhythmic MOA
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decreases cAMP shich decreases calcium currents.
suppress abnormal pacemakers by decreasing the slope of phase 4 |
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what part of the heart is particularly sensitive to beta blockers?
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AV node so increases PR interval
|
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use of beta blockers in arrhythmias?
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V tach, SVT, slowing ventriuclar rate in atrial fibrillation adn flutter
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sotalol class?
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potassium channel blocker - class III antiarrhythmic
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ibutilide class
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potassium channel blocker - class III antiarrhythmic
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bretylium class
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potassium channel blocker - class III antiarrhythmic
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dofetilide class
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potassium channel blocker - class III antiarrhythmic
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amiodarone class
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potassium channel blocker - class III antiarrhythmic
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class III have what effects?
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increase AP duration, increase ERP, increase QT interval
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when are class III antiarrhythmics used
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when others fail
|
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amiodarone main toxicities?
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remember to check PFT's, LFT's, TFT's
pulmonary liver thyroid |
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effective pharmoccologic agent for WPW
|
amiodarone
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