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Cardiovascular Pharm
First Aid: Cardiovascular Pharmacology
| Question | Answer |
|---|---|
| This diuretic, in addition to being known for potassium wasting, can also be ototoxic. | Furosemide |
| This diuretic, in addition to being known for potassium wasting, can also cause hypercalcemia. | Hydrochlorothiazide |
| This adrenergic agonist is notable for severe rebound hypertension. | Clonidine and Methyldopa; centrally acting alpha 2 agonist suppresses sympathetic outflow |
| This adrenergic agonist is notable for postive Coomb's test leading to hemolytic anemia. | Methyldopa |
| This ganglionic blocker no longer in use had a preference for preganglionic nicotinic receptors. | Hexamethonium |
| This vasodilator which increases cGMP leading to smooth muscle relaxation (arterioles>veins) is notable for a lupus-like side effect. | Hydralazine; first line for HTN in pregnancy w/ methydopa |
| This vasodilator with a preference for veins is related to cyanide toxicity. | Nitroprusside |
| This antihypertensive is associated with fetal renal toxicity. | ACE inhibitors |
| These drugs block voltage dependent L-type calcium channels of cardiac and smooth muscle to reduce contractility. Which one is not used to treat arrhythmias? | Verapimil, diltiazem, nifedipine; Nifedipine is not used on arrhythmias |
| This drug increases cGMP leading to smooth muscle relaxation (veins>arterioles). | Nitroglycerin |
| Why are beta blockers and nitrates commonly used together? | Beta blockers reduce the baroreceptor response which is initated by the drop in blood pressure seen with nitrates. |
| This lipid lowering agent decreases LDL and triglycerides (LDL > TG) while increasing HDL. Notable side effect is myositis. | Statins (HMG-CoA reductase inhibitor) |
| This lipid lowering agent decreases LDL and triglycerides while increasing HDL. Notable side effect is flushing. | Niacin |
| This lipid lowering agent decreases LDL, mildly elevates TG's and has no effect on HDL (patients hate it). | Bile acid resings (cholestyramine and colestipol); patients hate it cuz it tastes bad |
| This lipid lowering agent decreases LDL and has no effect on HDL or TG's. May raise LFT's | Ezetimibe (cholesterol absorption blocker) |
| This lipid lowering agent decreases LDL and triglycerides (TG > LDL) while increasing HDL. Notable side effect is myositis. | Fibrates (gemfibrozil, clofibrate); Similar action on lipids and SE to statins but they decrease LDL>TG's |
| These antiarrhythmics are used to treat both atrial and ventricular arrhythmia's expecially reentrant and ectopic SVT and ventricular tachycardia. | Class 1A; sodium channel blockers (Quinidine, amiodarone, procainamide, disopyramide); increase QT interval so can cause torsade de pointes |
| Patient presents with headache, tinnitus, and thrombocytopenia. History of arrhythmia. Diagnosis? | Cinchonism from qunidine toxicity |
| This antiarrhythmic is notable for a lupus like syndrome. | Procainamide; |
| These antiarrhythmics decrease cAMP leading to lowered calcium current, suppressing automaticity of pacemakers resulting in prolonged conduction through the AV node. | Class II; Beta blockers (propranolol, esmolol, metoprolol); esmolol is very short acting |
| These agents seek to decrease the action potential duration and are useful in ventricular arrhythmias as well as digitalis induced arrhythmias. | Class IB; Na channel blockers (lidocaine, mexiletine, tocainide) |
| These drugs of last resort is used to treat refractory ventricular arrhythmias and rapid atrial arrhthmias associated with WPW. | Class IC; flecainide, propafenone, encainide (proarrhythmic, especially post MI) |
| These drugs of last resort are used to treat recurrent ventricular arrhythmias, but may precipitate torsade de pointe arrhythmias. | Class III; potassium channel blockers (sotalol, ibutilide, bretylium, amiodarone) |
| This class III antiarrhythmic has the notable side effects of pulmonary fibrosis and corneal microdeposits. | Amiodarone |
| This extremely short acting agent is the drug of choice in diagnosing/abolishing AV nodal arrhythmias. | Adenosine |
| This agent depresses ectopic pacemakers, especially in digoxin toxicity. | Potassium |
| This agent is effective in treating torsade de pointes and digoxin toxicity. | Magnesium |
| This drug is used for treatment of ventricular arrhythmias following MI because it works only on ischemic tissue. | Lidocaine |
| This antihypertensive blocks the release of norepinephrine by displacing it from intracellular vesicles. | Guanethidine |
| This rarely used antihypertensive agent blocks the storage and release of catecholamines and serotonin from neurons. | Reserpine |
| This antihyperlipidemic agent may prevent atherosclerosis by acting as an antioxidant. | Probucol |
Created by:
rahjohnson
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