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USMLE
CV 6
| Question | Answer |
|---|---|
| flow of blood through PDA? | aorta to left pulmonary artery |
| ACE inhibitors can cause what type of electrolyte disturbance? | hyperkalemia |
| small mass on mitral valve with finger-like projections; non-neoplastic | papillary fibroelastoma |
| calcium channel blocker associated with accelerated progression of CHF? | verapamil |
| drug to slow ventricular response in Wolff-Parkinson White? | ibutilide |
| hypersensitivity angiitis or microscopic polyarteritis nodosa (can be caused by penicilin) | leukocytoclastic angiitis |
| in which part of the systemic circulation does the greatest decrease in blood pressure occur? | arterioles |
| vasodilator with lupus-like syndrome as side effect? | hydralazine |
| mechanism of hydralazine? | increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload |
| what calcium channel blocker is most selective for peripheral vasculature? | nifedipine |
| mechanism of calcium channel blockers? | block voltage-dependent L-type calcium channels of cardiac and SM and thereby reduce contractility |
| which calcium channel blocker is not used to treat arrhythmias? | nifedipine |
| what is the goal of antianginal therapy? | reduce myocardial O2 consumption by decreasing 1 or more of the determinants of MVO2: EDV, BP, HR, contractility, ejection time |
| what do nitrates affect in antianginal therapy? | preload |
| what happens to contractility and HR in nitrate therapy? | increase - reflex response |
| what do beta blockers affect in antianginal therapy? | afterload |
| how do nitrates affect ejection time and MVO2? | decrease |
| how do beta blockers affect ejection time? | increase it |
| what do beta blockers do to EDV? | increase it |
| what do beta blockers do to BP, contractility, and HR? | decrease them |
| what is digitoxin used for? | CHF (increases contractility) and atrial fibrillation (decreases conduciton at the AV node) |
| toxicities of digitoxin are increased by what? | renal failure, hpokalemia, and quinidine |
| blurry yellow vision is side effect of what? | digitoxin |
| what is the antidote for digitoxin? | slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments |
| lupus-like syndrome is associated with what class IA antiarrythmic? | procainamide |
| what are the class IA antiarrythmics? | Na+ channel blockers: quinidine, amiodarone, procainamide, disopyramide (queen amy proclaims disco pyramids) |
| this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval) | quinidine |
| what class of antiarrhythmics are contraindicated post-MI | class IC - proarrhythmic |
| what beta blocker is very short acting? | esmolol |
| what is the antiarrhythmic action of beta blockers? | decrease cAMP and calcium currents; suppress abnormal pacemaker by decreasing slope of phase 4 - AV node particularly sensitive - increased PR interval |
| toxicity of amiodarone? | pulmonary fibrosis, hepatotoxicity, hypo/hyperthroidism;corneal deposits, skin deposits resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF |
| K+ channel blockers that can cause torsades de pointes | soltalol, ibutilide |
| K+ channel blocker that can cause new arrhythmias and hypotension? | bretylium |
| wha type of cells do Ca2+ channel blockers primarily affect? | AV nodal cells |
| what type of antiarrhythmics are used for prevention of nodal arrhythmias? | class IV - Ca2+ channel blockers |
| what class IV antiarrhythmic can cause torsades de pointes? | bepridil |
| what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias? | adenosine |
| what depresses ectopic pacemakers, especially in digitoxin toxicity? | K+ |
| Mg+ is effective for treating what? | torsades de pointes and digitoxin toxicity |
| drug for hypertension in patient with PKD? | ACE inhibitor |
| anti-hypertesive for pregnant woman? | methyldopa |
| in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do? | enhance transmission through accessory pathways that can predispose to v-tach |