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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 |