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USMLE - More CVD, Pharm, Path, etc.

N-acetyltransferase is a Phase I or Phase II drug metabolism reaction? Phase II
How is procainamide metabolized? N-acetyltransferase (Phase II)
Slow acetylators on procainamide can develop what? drug induced SLE-like symptoms
Slow acetylators taking what types of drugs can develop SLE-like symptoms? All drugs metabolized by N-acetyltransferase can produce SLE-like sx's (procainamide, INH, hydralazine)
amiodarone Class III anti-arrhythmic, blocks K channels and slows repolarization
what do we have to monitor when administering amiodarone? PFTs (pulm), LFT's (liver), TFT (thyroid)
with which drug would you get smurf skin? amiodarone
which anti-arrhythmic would you use for Wolff Parkinson White syndrome? amiodarone
Most common lidocaine toxicity CNS dysfunction (drowsiness, excitation, seizures) because it can enter the CNS -- only given IV
why is the use of propranolol particularly good for hyperthyroidism? 1. opposes SANS stimulatory effect 2. inhibits 5'deiodinase --> prevents conversion of T4 to T3
why is metoprolol better than propranolol in some patients? met is B1 selective --> doesn't block B2 functions to cause bronchoconstriction
drugs that have both a and B antagonist actions carvedilol and labetalol
what do CaCB's do to the heart? decreases contractility
digoxin toxicity would include hyper or hypo K+? cardiac glycosides inhibit the Na/K ATPase, so it would inhibit K+ from coming into the cell --> increased K+ in the blood --> hyPERK+
what are some digoxin toxicity sx's? GI distress (nausea), EKG changes (premature ventricular beats, bigeminy), visual abnormalities such as halos around lights
why does having high levels of K+ in blood complicate digitalis toxicity? high K+ can lead to reentrant arrhythmias
what is bigeminy repeated sequence of abnormal followed by normal beat
nimodipine CaCB, the only FDP approved drug for subarachnoid hemorrhage; vasodilates cerebral vascular beds; prevents post-hemorrhagic vasospasm
cholestyramine bile acid sequester --> decrease bile acids in liver --> no more inhibition of 7a-hydroxylase --> liver uses cholesterol to synthesize more bile acids --> more LDL uptake --> less LDL in plasma
what does cholestyramine do to LDL, HDL, TG plasma levels? decreases LDL, increases both HDL and TG
ecainide class 1C anti arrhythmic
what does niacin do to VLDL, cholesterol, TG's and HDL? decreases VLDL --> decreases in cholesterol and TG's; increases HDL more than any other antihyperlipidemic drug
what is a common side effect of HTN meds? sexual dysfunction
which HTN drug can cause severe depressive disorder? reserpine. It decreases NE packaging into storage granules, but also depletes the brain of amines (NE and serotonin). Low levels of NE/serotonin --> depressive sx's
what are the two main effects of ANGII? vasoconstriction via AT1 receptors and increased aldosterone formation
what are the side effects of increased bradykinin? cough and angioedema
if post-MI and HTN, what drug should be used? B blockers
if post-MI and ventricular arrhythmia, what drug should be used? IV lidocaine (Class 1B concentrate on ventricular muscle and lidocaine focuses on ischemic tissue)
what drug to use for supraventricular and nodal tachycardias? Adenosine
what drugs to use on atrial arrhythmias? ventricular arrhythmias? adenosine for atrial, lidocaine for ventricular
where do B blockers act when treating arrhythmias? AV node
where do CaCB's act when treating arrhythmias? AV node
what should diabetics with HTN always be on? ACEi's -- slows the progression of diabetic nephropathy
don't prescribe losartan for which patients? pregnant patients -- teratogenic effects
don't prescribe ACEi's for which patients? pregnant patients -- teratogenic effects
what is pheochromocytoma? tumors of the adrenal gland --> excess adrenaline
congenital defects such as uni/bicuspid aortic valve causes what? aortic stenosis
L ventricular hypertrophy - aortic insuff or stenosis? either/both
crescendo decrescendo murmur aortic stenosis
tardus et parvus aortic stenosis
L ventricular dilation- aortic insuff or stenosis? aortic insuff due to increased preload
how do you tell the difference between chronic and acute aortic insufficiency? chronic - dilation of L ventricle; acute - pulmonary edema because everything is backed up into the lungs
wide pulse pressure aortic insufficiency
water-hammer pulse aortic insufficiency
Austin Flint rumble aortic insufficiency
diastolic and systolic murmur aortic insufficiency
caused by rheumatic heart disease mitral stenosis
L atrial hypertrophy and dilation mitral stenosis
systolic murmur mitral insuff or aortic stenosis
diastolic murmur mitral stenosis or aortic insuff
jugular venous distension think mitral stenosis
prominent a wave greater pressures in atrial contraction - mitral stenosis
RV hypertrophy mitral stenosis
L atrial enlargement and L ventricular dilation mitral insufficiency
increased preload and decreased cardiac output mitral insufficiency
very high v-wave mitral insufficiency due to increased volumes in both LA and LV
c wave ventricular contraction that closes the mitral and tricuspid valves
holosystolic mumur mitral insufficiency
mid-systolic click mitral valve prolapse in mitral insufficiency
Created by: christinapham
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