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USMLE - CVD Stuff
USMLE - More CVD, Pharm, Path, etc.
| Question | Answer |
|---|---|
| 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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