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USMLE - CVD Drugs
USMLE - CVD Drugs, Kaplan Pharmacology
| Question | Answer |
|---|---|
| Orthostatic hypotension | a1 block or decrease in SANS tone --> venular dilation |
| what drugs cause SLE-like syndromes? In what type of people do they occur? | Hydralazine > Procainamide > INH. In slow acetylators (can't break down/conjugate the drug). |
| Drugs that relax uterine smooth muscle | Diazoxide (vasodilator) and Ritodrine (B2 agonist) |
| -olol | B blockers |
| -prils | ACEi |
| -sartans | AT1 receptor antagonists (adrenal gland and vessels) |
| -dipines | vascular selective Ca channel blockers |
| if angina and HTN, what drug should be used? | B blockers and CCBs |
| if diabetes and HTN, what drug should be used? | ACEi and AT-1 antag |
| if CHF and HTN, what drug should be used? | ACEi and AT-1 antag |
| if post-MI and HTN, what drug should be used? | B blockers |
| if BPH and HTN, what drug should be used? | a blockers |
| if dyslipidemias and HTN, what drug should be used? | a blockers, CCBs |
| what breaks down bradykinin? | ACE |
| what does bradykinin do? | vasodilator and increases vascular permeability |
| What is a common side effect of pts on ACEi's? | cough caused by bradykinin because it is no longer metabolized by ACE since ACE is being inhibited |
| what do cardiac glycosides do for the heart? | increase contractility and vagal tone (slows the reflex tachy in CHF), stimulates B1 receptors (increases HR and conduction velocity) |
| what is the mechanism of cardiac glycosides? | binds to and inhibits Na/K ATPase --> decreases 3Na/Ca exchange --> more Ca stays in the sarcoplasmic reticulum and is available for use by actin and myosin in contraction --> increased contractility |
| digoxin is what type of drug? | cardiac glycoside from digitalis plant |
| If pt has Wolff-Parkinson-White arrhythmias, what drug should you avoid if they have CHF? | digitalis (wolves can't eat digitalis) |
| -rinone | bipyridines |
| what is the mechanism of bipyridines? | inhibit PDE --> increase cAMP --> increase contractility and vasodilation |
| milrinone and CHF | decreases survival! |
| for CHF, what drugs would you use to decrease preload? | DAAV: Diuretics, ACEi, AT-1 antag, Vasodilators |
| for CHF, what drugs would you use to decrease afterload? | AAV: ACEi, AT-1 antag, Vasodilators |
| for CHF, what drugs would you use to increase contractility? | DuBBi: Diuretics, B agnoists, bipyridines |
| what is DOC for treating CHF? | ACEi |
| what does Nesiritide do? | used in CHF, is recombinant ANF, relaxes veins and arteries by increasing cGMP |
| what is angina? | sx of ischemic heart dz (not enough O2 to the heart) |
| name the three types of angina | classic, vasospastic/Prinzmetal, unstable/crescendo |
| What is classic angina? | angina of effort/exercise due to atherosclerosis of the coronary vessels |
| what is Prinzmetal/vasospastic angina? | decrease in coronary blood flow that is reversible |
| what is unstable angina? | not enough O2 due to platelet aggregation |
| what are the three things you want to do to treat CHF? | decrease preload, decrease afterload, increase contractility |
| what are the two things you want to do for classic/vasospastic angina? | increase O2 delivery or decrease O2 requirement |
| What drugs would you use to increase O2 delivery to anginal heart? | decrease vasospasm with CaCB and nitrates |
| What drugs would you use to decrease O2 requirement in anginal heart? | decrease TPR and/or decrease CO with CaCB, nitrates, and B blockers |
| what is contraindicated for the administration of nitrates? | sildenafil (viagra) |
| what is methemoglobin? | a form of Hb (Fe3+ instead of Fe2+) that doesn't bind O2 --> anemia and tissue hypoxia |
| what is the mechanism of sildenafil? | inhibits PDE5 --> increases cGMP --> vasodilation --> increase blood flow to corpora cavernosa --> strengthen eretile response |
| Why shouldn't sildenafil be used with nitrates | both are vasodilators --> excessive decrease in BP --> sudden death |
| what causes torsades? | anything that prolongs phase III of the action potential (repolarization, K+ channels) |
| acetazolamide | carbonic anhydrase inhibitor --> diuretic |
| what does acetazolamide do in terms of electrolytes? | CAi's inhibit HCO3- absorption in the proximal convoluted tubule (PCT) --> decreases Na absorption in PCT --> increases the load of Na to be reabsorbed later in the tube --> hyperCl-, hyperCa+, hypoK+, acidosis (because you lose a lot of HCO3-) |
| furosemide | loop diuretic (thick ascending limb), inhibits Na/Cl/K cotransporter |
| what does furosemide do in terms of electrolytes? | hypoCa2+, hypoMg2+, hypoK+, alkalosis (lose H+) |
| hydroclorothiazide | thiazide diuretic, inhibits Na/Cl cotransporter in distal convoluted tubule |
| what does hydrochlorothiazide do in terms of electrolytes? | hypoK+, alkalosis, hypo Cl-; possible hyperCa2+ due to increased PTH levels trying to maintain blood Ca2+ levels |
| spironolactone | K-sparing, aldosterone receptor antagonist |
| amiloride | K-sparing, Na channel blocker in CT |
| triamterene | K-sparing, Na channel blocker in CT |
| K sparing diuretics cause what? | retention of K+ and H+ ions, loss of Na+ |
| mannitol | osmotic diuretic - inhibits the reabsorption of H2O in the PCT |
| what is cinchonism? | tinnitus, hallucinations, dizzy, nausea, bothered by bright lights, diplopia |
| what is cinchonism caused by? | quinidine (class IA antiarrhythmic) or quinine (anti malarial) |
| quinidine | class 1A anti arrhythmic, causes cinchonism |
| procainamide | class 1A anti arrhythmic |
| lidocaine | class 1B anti arrhythmic |
| phenytoin | class 1B anti arrhythmic |
| flecainide | class 1C anti arrhythmic |
| propranolol | B blocker, Class II anti-arrhythmic |
| acebutolol | B blocker, Class II anti-arrhythmic |
| esmolol | B blocker, Class II anti-arrhythmic |
| bretylium | Class III anti-arrhythmic |
| amiodarone | Class III anti-arrhythmic |
| verapamil | CaCB, Class IV anti-arrhythmic |
| diltiazem | CaCB, Class IV anti-arrhythmic |
| adenosine | anti arrhythmic, DOC for AV node arrhythmias and PSVT's (causes membrane hyperpolarization -- K+ flows out of cell) |
Created by:
christinapham
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