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CV Pharm (merged123)
CV Pharm (Merged former CV Pharm 1, 2, 3)
| Question | Answer |
|---|---|
| sotalol toxicity | torsades, excessive beta-block |
| ibutilide toxicity | torsades |
| bretylium toxicity | new arrhythmias, hypotension |
| amiodorone toxicity | hypothyrodism/hyperthyrodism, pulmonary fibrosis, hepatic toxicity, corneal deposits, skin deposits (photodermatitis), neurologic defects, constipation, bradycardia, heart block, chf |
| what 3 tests to do before using amiodarone? | PFT, LFT, TFT |
| name 2 class IV antiarrhytmics | verapamil, diltiazem |
| mechanism for class IV antiarrhythmics | blocks Ca channels; affect AV nodal cells, decrease conduction velocity, incrase ERP, increase PR. |
| what are class IV antiarrhythmics used for | prevent nodal arryhtmias (SVT) |
| what are 4 general side effects for class IV | constipation, flushing, edema, cv (chf, av block, sinus node depression) |
| bepridil toxicity | torsades |
| adenosine function | hyperpolarizes cells by facilitating K movement out of cells. drug of choice in diagnosing/abolishing AV nodal arryhtmias |
| potassium function | depress ectopic pacemaker, esp in dig toxicity |
| magnesium function | torsades and dig toxicity use |
| what are the adverse effects of nifedipine and verapamil? (5) | dizziness, flushing, nausea (verapamil also has constipation and AV block) |
| adverse effects of Diazoxide? | hypoglycemia - reduces insulin release |
| what is the first-line treatment of hypertension in pregnancy? | hydralazine with methyldopa |
| what is the mechanism of minoxidil? | K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
| what is the toxicity of minoxidil? | hypertrichosis, pericardial effusion |
| what is the treatment for malignant hypertension? | nitroprusside, fenoldopam and diazoxide |
| what is the mechanism of action of fenoldopam? | Dopoamine D1 receptor agonist --> relaxes renal vascular smooth muscle |
| what is the mechanism of diazoxide? | K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
| what are the HMG-CoA reductase inhibitors? | lovastatin, pravastatin, simvastatin, atorvastatin |
| What effects do the statins have on LDL, HDL and TGs? | greatly decreases LDL, increases HDL and decreases TGs |
| what is the mechanism of action of the Statins? | inhibit cholesterol precursor, mevalonate |
| side effects of statins? | reversible increase in LFTs and myositis |
| What effect does Niacin have on LDL, HDL and TGs? | decreases LDL, increases HDL, lesser decrease in TGs |
| what is the mechanism of action of niacin? | inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation |
| what effect do the Bile acid resins have on LDL, HDL, and TGs? | decrease LDL, slight increase in HDL, slight increase in TGs |
| what are the bile acid resins? | cholestyramine, colestipol |
| what is the mechanism of action of cholestyramine and colestipol? | prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more |
| what are side effects of cholestyramine and colestipol? | bad taste, causes GI discomfort, decreased absorption of fat-soluble vitamins |
| What effect does ezetimibe have on LDL, HDL and TGs? | decreases LDL; no effect on others |
| what is the mechanism of action of ezetimibe? | prevents cholesterol reabsorption at small intestine brush border |
| What are the Fibrates? | gemfibrozil, clofibrate, bezafibrate, fenofibrate |
| what effect do the fibrates have on LDL, HDL and TGs? | mainly decrease TGs, lesser decrease LDL and increase HDL |
| what is the mechanism of action of the fibrates? | upregulate LPL --> increase TG clearance |
| what are the side effects of fibrates? | myositis, and increase in LFTs |
| what Beta blockers are contraindicated in angina and why? | labetalol, pindolol and acebutolol, due to partial agonist effects |
| goal of antianginal therapy | reduce myocardial oxygen consumption |
| name 5 determinants of antianginal therapy | end diastolic volume, blood presure, heart rate, contractility, and ejection time |
| how do nitrates effect end diastolic volume, blood pressure, contractility, heart rate, and ejection time | decrease EDV, decrease BP, increase contractility (reflex), increase HR (reflex), decrease Ejection time |
| how does beta-blocker affect end-diastolic volume, blood pressure, contractility, heart rate, ejection time | increase EDV, decrease BP, decrease contractility, decrease HR, increase ejection time |
| name 3 factors that combo beta-blockers + nitrates will decrease | blood pressure, heart rate, and overall myocardial oxygen consumption |
| for calcium channel blockers, what drug is similar to nitro | nifedipine |
| for calcium channel blockers, what durg is similar to beta-blockers | verapamil |
| define bioavailability, protein bound percentage, where excreted, and 1/2 life for digoxin | 75% availability, 20-40% bound, excreted in kidney, 40 hours t(1/2) |
| mechanism for digoxin | block Na/K ATPase, increase Na, slow Na/Ca antiport, increases Ca in ECM, positive inotrope |
| how does digoxin affect ECG readings | vagal effects increase PR, decrease QT, T wave inversion on ECG, and scooping of ST segment |
| name 2 uses for digoxin | CHF (increase contractility) and A-Fib (decrease conduction at AV node) |
| 5 major general digoxin side efects | nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia |
| name 3 contraindications with digoxin | renal failure, quinidine (will displace dig on protein, potentiate effect), hypokalemia (potentiate effect) |
| what is the antidote for digoxin | slowly normalize K, lidocaine, cardiac pacer, anti-dig Fab fragments |
| describe function that all class I antiarrhythmics have | decrease slope of phase 4 depolarization by blocking Na channels |
| define state dependency and state what drugs are state dependent | class I antiarryhtmics. selectively depress tissue that is depolarized |
| name 4 class Ia antiarrhythmics | Queen Amy Proclaims Diso's pyramid: quinidine, amiodarone, procainamide, disopyramide |
| name 3 mechanisms of class Ia antiarrhythmics | increase AP duration, increase ERP, increase QT interval |
| what do you use class Ia antiarrhythmics for? | atrial and ventricular arrhythmias |
| quinidine toxicities | cinchonism: headache, tinnitisum, thrombocytopenia plus torsades |
| procainamide toxicity | reversible lupus like side effect |
| name 3 class IB antiarrhythmics | lidocaine, mexiletine, tocainide |
| mechanism for class IB | decrease AP duration by blocking Na channel |
| where does class IB affect? | affect ischemic or depolarized purkinje and ventricular tissue. |
| what is class IB useful for? | acute ventricular arrhythmias (post-MI) and digitalis induced arrhythmia |
| name 4 side effects of class IB | local anesthetic, cns stimulation, cns depression, cardiovascular depression |
| name 3 class IC antiarrhythmics | flecainide, encainide, propafenone |
| name mechanism of class IC | no effect on AP |
| what is class IC sueful for? | v-tach that progress to V fib and also for SVT. usuaully only last resort for refractory tachyarrhythmias |
| class IC toxicities | proarrhythmitic, especially post-MI (contraindiciated) |
| name 5 class II antiarrhythmics | propanolol, esmolol, metoprolol, atenolol, timolol |
| mechanism of class II antiarrhythmics | Beta-blockers; decrease cAMP, decrease Ca currents, decrease slope phase 4, increase PR interval at AV node |
| what is a short acting class II | esmolol |
| name 5 side effects of class II drugs | mask hypoglycema, impotence, asthma, CV effects (bradycardia, av block, chf). sleep alterations |
| name 4 class III antiarrhythmics | sotalol, ibutilide, bretylium, amiodarone |
| mecanism of class III | block K channels; increase AP duration, increase ERP, increase QT, used when others fail |
| 5 major side effects for hydrochlorothiazide | hypokalemia, slight hyperlipidemia, hyperuricemia, hypercalcemia, hyperglycemia |
| 4 major side effects for loop diruetics | potassium wasting, metabolic alkalosis, ototoxicity, hypotension |
| clonidine side effects (2) | dry mouth, severe rebound hypertension |
| methyldopa side effects (2) | sedation, positive Coombs test |
| hexamethonium side effects (4) | severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction |
| reserpine side effects (4) | sedation, depression, nasal stuffiness, diarrhea |
| guanethidine side effects (4) | orthostatic/exercise hypotension, sexual dysfunction, diarrhea |
| prazosin side effects (3) | 1st-dose orthostatic hypotensoin, dizziness, headache |
| beta-blocker major side effects (6) | asthma, impotence, sleep problems, bradycardia, CHF, AV block |
| hydralazine side effects (4) | lupus like syndrome, reflex tachycardia, angina, salt retention |
| minoxidil side effets (5) | hair, pericardial effusion, reflex tachycardia, angina, salt retention |
| vasodilator: calcium blocker side effects (3) | flushing, constipation, nausea |
| nitroprusside major side efect | cyanide toxicity |
| captopril side effects (8) | hyperkalemia, cough, angioedema, proteinuria, taste changes, hypotension, pregnancy problems (fetal renal damage), rash |
| ARB side effect (losartan) | fetal renal toxicity, hyperkalemia |
| two drugs that cause hyperkalemia | losartan and captopril |
| what do you have to do with hydralazine and minoxidil? | use beta blockers to treat reflex tachy, diuretic to block salt retention |
| mechanism of hydralazine | increase cGMP, smooth muscle relaxation, vasodilation, afterload reduction |
| hydralazine selectively dilates which vessels? | arterioles |
| clinical use for hydralazine (2) | severe hypertension, CHF, first-line therapy for HTN in pregnancy |
| mechanism for clonidine | alpha2 agonist |
| mechanism for methyldopa | alpha2 agonist |
| mechanism for prazosin | alpha1 blocker |
| mechanism for reserpine | blocks re-uptake of NE, E and Serotonin back into pre-synaptic vesicles --> allows degradation by MAO |
| mechanism for guanethidine | blocks the release of catecholamines from the presynaptic terminal by inhibiting Mg/ATPase dependent pump |
| what is the mechanism of hexamethonium? | it is a neronal ACh receptor antagonist in autonomic ganglia |
| name 3 calcium channel blockers | nifedipine, verapamil, diltiazem |
| mechanism of calcium blockers | block voltage-dependent calcium channels on cardiac/smooth muscle and reduce muscle contractility |
| rank vascular smooth muscle block by calcium blocker | nifedipine>diltiazem>verapamil |
| rank heart smooth muscle block by calcium blocker | verapamil>diltiazem>nifedipine |
| use for calcium blockers | hypertension, angina, arrhythmia (not nifedipine) |
| calcium blocker toxicity (3) | cardiac depression, peripheral edema, flushing, |
| mechanism for nitro drugs | vasodilate by releasing nitric oxide, increase cGMP, smooth muscle relaxation, decrease preload |
| rank the preference for dilation of vascular beds in nitro drugs | veins >> arterioles |
| clinical use for nitro drugs (4) | angina, pulmonary edema, aphrodisiac, erection enhancer |
| name side effects for nitro (4) | tachycardia, hypotension, headache, monday disease |
| define monday disease | build tolerance to nitro during occupational exposure, resensitize on weekend and get tachy and dizzy when returning to work Monday |
Created by:
doctaJ1230
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