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CV Pharm (merged123)

CV Pharm (Merged former CV Pharm 1, 2, 3)

QuestionAnswer
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