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74 Cards in this Set
- Front
- Back
drug class that prevents renin release
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Beta blockers
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drug class that blocks renin actions
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ACE-inhibitors
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drug class that blocks the increase in preload with angiotensin II
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diuretics
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drug class that blocks the increase in afterload with angiotensin II
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vasodilators
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class and adverse side effects of this antihypertensive drug: hydrochlorothiazide
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diuretic- hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
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class andadverse side effects of this antihypertensive drug: loop diuretics
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diuretic- potassium wasting, metabolic alkalosis, hypotension, ototoxicity
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class andadverse side effects of this antihypertensive drug: clonidine
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sympathoplegics- dry mouth, sedation, severe rebound HTN
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class andadverse side effects of this antihypertensive drug: methyldopa
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sympathoplegics- sedation, + coombs test
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class andadverse side effects of this antihypertensive drug: hexamethonium
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sympathoplegics- severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
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class andadverse side effects of this antihypertensive drug: reserpine
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sympathoplegics- sedation, depression, nasal stuffiness, diarrhea
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class andadverse side effects of this antihypertensive drug: guanethidine
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sympathoplegics- ortho/exercise hypotension, sexual dysfunction, headache
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class andadverse side effects of this antihypertensive drug: prazosin
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sympathoplegics- 1st dose ortho hypotension, dizziness, headache
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class andadverse side effects of this antihypertensive drug: beta blockers
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sympathoplegics- impotence, asthma, CV effects, CNS effects
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class andadverse side effects of this antihypertensive drug: hydralazine
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vasodilators- N, headache, lupus-like syndrome, reflex tachy, angina, salt retention
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class andadverse side effects of this antihypertensive drug: minoxidil
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vasodilators- hypertrichosis, pericardial effusion, reflex tachy, angina, salt retention
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class andadverse side effects of this antihypertensive drug: nifedipine, verapamil
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vasodilators- dizziness, flushing, nausea, constipation (verapamil), AV block (verapamil)
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class andadverse side effects of this antihypertensive drug: nitroprusside
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vasodilators- dcyanide toxicity (releases CN)
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class andadverse side effects of this antihypertensive drug: diazoxide
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vasodilators- hyperglycemia (reduces insulin releas, hypotension)
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class andadverse side effects of this antihypertensive drug: captopril, enalapril, fosinopril
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ACE-inhibitors- hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increase renin
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class andadverse side effects of this antihypertensive drug: losartan
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fetal renal toxicity, hyperkalemia
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MOA and AE's for hydralazine
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increase cGMP--> smooth muscle relaxation---> vasodilates arterioles> veins--> decreases afterload Aes- compensatory tachy, fluid retention, lupus-like syndrome
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MOA and AE's for minoxidil
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K+ channel opener--> hyperpolarizes and relaxes vascular smooth muscle AE's = hypertrichosis, pericardial effusion
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MOA and AE's for calcium channel blockers as antihypertensive
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block voltage-dependant L-type channels of cardiac and smooth muscle --> reduce muscle contractility. AE's = cardiac depression, peripheral edema, flushing, dizziness, and constipation
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MOA and AE's for nitroglycerin, isosorbide dinitrate
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vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation- dilates veins>>>arterioles decreases preload. AE's tachycardia, hypotension, flushing, headache. "Monday disease"
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3 drugs for malignant HTN treatment:
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nitroprusside (NO cGMP), fenoldapam (D1 agonist relaxes renal smooth muscle), diazoxide(K+ channel opener- hyperpolarizes and relaxes smooth muscle)
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goal of antianginal therapy:
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reduce myocardial O2 consumption via decreaseing one of the following: EDV, BP, HR, contractility, ejection time
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of the Ca+ channel blockers, which ones work more at vascular smooth muscle vs heart
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vascular smooth muscle- nifedipine>diltiazam>verapamil heart verapamil>diltiazam>nifedipine
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as an antianginal agent, nitrates primarily work to affect _____
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preload- thereby reducing EDV, BP, ejection time, and MVO2 consumption
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as an antianginal agent, beta blockers primarily work to affect _____
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afterload- thereby reducing BP, contractility, HR, and MVO2
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combined effect of nitrates and beta blockers on EDV, BP, HR, contractility, ejection time, MVO2:
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no effect or decreased EDV, decreased BP, decreased HR, little or no effect on contractility, little or no effect ejection time, big decrease in MVO2 consumption!!!! Yeah!!!!
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best drug at lowering LDL
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statins- HMG-CoA reductase inhibitors
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Side effects of statins
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expensive, reversible increase in LFTs, myositis
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MOA of niacin as a lipid lowering agent
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inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
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what do you coadminister with niacin to reduce side effect?
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ASA- reduces facial flushing
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MOA of cholestyramine, colestipol
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(bile acid resins) prevent intestinal reabsorption of bile acids- liver must use cholesterol to make more
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Adverse effects of cholestryamine, colestipol
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bile acid resins tast like- well, yeah- GI discomofrt, decreased absoprtion of fat soluble vitamins
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ezetimibe MOA
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prevents cholesterol reabsortion at small intestine brush border- only effects LDL
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gemfibrozil, clofibrate, bezafibrate, fenofibrate MOA
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upregulate Liproprotein lipase LPL to induce TG clearance- good at lowering triglycerides
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gemfibrozil, clofibrate, bezafibrate, fenofibrate side effects
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myositis, increas LFTs
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MOA of cardiac glycosides
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digoxin- direct inhibitor of Na/K/ATPase leads to indirect inhibition of Na/Ca+ exchanger/intipor--> increase inctracellular Ca = positive inotropy
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uses of digoxin
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CHF (increases contractility), atrial fib- decreases conduction at AV node and depression of SA node)
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ECG side effects of digoxin
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increase PR interval, decreased QT interval, scooping of ST segment, T-wave inversion
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non ECG side effects of digoxin
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increased parasympathetic activity: N, V, D, blurry yellow vision. Arrythmia. Toxicities increased by renal failure, hypokalemia potentiates effects, and quinidine (decreases clearance, displaces from tissue binding sites)
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digoxin OD antidote
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slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg++
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class I antiarrhythmics are all ____ channel blockers
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Na+
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common MOA of all Class I antiarrhythmics
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Na+ channel blockers- slow/block conduction. Decrease the slope of phase 4 depolarization and increase the threshold for firing in abnormal pacemaker cells. (state dependent)
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what are the class IA antiarrhythmics?
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Quinidine, Amiodarone (also class III), procainamide, disopyramide Queen Amy Proclaims Diso's Pyramide
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Class IA antiarrhythmics ___ AP duration, ____ effective refractory period, and ___ QT interval
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increase, increase, increase
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which class IA antiarrhythmic has a reversible SLE-like side effect?
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procainamide
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which class IA antiarrhythmic can produce cinchonism- headache, tinitis; thrombocytopenia, torsades de pointes (increased QT interval)?
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quinidine
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what are the class IB antiarrhythmics?
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Lidocaine, mexiletine, tocainide I'd Buy Lidy's Mexican tacos (phenytoin also fits this)
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what are the class IC antiarrhythmics?
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flecainide, encainide, propafenone
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what are the class II antiarrhythmics?
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propranolol, esmolol, metoprolol, atenolol, timolol (beta blockers)
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what are the class III antiarrhythmics?
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sotalol, ibutilide, bretylium, amiodarone (also class IA)
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what are the class IV antiarrhythmics?
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verapamil, diltiazem
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class IB antiarrhythmics ____ AP duration
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decrease- affect ischemic or depolarized purkinje and ventricular tissue
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uses for class IB antiarrhythmics
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acute ventricular antiarrhythmias -especially post MI- and digitalis induces arrythmias
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side effects for class IB antiarrhythmics
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local anesthetic- CNS stimulation/depression, CV depression
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class IC antiarrhythmics ____ AP duration
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have no change on
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class IC antiarrhythmics are used as a last resort in refractory ____ and intractable ____.
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Vtachs that progress to Vfib, SVT
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toxicity of class IC antiarrhythmics:
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proaarhythmic- especially post MI (contracindicated)- significantly prolongs refractory perios in AV node
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common toxicity for all class I drugs-
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hyperkalemia
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MOA for class II antiarrhythmics
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beta blockers-decrease cAMP leads to decrease Ca++ currents- suppress abnormal pacemakers by decreasing slope phase 4. AV node esp. Increase PR interval.
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clinical use of class II antiarrhythmics
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V-tach, SVT, slowing ventricular rate during a-fib and atrial flutter
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toxicity of class II antiarrhythmics
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impotence, exacerbation of asthma, bradycardia, AV block, CGF, sedation, sleep alteration. May mask signs of hypoglycemia- metoprolol can cause dysliidemia
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MOA for class III antiarrhythmics
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K+ channel blocker increase AP duration, increase ERP- used when other antiarrhythmics fail. Increased QT interval
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sotalol (class III antiarrhythmic) side effects:
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torsades de pintes, excessice beta block
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amiodarone (class IA/III antiarrhythmic)
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pulmonary fibrosis, conreal deposits, hepatotoxicity, skin deposits in photodermatitis, neuro effects, bradycardia, heart block, CHF, hypothyroidism/hyperthyroidism
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wolff--parkinson-white syndrome (class III antiarrhythmic)
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amiodarone
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what labs need to be checked when on amiodarone?
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PFTs, LFTs, TFTs (thyroid)
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MOA of class IV antiarrhythmics
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Ca ++ channel blockers affect AV nodal cells-- decreasing conduction velocity, increasing ERP, PR interval. Used in prevention of nodal arrythmias
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AE's of class IV antiarrhythmics
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constipation, flushing, edema, CHF, AV block, sinus node depression, torsades de pointes (bepridil)
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MOA of adenosine on heart
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increase K+ out of cell hyperpolarizes it. Drug of choice in diagnosing/abolishing AV nodal arrhythmias. Very short acting- flushing, hypotension, chest pain
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Mg++ is effective as an antiarrhythmic in treating ______ and _____ toxicity
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torsades de pointes, digoxin
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