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65 Cards in this Set
- Front
- Back
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classification of:
nitroglycerin |
organic nitrates
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classification of:
isosorbide dinitrite |
organic nitrates
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classification of:
isosorbide mononitrate |
organic nitrates
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classification of:
propranolol |
beta adrenergic antagonists
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classification of:
nadolol |
beta adrenergic antagonists
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classification of:
metoprolol |
beta adrenergic antagonists
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classification of:
labetalol |
beta adrenergic antagonists
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classification of:
pindolol |
beta adrenergic antagonists
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classification of:
carvedilol |
beta adrenergic antagonists
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classification of:
diltiazem |
calcium channel blocker
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classification of:
nifedipine |
calcium channel blockers
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classification of:
verapamil |
calcium channel blocker
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first drug in 15 years to treat chronic angina
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ranolazine
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prototype for organic nitrates
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nitroglycerin
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mechanism of nitroglycerin
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1. nitrates activate GC and increase cGMP which activates cGMP kinases, leading to dephosph of myosin light chain and relaxation of contractile apparatus
2.dilate all vessels |
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effects of nitroglycerin on angina tx
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1. peripheral venodilation decreases cardiac preload and myocardial wall tension
2. arterial dilation decreases afterload 3. both of these actions lower oxygen demand by decreasing the work of the heart -redistribution of coronary blood flow to subendocardial areas of the heart vulnerable to ischemia is increased in nitrate-treated pts -decrease platelet aggregation -dilation of constricted coronary vessels |
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indirect effects of nitroglycerin
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-relax smooth m of bronchi, GI tract, GU tract
-compensatory baros response -hormonal responses to dec BP -rentention of salt and water compensatory response: 1)symp discharge 2) tachycardia 3)increased contractility |
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nitroglycerin absorption
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rapid
sublingual |
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nitroglycerin metabolism
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inactive metabolites
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isosorbide dintrate metabolism
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2 active metabolites: isosorbide 2 and 5-mononitrite
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administration of nitroglycerin
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PO
topically ointments transdermal patches |
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metabolism of nitrcoglycerin
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inactive metabolites
-rapidly and efficiently by liver enzyme, glutathione organic nitrate reductase -considerable 1st pass effect -SL bypasses this effect |
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major acute effects of therapeutic vasodilation (nitroglycerin)
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orthostatis hypotension
tachycardia throbbing headache blushing and burning sensation large doses: methemoglobinemia and cyanosis |
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tolerance of nitroglycerin
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activation of guanyl cyclase is decreased by exposure to organic nitrates
partially reveresed by thiol compounds diminished release of nitric oxide plays a tole systemic compensatory mechanisms contribute |
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what effects of nitrates results in:
decreased myocardial oxygen requirement |
dec ventricular volume
dec BP dec Ejection time |
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what effects of nitrates results in:
relief of coronary artery spasm |
vasodilation of epicardial coronary arteries
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what effects of nitrates results in:
improved perfusion to ischemic myocardium |
increased collateral flow
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what effects of nitrates results in:
improved subendocardial perfusion |
decreased LV diastolic pressure
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what effects of nitrates results in:
increased myocardial osygen requirement |
reflex tachycardia
reflex increase in contractility |
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what effects of nitrates results in:
decreased myocardial perfusion |
decreased diastolic perfusion time due to tachycardia
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prototypes for beta-adrenergic antagonists
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propranolol
nadolol |
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major results of beta-adrenergic antagonist use in angina tx
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dec in frequency of angina attacks
dec in nitroglycerin consumption inc in exercise tolerance dec magnitude of S-T segment depression on ECG during exercise |
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mechanism of beta-adrenergic antagonist
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-antagonize the effect of catecholamines on the heart and thereby attenuate the myocardial response to exercise and stress
-decrease heart rate and ventricular contractility (w/ vent wall tension) determininats of myocardial oxygen demand -dec BP; dec afterload -**increase exercise tolerance and reduce frequency of angina attacks -increase in O2 supply to subendocardium of ischemic areas - due to dec in HR, inc diastolic perfusion time |
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determinants of myocardial oxygen demand
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HR
ventricular contractility ventricular wall tension |
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clinical uses of beta-adrenergic antagonists
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-frequent, unpredictable despite use of organic nitrates angina pts
-prop used with nitroglycerin -atherosclerotic angina: prop, nadol with caclium channel blockers |
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proposed mechanisms to explain antiHTN of B-blockers
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-dec CO
-CNS red sympathetic tone -inhibit renin -dec venous return and BV -dec in PVR -improvement in vascular compliance -reset baros -effects on prejunctional B-receptors : dec in NE release -attentuation of pressor response to CA with exercise and stress |
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effects of B-blockers in angina
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-dec frequency of attacks
-decrease nitro consumption -inc exercise tolerance -dec the magnitude of S-T depression during exercise |
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mechanism of Ca+ channel blockers
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produce blockade of L-type (slow) Ca+ channels, which decreases contractile force and O2 requirements
-inhibition of Ca+ entry into arterial smooth m. is assoc. with dec arteriolar tone and systemic vascular resistance (dec arterial and intraventricular pressure) |
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effect of Ca+ channel blockers
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left ventricular wall stress declines
dec HR reduce and prevent focal coronary artery spasm (variant) |
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clinical uses of Ca+ channel blockers
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variant and chronic stable angina; also used when nitrates are ineffective or when B-antags are contraindicated
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contraindications:
verampamil |
-severe LV dysfunction
-hypoTN or cardiogenic shock -sick sinus syndrome or 2/3rd degree AV-block -Atrial flutter or atrial fib -accessory bypass tract -hypersenstivity |
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contraindications:
verampamil |
-severe LV dysfunction
-hypoTN or cardiogenic shock -sick sinus syndrome or 2/3rd degree AV-block -Atrial flutter or atrial fib -accessory bypass tract -hypersenstivity |
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contraindications:
nifedipine |
known hypersensitivity to nif
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contraindications:
nifedipine |
known hypersensitivity to nif
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contraindications:
diltiazem |
-sick sinus syndrome
-2/3rd degree AV-block -hypoTN <90 systolic -acute MI -pulmonary congestion |
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effect of verapamil
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-slowed conduction thru the AV node
-AV block with b-blocker -peripheral vasodilating effects that reduce afterload and BP |
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side effects of verapamil
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toxic: myocardial depression, HF, edema
peripheral effects: headahce, reflex tachycardia, fluid retention |
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contraindications:
diltiazem |
-sick sinus syndrome
-2/3rd degree AV-block -hypoTN <90 systolic -acute MI -pulmonary congestion |
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nifedipine effects
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in peripheral vasculature: decrease afterload and lower BP
significantly less direct effect on the heart than verapamil |
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effect of verapamil
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-slowed conduction thru the AV node
-AV block with b-blocker -peripheral vasodilating effects that reduce afterload and BP |
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diltiazem used to treat
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variant angina, either naturally occuring or drug-induced and stable angina
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absorption of ranolazine
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-PO well absorbed
-t1/2 7 hours |
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side effects of verapamil
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toxic: myocardial depression, HF, edema
peripheral effects: headahce, reflex tachycardia, fluid retention |
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metabolism of ranolazine
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extensively in GI tract and liver by CYP3A4 and to a lesser degree by CYP2D6
substrate for P-glycoprotein |
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nifedipine effects
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in peripheral vasculature: decrease afterload and lower BP
significantly less direct effect on the heart than verapamil |
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mechanism of ranolazine
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inhibit the Na+ current and this may reduce the energy required for myocardial repolarization
inhibits the delayed retifier K+ current |
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diltiazem used to treat
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variant angina, either naturally occuring or drug-induced and stable angina
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absorption of ranolazine
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-PO well absorbed
-t1/2 7 hours |
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metabolism of ranolazine
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extensively in GI tract and liver by CYP3A4 and to a lesser degree by CYP2D6
substrate for P-glycoprotein |
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mechanism of ranolazine
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inhibit the Na+ current and this may reduce the energy required for myocardial repolarization
inhibits the delayed retifier K+ current |
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therapeutic uses of ranolazine
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improves exercise capacity and reduces anginal events with chronic pts
in pts who have not achieved adequate response with other drugs used with B-blockers, amlodipine, and nitrates |
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side effects of ranolazine
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nausea
constipation headache dizziness prolong QT interval (use in caution with other drugs that do this) use with caution in CYP3A4 inhibitors |
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classica angina
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O2 demand exceeds O2 supply, usually because of diminished coronary flow
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vasospastic angina
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reversible coronary vasospasm that decreases O2 supply and occurs at rest
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goal of antianginal therapy
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restore balance between O2 supply and demand in the ischemic region of myocardium
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