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37 Cards in this Set
- Front
- Back
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what are the 2 general treatments for CAD? |
decrease myocardial 02 demand or increase myocardial 02 supply |
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how do agents that reduce 02 demand work? |
decres HR, contractility, and ventricular wall stress (preload) |
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what do agent that treat unstable angina do? |
increase myocardial blood flow |
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name the only myocardial metabolic modulator |
ranolazine |
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name all the thrombolytics. |
t-PA, tenecteplase, reteplase, streptokinase, urokinase |
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name all the anitplatelet agents that work in platelet signaling platelet adhesion |
signaling- aspirin, clopedigrel, ticlopididne, prasugrel, adhesion- abciximab, tirofiban, eptifibatide |
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why do nitrates need to be stored specifically? |
because moisture can hydrolyze the ester bond |
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how can you tell if a nitrate is to be taken sublingually, if you look at the chemical structure? |
it should have at least two nitro groups |
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how do nitrates work? |
they are all progdrugs, the NO groups on the compound are liberated and acts like endogenous nitric oxide (not nitrous), activate guanylyl cyclase, increase cGMP, and reduces Ca, leading to smooth muscle relaxation |
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what are the nitrates primary method of alleviating symptoms of angina? why? |
venodilation, more active enzyemes in the veins to liberate the NO |
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do nitrates cause any coronary artery dilation? are there any unique effects at high doses? |
yes at high doses slight increase in TPR and increase in HR |
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how does a decrease in preload lead to a decrease in angina |
less preload = less wall tension= greater coronary artery diameter and less o2 demand=increase o2 supply=less angina |
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what can complicate the diagnosis of angina? |
biliary or esophageal spasm can cause perceived angina...true angina is pressure, while this causes pain |
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how do the BB treat angina? what are the best to treat? |
decrease the SNS to have negative chronotropy and inotropy effects, reduces 02 consumption at rest and during excercise exertional angina |
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general mechanism of a CCB? are dhp or non dhp more effective for monotherapy? |
blocks L type calcium channel to reduce heart rate, and decreases afterload non dhp |
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MOA of ranazoline? |
shifts the energy source of tthe myocardium from fatty acids to glucose which yields more ATP per o2 consumed so energy is produced more efficiently and o2 consumption is slowed |
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what is the main benefit of ranazoline? |
no hemodynamic, contraction, conduction effects |
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yup
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when using drug therapy in CAD, are we modulating the extrinsic or intrinsic pathway? |
intrinsic |
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how is fibrin created? what does it cause? |
thrombin cleaves fibrinogen to create fibrin which forms a network the stablizes the platelet |
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what is the mechanism of heparin? what two things does it inhibit? |
enhances antithrombin activity which enhances inhibiton of coagulation and prevents fibrin generation thrombin and and factor Xa |
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what exactly to platelets bind to on smooth muscle of the vasculature if it is damaged? what starts the clotting cascade? |
von willibrand factor, this starts the plug tissue factor |
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how do platelets bind/crosslink eachother? how are these recptors activated? |
via Gp IIb/IIIa receptor that are bound together by fibrinogen after they bind vWF they release TxA2 and ADP to activate the receptor |
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platelet activation leads to an increase of Ca entry and activation of PKC? what are the pivotal roles of this enzyme? |
activates more receptors for fibrinogen GpIIb/IIIa activates PLA2 which create AA which can be made into Txa2 from cox1 |
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what does TXa2 bind and what are the effects? |
binds a TP recpetor which results in more txa2 and adp to signal more platelets |
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what does ADP bind to and what are the effects? |
binds to P2y1 to start platelet activation over again binds P2y12 to reduces cAMP levels and results in more effective integrin activation and better platelet adhesion |
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what is the MOA of ASA? |
irreversibly inhibits cox1 by acetylating the active site to prevent txa2 production and decrease platele activation via TP receptor on other plateletes |
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how long do ASA effects last after d/c |
7 to 10 days |
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MOA of clopidogrel and others? how long until they work? what happens when they are discontinued? |
prodrugs, form an irreversible disulfide bond to inhibit the P2Y12 ADP receptor which increases cAMP and causes indirect inhibition of GpIIb/IIIa 2 to 8 days still get PD effect even though they are cleared, require new plateletes |
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what is unique about abciximab? |
does not have a Fc fragment, so no immune response |
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what GpIIb/IIIa inhibitor is peptide? |
eptifbatide |
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MOA of gpIIb/IIIa? |
directly inhibit platelet platelet adhesion that occurs from fibrin, fibrinogen, or vWF |
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what does plamin do? where does plasmin come from? |
digest fibrin and fibrinogen and clotting factors enothelium releases plaminogen and tissue plasminogen activator (t-PA), these both bind fibrin, and t-Pa turns plasminogen into plasmin |
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MOA of streptokinase? is it specific for fibrin? |
streptokinase binds plasminogen, conformationl change in active site, then this complex cleaves other plasminogen into plasmin, aka it turns plaminogen into t-PA no this one is not fibrin specific |
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what is urokinase? is it fibrin specific? |
a protease from kidney cells, converts plsmingoen to plasmin not fibrin specific |
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what drug is basically endogenous t-PA? what is the mutated form called? are they fibrin specific? |
alteplase, it is fibrin specific reteplase and tenecteplase |
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what is the purpose of the mutations used in reteplase and tenecteplase? |
increase half life, more specifity, resist inactivation |
