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MOA of anti platelet actions of aspirin
irreversibly inhibiting the enzymes COX1 and COX2 --> prevents formation of the platelet-aggregating agent thromboxane and suppress platelet function for its lifetime
how long do aspirin action affect the platelet?
the platelet's lifetime --> approx. 10 days
what are the indications for aspirin antiplatelet therapy?
-acute coronary syndromes (unstable angina and MI)
-post-ACS --> secondary prevention of Cv death, MI, and stroke
-stable angina --> reduces risk of MI or sudden death
-TIA or minor noncardioembolic stroke --> reduces risk of stroke or death, MI
-post-coronary stent --> prevents stent thrombosis
what formulation of aspirin is preferred for acute coronary syndrome?
why should you avoid enteric coated aspirin?
unpredictable release and no guarantee as to how long it will take to begin working
-if MI is occurring, immediate platelet inhibition needs to be achieved
What is the major ADR of aspiring?
what are the associated drug interactions for aspirin?
-primarily has additive drug-drug interactions that increase risk of bleeding:
what is the major warning related to aspirin use in children and teenagers?
taken with viral infection --> at risk for Reyes Syndrome
what is Reyes syndrome?
rapidly progressive encephalopathy with hepatic dysfunction that begins days after recovery from a viral illness
what are signs and symptoms of reyes syndrome?
vomiting, fatigue, confusion, seizures/coma
what are the GI- related effects of aspirin?
dyspepsia, heartburn, nausea
what are the methods for reducing GI-related side effects of aspirin?
-use enteric coated aspirin to limit dyspepsia (will not reduce bleeding)
-take with food
what is the MOA for oral dipyridamole?
-increase level of cAMP in platelets by 1) blocking the reuptake of adenosine 2) inhibiting phosphodiesterase-mediated cAMP degradation
-by promoting calcium uptake, cAMP reduces intracellular levels of calcium which inhibits platelet activation and aggregation
what are the approved indications for oral dipyridamole?
heart valve replacement: prevention of post-op thromboembolic complications
-used as an adjunct to warfarin
does ticlopidine have cross-reactivity with aspirin?
does clopidogrel have cross-reactivity with aspirin?
what is the MOA for ticlopidine?
irreversible platelet aggregation inhibitor --> inhibits preimary and secondary phases of aggregation induced by ADP and fibrinogen
-inhibits ADP-induced platelet-fibrinogen binding and blocks that action of fibrinogen that links platelets to form an aggregated plug
what is the MOA for clopidogrel?
-ADP-selective platelet aggregation inhibitor with 3 times the potency of ticlopidine
-irreversibly inhibits ADP-induced aggregation by inhibiting the binding of AMP to its P2Y12 receptor
-prevent subsequent activation of GCP 2b/3a
what is the incidence of severe hematological ADR of ticlopidine?
-can cause life threatening adverse reactions (7%) including: neutropenia/agranulocytosis, thrombotic thrombocytopenia purport (TTP), aplastic anemia
-should be reserved for patient who are intolerant or allergic to aspirin
what is the incidence of severe hematological Air of clopidogrel?
-much lower incidence of bleeding disorders (2%)
-lower incidence of neutropenia
what is the efficacy of ticlopidine compared to aspirin?
-equally as effective
-has a higher cost and toxicity
what is the efficacy of clopidogrel compared to aspirin?
marginally more effective than aspirin, but safer than ticlopidine
-3-4 days required for maximal activity
what are the potential problems for patients taking clopidogrel if they are deficient in the normal amount of CYP2C19?
-significantly reduced responses to clopidogrel and an increased risk for death, MI, or stroke compared to patients without these variants
-loss of function or decreased amount of P450 isoenzyme --> clopidogrel cannot be activated
what are the potential problems for patients taking clopidogrel if they are taking omeprazole or esomeprazole concurrently?
the PPI omeprazole inhibits 2C19 and may reduce the anti platelet effect by blocking the formation go the active metabolite (up to 50%), even if drugs are given 12 hours apart
what are the indications for combined aspirin/clopidogrel therapy?
-ACS medically treated with no fibrinolysis or revascularization
-STEMI treated with fibrinolysis
what is the MOA for eptifibatide and tirofiban?
-reversible receptor blockers
-inhibit the final step in platelet aggregation by: 1) blocking the platelet GCP 2b/3a receptor on platelets 2)inhibits cross-binding of fibrinogen across platelets
what are the indications for eptifibatide and tirofiban?
-treatment of ACs
-patients undergoing percutaneous coronary intervention, with to without stent placement --> reduced risk of death, new MI, or refractory ischemia
what is the MOA of abiximab?
irreversible receptor blockade that inhitbis platelet aggregation by binding to GCP 2b/3a platelet receptor sites involved in binding of fibrinogen, vWF, and other adhesive factors
what is the indication for abiximab?
-used as an adjunct to PCI for the prevention of cardiac ischemic complications
-patients with unstable angina not responding to conventional medical therapy when PCI is planned within 24 hours
-given with heparin
what is the MOA of vorapaxar?
-PAR1 is the primary receptor for thrombin which is the most potent platelet activator
-inhibits the PAR1 receptors and removes this pathway
-long half-life results in duration of platelet inhibition lasting about 4 weeks
what are the indications for vorapaxar?
reduction of the risk of thrombotic and CV events (heart attack, stroke, CV death) in patents with a history of MI or peripheral arterial disease
-combined wit slow-dose aspirin and/or clopidogrel
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