Pharm: Coagulation, Cardiac Arrhythmias
and Dyslipidemia
Coagulation - ANS
treating overactive clotting: name three primary drugs used and know their mechanism of action
- ANS -anticoagulants (preventing clotting in veins)
-antithrombotics (inhibits platelet function --> prevents clot from forming)
-thrombolytic agents (destroy clots already formed)
Warfarin (coumadin): effect what type of clotting factors? half lives of factor 7 vs 9 vs 10 vs 2?
pharmacokinetics - half life of Warfarin vs max effect of dose vs effect lasts for how long ? What
is the International normalized ratio and Prothrombin time...how to make sure these lab values
are within an acceptable range after starting Warfarin? the half lives of which clotting factors are
affected first by taking blood thinner? - ANS -vitamin K dependent clotting factors
-4-6 hours vs 8-24 vs 24-36 vs 36-60
-36-42 hours vs 40 hours vs 5 days
-essentially the same thing - concerned with the amount of time it takes for blood to clot...this is
measured daily until stable then periodically after that when on Warfarin
-shortest lasting ones (7 and 9)
Warfarin: adverse effects? how to predict this based off INR value? risk vs reward ratio? - ANS
-bleeding
-high INR = high chance of bleeding
-overall major/fatal bleeding is rare and prevents 20 strokes for every major bleeding event it
causes
pharmacokinetics - enters the body by which routes vs half life vs what does nonlinear response
mean (applies to this drug)?
monitoring - this drug targets which clotting factors? monitor aPTT (partial prothrombin time)
how long after the last dose adjustment?
adverse effects? early vs late stage thrombocytopenia? - ANS -prophylaxis and tx of DVT and
PE
-acute myocardial events
-acute coronary syndrome (Ex: unstable angina)
, -IV (quick action) or sub-q (delayed time)
-30-60 minutes
-give pt a second injection = effect increases more than proportion to just taking one (more than
a 100% increase)
pharmacokinetics - half life compared to UFH (unfractionated heparin) vs how is this eliminated
vs use in pregnant females?
advantages? - ANS -arin
-half life is much longer
-renally
-its safe (doesn't cross the placenta)
-longer half life, predictable anticoagulant response to drug = no routine monitoring due to low
incidence of hemorrhaging
antiplatelet (antithrombotic) agents: where/when are white clots (arterial thrombi) formed? -
ANS -in arteries (with atherosclerotic plaques that have ruptured) --> clot initiation
antithrombotic agents: Aspirin: mechanism of action? effect on TXA and PGI and what are the
functions of these? length of time effects lasts for? - ANS -IRReversible COX inhibitor (stop
production of prostaglandins and thromboxanes which are pro-aggregation substances)
-blocks their formation - TXA = platelet aggregation and vasoconstriction - PGI = platelet
aggregation and vasodilation
-at least one week
antithrombotic agents: thienopyridines: name two (common)? what do these inhibit? good use
for what pt populations? - ANS -clopidogrel and prasugrel
-ADP induced platelet aggregation and adhesion
-recent stroke, recent MI, etc ****think secondary prevention
antithrombotic agents: thienopyridines: clopidogrel: action of this? indications? - ANS
-IRReversibly blocks P2Y component of ADP receptor on platelets
-secondary prevention ***see previous card
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