DA5 thrombolytics

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HUSOP2014
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170751
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DA5 thrombolytics
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2012-09-14 08:47:01
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HUSOP DA5 thrombolytics STEMI
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HUSOP DA5 thrombolytics
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  1. Genetic fisk factors of MI include:
    • glucose metabolism
    • lipid metabolism
    • platelet function
    • blood pressure/growth regulation
    • coagulation/ fibrinolysis
  2. Fibrinogen is converted by _______ into fibrin during blood
    coagulation.
    thrombin
  3. Fibrin iscross linked by _______   to form a clot.
    factor XIII
  4. FXIIIa stabilizes fibrin further by incorporation of the __________
    fibrinolysis
  5. Fibrin specifically binds the activated coagulation factors __________ and _________ and entraps them in the network of fibers, thus functioning as a temporary inhibitor of these enzymes, which stay active and can be released during _________.
    • factor Xa
    • thrombin
    • fibrinolysis
  6. Fibrinolysis refers to the process of fibrin digestion by the fibrin-specific protease, __________.
    plasmin
  7. What class of drugs activate the fibrinolytic system by converting plasminogen to plasmin?  Name 2 drugs and its specificity.
    • tissue plasminogen activator
    • tenecteplase, alteplase, reteplase, lanoteplase - fibrin specific
    • streptokinase - non specific
  8. How does a fibrin specific differ from a non specific tpa?
    the non specific degrades fibrinogen, factor V, & factor VIII
  9. Fibrinolytics are used only for what indication?
    STEMI
  10. Which tpa has the highest incidence of noncerebral bleeding complications and need for transfusion.
    alteplase
  11. Survival benefit greatest when lytics administered within first _______ after onset of symptoms, particularly within the first ________.
    • 4 hours
    • 70 minutes
  12. Never use eptifibatide with which class of drugs?
    tpa
  13. What dose of clopidogrel should be used with a CABG?
    300-600mg
  14. Fibrinolytic therapy should be started within _______ after the diagnosis of STEMI is made
    30 minutes
  15. In STEMI, fibrinolytic agents offer a trade-off between reduced mortality and increased incidence of ___________ bleeding
    intracerebral
  16. Absolute contraindications to thrombolytics
    • Previous ICH
    • Known structural cerebral vascular lesion
    • Known malignant intracranial neoplasm
    • Ischemic CVA (stroke) within 3 months prior
    • Suspected aortic dissection
    • Active bleeding or bleeding diathesis
    • Significant closed-head or facial trauma within 3 months prior
  17. Relative contraindications to thrombolytics
    • Poorly controlled or chronic sustained HTN
    • Ischemic CVA (stroke) >3 months prior
    • Dementia
    • Traumatic or prolonged CPR or major surgery within <3 wk prior
    • Recent (within 2-4 wk) internal bleeding
    • Noncompressible vascular puncture
    • Allergy to lytic agents
    • Pregnancy
    • Active peptic ulcer
    • Current use of anti-coagulants
  18. _________ cleaves fibrinogen to fibrin.
    thrombin (factor IIa)
  19. Alteplase, reteplase, tenecteplase adjunctive therapy:  Unfractionated heparin (UFH) at ________ bolus followed by ________ infusion; maintain PTT b/w ________ sec for 48hr.
    • 60units/kg
    • 12u/kg/hr
    • 50-70
  20. LMWH also effective w/ tenecteplase, although don’t use it in pts ______ y/o (increased risk of ICH) or those with CrCl less
    than ________- Enoxaparin dose _______ q ______ hrs
    • >75
    • 30ml/min
    • 1mg/kg
    • 12
  21. Heparin binds to the enzyme inhibitor ___________ causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop. 
    antithrombin III (AT)
  22. The activated antithrombin III (AT) then inactivates ________ and other proteases involved in blood clotting, most notably __________. The rate of inactivation of these proteases by AT can increase by up to 1000-fold due to the binding of ________.
    • thrombin
    • factor Xa
    • heparin
  23. Antithrombin is a ________________
    serpin (serine protease inhibitor)
  24. The physiological target proteases of antithrombin are 
    ________, ___________, ________, ________, and, to a greater extent, __________(thrombin), and also __________ 
    • Factor XIIa
    • Factor XIa
    • Factor IXa
    • Factor Xa
    • Factor IIa
    • Factor VIIa
  25. Heparin dose: LD ________ iv bolus (Max 5000 units if > 65kg or 4000 u if < 65 kg)
    60u/kg
  26. Heparin Maintenance dose: ________ iv with max of 1000 u/hr if > 65kg or 800 u< 65kg 
    12 u/kg/hr
  27. Heparin titration goal is ______ PTT
    50-70 sec
  28. LMWH dose : enoxaparin ________ sc q12h
    100 u/kg (1mg/kg)
  29. DO NOT administer concurrent GP IIb/IIIa inhibitors with thrombolytics
    DO NOT administer concurrent GP IIb/IIIa inhibitors with thrombolytics
  30. Clopidogrel is a ________ which must undergo hepatic conversion to its active metabolite for platelet inhibition, a process taking several hours.
    prodrug
  31. Thienopyridines (P2Y12 ADP receptor platelet inhibitor)
    • ticlopidine
    • clopidogrel
    • prasugrel
    • Tricagrelor
  32. Direct thrombin inhibitors
    • heparin
    • bivalirudin
    • argatroban
    • Dabigatran
    • Lepirudin
  33. GP IIb/IIIa inhibitors
    • abciximab
    • eptifibatide
    • tirofiban
  34. Low molecular weight heparin
    Enoxaparin
  35. Aspirin inhibits __________ (prostaglandin G/H synthase) that mediates the first step in the biosynthesis of prostaglandins and thromboxanes (including _________) from arachidonic acid. ________________ is a potent stimulator of platelet aggregation.
    • cyclooxygenase 
    • TXA2
    • Thromboxane A2
  36. The platelet P2Y12 receptor blockers ________, __________, __________, and __________ block the binding of ________ to a specific platelet receptor P2Y12, thereby inhibiting activation of the ________ complex and _____________.
    • clopidogrel
    • ticlopidine
    • ticagrelor
    • prasugrel
    • ADP
    • GP IIb/IIIa
    • platelet aggregation
  37. Glycoprotein IIb/IIIa (GP IIb/IIIa) antibodies and receptor antagonists inhibit the ___________ of platelet aggregation (the cross-bridging of _________ by ________ binding to the GP IIb/IIIa receptor).
    • final common pathway
    • platelets
    • fibrinogen
  38. Ticarelor (Brilinta ®) _____ LD, then ______ BID, indicated STEMI and NSTEMI (BID dosing)
    • 180mg
    • 90mg
  39. Prasugrel (Effient ®) _____ LD, then _____ qd
    NSTEMI or STEMI with planned PCI indicated qd
    •  60mg
    • 10mg
  40. •Clopidogrel (Plavix ®) ________ LD, then ________
    daily- STEMI or NSTEMI
    • 300-600mg
    • 75mg
  41. Myocardial infarction complicatons
    • heart failure
    • myocardial rupture
    • arrhythmias
    • pericarditis
    • cardiogenic shock
  42. GPIIB/IIIA inhibitors may be beneficial during coronary interventions among ___________ including _________ and ________ myocardial infarctions, particularly in the absence of adequate pretreatment with _____________ drugs or when __________________ are not utilized. 
    • high-risk patients
    • acute ST-elevation
    • non-ST-elevation
    • oral antiplatelet
    • direct thrombin inhibitors

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