DA5 thrombolytics

Genetic fisk factors of MI include:

Fibrinogen is converted by _______ into fibrin during blood
coagulation.

Fibrin iscross linked by _______   to form a clot.

FXIIIa stabilizes fibrin further by incorporation of the __________

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 _________.

Fibrinolysis refers to the process of fibrin digestion by the fibrin-specific protease, __________.

What class of drugs activate the fibrinolytic system by converting plasminogen to plasmin?  Name 2 drugs and its specificity.

How does a fibrin specific differ from a non specific tpa?

Fibrinolytics are used only for what indication?

Which tpa has the highest incidence of noncerebral bleeding complications and need for transfusion.

Survival benefit greatest when lytics administered within first _______ after onset of symptoms, particularly within the first ________.

Never use eptifibatide with which class of drugs?

What dose of clopidogrel should be used with a CABG?

Fibrinolytic therapy should be started within _______ after the diagnosis of STEMI is made

In STEMI, fibrinolytic agents offer a trade-off between reduced mortality and increased incidence of ___________ bleeding

Absolute contraindications to thrombolytics

Relative contraindications to thrombolytics

_________ cleaves fibrinogen to fibrin.

Alteplase, reteplase, tenecteplase adjunctive therapy:  Unfractionated heparin (UFH) at ________ bolus followed by ________ infusion; maintain PTT b/w ________ sec for 48hr.

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

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. 

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 ________.

Antithrombin is a ________________

The physiological target proteases of antithrombin are 
________, ___________, ________, ________, and, to a greater extent, __________(thrombin), and also __________ 

Heparin dose: LD ________ iv bolus (Max 5000 units if > 65kg or 4000 u if < 65 kg)

Heparin Maintenance dose: ________ iv with max of 1000 u/hr if > 65kg or 800 u< 65kg 

Heparin titration goal is ______ PTT

LMWH dose : enoxaparin ________ sc q12h

DO NOT administer concurrent GP IIb/IIIa inhibitors with thrombolytics

Clopidogrel is a ________ which must undergo hepatic conversion to its active metabolite for platelet inhibition, a process taking several hours.

Thienopyridines (P2Y₁₂ ADP receptor platelet inhibitor)

Direct thrombin inhibitors

GP IIb/IIIa inhibitors

Low molecular weight heparin

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.

The platelet P2Y₁₂ receptor blockers ________, __________, __________, and __________ block the binding of ________ to a specific platelet receptor P2Y₁₂, thereby inhibiting activation of the ________ complex and _____________.

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).

Ticarelor (Brilinta ®) _____ LD, then ______ BID, indicated STEMI and NSTEMI (BID dosing)

Prasugrel (Effient ®) _____ LD, then _____ qd
NSTEMI or STEMI with planned PCI indicated qd

•Clopidogrel (Plavix ®) ________ LD, then ________
daily- STEMI or NSTEMI

Myocardial infarction complicatons

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.