Antithrombolytic therapy Flashcards Preview

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Flashcards in Antithrombolytic therapy Deck (13):

What is the difference between arterial clots and venous clots?

Arterial = primarily platelets, treat with antiplatelet meds

Venous = primarily fibrin, treat with anticoagulants - inhibit coagulation cascade


What are the 4 major antiplatelet therapies?

Cyclooxygenase inhibitors: aspirin (irreversible), NSAIDS (competitive inhibitors- used more for pain relief)


GP IIb/IIa inhibitors (this complex is important for getting platelets to stick together)

ADP receptor inhibitors - ticlopidine, clopidogrel, prasugrel, ticagrelor


Aspirin mechanism of action

Low doses: blocks thromboxane A2 production --> block platelet aggregation & vasoconstriction

Higher doses: also blocks PGI2 --> blocks prostacyclin production too! Inhibits platelet aggregation & causes vasodilation


Dipyridamole mechanism

Increases cAMP production

Blocks Ca release from dense granules, blocking AA production & decreasing thromboxane A2 production

Enhances aspirin's effect on platelet aggregation


Glycoprotein IIb/IIIa inhibitors mechanism of action

Interfere with fibrinogen-induced platelet aggregation

3 classes:
Fab fragments- abciximab
Peptide-bast antagonists - eptifibatide
Small molecule inhibitors- tirofiban

Potent: platelet count --> 0

Abciximab: 30 min half life
Eptifabatide/tirofaban: 2-2.5 hours

Best for short term bc too potent for long term!


ADP receptor inhibitors- mechanism? use? SE?

Block P2Y-12 receptor which inhibits ADP-induced activation of platelets

Ticlopidine (rarely used-SE), clopidogrel (major agent), prasugrel, ticagrelor

Long half life, no reversing agent

Used for unstable angina, MI, percutaneous coronary intervention, secondary stroke prophylaxis, periph vasc dis

Synergy with aspirin

SE=bleeding, thrombotic thrombocytopenic purpura (TTP- dangerous), neutropenia


What are the anticoagulant?

Older Meds:

Newer meds:
LMW heparins
Factor Xa inhibitors
Direct thrombin inhibitors


What is rivaroxaban?

Oral Factor Xa inhibitor

VTE (venous thromboembolism) prophylaxis, stroke prevention in non-valvular Afib, VTE treatment


What is apixaban?

Treat non-valvular Afib

Problematic in renal dysfunciton bc renally excreted


What are the direct thrombin inhibitors?

Block thrombin, more potent than heparin

Includes: Argatroban (small molecule blocker of thrombin, problematic in liver disease), bivalirudin=angiomax (unstable angina/angioplasty), desirudin (VTE prophylaxis),  Dabigatran=Pradaxa (oral direct thrombin inhibitor- lots of press, no DDI/food, bleeding possible-- stroke prevention in nonvalvular AFib)



Inhibits Vitamin K dependent carboxylase activity by preventing reduction of Vitamin K

Doesn't affect proteins already synthesized

Multiple DDI's

Antidote = Vitamin K


What is thrombolytic therapy?

Lysing clots that have already formed

Problem: doesn't discrimiate between therapeutic and pathologic thrombosis --> increased risk of hemorrhage compared with other antithrombotic therapties

Only therapy that prevents tissue death in acute aterial thrombosis (in MI and stroke-- more important in stroke!)

Lyses hemostatic plugs everywhere --> SE= bleeding, esp CNS


What are the 3 classes of thrombolytic therapy?

Streptokinase: binds plasminogen, activates a second plasminogen molecule to plasmin

Urokinase: activates plasminogen directly

TIssue plasminogen activator: activates plasminogen directly