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15 Cards in this Set

  • Front
  • Back
Thrombotic Treatment
Prevention: anticoagulants, anti-platelet drugs (after MI or Afib and during angiplasty)

Treatment: Fibrinolytics (PE, DVT, MI)

Replacement: Help clotting (hemophilia, aneurysm, postop GI bleed)
Physiological Regulatory Mechanism
1. Inhibition of platelet aggregation by increasing cAMP (PFI2, prostacyclin)
2. Inhibition of clotting enzymes by plasma protease inhibitors.
3. Fibrinolysis by plasmin (controlled by t-PA)
Mechanism: irreversible COX inhibitor, block formation of thromboxane A2

Clinical Use: stable and unstable angina, acute MI, trasient ischemic attack (TIA), stroke prevention after carotid artery surgery

Side Effects: GI bleed
Mechanism: oral anti-platelet, increases cAMP by blocking uptake of adenoise and inhibits phosphodiesterase

Clinical Use: prophylaxis of thrombemboli with prostethic heart valves, stroke survivors
Mechanism: irreversibly inhibits ADP receptors, 4-7 days for 50-60% platelet inhibition

Clinical Use: better than aspirin in preventing MI and stroke, acute coronary syndrome (ACS: unstable angine and MI), recent stroke, peripheral arterial disease

Side Effects: contraindicated in patients with bleeds e.g. ulcer or intracranial hemorrhage
Mechanism: I.V. anti-platelet, monoclonal AB that blocks glycoprotein IIb/IIIa -> prevents fibrinogen binding

Clinical Use: adjunct to heparin and aspirin, percutaneous coronary interventions (PCI: angioplasty, stenting), prevention of acute cardiac ischemia, refractory unstable angina
Mechanism: I.V. antiplatelet, KGD sequence, more specific for GP IIb/IIIa

Clinical Use: acute coronary syndrome, PCI
Side Effects:
Mechanism: I.V. anti-platelet, GP IIb/IIIa inhibitor, basedon RGD sequence

Clinical Use: use with heparin for ACS and PCI
LMWH- Enoxaparin, Dalteparin
Mechanism: injectable Anticoagulant, binds antithrombin III to stimulate anti-protease activity

Clinical Use: prevention DVT, PE, thrombosis after MI, used in unstable angina, non-Q wavw MI, coronary stents

Side Effects: Bleeding, Heparin Induced Thrombocytopenia (HIT)
Less side effects with LMWH
Mechanism: direct thrombin inhibitor

Clinical Use: patients with HIT
Mechanism: oral anticoagulants; structure related to vit K act as competetive inhibitor -> prevents gamma-carboxylation of factors II, VII, IX, X

Clinical Use: prevention of DVT, thromboembolism, Afib, MI
start low, stabilize, monitor, adjust

Side Effects: bleeding, antidote is vit K and hold warfarin
Mechanism: Fibrinolytic, when complexed with plasminogen can convert other plasminogen to plasmin (autocatalytic reaction

Clinical Use: not used much anymore for VTE, MI

Side Effects: bleeding
Mechanism: recombinant t-PA
short T1/2 of 3min

Clinical Use: DVT, PE, MI

Side Effects: lysis at vascular injury sites, excessive plasmin, hemorrhage
Mechanism: t-PA with 176 a.a. deleted -> longer T1/2 (15 min)

Clinical Use: specificity for coronary thrombi
Mechanism: t-PA with 3 mutations, more resistant to PAI-1, prolonged T1/2 enables single bolus dosing and 14x specificity for fibrin