Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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) |
|
Aspirin
|
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 |
|
Dipyridamole
|
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 |
|
Clopidogrel
|
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 |
|
Abciximab
|
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 |
|
Eptifibatide
|
Mechanism: I.V. antiplatelet, KGD sequence, more specific for GP IIb/IIIa
Clinical Use: acute coronary syndrome, PCI Side Effects: |
|
Tirofiban
|
Mechanism: I.V. anti-platelet, GP IIb/IIIa inhibitor, basedon RGD sequence
Clinical Use: use with heparin for ACS and PCI |
|
Heparin
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 |
|
Lepirudin
Bivalirudin Argatroban |
Mechanism: direct thrombin inhibitor
Clinical Use: patients with HIT |
|
Warfarin
|
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 |
|
Streptokinase
|
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 |
|
Alteplase
|
Mechanism: recombinant t-PA
short T1/2 of 3min Clinical Use: DVT, PE, MI Side Effects: lysis at vascular injury sites, excessive plasmin, hemorrhage |
|
Reteplase
|
Mechanism: t-PA with 176 a.a. deleted -> longer T1/2 (15 min)
Clinical Use: specificity for coronary thrombi |
|
Tenecteplase
|
Mechanism: t-PA with 3 mutations, more resistant to PAI-1, prolonged T1/2 enables single bolus dosing and 14x specificity for fibrin
|