Blood Agents Flashcards
HMWH (standard)
MOA: Activation of AT3 causing inhibition of IXa, Xa, XIa, XIIa does not affect thrombin bound to fibrin or Xa bound to PLT
PK: Short duration & t1/2 (IV or deep SC only)
ADEs: high risk of bleeding, HIT, osteoporosis, high [K] in patients with MC deficiency
Uses: Ppx & Tx of DVT. PE, Acute MI. Ok for pregnancy
UFH
MOA: Activation of AT3 causing inhibition of IXa, Xa, XIa, XIIa does not affect thrombin bound to fibrin or Xa bound to PLT
PK: unpredictable; IV only
ADEs: high risk of HIT; rebound ischemia
- requires regular monitoring
LMWH (enoxaparin, tinzaparin, fondaparinux, danaparoid)
MOA: activation of AT3 causing inhibition of mostly Xa
does not affect Xa already bound to PLT
PK: higher BA, longer duration
ADEs: lower HIT incidence
Uses: possible improvement in outcomes of acute coronary syndrome
Other: No monitoring, easy SC inj
Direct Thrombin Inhibitors (Hirudin, Lepirudin, Bivalirudin)
MOA: directly inhibits fibrin binding to thrombin with little effects on PLT (except bivalirudin)
3 advantages for DTIs over Heparin
- MOA of DTIs is AT3 dependent
- Hemorrhage is dose related (more predictable)
- no HIT!!!
Warfarin
MOA: block the function of the vitamin K epoxide reductase complex in the liver, leading to depletion of the reduced form of vitamin K that serves as a cofactor for gamma carboxylation of vitamin K-dependent coagulation factors 2, 7, 9, 10, protein C & S
PK: slow onset (8-12 hr) and long duration (36 hr cl)
ADEs: fetal hemorrhagic disorder, cutaneous necrosis d/t depletion of protein C, diarhhea & flatulence, bone defects and hemorrhagic disorders in infants
Uses: DVT, PE, Afib, rodenticides
- CI in pregnancy. Requires routine labs/monitoring
Warfarin drug interactions
increases warfarin:
- ASA & sulfonamides: decrease protein binding
- SSRIs & cimetidine: decrease degradation
- Antibiotics: decrease synthesis of clotting factors
- Sulfinpyrazone and phenylbutazone: inhibit S-warfarin and decrease albumin binding
