Hemostatic drugs and fibrinolytics Flashcards
T/F: Platelet transfusion works best for irreversible inhibitors
True
Desmopressin (DDAVP)
MOA: triggers release of VWF and causes platelet activation, cross-linking, and prolongs t1/2 of factor VIII
Indications: VWF deficiency (von willebrands disease), factor VIII deficiency (hemophilia A), platelet dysfunction (uremia)
What different clotting factors can be used to treat clotting factor diseases?
Factor VII= hemophilia A
Factor VIII= hemophilia A
Factor IX= hemophilia B
T/F: In cirrhosis we use PCC because all clotting factors needs to be depleted
False, we would use Cryo or FFP
What are approaches for anticoagulant reversal?
You can either overwhelm the anticoagulant with PCC or neutralize it
T/F: Dabigatran reversing can be treated with PCC
False, this drug is least reversible by PCC and we need to use idarucizumab instead
Idarucizumab
MOA: monoclonal antibody that binds and inactivates dabigatran
Indications: reverses anticoag effect of dabigatran only
Andexanet alfa
MOA: recombinant factor that binds and inactivates factor Xa inhibitors
Indications: reverses anticaog effect of factor Xa inhibitors
Duration of action: 4 hours (short)
Clotting after use is 10% (more effective at reversal)
Protamine
MOA: weak anticoag effect on its own (inhibits thrombin) but chemically neutralizes heparin (greater acting in UFH) by binding together (positive and negative charge) so that ATIII cannot be activated anymore
Indications: reversal of heparin
Ciraparantag
MOA: synthetic molecule capable of H bonding and binds + inactivates heparin along with factor Xa & IIa inhibitors
Indications: reverses a lot of dif anticoags
Downside: not FDA approved
Which two targets can we use in reversal of warfarin?
PCC or FFP
Phytonadione (vitamin K)
MOA: allows synthesis of clotting factors depleted in warfarin and restores vit K (increases)
Indications: restores vitamin K levels and is given after PCC
Anti-fibrinolytics (aminocaproic acid and tranexamic acid)
MOA: competitive inhibitor of plasminogen and plasmin; stabilizes clots in all patients even if not taking an anticoagulant
Clinical use: control of bleeding from various causes and can be given in many dif formulations
Which hemostatic agents are topical?
Tranexamic acid, aminocaproic acid, and thrombin
T/F: when plasmin is activated it increases fibrin levels
False, when plasmin is activated it causes fibrin to be degraded