Hemostasis/WBC/Anticoag Flashcards
Platelet Plug
- Plts adhere to vWF through GPIb
- Plts adhere to collagen through GPIa
- Plts aggregate when GPLLb binds to fibrinogen after plts are activated (CAT)
- Act plts secrete ADP and thromboxane = vasoconstriction and factor Va
WCAFAT
Coag Cascade: Form a fibrin clot
- Endo makes TF
- TF activates VII
- VIIa activates X and IX
- II (pro) to IIa (thrombin)
- IIa makes fibrinogen into fibrin
- XIII crosslinks to make stable clot
T 7 910 2 2a F 13
TSNTTTFT
Prothrombin Time
-Time for conversion of prothrombin to thrombin
-VII dependent paths
-Performed by adding TF to plasma
-Often converted to INR (2-3)
-Best for Coumadin therapy
APTT
-Time to form clot
-Evaluates XII dependent paths
-Exposing blood to negative charged surface
-Best for Heparin therapy
-Screen for hemophilia A/B
Heparin
-Requires ATIII
-Inhibits thrombin (II), X primarily
Warfarin
-Antagonist of VK
-Inhibits II, VII, IX, and X (and C/S)
Factor Xa Inhibitors
-Riva, apixa, edoxa
-Safer than warfarin
-Dabi is direct thrombin inhibitor
Streptokinase
-Forms non-covalent attachment with plasminogen = free plasmin = digests fibrin clots
TPA
-Activates plasminogen bound to fibrin
-Reteplase is deletion mutant of TPA
Aspirin
-Prevent formation of thromboxane A2
Clopidogrel
-Blocks purine receptor
-May cause TTP
Abciximab
MAB against IIb/IIIa receptors
Platelets
-Increase in inflammation, disseminated cancer
-Decrease in ITP, TTP, bone marrow failure, DIC
place CI TI BD
White Blood Cells
-Increase in infection, inflammation
-Decrease in aplastic anemia (do not recover), hypoplastic anemia (recover)
IIAHA
Neutrophils
Increase in steroid use, inflammation (bacteria infection)
ISI is neutral