Coagulation Theoriescontinued Hematology Review 351
CASCADE MODEL* CELL-BASED OR PHYSIOLOGICAL MODEL
Comments
*For simplicity, Ca2+& platelet factor 3 not shown.
Common pathway (factors X, V, II, I):
- Xa:Va converts prothrombin (II) to thrombin (IIa).
- Thrombin cleaves fibrinogen (I) into fibrin & acti-
vates factor XIII to stabilize clot.
“Classic” theory. Explains in vitro coag (PT & APTT
tests) & helps ID factor deficiencies, but doesn’t fit cur-
rent understanding of coag in vivo. Pathways don’t
operate independently.
Propagation (on surface of activated platelet):
- Factor Xa binds to factor VIIIa on platelet.
- IXa:VIIIa activates factor X.
- Xa:Va converts prothrombin (II) to thrombin (IIa).
- Thrombin cleaves fibrinogen (I) into fibrin & activates factor
XIII to stabilize clot.
To compare models, think of extrinsic pathway as occurring on
TF-bearing cell & intrinsic pathway (without factor XII, HMPK,
PK) on platelet surface. (Factor XII, HMPK, PK aren’t needed in
vivo because factor XI is activated by thrombin produced in
initiation phase.)