Page 189 - Basic Monitoring in Canine and Feline Emergency Patients

(A) (B)
VetBooks.ir Cell Intrinsic factor tenase Cell
Cell
surface
surface
surface
Factor IX complex
VIII Factor X II
V
LOTS!!!!
Ca
Ca
Prothrombinase
complex

Factor X

(C)
II Crosslinked fibrin

Fibrin Fibrin (‘hard’ clot)

Fibrinogen
Fibrin
Fibrin

Fibrin

Fig. 9.4. Amplification and propagation of secondary coagulation. (A) The activated factor IX generated during
initiation binds to factor VIII and calcium (Ca) on a cell surface to form the intrinsic factor tenase complex. This
complex activates factor X. (B) The activated factor X combines with factor V and Ca to form the prothrombinase
complex. The prothrombinase complex causes the conversion of prothrombin to thrombin. Since this reaction is
occurring on many cell surfaces (including platelets) during amplification and propagation, large amounts of thrombin
are created, also known as the ‘thrombin burst.’ (C) Thrombin will in turn cause activation of fibrinogen to fibrin that, in
the presence of factor XIII (also activated by thrombin), will cause crosslinking of the fibrin to form the clot.

factor V on the cell surface (both usually released tors from their granules including V, VIII, vWF, and
from dense and alpha granules respectively) to Ca which are involved in the various stages of sec-
form more prothrombinase complexes and cleave a ondary coagulation. Also (and arguably most impor-
large volume of prothrombin to thrombin. tantly), the activated platelets provide more negatively
The final stage of secondary coagulation is termed charged phospholipid surfaces upon which coagula-
propagation and describes the recruitment of acti- tion can occur. This leads to further amplification
vated platelets to the area to further coagulation (see and more and more thrombin production (i.e. the
Fig. 9.4). The recruited activated platelets release fac- ‘thrombin burst’). A large quantity of thrombin

Coagulation 181