Page 205 - Veterinary Immunology, 10th Edition

by massive tissue damage or by exposure to bacteria and bacterial
VetBooks.ir endotoxins in Gram-negative sepsis. Virtually every bacterial

species can trigger TF release. The TF transforms prothrombin to
thrombin to form fibrin thrombi. Simultaneous downregulation of

anticoagulant systems results from reduced antithrombin synthesis
(it is a “negative” acute-phase protein). Activation of the clotting
cascade leads to the formation of fibrin and platelet microthrombi
in small blood vessels throughout the body. These clots can cause

intravascular thrombosis and can lead to ischemia, impaired organ
perfusion and widespread damage.

FIG. 7.7 The mechanism of disseminated intravascular
coagulation. Widespread injury to vascular endothelium results in
the production of microthrombi.

At same time, the excessive thrombin activates plasminogen to
generate plasmin, which causes fibrinolysis. When the
microthrombi break down they release anticoagulant fibrin

breakdown products that therefore promote hemorrhage. In
addition, the newly formed thrombi consume clotting factors and
platelets. As a result, normal clotting does not occur and
uncontrolled bleeding may result. Plasmin also activates the

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