2. Definition
DIC is characterized by widespread,
intravascular activation of
coagulation (leading to intravascular fibrin
deposition) and
simultaneous consumption of coagulation factors
and platelets
(potentially resulting in bleeding)
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3. Risk Factors and Etiology
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• Almost always a secondary event from
activation of one of the coagulation pathways
• Underlying pathology creates a triggering
event: Either-
– endothelial tissue injury (Extrinsic)
– blood vessel injury (Intrinsic)
(Porth, 2004)
5. Pathogenesis of DIC
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• A) Excessive formation of thrombin
• B) Suppression of natural anticoagulation
• C) Failure to remove excessive fibrin
(Failure of fibrinolytic system)
6. A) Excessive formation of thrombin
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• Increase activity of Tissue Factor (TF)
• IL-1, endotoxin, TNF alpha
Upregulate
TF mRNA Endothelium
• Damage tissue
8. B) Suppression of natural anticoagulation
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• Decrease antithrombin
About 30% reduction in severe
sepsis
9. C) Failure to remove excessive fibrin
(Failure of fibrinolytic system)
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tPA + plasminogen
Alpha 2 plasmin
inhibitor
Free plasmin
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Patients with chronic liver disease
with systemic hyperfibrinolysis
This occurs due to increased levels
of plasminogen activators
Secondary to decreased hepatic
clearance and
Lower circulating levels of PAI-1 and α2-plasmin
inhibitor.