Pathogenesis of disseminated intravascular coagulation.
Figure 5 summarizes the three different phases in the pathophysiology of disseminated intravascular coagulation exemplified by the effect of endotoxin. During the first phase, the coagulation system is activated to generate soluble fibrin. Fibrin kept in solution by fibrinogen or fibrinolytic degradation products can be cleared from the circulating blood. If the amount of soluble fibrin exceeds a certain threshold, soluble fibrin may precipitate or polymerize to fibrin clots. At this state, active fibrinolysis breaks down the precipitated fibrin to fibrinolytic degradation products preventing the preservation of fibrin. If the capacity of the fibrinolytic system is exhausted, or if fibrinolysis is inhibited, fibrin clots may be preserved, causing cell damage, as for instance bilateral renal cortical necrosis.
D000818:Animals; D001777:Blood Coagulation; D001792:Blood Platelets / Q000502:physiology; D003167:Complement Activation; D004211:Disseminated Intravascular Coagulation / Q000209:etiology* / Q000503:physiopathology; D004731:Endotoxins / Q000494:pharmacology; D005337:Fibrin / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D010974:Platelet Aggregation; D011817:Rabbits
D004731:Endotoxins; D005337:Fibrin