*Infections (viral, bacterial, protozoal) and post-infectious immunologic reactions.
*Infections (viral, bacterial, protozoal) and post-infectious immunologic reactions.
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Once coagulation begins a positive feedback loop is set up whereby coagulation inhibitors are consumed, allowing more coagulation. In this way coagulation continues and induces further coagulation.
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Once [[Normal_Mechanisms_of_Haemostatic_Control#Coagulation_physiology|coagulation]] begins a positive feedback loop is set up whereby coagulation inhibitors are consumed, allowing more coagulation. In this way coagulation continues and induces further coagulation.
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Thrombin levels are increased. Thrombin converts plasminogen into the active form, plasmin and initiates the fibrinolytic cascade. Fibrinolysis produces high levels of FDPs (fibrin degradation products) which are themselves anticoagulants, further fuelling the coagulation cascade.
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Thrombin levels rise; thrombin converts plasminogen into the active form, plasmin which initiates the fibrinolytic cascade. Fibrinolysis produces high levels of fibrin degradation products (FDPs) which are themselves anticoagulants, promoting further coagulation. As thrombi form in the vasculature, tissues become hypoxic leading to multisystemic organ failure in severe cases.
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As thrombi form in the vasculature tissues will become hypoxic leading to multisystemic organ failure in severe cases.
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As [[Thrombocytes|platelets]] are used up in the thrombi a [[Platelet Abnormalities#Thrombocytopaenia|thrombocytopaenia]] occurs, leading to a paradoxical haemorrhage and the patient starts to bleed. This is the mechanism by which most viral haemorrahgic diseases cause their clinical signs.
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As [[Thrombocytes|platelets]] are used up in the thrombi, a [[Platelet Abnormalities#Thrombocytopaenia|thrombocytopaenia]] occurs which leads to paradoxical haemorrhaging and the patient starts to shown symptoms of bleeding. This is the mechanism by which most viral haemorrahgic diseases induce clinical signs.