Local hemostasis, immunothrombosis, and systemic disseminated intravascular coagulation in trauma and traumatic shock

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ischemia 1 angiologydiseases
thrombosis 30 angiologydiseases

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ischemia 5216 patterns (DAMPs) are molecules produced in stressed or damaged tissues in connection with trauma, shock, ischemia , and reperfusion [[10]]. The innate immune responses start following the sensing PAMPs or DAMPs by pattern-recognition
thrombosis 44 Title: Critical CareLocal hemostasis, immuno thrombosis , and systemic disseminated intravascular coagulation in trauma and traumatic shockSatoshi GandoYasuhiro
thrombosis 495 patients. The aims of this review are to provide a summary of the recent advances in our understanding of thrombosis and hemostasis following trauma and to discuss the pathogenesis of disseminated intravascular coagulation
thrombosis 668 pathogenesis of disseminated intravascular coagulation (DIC) at an early stage of trauma. Local hemostasis and thrombosis respectively act to induce physiological wound healing of injuries and innate immune responses to damaged-self
thrombosis 1246 insufficient control of coagulation, and increased fibrin(ogen)olysis. Irrespective of microvascular thrombosis , the condition shows systemic thrombin generation as well as its activation in the circulation and extensive
thrombosis 1952 ridiculed to be an abbreviation for ‘disseminated international confusion’ because intravascular thrombosis was hardly ever found at autopsy. At the end of the 1970s, however, Spero and colleagues [[1]] correctly
thrombosis 2326 including trauma and sepsis [[2]]. Recent findings suggest that, under certain circumstances, local thrombosis as well as hemostasis is a physiological process that constitutes an intrinsic effector mechanism of
thrombosis 2477 process that constitutes an intrinsic effector mechanism of innate immunity, which is called immuno thrombosis [[3]]. DIC is now believed to be a result of the dysregulation of immunothrombosis. This suggests that
thrombosis 2560 is called immunothrombosis [[3]]. DIC is now believed to be a result of the dysregulation of immuno thrombosis . This suggests that all insults, irrespective of whether they are infectious (sepsis) or non-infectious
thrombosis 2736 infectious (sepsis) or non-infectious (trauma), can cause DIC when the control mechanisms of immuno thrombosis are overwhelmed.However, the new theory of acute coagulopathy of trauma shock (ACOTS) has completely
thrombosis 4291 patients [[2],[9]]. This review will provide a summary of the recent advances in our understanding of thrombosis and hemostasis following trauma and will discuss the pathogenesis of DIC, especially DIC with the fibrinolytic
thrombosis 6006 vessels to protect hosts from non-self (PAMPs) and altered-self (DAMPs). These processes are called immuno thrombosis , and the basic principles have been reviewed [[3]]. During the responses to PAMPs and DAMPs, monocytes
thrombosis 6555 DNA, histones, nucleosomes, and antibacterial machinery, including neutrophil elastase, which promotes thrombosis [[16]]. Histones induce platelet activation and cause profound thrombocytopenia [[17]]. Histones also
thrombosis 7005 [[20]], which then promotes the activation of complement pathways. The generated C3a and C5a also promote thrombosis and platelet activation [[21]]. In addition, extracellular RNA derived from damaged cells constitutes
thrombosis 7528 changes, including the activation of coagulation and insufficient control of coagulation, give rise to thrombosis at the sites of PAMP- and DAMP-induced inflammation. This local thrombus formation in microvessels impedes
thrombosis 8401 that restrict the hemostasis locally, DIC ensues [[28]]. In the same manner, DIC results when immuno thrombosis is no longer able to restrict the spread of pathogens or damaged cells at the inflamed injured sites
thrombosis 8636 processes are presented in Figure 1.Figure 1The pathophysiological processes of local hemostasis, immuno thrombosis , and systemic disseminated intravascular coagulation (DIC). Tissue injury promotes local hemostasis
thrombosis 8814 injury promotes local hemostasis and wound healing. Tissue injury also induces microvascular fibrin thrombosis called immunothrombosis to protect the host from altered-self (damage-associated molecular patterns;
thrombosis 8838 hemostasis and wound healing. Tissue injury also induces microvascular fibrin thrombosis called immuno thrombosis to protect the host from altered-self (damage-associated molecular patterns; DAMPs) and to restrict
thrombosis 9040 restrict the DAMPs in the injured vascular compartment. DIC results when local hemostasis and immuno thrombosis are no longer able to anchor thrombin or to restrict the spread DAMPs at the injured site. NET, neutrophil
thrombosis 10043 released by damaged and inflammatory cells at the site of injury promotes the development of microvascular thrombosis [[34]]. An important point is that HMGB1 inhibits the anticoagulant protein C pathway mediated by the
thrombosis 19051 antithrombin can significantly influence the coagulation processes, and are a potential risk factor for thrombosis [[56]]. Insufficient levels of antithrombin compared with the potential for thrombin generation in the
thrombosis 21895 alter the properties of the four hemostatic systems by affecting the endothelial function. Systemic thrombosis , namely DIC, ensues when these changes overwhelm the anticoagulation mechanisms that restrict the hemostasis
thrombosis 30443 protein C-mediated inhibition of PAI-1 is unlikely [[47],[80]].Solving the mystery of microvascular thrombosis Histological evidence of microvascular thrombosis in DIC, especially in DIC with the thrombotic phenotype,
thrombosis 30492 unlikely [[47],[80]].Solving the mystery of microvascular thrombosisHistological evidence of microvascular thrombosis in DIC, especially in DIC with the thrombotic phenotype, has been reported in clinical, experimental,
thrombosis 31003 hyperfibrin(ogen)olysis at an early stage of trauma and traumatic shock. Although arguments had been proposed, fibrin thrombosis [[87]], vein thrombi formation [[88]], platelet aggregation, and emboli formation [[89],[90]] had been
thrombosis 31209 had been repeatedly confirmed in hemorrhagic shock and trauma. Subsequently, the platelet and fibrin thrombosis became more prominent during antifibrinolytic therapy using tranexamic acid in a dog model of hemorrhagic
thrombosis 31844 DIC proposed by the SSC on DIC of ISTH, it is of limited interest to discuss whether microvascular thrombosis occurs in a situation of fibrin(ogen)olysis immediately after trauma and traumatic shock. However, it
thrombosis 32107 and anti-thrombotic states during the early stage of trauma. Therefore, the debate on microvascular thrombosis has major implications for the therapeutic strategies for patients with DIC after trauma [[95]].Figure
thrombosis 32313 [[95]].Figure 4The inhibition of the activation of fibrinolysis by tranexamic acid revealed microvascular thrombosis and thromboemboli formation in the large vessels in a dog model of hemorrhagic shock. (A) A section
thrombosis 36097 pathogenesis of DIC with the fibrinolytic phenotype is due to the dysregulation of local hemostasis and immuno thrombosis that are overwhelmed by the systemic inflammation caused by extensive tissue injury and tissue hypoperfusion.

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