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Postoperative Bleeding
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
The coagulation system is comprised of primary and secondary hemostasis. Platelet plug formation is the endpoint for primary hemostasis, while secondary hemostasis centers around thrombin. Thrombin is an enzyme that converts fibrinogen to fibrin and simultaneously activates platelet aggregation and the intrinsic and extrinsic pathways. Massive blood loss presents a challenge to the coagulation system. With loss of coagulation factors and thrombocytopenia comes coagulopathy (Curnow et al., 2016).
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
Ongoing problems with sepsis/septic shock require the patient to be transferred to a higher level of care, where continuous monitoring and circulatory support, with a nurse–patient ratio of 1:1, can be offered. The coagulation system is inappropriately activated, and clotting factors become depleted as a result of forming multiple clots in the capillary bed. This has several physiological effects: Depletion of clotting factors puts the patient at risk from spontaneous bleeding.Increase in clot formation increases the risk of thrombosis.
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Evidence for the role of lipid factors in thrombosis and atherosclerosis exists in Type IIa hyperlipidemic patients. These patients are highly sensitive to aggregating agents such as ADP, collagen, or epinephrine.369 The lipid composition of platelets is not different from normals, however, Type IIa subjects produce more thromboxane A2 from arachidonic acid than normals. Type IIa patients also exhibit increased kallikrein activation and have high levels of circulatory soluble fibrin complexes. This finding is consistent with platelet-mediated activation of the intrinsic coagulation system. Treatment of these patients with clofibrate or other lipid regulating agents returns the ADP-sensitivity of platelets to normal, while modifying the plasma lipid profile.
The antithrombosis effect of dehydroandrographolide succinate: in vitro and in vivo studies
Published in Pharmaceutical Biology, 2022
Bowen Yin, Shuhua Zhang, Yuxi Huang, Yuanzhu Long, Yiguo Chen, Shiyun Zhao, Aiqun Zhou, Minghua Cao, Xiaoming Yin, Daya Luo
In the detection of coagulation factors, we found that DAS activated many coagulation factors after administration to rats. The activation of FV, FVII, FVIII, FX and FXI was significant in the medium- and high-dose groups. The activation of these factors indicates that DAS effectively protects both the intrinsic and extrinsic pathways and confirms the results of coagulation function: PT and APTT are shortened. At the same time, a slight increase in the Fg content was observed both in vivo and in vitro. We speculated that the increase in Fg levels was due to the release of platelet α granules induced by related factors, which was verified by the shortening of TT in vitro. These phenomena in the secondary haemostatic system are encouraging. The current antiplatelet, anticoagulant and thrombolytic drugs all inhibit the haemostatic system, resulting in a low reaction within the coagulation system. In contrast, the appropriate protective effect of DAS on secondary hemostasis effectively avoids hypoactive coagulation function.
Factor IX(a) inhibitors: an updated patent review (2003-present)
Published in Expert Opinion on Therapeutic Patents, 2022
Daniel K. Afosah, Edward Ofori, Madhusoodanan Mottamal, Rami A. Al-Horani
The coagulation system and platelets are activated by vascular injury. In one hand, the vascular injury promotes the platelets adhesion by von Willebrand factor (vWF)-mediated bridging of the glycoprotein (GP) Ib–V–IX complex on the platelet surface to the subendothelial collagen [39]. Platelet receptors αIIβI (endogenous ligand is fibrinogen) and GPVI (endogenous ligand is collagen) are also important for platelet activation, aggregation at the site of injury, accumulation on collagen, and clot retardation which helps tightening the injury sealing and initiating wound healing [40,41]. Adhered platelets subsequently secrete soluble agonists (thromboxane A2 and adenosine diphosphate) to further recruit and activate circulating platelets [33]. Thrombin, a pivotal coagulation factor, can also activate platelets by binding to protease activated receptors 1 and 4, and thus, serves as the main linking protein between the platelet and coagulation pathways [42].
The Total Thrombus Formation (T-TAS) platelet (PL) assay, a novel test that evaluates whole blood platelet thrombus formation under physiological conditions
Published in Platelets, 2022
K.L. Zheng, H. Wallen, D. Aradi, T.C. Godschalk, C.M. Hackeng, J.R. Dahlen, J.M. Ten Berg
Both platelets and the coagulation system play a pivotal role in the pathogenesis of arterial thrombosis. Patients undergoing percutaneous coronary intervention with stenting, or with an acute coronary syndrome (ACS), are treated with dual antiplatelet therapy (DAPT, aspirin, and a P2Y12 inhibitor) to reduce (recurrent) thrombotic events[1]. The antiplatelet effect of P2Y12 inhibitors is, however, variable, and measuring this effect can be done with several tests [2]. However, currently available agonist-based platelet function assays have the limitation to reflect only one pathway of platelet activation, instead of a general measure of the effect of combined antiplatelet therapy. Unlike existing methods that rely on changes in light transmission and/or electric impedance after stimulation, the Total Thrombus Formation Analysis System (T-TAS) PL assay is a novel point-of-care whole blood test that uses shear flow in the presence of collagen-coated surface. The method allows for ex vivo evaluation of overall primary hemostatic ability in flowing whole blood mimicking physiological conditions without the addition of soluble agonist stimulation, and might better reflect the in vivo situation. As such, the T-TAS assay is able to measure the combined effect of antithrombotic therapy on platelet thrombus formation: von Willebrand factor (vWF) mediated platelet adhesion, the release of endogenous platelet agonists, and platelet activation and aggregation.