China
Africa
Explore chapters and articles related to this topic
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).
Heterocyclic Drug Design and Development
Published in Rohit Dutt, Anil K. Sharma, Raj K. Keservani, Vandana Garg, Promising Drug Molecules of Natural Origin, 2020
Garima Verma, Mohammad Shaquiquzzaman, Mohammad Mumtaz Alam
Hemostasis is known as a stoppage of bleeding from any blood vessel or body part. Agents which bring about hemostasis are known as hemostatic agents (Levy, 2009). Hemostasis is brought about by stimulation of fibrin formation or inhibition of fibrinolysis. Hemostatic agents derived from plants are given in Table 9.12.
Tranexamic Acid (TA)
Published in John C. Petrozza, Uterine Fibroids, 2020
John Storment, Camille Storment
Data show the presence of extensive fibrinolysis in the menstrual blood of women with heavy menstrual bleeding [3]. This has prompted investigation into the use of antifibrinolytic agents to decrease menorrhagia by increasing clot formation [4,5]. Activation of the clotting cascade occurs at the site of tissue injury. It involves the formation of thrombin, which cleaves fibrinogen to fibrin and produces hemostasis. Dissolution of this clot is then activated by fibrin in an effort to keep the vessel open. Fibrinolysis occurs when plasminogen (trapped within the clot) binds to lysine, resulting in a degradation of the fibrin clot. Excessive fibrinolysis can be prevented by tranexamic acid (TA) keeping the clot more stable [6]. TA, a synthetic derivative of the amino acid lysine, binds to plasminogen and blocks the interaction of plasmin with fibrin, thereby preventing clot dissolution [6]. Although its mechanism of action raises concern about an increased risk of thrombosis, this association has not been seen in clinical trials [7].
Hirudin versus citrate as an anticoagulant for ROTEM platelet whole blood impedance aggregometry in thrombocytopenic patients
Published in Platelets, 2023
Wasanthi Wickramasinghe, Bhawani Yasassri Alvitigala, Thisarika Perera, Panduka Karunanayake, Saroj Jayasinghe, Senaka Rajapakse, Praveen Weeratunga, Ananda Wijewickrama, Roopen Arya, Klaus Goerlinger, Lallindra Viranjan Gooneratne
Platelets play a crucial role in hemostasis.1 The rotational thromboelastometry (ROTEM) platelet module used together with the ROTEM delta device (TEM Innovations GmbH, Munich, Germany) assesses platelet aggregation by whole blood impedance aggregometry and displays platelet aggregation graphically and numerically.2 3.2% sodium citrate is the most widely used and conveniently available anticoagulant for platelet function tests (PFTs), although its chelation of ionized calcium in blood affects platelet function by the inhibition of platelet aggregation since intra-platelet calcium concentration is an important modulator of platelet function.3 Moreover, as a result of reduction in calcium levels, citrated samples have resulted in low reproducibility and sensitivity to tests associated with thrombin activation of platelets.4 The non-calcium chelating anticoagulant hirudin which was introduced subsequently, is a polypeptide present in the leech (Hirudo medicinalis) having a strong and direct antithrombin activity by inhibiting the conversion of fibrinogen to fibrin. Hence, hirudin maintains the physiological milieu of the sample.5 Thrombin-receptor activating peptide-6 is used in platelet function testing in order to provide a standardized activation.6–8
Computational modeling of hypercoagulability in COVID-19
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Ge Zhu, Susree Modepalli, Mohan Anand, He Li
The human blood coagulation cascade is a complex biochemical process (Schenone et al. (2004)). The primary function of human blood coagulation is to minimize blood loss during vascular injury due to physical trauma. Hemostasis refers to the process by which the body controls blood loss after an injury by secreting enzymes to form a clot and cover the injury sites. The human body maintains homeostasis by maintaining balance among three major hemostatic processes: vasodilation, blood coagulation and clot dissolution. The excessive progress of any of these three hemostatic processes can lead to abnormal hemostasis and potentially fatal consequences. For example, lack of sufficient concentration of coagulation factors (hemophilia) or abnormal fibrinolysis (Francis (1989)) can lead to rapid blood loss (Zimmerman and Valentino (2013)) and excessive generation of prothrombotic factors can lead to undesired blood clotting (thrombosis)(Zoller et al. (1999)). Both hemophilia and thrombosis can lead to fatalities. As a result, maintaining hemostasis is key to maintaining healthy physiology.
Application of anti-Xa assay in monitoring unfractionated heparin therapy in contemporary antithrombotic management
Published in Expert Review of Hematology, 2023
Michael Safani, Steve Appleby, Ryan Chiu, Emmanuel J Favaloro, Emanuel T. Ferro, Jimmy Johannes, Milan Sheth
The coagulation pathways represent a cascade of events intended to provide a balance between procoagulant and anticoagulant processes and maintain hemostasis. Primary hemostasis consists of platelet activation, aggregation, and thrombus formation and aims to form a plug at the site of exposed endothelial cells due to tissue damage. Secondary hemostasis, as measured by the pathology laboratory, conventionally comprises three coagulation pathways. The intrinsic pathway is activated by endothelial damage and collagen exposure and includes factors I, II, IX, X, XI, and XII. The extrinsic pathway is activated by release of tissue factor by damaged endothelium and includes factors I, II, VII, and X. The common pathway consists of factors I, II, V, VIII, X. The intrinsic and extrinsic pathways converge to form a common pathway and at a specific point to activate fibrinogen to form fibrin polymer. In vivo, the final stages of primary and secondary hemostasis are marked by binding of fibrin polymers to platelets to secure and stabilize the platelet plug [37–41].