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Shock Management
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Anti-coagulation must be rapidly reversed in anti-coagulated patients who have major trauma with haemorrhage. Prothrombin complex concentrate should be administered immediately in adults (age 16 years or over) with major trauma who have active bleeding and need emergency reversal of a vitamin K antagonist. A haematologist should be consulted at the earliest opportunity for advice on adults who have active bleeding and need reversal of any anti-coagulant agent other than a vitamin K antagonist.28
Studies of the Primate Inflammatory Hemostatic Axis and Its Response to Inflammatory Mediators
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Figure 1A shows the four functional domains of the hemostatic system. The anticoagulant and coagulant domains acting through the vascular endothelium and platelets, respectively, compete to control clot formation. The fibrinolytic and antifibrinolytic domains compete in the same manner to control clot removal. All four domains respond to thrombin through its action on the vascular endothelium, platelets, and fibrinogen (2). The key to understanding this integrated system is that there is a hierarchy of responses to thrombin. The vascular endothelium and its associated anticoagulant/fibrinolytic domains are the most responsive, platelets are next, and fibrinogen is the last and least responsive. Under normal circumstances the small amounts of thrombin that are generated “spontaneously” in the microvasculature bind to receptors on the vascular endothelium such as thrombomodulin (TM) (3,4). These interactions lead to the generation of activated protein C (APC) (3) and the release of tissue plasminogen activator (t-PA) (5,6). The activated protein C inhibits further production of thrombin by inactivating factors Va and Villa in a negative feedback (3,4). The tissue plasminogen activator lyses any fibrin (fdp) that might have formed by activating plasminogen to plasmin (7).
Disorders in tHemostasis System and Changes in the Rheological Properties of the Blood in Ischemic Heart Disease and Diabetes Mellitus Patients
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
In the appearance of pathological processes such as DIC and IHD, both qualitative and quantitative changes occur in the system of blood coagulation. First of all, the sensitivity to thrombin lowers and the process of polymerization of the fibrin monomers is disturbed. They partly form complex compounds with fibrinogen, probably with early products of the decomposition of fibrinogen by plastin. Products of paracoagulation appear — soluble fibrin-monomer complexes (SFMC). These large and medium-size molecular SFMC coagulate poorly under the influence of thrombin. This thrombin resistance of the complexes disturbs the normal transformation of fibrinogen into fibrin and may produce the phenomenon of the DIC syndrome (syndrome of disseminated intravascular coagulation).
Erroneous computer-based interpretations of atrial fibrillation and atrial flutter in a Swedish primary health care setting
Published in Scandinavian Journal of Primary Health Care, 2019
Thomas Lindow, Josefine Kron, Hans Thulesius, Erik Ljungström, Olle Pahlm
Patient records for those patients who had an incorrect computer-based diagnosis of atrial fibrillation or atrial flutter were studied to find out whether (a) the incorrect computer diagnosis was corrected; (b) treatment with anti-coagulant therapy was initiated; (c) anti-arrhythmic therapy was initiated; (d) the patient was admitted to a hospital or (e) the patient was referred for follow-up tests. Data on b–e were not included if reasons other than atrial fibrillation or flutter were present for initiation of medical therapy (b, c), admittance to the hospital (d) or follow-up investigations were present (e). If the primary care physician interpreted an ECG with a computer diagnosis of atrial fibrillation as atrial flutter or vice versa, the diagnosis was considered to be correct in this study.
Chronic testosterone administration improves cardiac contractility and has a beneficial effect on the haemostatic system by enhancing fibrinolytic activity and inducing hypocoagulation in healthy rats
Published in Archives of Physiology and Biochemistry, 2019
Naif M. Alhawiti, Sultan A. Alqahtani
A delicate balance exists between the pro-coagulant and anticoagulant components of the haemostatic system (Gale 2011). Any discrepancy in this balance participates in either thrombosis or haemorrhage as a result of hyper-coagulation or hypocoagulation, respectively (Rodak 2002, Gale 2011). Currently, accumulating evidence suggests an increasing importance of haemostatic disturbance as cardiovascular (CV) risk factors. Indeed, the link between acute variations in haemostatic variables and the risk of cardiovascular disease (CVD) has been strengthened by the identification of certain CVD biochemical markers including hyper-coagulation, enhanced platelet reactivity, increased blood viscosity as well as decreased fibrinolytic activity (Juhan-Vague et al.1996, Ernst and Koenig 1997, Koenig 1998, Pop et al.2002, Campo et al.2006, Doggen et al.2006, Chan et al.2008).
A vaccine targeting blood clot formation: what is the potential?
Published in Expert Review of Vaccines, 2019
Munehisa Shimamura, Hironori Nakagami
Antithrombotic agents are generally classified as anti-platelet agents for non-cardioembolic stroke and anti-coagulants for cardio-embolic stroke. Although several types of anti-platelet and anti-coagulant agents are available in the clinic which targets different molecules in the thrombosis pathway, most agents cause increased the risk of bleeding. For example, aspirin and a P2Y12 receptor antagonist (clopidogrel), commonly used for secondary prevention of ischemic stroke, prasugrel, ticagrelor, and other glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, and eptifibatide) in heart diseases increase the risk of bleeding [5]. In contrast, protease-activated receptor (PAR)-1 inhibitor is an anti-platelet medication reported to prevent thrombotic formation without affecting coagulation and bleeding time in animal models [6] and a phase 2 clinical trial [6]. However, patients administered the PAR-1 inhibitor in addition to standard of care antiplatelet therapy showed an increased incidence of bleeding events compared to the placebo group in phase 3 trials [7,8]. Thus, we focus on the recently reported novel thrombotic agent S100A9 [9].