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I need some assistance with these assignment. the use of tranxamic acid for haemorrhage vontrol in a pre-hospital environment Thank you in advance for the help!
I need some assistance with these assignment. the use of tranxamic acid for haemorrhage vontrol in a pre-hospital environment Thank you in advance for the help! Dawkins and Deakin (2004 P.93) note that Kallikrein catalyzes activation rate of factor XII, which in turn activates factor XI, then factor IX. They also reveal that factor X speeds up the activation of prothrombin (Factor II) to thrombin. The thrombin form plays two major roles: it breaks the arginine-glycine bonds found in fibrinogen (factor I) to form fragment that polymerizes to form fibrin. It also activates factor XIII whose role is to strengthen the fibrin to form a stable fibrin. Dawkins and Deakin (2004 P.93) note that it is this fibrin that forms the rigid layer of the clot. Physiology of Fibrinolysis Fibrinolysis refers to the process of breaking down of fibrin clot. It is generally catalyzed by serine protease plasmin found in the blood as the inactive proenzyme plasminogen. Dawkins and Deakin (2004 P.94) argue that plasminogen is activated by a plasminogen activator. Since the plasminogen activator also contains fibrin binding site, it also aids in the activation of plasminogen in the presence of fibrin. Tissue plasminogen activator (tPA) is the major plasminogen activator found in vivo, which is released from vascular endothelial cells when stimulated by urokinase and thrombin. The complex plasmin-activator binds to plasmin through lysine binding sites and breaks down fibrin to fibrin degradation products according to Dawkins and Deakin (2004 p.93). Learning outcome 2 How hyperfibrinolysis occurs in massive hemorrhage Blood clots are removed through a process known as fibrinolysis. Enhanced fibrinolytic activity in the blood is referred to as hyperfibrinolysis. Hyperfibrinolysis leads to increased bleeding, which can lead to trauma and death in patients. Lack of alfa-2-antiplasmin in the body is the main cause of hyperfibrinolysis. In addition, hyperfibrinolysis can also be a result of lack of plasminogen activator inhibitor type 1. Severe trauma cases have witnessed the ineffective outcome of hyperfibrinolysis (Akahashi, Tanaka, Minowa, 1996: 61). In trauma patients, bleeding is as a result of the production of fibrinogen degradation products. These fibrinogen degradation products normally affect the regular fibrin polymerization and interfere with the production of platelets. Hyperfibrinolysis leads to the production of plasmin. Plasmin has the ability to proteolytically activate or deactivate several plasmatic and cellular proteins which are important in the process of homeostasis. The degradation of fibrinogen is the main cause of excessive bleeding in trauma patients and other injury victims (Akahashi, Tanaka, Minowa, 1996: 61). Tranexamic acid is the best treatment for hyperfibrinolysis. Several deaths of both citizens and military officers take place in the pre-hospital setting. Tourniquet placement was the treatment method used in the pre-hospital setting before the introduction of Tranexamic acid (Sauaia, Moore, Moore, Moser, Brennan, Read, Pons, 1995: 188). Tourniquet placement has proved to be ineffective due to the number of soldiers and other individual who succumb to survivable injuries. The use of Tourniquet has not been able to control injuries leading to torso exsanguinations. In addition, Tourniquet placement has not also been able to control deaths that result from functional haemorrhage (Spahn & Rossaint, 2005: 130).
