The Human Body Transports Oxygen And Nutrients Throughout The Body Using The Vascular

Enoxaparin is a low molecular weight heparin used to prevent thrombosis, particularly post surgery. Enoxaparin binds to antithrombin III which is responsible for inhibiting coagulation by acting on factor Xa. Enoxaparin accelerates the activity of antithrombin III therefore preventing clot formation (McKenna & Lim, 2014 p766). When a blood vessel is damaged, platelets in circulating blood stick to the site of injury and release chemicals that attract more platelets causing aggregation. There are both intrinsic and extrinsic pathways causing thrombi to form to maintain a closed cardiovascular system (Hollar, 2017). Immobility increases risk of thrombus formation as the blood becomes stagnant with gravity and decreased

The dabigatran etexilate (DE) is a prodrug that directly competes for the active site of thrombin.1 This direct inhibition inactivates both fibrin-bound and free form of thrombin. Because of its rapid onset and offset of action, there is no need for the initial parenteral anticoagulant treatment in patients with acute thrombosis.1 On the other hand, the enoxaparin indirectly inhibits factor Xa.2 It has a shorter duration of action (12h vs 24h) and a shorter half-life (4.5-7h vs 12-14h) in comparison to DE. The DE and the enoxaparin have no interaction with diet and alcohol. There is no routine monitoring required

Disseminated intravascular coagulation (DIC) is an acquired syndrome that occurs when a stimulus pathologically activates intravascular coagulation and fibrinolysis resulting in an unbalanced hemostasis (Cunningham, 1999; Huether & McCance, 2008; Wada, 2008). The initiation of DIC starts with the release of tissue factor (TF) by the endothelial cells or white blood cells (WBCs). TF are present on many different cell types including lungs, brain, and placenta. The release of TF is subsequent to a variety of causes including trauma, ischemia, excessive metabolic stress, tumors, infectious organisms, exposure to cytokines and endotoxins (Baglin, 1996; Vinay, Abul, Nelson, & Richard, 2007). The release of endotoxin is the means by which

It inhibits thrombosis by inactivating co-factors Va, and VIIIa (Neyrinck, 2009). When deficient, Factor V can cause excessive blood clotting and Factor VIII, being an essential clotting factor, can cause blood to profusely move out of tissues once cut or damaged (Faust, 2001 and Yan, 2001). Thrombin may become limited, one reason being the decrease of plasma D-dimer, which again stimulates fibrinolysis (Bernard, 2001).

A: Potentiates the action of antithrombin III and thereby inactivates thrombin (as well as activated coagulation factors IX, X, XI, XII, and plasmin) and prevents the conversion of fibrinogen to fibrin; heparin also stimulates release of lipoprotein lipase (lipoprotein lipase hydrolyzes triglycerides to glycerol and free fatty acids)

Each treatment should be treated case-by-case to ensure that the patient is receiving the best possible care. Suggested treatments consist of regular infusions of DDAVP and/or clotting factor, first aid for minor cuts, physical therapy, fibrin sealants and clot-preserving medications. For Hemophilia C, clotting factor XI is available only in Europe and in the United States bleeding episodes are treated through plasma infusions. Clotting factor XI is not available in the United States because Factor XI concentrates are blood products with a concentrated form of Factor XI. Meanwhile, available only in certain areas of Europe, these blood concentrates are made through a series combining thousands of different blood donors. Therefore, the United States only keeps frozen plasma instead. Fibrin sealants work by applying the medication directly to the site of the wound, from there the Fibrin promotes clotting and healing. Clot-preserving medications can also be applied directly to the wound. However, this time the medication preserves the clot from breaking down and assists in ending the

This organ system has a number of functions namely, to keep a constant body temperature as well as to ensure coagulation occurs specifically at the site of injury, as well as to ensure no added blood loss occurs to cause life-threatening effects. This process of blood coagulation is explained in three interconnected phases. In the first phase, the enzyme thrombokinase is activated due to the damage of tissue and the breaking down of platelets. Prothrombin is converted into thrombin by the disintegration of the thrombocytes, electrically charged calcium ions and other coagulation factors, as well as the blood activator and tissue activator which become involved in the coagulation process. The second phase includes production of the thrombin that transforms fibrinogen in the blood plasma into fibrin. The thrombus (or blood clotting) is formed by a fibrilliform mesh that encloses the blood cells. Lastly, the third phase, which takes place as retraction occurs of the fibres of the fibrin mesh. Solidification of the fibrous mesh takes place which closes the defect in the vascular wall. Coagulation is then followed by fibrinolysis (re-dissolution of the clot).

Tranexamic acid is anti-fibrinolytic agent which prevents breakdown of fibrin clots. The mechanism of action of the drug is a complex one. The acid initially acts by hindering the binding of plasminogen and plasmin. Tranexamic acid has more potency and efficacy than aminocaproic acid. Tranexamic acid is used in multiple emergency medical conditions. The drug is used in prevention of postoperative bleeding disorders such as hemophilia. The drug proves to very useful in treating conditions such as menorrhagia, epistaxis, angioedema, and surface bleeding from tumors. In conditions such as DIC, tranexamic acid should not be used. The acid should not be used because it works against clots and hence activates

After injury Platelets adhere to the site of injury, then platelet gets activated and aggregated followed by activation of coagulation cascade and formation of clot.28,29

Rotational Thromboelastometry (ROTEM, TEM Innovations GmbH, Munich, Germany) and thromboelastography (TEG, Haemoscope, Braintree, MA) are whole blood coagulation analyzers that measure viscoelastic changes of the entire clotting process. Compared to the prothrombin time (PT/INR) and partial thromboplastin time (aPTT), which measure coagulation factor function, TEG/ROTEM can evaluate platelet function, clot strength, and fibrinolysis, (de Laz, Nascimento, & Rizoli, 2013). This additional information can help guide resuscitation efforts by classifying bleeding due to coagulopathy. As a result, the need for platelets, cryoprecipitate (fibrinogen, Factor VIII, von Willebrand factor, &

Vasoconstriction of the blood vessel is the initial stage in which it limits the blood flow at the site of injury. With the help of thrombin platelets become activated and aggregated via activation of protease-activated receptors (PARs) on the surface of the platelet cell membrane. During coagulation, prothrombin is converted to thrombin in the presence of Ca2+, though these functions involve numerous cleavage reactions. Thrombin has a vital role in clot promotion and inhibition,

Hemostasis is the process that causes bleeding to stop. It also changes blood from a liquid to a gel. It consists of three processes, vascular spasm, platelet plug formation and blood coagulation. Vascular spasm is the first step in heeling in the wound. Vascular spasm is when the damaged blood vessels constrict due to tightening of muscle cells on the inside wall. This helps decrease blood flow, thus minimizing blood loss. Then platelet plug formation occurs. This is when platelets adhere to the damaged endothelium and form a plug. Normally platelets do not stick to the endothelial lining but during an injury collagen is exposed. The exposed collagen activates the platelets to stick together and form a plug. Once the platelets are stuck together

Hemostasis is the process of blood coagulation. The first thing that happens is the contraction of the smooth muscles in the blood vessel wall. next is the formation of the platelet plug, which become sticky and adhere to the defect to form a temporary plug. Formation of a blood clot then happens. The substance needed for coagulation are normally inactive in the bloodstream. some substances in clotting are ones such as, calcium ion, enzyme precursors, vitamin k, fibrinogen, calcium. After these substances are obtained then the final steps begin. First substance released from the damaged tissue and sticky platelets initiate a reaction that leads to the formation of prothrombinase. Next the prothrombinase converts prothrombin in the blood to

FXI play a crucial role in coagulation, thromboembolism, and peripheral vascular disease mediated by venous thrombus growth in an endothelial denudated vessel and/or blood stasis. Promotion of the platelet aggregation and fibrin formation at low shear stress by the interaction of FXI and thrombin signify the role of FXI in thromboembolism [47]. Further, reduction in the thrombus formation in a denuded vessel with anti-FXI antibody indicates FXI to be a promising target in coagulation cascade to prevent thromboembolic events [47,48]. Many studies has demonstrated the reduced thrombus formation without increasing the risk of bleeding with antisense oligonucleotide (ASO) along with increased number of fluorescent platelets shed from the

Heparin act by binding to the natural anticoagulant antithrombin, thereby consequently increasing the activation of thrombin by antithrombin and several others activated coagulation factors.