To stop the blood flow after damage, body uses three ways to maintain hemostasis; vascular spasm, platelet plug formation, and coagulation. Coagulation is an important process to prevent loss of blood when blood vessels are cut or damaged. Blood clot is a plug of platelet reinforce with the mesh of fibrin. However, a person with Disseminated intravascular coagulation, DIC, the blood clots have formed throughout the blood vessels when does not necessary. It leads to organ damages due to blocked blood vessels; furthermore, it leads to life-threatening bleeding due to wasting clotting factors and platelets when they are needed.
According to Marieb and Hoehn, to do the blood clot, the enzyme, thrombin, and clotting factors are required. The clotting factors are represented with Roman numerals. There are thirteen different types of clotting factors. There are two ways to initiate the blood clot; the extrinsic pathway and intrinsic pathway. With the extrinsic pathway, the faster coagulation occurred in outer tissues. With the cut, cells get damaged, and more tissue factors, TF, are produced on the surface protein. This TF then binds to factor VII, form TF/VIIa complex, and it substrates into factor IX and factor X. With the intrinsic pathway slower but broader coagulation occurred within the damaged vessels. Factor XII is regularly circulates in the blood, but when the blood vessel gets cut, the blood flow into the tissue space. The collagens in the tissue activate the factor XII. This activated factor XIIa trigger factor XI which then activates factor IX, and factor X. The factor X from both of the pathways binds and activates factor V. This combination is called as prothrombinase because it converts prothrombin, factor II, to throm...
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Another projection mechanism is what is called Arterial spray, this is one of the more serious mechanisms, although all are serious, but this type indicates that a major artery has been detached. The continuous pumping of the heart gushes blood form the severed artery. The patterns are more inconsistent here, because each time the heart pumps it will leave an entirely new blood stain
In some individuals with severe hemophilia, the factor VIII replacement therapy is identified as a foreign substance by their immune system. If this happens, their immune system will make antibodies against factor VIII. These antibodies will inhibit the ability of the factor to work in the clotting process. The higher the antibody or inhibitor level, the more factor VIII replacement therapy it takes to overcome the inhibition and produce clotting. This can complicate the treatment of a bleed. The good news is that there are different types of therapies available to successfully treat most individuals who develop inhibitors.
Signs of DIC are as varied as the diseases and conditions which precipitate it; the most universal sign is abnormal bleeding, such as excessive bleeding from venipuncture sites and petechiae or ecchymoses occurring spontaneously along the ventrum and inguinal body regions (Bassert 1161, Tilley 373). Three distinct phases of DIC are recognized: the chronic silent phase, the peracute hypercoagulability phase, and the acute consumptive phase (Bruchim). Each phas...
...-1 (PAI-1) from the endothelial cells and monocytes, activating the extrinsic coagulation pathway. This also leads to activation of factor X and fibrin production.
Hemophilia is a rare bleeding disorder that slows the blood clotting process, which is not normal. Some people with Hemophilia may just have a little bit of “clotting factor” or no clotting factor at all (National Institute of Health [NIH], 2013). Clotting factor is a protein in blood that controls bleeding and they are needed the blood to clot normally. In order to help the blood clot, clotting factors work with “platelets” (National Institute of Health [NIH], 2013). Platelets are small blood cell fragments that form in the bone marrow, a tissue in the bones that is similar to a sponge. The functions of platelets have a very important role in blood clotting; the role of a platelet is to stick together (by the help of clotting factors) to block cuts, break on the carriers of blood (veins or arteries) throughout the body, and stop the bleeding when “blood vessels” (National Institutes of Health [NIH], 2013) are injured. Blood vessels are tube like structures carrying blood through the tissues and organs, like a vein, artery, or capillary. People with hemophilia do not have enough “clotting factor VIII or IX” (World Federation of Hemophilia [WFH], 2013) in their blood, which results to prolonged bleeding or oozing, meaning that bleeding can last longer (though, not faster) than usual after surgeries, accidents, or having teeth pulled out at the dentist. Clotting factor VIII, which can also be called as “anti-hemophilic factor” (AHF, for short) (Patient.co.uk, 2011), is a blood clotting protein that is necessary for humans to have. Clotting Factor IX is a protein that i...
...n of the valves. ClfA mediates the attachment to nonbacterial thrombotic endocarditis (NBTE) followed by FnbpA causing endothelial cell internalisation, inflammatory and coagulation responses[12].
Deep Vein Thrombosis (DVT), is a blood clot that forms in a deep vein inside the body. DVT can occur when the blood thickens, because the thickening of the blood can cause a clot to form. DVT will generally occur within the lower leg or thigh, as well as other parts of the body. A clot that occurs in a deep vein can possibly break off from the original vein. When it breaks off it can travel throughout the body’s bloodstream. It is called an embolus when the clot breaks off. The clots that broke off throughout the thighs, are more likely to cause Pulmonary Embolism, rather than the other blood clots within the remainder of the body. Pulmonary Embolism is a serious condition which can be caused by blood clots. It can damage your organs, more likely to be the lungs, and cause death of an individual.
Whenever an injury cannot be avoided, however, it activates a series of mechanisms to repair the organism. Evidence of these systems comes from blood platelets that clot wounds to prevent bleeding out.
Immediately after wounding, the first phase of hemostatsis sets in motion with vascular constriction which restricts the blood flow in the blood vessels followed by the platelets plug formation which creates a temporary blockage of blood flow and then coagulation takes place with fibrin clot formation. The clot and surrounding tissue release pro-inflammatory growth factors and cytokines such as transforming growth factor (TGF)-13, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and epidermal growth factor (EGF).
Von Willebrand disease is due to an abnormality, either quantitative or qualitative, of the von Willebrand factor, which is a large multimeric glycoprotein that functions as the carrier protein for factor VIII (FVIII) (1). Von Willebrand factor is also required for normal platelet adhesion. As such, von Willebrand factor functions in both primary (involving platelet adhesion) and secondary (involving FVIII) hemostasis. In primary hemostasis, von Willebrand factor attaches to platelets by its specific receptor to glycoprotein 1b on the platelet surface and acts as an adhesive bridge between the platelets and damaged sub-endothelium at the site of vascular injury. In secondary hemostasis, von Willebrand factor protects FVIII from degradation and delivers it to the site of injury.
Proteins, a macromolecule in the blood, serve many functions. One of these is to assist in blood clotting. There are 13 proteins that make up the clotting cascade. After a bleeding episode or injury, the clotting cascade is activated. These proteins work together in the blood to create what is known as a fibrin clot. A fibrin clot is what most people know as a scab. This clot stops the loss of blood and keeps it circulating inside the veins to continue its mission of carrying oxygen and other vital things to our organ systems.
Von Willebrand factor is the protein that allows for the forming of blood clots that will seal off broken blood vessels and form a clot that will slow down or stop bleeding. If an abnormality of this protein occurs then the sticking of platelets does not happen which then does not allow them to stick to the broken blood vessels and clot them.
There are the three pathways in which coagulation occurs: Intrinsic, Extrinsic and Common. The intrinsic pathway is once a substance within the vessel wall (collagen that ordinarily hidden from the blood however exposed if the vessel is damaged) meets a unique chemical within the blood (Factor XII) a series of chemical changes occur that end in the formation of protein and a blood clot. The foreign pathway is ready in motion once blood leaves a broken vessel and enters the tissues around it. Then a chemical within the blood (Factor VII) comes into contact with a chemical within the tissues (Tissue Factor). Once these 2 rest a series of chemical changes occur that results in the formation of protein and a blood clot.
Once the vascular component has been assessed, we get a clear idea of the main limiting organic factor in wound healing. We can then build on this information by assessing the patient 's cofactors in healing. This step is essential in order to maximize the vascular network the patient possesses. Those cofactors are:
The second and more serious type of bleeding is venous bleeding, which transpires when a vein has been severed and blood flows steadily. Most veins collapse when cut, which aids in controlling this type of external bleeding until medical attention can be received.