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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...-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.
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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.
“Chronic diseases and illnesses are the leading causes of death and disability in the United States” (CDC.gov, 2014). These types of illnesses are the most common health problems that people in this country face today and they are also the most preventable (CDC.gov, 2014). Every year the cost to help care for and manage people with these types of illnesses increases and there is less being done about educating people about prevention. Venous Thromboembolism is one such chronic disease that is very deadly but also very preventable if the right precautions are taken. This paper will aim to educate about the disease, courses and costs of treatment, clinical microsystems that are involved and what barriers if any exist to achieving generative relationships among the various clinical microsystems involved.
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Many great historical figures of the scientific community have written on the subject of the same perplexing disease over the centuries (Angus, van der Poll, Finfer, Vincent 2013). Sepsis has been given many names, origins, and etiologies. In the 4th century, Hippocrates declared the disease the cause of organic decomposition, wound festering, and swamp gas (Angus et al. 2013). During the 19th century, Louis Pasteur theorized the disease was the outcome of a pathogenic microorganism in the bloodstream, which resulted in a body-wide infection (Angus et al. 2013). In the 21st century, the medical community made a breakthrough with the discovery of the disease’s link to the inflammatory response system and devised a plan of action to combat the high mortality rates among those infected (Angus et al. 2013). According to Hotchkiss, Monneret, & Payen (2013) the effects of sepsis are well documented, while the molecular processes it utilizes are still being explored; however, new studies are helping to expand our understanding of the centuries old disease.
...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].
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.
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Sepsis is defined as a systemic inflammatory response caused by an infective process such as viral, bacterial or fungal (Holling, 2011). Assessment on a patient and starting treatment for sepsis is based on identifying several factors including the infective source, antibiotic administration and fluid replacement (Bailey, 2013). Because time is critical any delay in identifying patients with sepsis will have a negatively affect the patients’ outcome. Many studies have concluded every hour in delay of treatment mortality is increased by 7% (Bailey, 2013). Within this assignment I will briefly discuss the previous practice and the recent practice including the study based on sepsis. I will show what enabled practice to change and I will use the two comparisons of current practice and best practice.
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).
External bleeding is divided into three types. Capillary bleeding is the most common type of external bleeding, which occurs when blood oozes from the capillary. It is easiest form of external bleeding to control and is typically not serious.
platelets on a slide, you would need to have the specimen recollected because of a clot, or
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 white blood cells destroy any unfamiliar pathogens in the bloodstream and can cause inflammation. Therefore, the inflammation causes a surplus of white blood cells to clot the wound for healing.