Thrombin Research Paper

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

Venous thrombi, composed predominately of red blood cells but also platelets and leukocytes bound together by fibrin, form in sites of vessel damage and areas of stagnant blood flow such as the valve pockets of the deep veins of

Heparin, also known as a blood thinner is given to people to help reduce and stop blood clots that have yet begun to form. It is one of the most common medications given to help thin blood by entering the thrombus and speeding up the activity of one of the body's natural anticoagulant by 2000 times. Heparin may also be given to people who about to undergo surgeries such as: open heart, heart transplant, lung

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)

During this step, the body has one primary goal; Stop the bleeding (coagulate the blood). In order to reach this goal, as series of clotting factor proteins have

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

Hemophilia is a rare blood condition in which an individual’s blood cannot clot appropriately to stop bleeding. There are two types of Hemophilia, Hemophilia A and Hemophilia B. This paper will be focusing on Hemophilia A, also known as classic hemophilia. “Hemophilia A is a genetic disorder caused by a missing or defective factor VIII, a clotting protein” (National Hemophilia Foundation, n.d., para. 1). Clotting proteins work with cell fragments called platelets to stop bleeding. “When blood vessels are injured, clotting factors help platelets stick together to plug cuts and breaks on the vessels and stop bleeding (National Heart, Lung, and Blood Institute, 2013, para.

The occlusion, caused by a haemostatic plug or thrombus is comprised of a fibrous protein called fibrin. This protein polymerises to create a tightly woven mesh, trapping platelets within the fibrin fibre meshwork, resulting in the

Platelets are small fragments of cells. Platelets process coagulation. This is done by them gathering at the site of an injury and in turn sticking to the lining of the injured blood vessel. This is a platform on which blood coagulations occur, resulting in the formation of a fibrin clot. This covers the wound and prevents blood from leaking out. Fibrin also forms the initial building blocks from which new tissue are formed, in- turn promoting the healing process. If there is an imbalance, for example to high of a number of platelets may result in clotting not necessary in the body that can lead to health risks or a lower than normal counts can lead to extensive bleeding. So they protect us by clotting and aiding in healing by producing

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

Thrombolytic therapy is the use of drugs to break up or dissolve blood clots, which are the main cause of both heart attacks and stroke.

It is amazing to see how this simple protein can have such a large positive impact on the general population; especially to those who have diabetes. This is entire new to me; that is people who are diabetics have a hard time to the heal wounds. My answer to the question is that I believe there are other factors that plays a role in blood clotting. Hsp60 protein may be an important factor, but those that lack Hsp60, I assume can still clot blood, just in the matter of time. I thought this article is relevant to me because my great grandmother suffered from diabetes and my mom is also diabetic, however, it does not seem as if they are having trouble with any wound healing problem. That’s why I hypothesized that there are other factors that plays

Coagulation is a natural physiological process and is required for the normal functioning of the body. At sites where there is injury to the blood vessels, blood clots are formed as a result of activation of coagulation pathway. Platelets are attracted to the site of injury and a network of tissues is formed. It gets dissolved as the wound heals. However, if the clotting plug increases in size and does not dissolve, there are chances of thrombotic episodes. LMWH are modulators of the coagulation pathway. Enoxaparin is a LMWH, hance, used to treat patients with myocardial infarction or related thrombotic disorders. An effective dose of the drug need to be provided to the patient. ‘Therapeutic dosing period’ is the time period calculated on a

Coagulation is a process where there is a blood clot formation at the site of an injured blood vessel. Once there has been an injury to the blood vessel wall, vasoconstriction immediately occurs, and then we get primary haemostasis. Platelet activation occurs in this process and they adhere to the subendothelial complex. There is a formation of fibrin in this process and this leads to a haemostatic plug being formed at the site of injury. Secondary haemostasis also occurs simultaneously with primary haemostasis. In this process, tissue factors are involved in the initiation of the coagulation cascade. The end result of the coagulation cascade is the activation of thrombin. Thrombin is an important enzyme in haemostasis as it is needed for the conversion of fibrinogen to an insoluble fibrin monomer to form the matrix of the clot and also it is important for further platelet activation. (Khan and Dickerman, 2006; Hoffman, 2003; Clemetson, 2012; Arnout et al., 2006; Hawiger, 1987; Green, 2006)

Physiology is the study of how body of living things function. There are many issues in this topic but the issue of blood clotting is a unique area of study. Blood clotting is also known as blood coagulation and it has two definitions which vary because of its occurrences. Blood clotting is first defined as natural sealing of an injured part of the body by blood for the purpose of preventing blood loss. The second meaning of blood is concentration of blood in one part of the body like in lungs or veins. Many researchers and physician concentrate more on veins clotting (inner clotting) of blood because it is a threat to lives of many people. However, the paper will explore the two types of blood clotting and come up with a conclusion on how the two types of blood clotting occur and how they are threat to human life. The general objective of the paper is to research on the whole concept of physiology blood clotting in human beings.