Thrombus Formation

Venous thrombosis and arterial thrombosis are considered to be distinct pathophysiological processes due to their evident anatomical variances. With one having to deal with platelet activation while the other involving the clotting system activation, arterial thrombosis and venous thrombosis are similar yet vastly different when it comes to the processes that are performed for the body. These same processes that help the body have to be performed accordingly or the signs and symptoms begin to show. For instance, venous thrombosis can lead to Chronic Venous Insuffiency and other issues when a body part is congested. This is most commonly causes by valvular incompetence in the low-pressure superficial venous system; however, it can also be causes

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

Blood coagulation is the process whereby a blood clot (thrombus) is formed. The formation of a thrombus represents the second stage of hemostasis, following vasoconstriction and platelet aggregation at the site of injury. The clotting process is very complex and its role is to maintain vascular integrity and to induce rapid clot formation after a vascular injury. It is vital to be able to regulate the production of thrombin, in order to prevent thrombosis, as well as maintaining normal blood circulation.

Thrombus formation, stabilisation and dissolution is process that requires a balance of procoagulant and anticoagulant processes. Coagulation is used to control haemorrhage from the vascular endothelium. There are four main steps in this process: initial vascular injury, primary hemostasis, secondary hemostasis and clot formation. The first step, initial vascular injury, begins when the vascular endothelium has become damaged or inflamed. Anticoagulants and fibrinolytic mechanisms are introduced to help preserve adequate blood flow. The injury then results in vasoconstriction. Smooth muscle contractions begin before myogenic spasms occur which is then followed by endothelial and platelet release of autacoid vasoconstrictive substances (endothelin

Nurden AT, Pillois X, Wilcox, DA. Glanzmanns thrombasthenia: state of the art, and future directions. Semin Thromb Hemost. 2013; 39: 642-55

We present a case of a 31-year-old Caucasian woman with a massive recurrent venous thrombosis, including central venous thrombosis and vena cava thrombosis. She presented to our emergency department with persistent headache. Neurologic examination revealed bilateral papilledema. Brain computed tomographic venography confirmed venous thrombosis. Headaches were improved after treatment of heparin and warfarin. One month later the patient was readmitted with facial edema and venous engorgement with extensive collateral circulation. The Computed tomography angiography revealed signs of extensive cervical, thoracic and abdominal collateral circulation as well as superior vena cava thrombosis superior. A composed heterozygosity mutations were found

There was no effect on the initial formation of the thrombus, however, the size of the thrombus at a later time (2 and 10 minutes after plaque rupture) and stability were reduced with the use of corn trypsin inhibitor or r-HA-infestin-4 to inhibit factor XIIa [32] (Figure 2).

The purpose of this experiment was to observe the differences in the formation of simulated blood clots when different amounts of sodium citrate, an anticoagulant, was added to the coagulation process, which would help gain information about the process that could potentially be used to create medications for different blood clotting disorders.

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

As it was defined in Oxford Concise Medical Dictionary, phlebothrombosis is “an obstruction of a vein by a blood clot, without preceding inflammation of its wall. It is most common within the deep veins of the calf of the leg - deep vein thrombosis (DVT) - in contrast to thrombophlebitis, which affects superficial leg veins. Prolonged immobility, heart failure, pregnancy, injury, and surgery predispose to thrombosis by encouraging sluggish blood flow. Many of these conditions are associated with changes in the clotting factors in the blood that increase the tendency to thrombosis; these changes also occur in some women taking oral contraceptives. The affected leg may become swollen and tender. The main danger is that the clot may become detached and give rise to pulmonary

Thrombophilia is a disorder that contains several genetic components that can cause an individual to form arterial and venous thrombi more readily. Many serious medical complications can result from thrombus formations that are often times fatal. In fact, a venous thromboembolism (VTE) is relatively common and a thrombosis of the deep veins of the legs or pelvis can lead to morbidity and mortality. Small portions of this patient population even develop pulmonary emboli (PE), which can be fatal. This major medical problem affects 1 in 1,000 persons per year and approximately 1 in 130 Americans younger than age 65 develop a VTE (Crow, 2003; Kujovich, 2011). Interestingly enough, inherited thrombophilia can be identified in half of the patients presenting with VTE (Kujovich, 2011).

Von Willebrand Disease, Glanzmann’s Thrombasthenia and Bernard-Soulier Syndrome are three frequently referenced inherited forms of platelet dysfunction due to the inability of platelets to adhere or aggregate during primary hemostasis. (1, 7) These hereditary abnormalities would give prolonged closure times in both cartridges. (1, 6, 7) Frequently, platelet dysfunction is secondary due to another disease state, such as liver disease, kidney failure or myelodysplatic syndromes – which will also give abnormally prolonged closure times in both cartridges. (6,

Haemostasis occurs in three stages, vascular platelet phase, activation of coagulation cascade producing a clot and initiation of control mechanisms. Coagulation tests are used measure the functions associated with clotting, which involves drawing blood, chelating out the calcium and beginning the clot in a controlled environment, to discover if an individual has a clotting disorder or a factor deficiency. There are many disorders that cause problems with coagulation for example thrombophilia and haemophilia. (Hillyer 2009)

If one of the in vivo processes is altered within the cascade the cycle cannot complete with the formation of Thrombin.

Diagnosing prothrombotic diseases early and preventing its complications are significantly essential. Therefore, this study sought to investigate whether MPV contain diagnostic value that can prompt it to be utilized as a platelet activation marker and as marker of evidence of thrombotic risk. Platelet activation is widely acknowledged to be an indicator of likely prothrombotic diseases. Platelet size, measured as MPV, has been shown to be an indicator of platelet function and is positively linked to platelet activity indicators (Tsiara et al., 2003). The correlation between platelet size and function can be attributed to the larger platelets that activated megakaryocyte produce in the bone marrow likely to be more reactive and easier to aggregate than the normal platelets. Such is because the larger platelets secret more β-thromboglobulin and serotonin, have denser granules, generate more thromboxane in comparison to the smaller platelets while also showing more activity than the smaller platelets (Dastjerdi et al., 2006). Therefore, the hyperactive large platelets contribute considerably in speeding the formation and spread of intracoronary thrombus. This causes acute thrombotic events to occur (Smith et al., 1999). Increased MPV levels are exhibited to constitute an independent predictor for recurrent MI, ischemic vascular events or even death caused by coronary artery disease (Wang et al., 2011; Chu et al., 2010; Huczek et al., 2005). Dogan et al. (2012) linked MPV