Coagulation Cascade Research Paper

The liver becomes so diseased and damaged that it can no longer produce appropriate amounts of clotting factor and hormones to make platelets. “Vitamin K must be present in order for the liver to synthesize some of the clotting factors, including prothrombin, interleukin-6, multi-CSF, and fibrinogen.” p 664 If the blood is unable to clot then the patient will continue to bleed to the point that a liver transplant is necessary. Prothrombin a peptide hormone produced in the kidneys that accelerates platelet formation. Interleukin-6 is a hormone that stimulates platelet formation. Multi-CSF is a hormone that stimulates platelet production by promoting the formation and growth of megakaryocytes. p.660 If all of these hormones are

Platelets 1)Transport chemicals important to clotting, 2)Form a temporary patch in the walls of damaged blood vessels, and 3)Actively contract after the clot has formed.

Venous thrombosis is a multifactorial disease. In the majority of thrombosis patients a risk factor is not detectable. Virchow's triad refers to three primary influences for thrombus formation, endothelial injury, stasis, turbulence or abnormal blood flow, and blood hypercoagulability (Kyrle, 2009). A shift in balance between procoagulant and anticoagulant of the endothelium is responsible for thrombotic state (Kyrle, 2009). Endothelial injury is the physical loss of endothelium leading to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, depletion of PGI2 and plasminogen activators (Kumar, 2010). Abnormal blood flow refers to turbulence that causes endothelial injury, which is a major influence

Hemophilia is a rare genetic blood clotting disorder that primarily affects males. People living with hemophilia do not have enough of, or are missing, one of the blood clotting proteins naturally found in blood. Two of the most common forms of hemophilia are A and B. In persons with hemophilia A (also called classic hemophilia), clotting factor VIII is not present in sufficient amounts or is absent. In persons with hemophilia B (also called Christmas disease), clotting factor IX is not present in sufficient amounts or is absent. People with hemophilia do not bleed more profusely or bleed faster than normal; they bleed for a longer period of time.

7.b) Damaged endothelium present an increased risk of blood clotting because it exposes the underlying collagen. Platelets bind to the collagen, and the clotting process is then

Proteins form over the platelets called fibrin that make the blood clot and stick the platelets together. When this process gets repeated it can cause a clot, or thrombus. As a result, this forces the heart to work much harder to pump blood efficiently due to the arteries becoming narrower. Continued buildup of plaque can lead to heart disease and cause a heart attack as well as many other health complications.

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)

Both conditions increase coagulability. Atherosclerosis increases platelet function by encouraging aggregation and adherence. Immobility, in contrast, contributes to hypercoagulability by increasing procoagulation factors.

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).

Check your levels of fibrinogen and other clotting factors. Fibrinogen is a protein produced by the liver, and it helps blood to clot.

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

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, &

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

Thrombosis is the leading cause of morbidity and mortality worldwide and is also associated with the three major cardiovascular diseases: ischemic heart disease, stroke, and venous thromboembolism (VTE). In 2010, GBD documented 52.8 million deaths worldly, 12.9 million deaths were caused by ischemic heart disease and stroke collectively [56]. Thrombosis is the accumulation of blood clot in blood vessels and can be arterial or venous thrombosis. Arterial thrombosis is a thrombotic event in the artery wall and the primary trigger for such event is the rupture of an atherosclerotic plaque which formed because the accumulation of lipid deposits and lipid-laden macrophages (foam cells). On the other hand, venous thrombosis is the thrombotic event