Hemostasis coagulation

Antihemophilic factor [9001-28-9] (AHF) is a protein found in normal plasma that is necessary for clot formation. It is needed for transformation of prothrombin to thrombin. Administration of AHF by injection or infusion can temporarily correct the coagulation defect present in patients with hemophilia. Antihemophilic factor VIII (Alpha Therapeutic) has been approved by the FDA as replacement therapy in patients with hemophilia B to prevent bleeding episodes, and also during surgery to correct defective hemostasis (178). 

Kleinschnitz C, Stoll G, Bendszus M et al (2006) Targeting coagulation Factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis. J Exp Med 203 513-518... 

Primary hemostasis is the first phase of hemostasis consisting of platelet plug formation at the site of injury. It occurs within seconds and stops blood loss from capillaries, arterioles, and venules. Secondary hemostasis, in contrast, requires several minutes to be complete and involves the formation of fibrin through the coagulation cascade. 

Hemostasis is the process that stops bleeding in a blood vessel. Normal hemostasis involves a complex process of extrinsic and intrinsic factors. Figure 44-1 shows the coagulation pathway and factors involved. The copulation cascade is so named because as each factor is activated it acts as a catalyst that enhances the next reaction, with the net result being a large collection of fibrin that forms a plug in the vessel. Fibrin is the insoluble protein that is essential to clot formation. 

Hemostasis is the cessation of bleeding from a cut or severed vessel, whereas thrombosis occurs when the endothelium lining blood vessels is damaged or removed (eg, upon rupmre of an atherosclerotic plaque). These processes encompass blood clotting (coagulation) and involve blood vessels, platelet aggregation, and plasma proteins that cause formation or dissolution of platelet aggregates. 

We shall first describe the coagulation pathway leading to the formation of fibrin. Then we shall briefly describe some aspects of the involvement of platelets and blood vessel walls in the overall process. This separation of clotting factors and platelets is artificial, since both play intimate and often mutually interdependent roles in hemostasis and thrombosis, but it facifitates description of the overall processes involved. 

Hemostasis and thrombosis are complex processes involving coagulation factors, platelets, and blood vessels. 

The chapter on plasma proteins, immunoglobulins, and blood coagulation in the previous edition has been split into two new chapters on plasma proteins and immunoglobuhns and on hemostasis and thrombosis. 

Describe the processes of hemostasis and thrombosis, including the role of the vascular endothelium, platelets, coagulation cascade, and thrombolytic proteins. 

The main goal of recessively inherited coagulation disorder (RICD) treatment is to prevent and control spontaneous and surgery-related bleeding episodes. Specifically, therapeutic options improve hemostasis via replacement of deficient blood coagulation factors while minimizing the development of immune tolerance.20... 

Platelets play a role in each of the mechanisms of normal hemostasis vasoconstriction, formation of the platelet plug, and blood coagulation. However, they are also involved in pathological processes that lead to atherosclerosis and thrombosis (formation of a blood clot within the vascular system). Antiplatelet drugs interfere with platelet function and are used to prevent the development of atherosclerosis and formation of arterial thrombi. 

Blood coagulation. The third major step in hemostasis is coagulation, or the formation of a blood clot. This complex process involves a series of reactions that result in formation of a protein fiber meshwork that stabilizes the platelet plug. Three essential steps lead to clotting (see Figure 16.1) ... 

Self-protection. To prevent blood loss when a vessel is injured, the blood has systems for stanching blood flow and coagulating the blood (hemostasis see p. 290). The dissolution of blood clots (fibrinolysis) is also managed by the blood itself (see p. 292). 

Following injury to blood vessels, hemostasis ensures that blood loss is minimized. Initially, thrombocyte activation leads to contraction of the injured vessel and the formation of a loose clot consisting of thrombocytes (hemostasis). Slightly later, the action of the enzyme thrombin leads to the formation and deposition in the thrombus of polymeric fibrin (coagulation, blood clotting). The coagulation process is discussed here in detail. 

Hematologic effects Aspirin interferes with hemostasis. Avoid use if patients have severe anemia, history of blood coagulation defects, or take anticoagulants. Long-term therapy To avoid potentially toxic concentrations, warn patients on long-term therapy not to take other salicylates (nonprescription analgesics, etc). Salicylism Salicylism may require dosage adjustment. 

Little intravascular coagulation of blood occurs in normal physiological conditions. Hemostasis involves the interplay of three procoagulant phases vascular, platelet, and coagulation) that promote blood clotting to prevent blood loss (Fig. 22.1). The fibrinolytic system prevents propagation of clotting beyond the site of vascular injury and is involved in clot dissolution, or lysis (Fig. 22.2). 

Hemophilia A Determine factor VIII coagulant activity before injecting desmopressin for hemostasis if activity is <5% of normal, do not rely on desmopressin... 

Hemostasis begins with the formation of the platelet plug, followed by activation of the clotting cascade, and propagation of the clot. One of the major multicomponent complexes in the coagulation cascade consists of activated factor IX (factor IXa) as the protease, activated factor VIII (factor Villa), calcium, and phospholipids as the cofactors, and factor X as the substrate. Factor IXa can be generated by either factor Xa activation of the intrinsic pathway or by the tissue factor/factor Vila complex. 

G. Other applications NovoSeven may be effective for acute bleeding or hemostasis during surgery. In one study NovoSeven reversed the effects of the oral anticoagulant acenocoumarol on the prothrombin time and International Normalized Ratio (INR) in healthy volunteers, without evidence of systemic coagulation. It may also transiently correct elevated prothrombin time in patients with cirrhosis-induced coagulopathy. 

To maintain hemostasis, blood must be retained in the vasculature as fluid. At the same time, blood components must be able to respond rapidly with a clot when a vascular injury occurs. To repair a vascular injury, platelets in blood first adhere as aggregates to the endothelial cells at the affected site and form an initial blood clot. Platelets then stimulate and activate coagulation factors found in plasma to form a more stable fibrin clot. As the injury is resolved and healed, the clot is degraded. Thrombosis is a pathological event wherein a blood clot occludes a blood vessel, resulting in ischemic necrosis of the tissue fed by the blood vessel. Ischemic necrosis involves local anemia and oxygen deprivation. Thrombosis of a coronary artery may lead to myocardial infarction or unstable angina [20]. 

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