Coagulation platelets

Plasma Inhibitors, In Vivo Anticoagulants. Fourteen naturally occurring compounds that normally exert an inhibiting effect on the activity of coagulation, platelet function, and fibrinolytic activity and complement systems have been identified within the circulating blood. 

Hemocompatibility tests evaluate effects on blood and/or blood components by blood-contacting medical devices or materials. In vivo hemocompatibility tests are usually designed to simulate the geometry, contact conditions, and flow dynamics of the device or material in its dinical application. From the ISO standards perspective, five test categories are indicated for hemocompatibility evaluation thrombosis, coagulation, platelets, hematology, and immimology (complement and leukocytes) (Table 12). 

Hemocompatibility testing includes a full battery of tests required of anything that comes into contact with blood. ISO 10993-4 clearly defines the categories of evaluations to be performed, as well as which types of medical devices need to have which tests performed. The five categories of hemocompatibility testing are thrombosis, coagulation, platelets, hematology, and the complement system. With the exception of thrombosis, all of these tests are in vitro assays. 

Fig. 1. Influence of feeding various diets to rats for 10 weeks on cholesterolemia, coagulation, platelet aggregation, and on severity of thrombosis initiated by S. typhosa lipopolysaccharide (0.3 mg/Kg). PCT- plasma clotting time CEP-CT - cephalin clotting time F3-CT - factor 3 clotting time (Courtesy of S. Renaud and F. Lecompte, Circulat. Res. 37 1003, 1970).

Effect of different dietary fats on blood coagulation, platelet economy and blood lipids. 

In addition to their role in coagulation, platelets are of the utmost importance in the hemostatic and thrombotic processes. The structure of an arterial thrombus resembles that of a hemostatic platelet plug. 

Primary blood components iaclude plasma, red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes), and stem cells. Plasma consists of water dissolved proteias, ie, fibrinogen, albumins, and globulins coagulation factors and nutrients. The principal plasma-derived blood products are siagle-donor plasma (SDP), produced by sedimentation from whole blood donations fresh frozen plasma (FFP), collected both by apheresis and from whole blood collections cryoprecipitate, produced by cryoprecipitation of FFP albumin, collected through apheresis and coagulation factors, produced by fractionation from FFP and by apheresis (see Fractionation, blood-plasma fractionation). 

The calcium ion, necessary for blood-clot formation, stimulates release of bloodclotting factors from platelets (see Blood, coagulants and anticoagulants) (25). Neuromuscular excitabihty also depends on the relative concentrations of Na", Ca ", Mg ", and (26). Upon a decrease in... 

Hematology. The functional status of blood and of the blood-forming tissues can be assessed by tests which include red and white blood cell counts, platelet counts, clotting time, coagulation tests, and examination of bone marrow. Such tests, in addition to detecting abnormahties, may also allow differentiation between primary and secondary effects on blood and blood-forming tissues (75). 

Blood Plasma and Serum. The terms plasma and semm are frequendy confused. Plasma refers to the Hquid that suspends the red cells within the body. Semm is that Hquid, removed from the body, from which the coagulum has been removed semm contains no coagulation factors and is severely depleted of platelets. 

The hemorrhagic diathesis in patients with coagulation disorders is because of either an abnormaUty of one or more plasma proteins and/or platelets necessary for normal blood coagulation or the spontaneous presence of a circulating anticoagulant. Specific laboratory techniques are required for the precise identification of these disorders. 

Dismption of the endothehal surface of blood vessels expose coUagen fibers and connective tissue. These provide surfaces that promote platelet adherence, platelet release reaction, and subsequent platelet aggregation. Substances Hberated from the platelets stimulate further platelet aggregation, eg, adenosine diphosphate maintain vasoconstriction, eg, serotonin and participate in blood coagulation, eg, platelet Factors III and IV. In addition, the release reaction modifies platelet membranes in a manner that renders phosphoHpid available for coagulation. The thrombin [9002-04-4] elaborated by the coagulation mechanism is a potent agent in the induction of the platelet release reaction. 

Thrombin, the two-chain derivative of the prothrombin molecule, has a molecular weight of approximately 37,000 daltons. Its proteolytic properties induce the conversion of fibrinogen to fibrin to produce the initial visible manifestation of coagulation, the soluble fibrin clot. In addition, thrombin influences the activity of Factors V, VIII, and XIII and plasmin. Thrombin affects platelet function by inducing viscous metamorphosis and the release reaction with subsequent aggregation. 

Factor V. High in sialic acid content. Factor V is a large asymmetric single-chain glycoprotein that becomes an active participant in the coagulation cascade when it is converted to its active form by a-thrombin. Approximately 25% of human Factor V is found in the whole blood associated with platelets. Factor V is an essential cofactor along with Factor Xa plus phosphohpid plus Ca " in the conversion of prothrombin to thrombin. 

Coagulation factors are glycoproteins named by roman numbers (the numbers being ascribed at the time of the components definition, not sequence of activation) (Table 1). Besides von Willebrand factor (vWF), the coagulation factors are synthesized in the liver. They have very different half-lifes and different concentrations in the plasma. Several coagulation factors are stored in platelets and endothelial cells and can be released during activation of these cells, which can result in a much higher local concentration of the respective factor (e.g., vWF). 

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. 

FAT EMULSIONS. When a fat emulsion is administered, the nurse must monitor the patient s ability to eliminate the infused fat from the circulation. The lipidemia must clear between daily infusions. The nurse monitors for lipidemia through assessing the result of the following laboratory exams hemogram, blood coagulation, liver function tests, plasma lipid profile, and platelet count. The nurse reports an increase in any of these laboratory examinations as abnormal. 

Basic aspects of the proteins of the blood coagulation system and of fibrinolysis are described in this chapter. Some fundamental aspects of platelet biology are also presented. Hemorrhagic and thrombotic states can cause serious medical emergencies, and thromboses in the coronary and cerebral arteries are major causes of death in many parts of the world. Rational management of these conditions requires a clear understanding of the bases of blood clotting and fibrinolysis. 

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. 

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