Blood coagulation platelets

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

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... 

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. 

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. 

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. 

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) ... 

The first aspect of biocompatibility is a natural immune response. When a foreign object enters the blood stream, it can be attacked by the body s defense system. The first step is protein adsorption on an object surface. It is believed that the amount and type of protein adsorption is one of the most important steps determining whether the object is tolerated or rejected by the body. The next step is cell adhesion, which may cause aggregation and activation of platelets and triggering of the blood coagulation system with resulting thrombus formation. It may not only lead to sensor failure via surface blocking but directly threatens the patient s health. 

Garcfa-Martfnez MC, Labios M, Hermenegildo C, Tarfn JJ, O Connor E, Cano A (2004) The effect of hormone replacement therapy on Ca2+ mobilization and P-selectin (CD62P) expression in platelets examined under flow cytometry. Blood Coagul Fibrinolysis 15 1-8... 

Blood coagulation —In vitro platelet aggregation In vitro hemolysis... 

Park, H. J., Lee, H. J., Song, Y. B., and Park, K. H. (1996b). Effects of dietary supplementation of lipophilic fraction from Panax ginseng on cGMP and cAMP in rat platelets and on blood coagulation. Biol. Pharm. Bull. 19,1434-1439. 

Blood coagulation resulting in the formation of a stable fibrin clot involves a cascade of proteolytic reactions involving the interaction of clotting factors, platelets, and tissue materials. Clotting factors (see table) exist in the blood in inactive form and must be converted to an enzymatic or activated form before the next step in the clotting mechanism can be stimulated. Each factor is stimulated in turn until an insoluble fibrin clot is formed. 

Gurbel P, Hayes K, Bliden K, Yoho J, Tantry U. The platelet-related effects of tenecteplase versus al-teplase versus reteplase. Blood Coagul Fibrinolysis 2005 16(1) 1-7. 

Platelet. Disc-like structure, 2-4 mm in diameter, found in the blood of all mammals and chiefly known for its role in blood coagulation. 

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]. 

The antithrombotic effects of NO are also mediated by NO-dependent inhibition of platelet aggregation. Both endothelial cells and platelets contain eNOS, which acts to regulate thrombus formation. Thus, endothelial dysfunction and the associated decrease in NO generation may result in abnormal platelet function. As in vascular smooth muscle, cGMP mediates the effect of NO in platelets. NO may have an additional inhibitory effect on blood coagulation by enhancing fibrinolysis via an effect on plasminogen. 

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