Blood coagulation extrinsic

Figure 51-1. The pathways of blood coagulation. The intrinsic and extrinsic pathways are indicated. The events depicted below factor Xa are designated the final common pathway, culminating in the formation of cross-linked fibrin. New observations (dotted arrow) include the finding that complexes of tissue factor and factor Vila activate not only factor X (in the classic extrinsic pathway) but also factor IX in the intrinsic pathway, in addition, thrombin and factor Xa feedback-activate at the two sites indicated (dashed arrows). (PK, prekallikrein HK, HMW kininogen PL, phospholipids.) (Reproduced, with permission, from Roberts HR, Lozier JN New perspectives on the coagulation cascade. Hosp Pract [Off Ed] 1992Jan 27 97.)...

Distinguish between the extrinsic and intrinsic mechanisms of blood coagulation... 

The extrinsic mechanism of blood coagulation begins when a blood vessel is ruptured and the surrounding tissues are damaged. The traumatized tissue releases a complex of substances referred to as tissue thromboplastin. The tissue thromboplastin further complexes with factor VII and Ca++ ions to activate factor X directly. 

Figure 12.1 Schematic diagram of the initial steps of the extrinsic blood coagulation pathway. See text for details (TF tissue factor)...

Peptide derivatives, (III), prepared by Shiraishi (3) selectively inhibited extrinsic blood coagulation by inhibiting factor Vila. a-Ketoamide peptides, (IV), while those prepared by Chatterjee (4) were effective as cysteine and serine proteases inhibitors and used in treating coagulation disorders associated with thrombophlebitis and... 

Initiation of blood coagulation (clotting) occurs through the contact activation pathway (intrinsic pathway) and the tissue factor (TF) pathway (extrinsic pathway). The contact activation pathway is quantitatively the most important, but is much slower to initiate the TF pathway is considered to be the primary pathway for the initiation of blood coagulation and affords a more rapid response (the so-called thrombin burst), which augments the contact activation pathway. Both pathways share a common pathway that converges at factor X with the production of thrombin (Figure 11.1). 

Following the recruitment and activation of platelets by injured capillaries, their soft clot aggregates provide a surface for plasma proteins to interact and activate thrombin, which transforms soluble fibrinogen to a fibrin clot. Thrombin is activated by two blood coagulation pathways, extrinsic and intrinsic. A defective extrinsic path is incompatible with life, whereas defects of the intrinsic path cause hemophilia. 

Fig. 11.13 Coagulation flow chart Blood coagulation events are divided into initiation, extrinsic and intrinsic path activation, and the common path to fibrin. Controls are fibrinolysis as healing begins and inhibition of clotting factors in a healthy (uninjured) blood vessel. Diseases are excessive bleeding (hemophilia) and excessive clotting (Original figure)...

During blood coagulation either an intrinsic (all blood) system or an extrinsic (tissue juice-lipoprotein) system is activated.. In either case the pathways meet at the activation of Factor X, forming a proteolytic enzyme Factor X. This enzyme in the presence of cofactors (calcium ion, phospholipid and Factor V) will form thrombin from prothrombin. Heparin is a cofactor for a protein called antithrombin III which circulates in the plasma and is an inhibitor of both Factor Xg and thrombin. Antithrombin III neutralizes these 2 enzymes by molecular combination heparin increases the rate of this neutralization. In the past 2 years work has continued on the mechanism of blood coagulation More... 

The answer is e. (Murray, pp 812-828. Scriver, pp 3-45. Sack, pp 121—144. Wilson, pp 23—98.) Hemophilia A is caused by deficiency of factor VIII and hemophilia B by deficiency of factor IX. Both factors are involved in the intrinsic blood coagulation pathway that results in activation of factor X. Alternatively, factor X can be activated by tissue factors through the extrinsic blood coagulation pathway Activated factors X and V produce thromin from prothrombin, which in turn cleaves fibrinogen to produce fi-... 

Factor X is a plasma protein involved in both the intrinsic and extrinsic pathways of blood coagulation. Factor X has a mass of 55kDa and the activated Xa of 40kDa. The normal concentration in plasma is 6-8 pg/ml. Post-translational modifications of the protein involve y-carboxylation of specific glutamic acid residues, 3-hydroxylation of one aspartic acid residue, and N- and 0-linked glycosylation. 

Activation of the blood coagulation cascade is triggered by the reaction of plasma proteins with the subendothelium at the same time that platelets are adhering to the subendothelial layer. Historically, two different pathways were discovered, one dependent on external stimuli (such as blunt trauma, which initiates the extrinsic pathway) and one using internal stimuli (the intrinsic pathway). As our understanding of blood clotting has expanded, it has become obvious that these distinctions are no longer correct, because there is overlap between the pathways, but the terms have persisted in the description of the pathways. 

Blood coagulation occurs as a "cascade" of proteolytic factors are activated. Each factor is proteolyzed into an active protease. The newly-formed protease in turn proteolyzes the next factor into an active protease. The cascade produces fibrin, which forms an insoluble network that entangles blood cells and platelets. The clotting cascade can be activated by factors that reside only in the bloodstream (intrinsic pathway) or by tissue factors that are not present in blood (extrinsic pathway). 

Stuart-Factor, Stuart Prower-Factor, Thrombokinase, Factor X, a serine protease and constituent of the blood coagulation cascade. It is either be activated by factor IX (intrinsic pathway) or by Factor Vila (extrinsic pathway). In complex with Factor V as the cofactor it cleaves prothrombin at Arg-Thr and Arg-Ile to give active thrombin. 

Figure 2. Intrinsic and extrinsic pathways in blood coagulation/...

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