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Louis VII
Its Edward VI, not Edward VII. Edward VI (12th October 1537 - 6th July 1553) aged 15. He died from tuberculosis.
King Henry VII died on the 21st April 1509 (aged 52) at Richmond Palace, England. Therefore: 2015 minus 1509 = 506 years ago.
During the reign of Edward VII, 1901-1910.
Prothrombin time (PT) measures the activity of coagulation factors in the tissue factor pathway of the coagulation cascade.
factor I (fibrinogen), factor II (prothrombin), factor III (tissue thromboplastin), factor IV (calcium), factor V (proaccelerin), factor VI (no longer considered active in hemostasis), factor VII (factor-vii), factor VIII (antihemophilicfactor), factor IX (plasma thromboplastincomponent; Christmas factor), factor X (stuart-factor-stuart-prower-factor), factor XI (plasma thromboplastinantecedent), factor XII (factor-xii), factor XIII (fibrin stabilizing factor).
prothrombin
the liver synthesizes all the clotting factors, and requires vitamin K to activate factors II, VII, IX and X. Reduced plasma concentration of coagulation factors occurs in liver damage, which is easily recognized by prolongation of prothrombin time, which depends on factors I, II, V, VII and X.
These are the three phases:Phase 1: Formation of prothrombin activatorThe prothrombin activator is formed through intrinsic and/or extrinsic pathway. Usually it is formed by both. Its formation is triggered by tissue-damaging events and it involves a series of procoagulants. Each pathway cascades towards Factor X (i.e. the Stuart Factor) that complexes with Ca2+, platelet factor 3 (PF3), and Factor V to form the prothrombin activator.The intrinsic pathway is triggered by negatively charged surfaces of activated platelets, collagen, and glass and it uses factors present within the blood. As for the extrinsic pathway, it is triggered by exposure to tissue factor (Factor III). The extrinsic pathway bypasses several steps of the intrinsic pathway so it is faster. Once the prothrombin activator is formed, the clot forms in 10-15 seconds.Phase 2: Prothrombin's conversion to thrombinThe prothrombin activator catalyses the transformation of prothrombin to thrombin.Phase 3: Fibrinogen conversion to fibrinThrombin (Factor II) converts soluble fibrinogen to the solid fibrin. The fibrin formed will cause the plasma to become a gel-like trap for formed elements, forming the structural basis of the clot. The thrombin along with Ca2+ activates Factor XIII to cross-link fibrin. This will strengthen and stabilise the clot.
http://web.indstate.edu/thcme/mwking/blood-coagulation.html Factor I = Fibrinogen Factor II = Prothrombin Factor III = Tissue factor Factor IV = Calcium Factor V = Labile factor Factor VI - Does not exist as it was named initially but later on discovered not to play a part in blood coagulation. Factor VII = Stable factor Factor VIII = Antihemophilic factor A Factor IX = Antihemophilic factor B or Christmas factor (named after the first patient in whom the factor deficiency was documented) Factor X = Stuart Prower factor Factor XI = Antihemophilic factor C Factor XII = Hageman factor Factor XIII = Fibrin stabilising factor
substance in blood and tissues which, in the presence of ionized calcium, aids in the conversion of prothrombin to thrombin. Extrinsic and intrinsic thromboplastin are formed as the result of the interaction of different clotting factors; the factors that combine to form extrinsic thromboplastin are not all derived from intravascular sources, whereas those that form intrinsic thromboplastin are.activated partial t. time - see http://www.answers.com/topic/activated-4 partial thromboplastin time.extrinsic t. - the prothrombin activator formed as a result of interaction of coagulation factors III, VII, and X which, with factor IV, aids in the formation of thrombin.t. generation time (TGT) - evaluates the first stage in blood coagulation by measuring the efficiency of prothrombinase formation.intrinsic t. - the prothrombin activator formed as a result of interaction of coagulation factors V, VII, IX, X, XI and XII and platelet factor 3 (PF-3), which, with factor IV, aids in the conversion of prothrombin to thrombin.plasma t. antecedent (PTA) - http://www.answers.com/topic/clotting-1 factor XI; deficiency occurs in cattle and dogs, causing mild to severe bleeding tendencies called hemophilia C.plasma t. component (PTC) - http://www.answers.com/topic/clotting-1 factor IX; deficiency causes http://www.answers.com/topic/haemophilia-b. Called also Christmas factor, antihemophilic factor B, autoprothrombin II.t. time - see http://www.answers.com/topic/activated-4 partial thromboplastin time.tissue t. - factor III, a material derived from several sources in the body (e.g. brain, lung), and is important in the formation of extrinsic prothrombin converting principle in the extrinsic pathway of blood coagulation. Called also tissue factor.
prothrombin time is a factor involved in the clotting process. the factors nearly all of which are produced in the liver.
There are 13 clotting factors identified in blood that work together in the coagulation cascade to form blood clots. These factors include Factor I (fibrinogen), Factor II (prothrombin), Factor III (tissue factor), Factor IV (ionized calcium), Factors V, VII, VIII, IX, X, XI, XII, XIII, and von Willebrand Factor.
Vitamin K deficiency is typically measured by assessing levels of prothrombin time (PT) and activated partial thromboplastin time (aPTT) in the blood. Additionally, measurement of vitamin K-dependent clotting factors, such as Factor II, VII, IX, and X, can also be used to diagnose deficiency. Specialized tests to directly measure vitamin K levels in the blood can also be performed.
Factor VII is one of the proteinsthat causes blood to clot in the coagulation cascade.
There are the intrinsic and extrinsic pathways in clotting. The intrinsic pathway is initiated when blood comes in contact with damaged endothelium or collagen, and involves clotting factors XII, XI, IX, and VIII. The extrinsic pathway is activated when being exposed to tissue factor from tissue injury or the addition of thromboplastin to blood, and involves clotting factor VII. The two pathways meet at the point of clotting factor X activation to lead the final common pathway. From here, factor X is converted to prothrombin, prothrombin to thrombin, thrombin to fibrinogen, fibrinogen to fibrin, and finally fibrin to fibrin clot. Platelets, activated by thrombin, adhere to the damaged endothelium wall or collagen to form a plug. At the same time, they activate clotting factors VII and X. More platelets are stimulated by fibrin clots, resulting in reinforcing the formed clots.