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A number of different mediating factors can cause this condition; either from within the blood cell itself (intrinsic factors) or outside of the cell (extrinsic factors). [39] Congenital hemolytic anemia: Fanconi anemia: D61.0: 4745: D005199 Fanconi anemia is a rare genetic autosomal recessive aplastic anemia that involves chromosomes 9q and ...
The coagulation factors are generally enzymes called serine proteases, which act by cleaving downstream proteins. The exceptions are tissue factor, FV, FVIII, FXIII. [28] Tissue factor, FV and FVIII are glycoproteins, and Factor XIII is a transglutaminase. [27] The coagulation factors circulate as inactive zymogens. The coagulation cascade is ...
286 Coagulation defects. 286.0 Hemophilia A; 286.1 Hemophilia B; 286.2 Hemophilia C; 286.3 Congenital deficiency of other clotting factors. Factor XIII deficiency; 286.4 Von Willebrand's disease; 286.5 Hemorrhagic disorder due to intrinsic anticoagulants; 286.6 Defibrination syndrome; 286.7 Acquired coagulation factor deficiency; 286.9 ...
The normal clotting process depends on the interplay of various proteins in the blood. Coagulopathy may be caused by reduced levels or absence of blood-clotting proteins, known as clotting factors or coagulation factors. Genetic disorders, such as hemophilia and Von Willebrand disease, can cause a reduction in clotting factors. [2]
Thrombosis (from Ancient Greek θρόμβωσις (thrómbōsis) 'clotting') is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel (a vein or an artery ) is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss.
The last category, alterations in the constitution of blood, [6] has numerous possible risk factors such as hyperviscosity, coagulation factor V Leiden mutation, coagulation factor II G2021A mutation, deficiency of antithrombin III, protein C or S deficiency, nephrotic syndrome, changes after severe trauma or burn, cancer, late pregnancy and ...
Essential thrombocythemia is sometimes described as a slowly progressive disorder with long asymptomatic periods punctuated by thrombotic or hemorrhagic events. [15] However, well-documented medical regimens can reduce and control the number of platelets, which reduces the risk of these thrombotic or hemorrhagic events.
The incorrectly glycosalated fibrinogen is dysfunctional and may cause pathological episodes of bleeding and/or blood clotting. [5] Congenital hypodysfibrinogenemia, an inherited disorder in which low levels of fibrinogen composed at least in part of a dysfunctional fibrinogen may cause pathological episodes of bleeding or blood clotting. [6]
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