Coagulation: Difference between revisions
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==Biochemistry== | ==Biochemistry== | ||
All coagulation factors are produced in the liver except for von Willebrand's factor.<ref name="pmid10533518">{{cite journal |author=Sallah S, Bobzien W |title=Bleeding problems in patients with liver disease. Ways to manage the many hepatic effects on coagulation |journal=Postgrad Med |volume=106 |issue=4 |pages=187–90, 193–5 |year=1999 |pmid=10533518 |doi=|url=http://www.postgradmed.com/issues/1999/10_01_99/sallah.htm}}</ref> However, Factor VIII levels may be normal in liver disease.<ref name="pmid10533518"/><ref name="pmid1333467">{{cite journal |author=Mammen EF |title=Coagulation abnormalities in liver disease |journal=Hematol. Oncol. Clin. North Am. |volume=6 |issue=6 |pages=1247–57 |year=1992 |pmid=1333467 |doi=}}</ref> The synthesis of coagulation factors II, VII, IX, and X and proteins C and S is dependent on vitamin K.<ref name="pmid1333467">{{cite journal |author=Mammen EF |title=Coagulation abnormalities in liver disease |journal=Hematol. Oncol. Clin. North Am. |volume=6 |issue=6 |pages=1247–57 |year=1992 |pmid=1333467 |doi=}}</ref> | All coagulation factors are produced in the liver except for von Willebrand's factor.<ref name="pmid10533518">{{cite journal |author=Sallah S, Bobzien W |title=Bleeding problems in patients with liver disease. Ways to manage the many hepatic effects on coagulation |journal=Postgrad Med |volume=106 |issue=4 |pages=187–90, 193–5 |year=1999 |pmid=10533518 |doi=|url=http://www.postgradmed.com/issues/1999/10_01_99/sallah.htm}}</ref> However, Factor VIII levels may be normal in liver disease.<ref name="pmid10533518"/><ref name="pmid1333467">{{cite journal |author=Mammen EF |title=Coagulation abnormalities in liver disease |journal=Hematol. Oncol. Clin. North Am. |volume=6 |issue=6 |pages=1247–57 |year=1992 |pmid=1333467 |doi=}}</ref> The synthesis of coagulation factors II, VII, IX, and X and proteins C and S is dependent on vitamin K.<ref name="pmid1333467">{{cite journal |author=Mammen EF |title=Coagulation abnormalities in liver disease |journal=Hematol. Oncol. Clin. North Am. |volume=6 |issue=6 |pages=1247–57 |year=1992 |pmid=1333467 |doi=}}</ref> The half-lives of the cofactors range from five to seven hours for factor VII to 3 days for factor II (prothrombin). | ||
===Intrinsic pathway=== | ===Intrinsic pathway=== | ||
Revision as of 01:20, 13 January 2008
Coagulation is "the process of the interaction of blood coagulation factors that results in an insoluble fibrin clot."[1]
Biochemistry
All coagulation factors are produced in the liver except for von Willebrand's factor.[2] However, Factor VIII levels may be normal in liver disease.[2][3] The synthesis of coagulation factors II, VII, IX, and X and proteins C and S is dependent on vitamin K.[3] The half-lives of the cofactors range from five to seven hours for factor VII to 3 days for factor II (prothrombin).
Intrinsic pathway
The intrinsic pathway uses Factors VIII, IX, XI, and XII. The partial thromboplastin time measures the function of the intrinsic pathway and the common pathway.
Extrinsic pathway
The extrinsic pathway uses Factors VII and X. The prothrombin time measures the function of the extrinsic pathway and the common pathway.
Final common pathway
The final common pathway used factors II (prothrombin) and I (fibrinogen).
Disorders of coagulation
Blood coagulation disorders are "hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as coagulation protein disorders; blood platelet disorders; blood protein disorders or nutritional conditions."[4]
Factor I deficiency
Deficiency of Factor I (fibrinogen) may be inherited (afibrinogenemia) or acquired.
Factor II deficiency
Deficiency of Factor II (prothrombin) leads to hypoprothrombinemia. The defiency may be acquired in due to prothrombin antibodies.[5]
Factor V deficiency
Factor V deficiency is a "(known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as Owren's disease or parahemophilia. It varies greatly in severity. Factor V deficiency is an autosomal recessive trait."[6]
Factor X deficiency
Factor X deficiency is a "blood coagulation disorder usually inherited as an autosomal recessive trait, though it can be acquired. It is characterized by defective activity in both the intrinsic and extrinsic pathways, impaired thromboplastin time, and impaired prothrombin consumption."[7]
Multiple factor deficiencies
Heparin therapy primarily affects Factors IX and X of the intrinsic pathway. Thus, its effect is monitored by the partial thromboplastin time. However, it can affect the prothrombin time as well.[8] and extend the prothrombin time by one to two seconds.[9]
Warfarin therapy reduces the vitamin K dependent cofactors II, VII, IX, and X. With the exception of Factor IX, these factors are from either the extrinsic pathway or the final common pathway. The effect of warfarin is measured by the prothrombin time (or the International Normalized Ratio derived from the prothrombin time) although warfarin can also affect the partial thromboplastin time.[10][11]
Cirrhosis affects all coagulation factors except von Willebrand's factor and Factor VIII.
Disseminated Intravascular Coagulation affects all coagulation factors.
References
- ↑ Anonymous. Blood coagulation. National Library of Medicine. Retrieved on 2008-01-10.
- ↑ 2.0 2.1 Sallah S, Bobzien W (1999). "Bleeding problems in patients with liver disease. Ways to manage the many hepatic effects on coagulation". Postgrad Med 106 (4): 187–90, 193–5. PMID 10533518. [e]
- ↑ 3.0 3.1 Mammen EF (1992). "Coagulation abnormalities in liver disease". Hematol. Oncol. Clin. North Am. 6 (6): 1247–57. PMID 1333467. [e]
- ↑ Anonymous. Blood Coagulation Disorders. National Library of Medicine.
- ↑ Bajaj SP, Rapaport SI, Fierer DS, Herbst KD, Schwartz DB (1983). "A mechanism for the hypoprothrombinemia of the acquired hypoprothrombinemia-lupus anticoagulant syndrome". Blood 61 (4): 684–92. PMID 6403077. [e]
- ↑ Anonymous. Factor V Deficiency. National Library of Medicine.
- ↑ Anonymous. Factor X Deficiency. National Library of Medicine.
- ↑ Schultz NJ, Slaker RA, Rosborough TK (1991). "The influence of heparin on the prothrombin time". Pharmacotherapy 11 (4): 312–6. PMID 1923913. [e]
- ↑ Lutomski DM, Djuric PE, Draeger RW (1987). "Warfarin therapy. The effect of heparin on prothrombin times". Arch. Intern. Med. 147 (3): 432–3. PMID 3827418. [e]
- ↑ Bell DF, Harris WH, Kuter DJ, Wessinger SJ (1988). "Elevated partial thromboplastin time as an indicator of hemorrhagic risk in postoperative patients on warfarin prophylaxis". J Arthroplasty 3 (2): 181–4. PMID 3397749. [e]
- ↑ Hauser VM, Rozek SL (1986). "Effect of warfarin on the activated partial thromboplastin time". Drug Intell Clin Pharm 20 (12): 964–7. PMID 3816546. [e]