Coagulation: Difference between revisions
imported>Robert Badgett |
imported>Robert Badgett No edit summary |
||
| Line 1: | Line 1: | ||
'''Coagulation''' is "the process of the interaction of blood coagulation factors that results in an insoluble fibrin clot."<ref name="MeSH-Coagulation">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?mode=&index=1700 |title=Blood coagulation |accessdate=2008-01-10 |author=Anonymous |authorlink= |coauthors= |date= |format= |work= |publisher=National Library of Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref> | '''Coagulation''' is "the process of the interaction of blood coagulation factors that results in an insoluble fibrin clot."<ref name="MeSH-Coagulation">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?mode=&index=1700 |title=Blood coagulation |accessdate=2008-01-10 |author=Anonymous |authorlink= |coauthors= |date= |format= |work= |publisher=National Library of Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref> | ||
==Biochemistry== | |||
The Vitamin K dependent coagulation factors are II, VII, IX, and X. | |||
===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== | ==Disorders of coagulation== | ||
| Line 5: | Line 17: | ||
===Factor II deficiency=== | ===Factor II deficiency=== | ||
Deficiency of Factor II (prothrombin) leads to hypoprothrombinemia. | Deficiency of Factor II (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.<ref name="pmid6403077">{{cite journal |author=Bajaj SP, Rapaport SI, Fierer DS, Herbst KD, Schwartz DB |title=A mechanism for the hypoprothrombinemia of the acquired hypoprothrombinemia-lupus anticoagulant syndrome |journal=Blood |volume=61 |issue=4 |pages=684–92 |year=1983 |pmid=6403077 |doi=}}</ref> | |||
===Factor V deficiency=== | ===Factor V deficiency=== | ||
Revision as of 11:33, 11 January 2008
Coagulation is "the process of the interaction of blood coagulation factors that results in an insoluble fibrin clot."[1]
Biochemistry
The Vitamin K dependent coagulation factors are II, VII, IX, and X.
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."[2]
Factor II deficiency
Deficiency of Factor II (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.[3]
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."[4]
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."[5]
References
- ↑ Anonymous. Blood coagulation. National Library of Medicine. Retrieved on 2008-01-10.
- ↑ 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.