Hemophilia A pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
*The ''F8'' gene associated with the development of Hemophilia A is located close to the tip Xq, and affects production of clotting factor VIII. Abnormalities in the ''F8'' gene cause a relative deficiency in factor VIII, resulting in improper hemostasis and abnormal or excessive bleeding. | |||
*This trait is inherited in an X-linked recessive manner, affecting males and homozygous females (very rare). | |||
*One-third of new cases of Hemophilia A are due to spontaneous mutations in the X-chromosome, not inherited from either parent. | |||
*In rare cases, individuals may develop hemophilia later in life. This acquired form of the disease results from development of antibodies to factor VIII. | |||
==References== | ==References== | ||
Revision as of 22:06, 29 July 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
- The pathogenesis of hemophilia A is characterized by genetic deficiency in Factor VIII.
Pathophysiology
- The F8 gene associated with the development of Hemophilia A is located close to the tip Xq, and affects production of clotting factor VIII. Abnormalities in the F8 gene cause a relative deficiency in factor VIII, resulting in improper hemostasis and abnormal or excessive bleeding.
- This trait is inherited in an X-linked recessive manner, affecting males and homozygous females (very rare).
- One-third of new cases of Hemophilia A are due to spontaneous mutations in the X-chromosome, not inherited from either parent.
- In rare cases, individuals may develop hemophilia later in life. This acquired form of the disease results from development of antibodies to factor VIII.