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Hub AI
Factor VII deficiency AI simulator
(@Factor VII deficiency_simulator)
Hub AI
Factor VII deficiency AI simulator
(@Factor VII deficiency_simulator)
Factor VII deficiency
Factor VII deficiency is a bleeding disorder characterized by a lack in the production of Factor VII (FVII) (proconvertin), a protein that causes blood to clot in the coagulation cascade. After a trauma factor VII initiates the process of coagulation in conjunction with tissue factor (TF/factor III) in the extrinsic pathway.[citation needed]
The condition may be inherited or acquired. It is the most common of the rare congenital coagulation disorders.
Symptoms may differ greatly, as apparently modifiers control to some degree the amount of FVII that is produced. Some affected individuals have few or no symptoms while others may experience life-threatening bleeding. Typically this bleeding disorder manifests itself as a tendency to easy bruising, nose bleeding, heavy and prolonged menstruation, and excessive bleeding after dental or surgical interventions. Newborns may bleed in the head, from the umbilicus, or excessively after circumcision. Other bleeding can be encountered in the gut, in muscles or joints, or the brain. Hematuria may occur.[citation needed]
While in congenital disease symptoms may be present at birth or show up later, in patients with acquired FVII deficiency symptoms typically show up in later life.[citation needed]
About 3-4% of patients with FVII deficiency may also experience thrombotic episodes.
Inherited or congenital FVII deficiency is passed on by autosomal recessive inheritance. A person needs to inherit a defective gene from both parents. People who have only one defective gene do not exhibit the disease, but can pass the gene on to half their offspring. Different genetic mutations have been described.
In persons with the congenital FVII deficiency the condition is lifelong. People with this condition should alert other family members may they also have the condition or carry the gene. In the general population the condition affects about 1 in 300,000 to 500,000 people. However, the prevalence may be higher as not all individuals may express the disease and be diagnosed.
In the acquired form of FVII deficiency an insufficient amount of factor VII is produced by the liver due to liver disease, vitamin K deficiency, or certain medications (i.e., Coumadin).
Factor VII deficiency
Factor VII deficiency is a bleeding disorder characterized by a lack in the production of Factor VII (FVII) (proconvertin), a protein that causes blood to clot in the coagulation cascade. After a trauma factor VII initiates the process of coagulation in conjunction with tissue factor (TF/factor III) in the extrinsic pathway.[citation needed]
The condition may be inherited or acquired. It is the most common of the rare congenital coagulation disorders.
Symptoms may differ greatly, as apparently modifiers control to some degree the amount of FVII that is produced. Some affected individuals have few or no symptoms while others may experience life-threatening bleeding. Typically this bleeding disorder manifests itself as a tendency to easy bruising, nose bleeding, heavy and prolonged menstruation, and excessive bleeding after dental or surgical interventions. Newborns may bleed in the head, from the umbilicus, or excessively after circumcision. Other bleeding can be encountered in the gut, in muscles or joints, or the brain. Hematuria may occur.[citation needed]
While in congenital disease symptoms may be present at birth or show up later, in patients with acquired FVII deficiency symptoms typically show up in later life.[citation needed]
About 3-4% of patients with FVII deficiency may also experience thrombotic episodes.
Inherited or congenital FVII deficiency is passed on by autosomal recessive inheritance. A person needs to inherit a defective gene from both parents. People who have only one defective gene do not exhibit the disease, but can pass the gene on to half their offspring. Different genetic mutations have been described.
In persons with the congenital FVII deficiency the condition is lifelong. People with this condition should alert other family members may they also have the condition or carry the gene. In the general population the condition affects about 1 in 300,000 to 500,000 people. However, the prevalence may be higher as not all individuals may express the disease and be diagnosed.
In the acquired form of FVII deficiency an insufficient amount of factor VII is produced by the liver due to liver disease, vitamin K deficiency, or certain medications (i.e., Coumadin).
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