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In the acquired form of FX deficiency an insufficient amount of factor X is produced by the liver due to liver disease, vitamin K deficiency, buildup of abnormal proteins in organs (amyloidosis) or certain medications (i.e. warfarin). [1] In amyloidosis FX deficiency develops as FX and other coagulation factors are absorbed by amyloid fibrils. [3]
Inborn deficiency of factor X is very rare (1:1,000,000), and may present with epistaxis (nosebleeds), hemarthrosis (bleeding into joints) and gastrointestinal blood loss. . Apart from congenital deficiency, low factor X levels may occur occasionally in a number of disease stat
Fresh normal plasma has all the blood coagulation factors with normal levels. If the problem is a simple factor deficiency, mixing the patient plasma 1:1 with plasma that contains 100% of the normal factor level results in a level ≥50% in the mixture (say the patient has an activity of 0%; the average of 100% + 0% = 50%). [3]
Glanzmann's thrombasthenia can be inherited in an autosomal recessive manner [3] [4] or acquired as an autoimmune disorder. [3] [5]The bleeding tendency in Glanzmann's thrombasthenia is variable, [3] some individuals having minimal bruising, while others have frequent, severe, potentially fatal hemorrhages.
Platelet storage pool deficiency is a family of clotting disorders characterized by deficient granules in platelets. Individuals with these disorders have too few or abnormally functioning alpha granules , delta granules , or both alpha and delta granules and are therefore unable to form effective clots, which leads to prolonged bleeding.
A mutation in factor II would essentially lead to hypoprothrombinemia. The mutation is presented on chromosome 11. [9] Areas where the disease has been shown to present itself at include the liver, since the glycoprotein is stored in this area. Acquired cases are results from an isolated factor II deficiency. Specific cases include:
Coagulopathy (also called a bleeding disorder) is a condition in which the blood's ability to coagulate (form clots) is impaired. [1] This condition can cause a tendency toward prolonged or excessive bleeding (bleeding diathesis), which may occur spontaneously or following an injury or medical and dental procedures.
Factor XII deficiency is a deficiency in the production of factor XII (FXII), a plasma glycoprotein and clotting factor that participates in the coagulation cascade and activates factor XI. FXII appears to be not essential for blood clotting, as individuals with this condition are usually asymptomatic and form blood clots in vivo .
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