Hypercoagulable Disorders
What is it?
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Activation problems
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Regulation problems
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Breakdown problems
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Other factors
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Laboratory tests
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Treatments
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Related Pages
Problems with clot breakdown (fibrinolysis)
Inherited:
- Congenital plasminogen deficiency - rare factor deficiency; plasminogen is activated to form plasmin. Plasmin helps break apart the clot's cross-linked fibrin net. Most of these patients have eye problems, not thrombotic complications.
- Dysfibrinogenaemia - abnormal fibrinogen; it leads to fibrin that does not break down normally. Most patients with dysfibrinogenaemia have laboratory results within normal limits, but some have bleeding symptoms, and a small number have been reported to have thrombotic complications.
Acquired:
- Plasminogen deficiency -- plasminogen is the precursor to plasmin, which helps to break down clots; may also be an acquired deficiency (see above)
- Decreased plasminogen activator
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