Hemostais and Thrombosis
9 important questions on Hemostais and Thrombosis
What is primary and secondary hemostasis?
- Secondary: stabilization of platelet plug by a fibrin network
Where is the von Willebrand factor (VWF) stored?
How do platelets adhere to a damaged vessel wall during primary hemostasis?
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How does a vitamin K antagonist work and what does it treat?
The vitamin K antagonist inhibits vitamin K epoxy-reductase thereby limiting the activity of the vitamin K dependent carboxylase. Reduced gamma-carboxylation of blood coagulation results in reduced ability to interact with phospholipids and a reduced activity. So less clotting.
What is hemophilia a and b and how can it be treated?
- Hemophilia b: Lack Factor IX
Result: bleeding in joints or muscle (joint bleeding may result in severe damage)
Patients are treated with:
- purified factor VIII or purified factor IX (intravenous administration)
(sometimes the proteins are recognized as foreign, which induces an immune reaction).
- Bispecific anitobody (Hemophilia a): brings FIXa and FX together (so does the same as FVIII). Is however still less effective than FVIII istself.
- Gene therapy
How does secondary hemostasis go?
- Complex VIIa activates factor X and factor IX.
- Factor Xa and IXa lead to the formation of thrombin and that leads to the formation of fibrin. (FIXa accelerates serine protease).
* Complex FXa and FVa converts prothotrobin into thrombin (which activates FV, FVIII and FXI --> amplification thrombin formation)
* Thrombin cleaves fibrogen which forms fibrin by releasing fibrinopeptiole A and B.
* Fibrin crosslinks due to Ca2+binding
How are fibrin clots degraded?
How can blood coagulation be controlled?
- APC (Activated Protein C) + ProtS (active component) cleave FVa and FVIIIa (cofactors) which lead to a limited thrombin formation.
What happens in Factor V Leiden?
* Treatment: vitamin K antagonist
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