LT 44-45
16 important questions on LT 44-45
What is secondary hemostasis?
- strengthen the platelet plug
- adherence and activation of cells involved in vascular repair (fibroblasts, smooth muscle cells)
Wat is de werking van thrombin (IIa)?
Je krijgt daardoor fibrin monomers
Deze fibrin monomers kunnen fibrin dimers worden en uiteindelijk ook fibrin polymers.
Hoe meer thrombin, des te meer side chains kunnen worden gevormd
What is the role of factor XIII?
Gives a solid isopeptid bond, cross linking between D-domains of fibrin
Dit geeft dus een strong insoluble fibrin network in between platelets
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What is tissue factor?
Non-enzymatic cofactor of FVIIa
Normally absent in the blood compartment
Produced by fibroblasts and smooth muscle cells (hemostatic envelope) -> blood is protected from TF by the endothelium
During inflammation expression on endothelial cells and monocytes (disseminated itnravascular coagulation (DIC))
In cancer expression on tumor cells and circualting tumor derived microparticles
What is the coagulation cascade of the intrinsic pathway?
Conversion of XI to XIa
XIa zet IX om in IXa
IXa zet X om in Xa
Xa zet II om in IIa (thrombin)
IIa zet V om in Va
IIa zet VIII om in VIIIa
VIIIa helpt IXa met omzetten van X in Xa
Welke cofactoren zijn belangrijk bij thrombin formation en dus fibrin network?
Factor Va and factor VIIa
Va helpt bij omzetting II in IIa
VIIIa helpt IXa bij omzetting X in Xa
How to measure efficacy of coagulation/
Centrifugation:
- platelet rich plasma
- platelet poor plasma
Waravoor is PT sensitive?
What is the regulation of thrombin generatino/
- contact with TF
- activation of pro-enzymes
Amplification:
- V and VII feedback activation of procofactors
- feedback activation of factor XI
Inhibition:
- inhibition of the enzymes
- inhibition of the cofactors
What kind of venous thrombosis can you get?
- deep vein thrombosis (DVT)
- pulmonary embolism (PE)
Different locations (mainly legs)
Genetic and environmental factors involved
What is the prevalence of deficiencies in natural anticoagulatns?
High relative risk of VTE (10-20 fold)
Genetic basis: loss of function mutations
Different mutations in different families
mostly partial deficiencies
What illness do you get if you have a complete deficience of the natural anticoagulants?
How is the activationa nd inactivation of factor V?
FV is activated by thrombin (IIa) -> arginine residues in FV are cleaved for activation
When FVa is activated, there are specific Arg where APC cleaves.
What are genetic risk factors for venous thrombosis?
anticoagulant yeans: AT, PC, PS, very severe in homozygotes
Pro-coagulatn genes: FV Leiden, PT20210A, moderate in homozygotes
What are non-genetic risk factors for venous thrombosis?
What relation between malignancies and venous thrombosis?
Tissue factor on cancer cells upregualted up to 1000 fold.
Upregulation after mutation (KRAS, p53)
Major cause of death in cancer patients
In cancer tissue factori is in the blood stream. those tumors have microparticles, these microparticles have tissue factor on their surface. it can bind VII and this can activate factor X and IX and in the end lead to fibrinogen to fibrin conersion
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