Haem: Coagulation Pt.2 Flashcards
(25 cards)
How is the common final pathway monitored?
Thrombin time (TT)
Assesses the activity of fibrinogen
Why is the prothrombinase complex important?
It allows activation of prothombin at a much faster rate
What is required for adequate production/absorption of vitamin K?
- Bacteria in the gut produce Vitamin K
- It is fat-soluble so bile is needed for viatmin K to be absorbed
What is the most common cause of vitamin K deficiency?
Warfarin
Name two factors that convert plasminogen to plasmin.
- Tissue plasminogen activator
- Urokinase
Name a factor that inhibits the tissue plasminogen activator and urokinase.
Plasmingoen activtor inhibitor 1 and 2
Name two factors that directly inhibit plasmin.
- Alpha-2 antiplasmin
- Alpha-2 macroglobulin
What is the role of thrombin-activatable fibrinolysis inhibitor (TAFI)?
Inhibitor of fibrin breakdown
Describe the action of antithrombins.
Bind to thrombin in a 1:1 ratio and this complex is excreted in the urine
How many types of antithrombin are there?
Five (antithrombin-III is the most active)
What is the most thrombogenic hereditary condition?
Antithrombin deficiency
Outline the role of protein C and protein S.
- Trace amounts of thrombin generated at the start of the clotting cascade activate thrombomodulin
- This allows protein C to bind to thrombomodulin through the endothelial protein C receptor
- Protein C is then fully activated in the presence of protein S
- Fully activated protein C will inactivate factors 5a and 8a
Why does Factor V Leiden cause a prothrombotic state?
The factor 5a will be resistant to breakdown by protein C.
State two causes of activated protein C resistance.
- Mutated factor 5 (e.g. factor V Leiden)
- High levels of factor 8
What is the role of tissue factor pathway inhibitor?
- TFPI neutralises the tissue factor-factor 7a complex once it has initiated the clotting cascade
List some categories of genetic defects that cause excessive bleeding.
- Platelet abnormalities
- Vessel wall abnormalities
- Clotting factor deficiencies
- Excess clot breakdown
List some acquired defects that cause excessive bleeding.
- Liver disease
- Vitamin K deficiency
- Autoimmune diseases (platelet destruction)
- Trauma
- Anti-coagulants/anti-platelets
List some genetic defects that cause excessive thrombosis.
- Clotting factor inhibitor deficiencies
- Decreased fibrinolysis
List the types of disorders of haemostasis.
- Vascular disorders (e.g. scurvy)
- Platelet disorders
- Coagulation disorders
- Mixed disorders (e.g. DIC)
What is the difference between immediate and delayed bleeding with regards to the underlying pathological process?
- Immediate - issue with the primary haemostatic plug (platelets, endothelium, vWF)
- Delayed - issue with the coagulation cascade
Describe the key clinical differences between platelet disorders and coagulation factor disorders.
Platelet disorders:
- Bleeding from skin and mucous membranes
- Petechiae
- Small, superficial ecchymoses
- Bleeding after cuts and scratches
- Bleeding immediately after surgery/trauma
- Usually mild
Coagulation factor disorders:
- Bleeding into soft tissues, joints and muscles
- No Petechiae
- Large, deep ecchymoses
- Haemarthroses
- No bleeding from cuts and scratches
- Delayed bleeding from surgery or taruma
- Often SEVERE
When is treatment for platelet disorders required?
Platelet count <30x109/L (this is associated with spontaneous haemorrhage)
Why is it important to look at platelets under the microscope in thrombocytopaenia?
- To check whether it is pseudothrombocytopaenia (platelets clump together giving an erroneously low result)
- Also allows identification of other abnormalities (e.g. Grey platelet syndrome - large platelets)
What can cause a decrease in platelet number?
- Decreased producton
- Decreased survival (TTP)
- Increased consumption (DIC)
- Dilution
