Haemostasis Flashcards
What are the main steps of Haemostasis?
1- Artery contacts
2- Primary Haemostatic plug forms (from platelets, fragile)
3-Secondary Haemostatic plug forms (fibrin filaments stabalise primary)
What is the role of platelets?
Stick to exposed subendothelium Aggregate with other platelets (plugs form) Swell and change shape Secreate factors (to aid plug growth)
What is the role of vessel walls?
Atrial media contracts
Subendothelium traps platelets
Endothelium (balances between opposing and favouring clotting)
What mediates platelet clotting?
Platelet receptors Von Willebrand factor (platelets adhear to it) Fribinogen (links platelets) Collagen (binds platelets) ADP & Thromboxine (make plug) Thrombin (fribinogen to fibrin)
What is the purpose of the clotting cascade?
Produce Thrombin (11a) to convert soluble fribinogen to insoluble fibrin
What are the two cascade pathways?
Intrinsic- from blood itself (factor 12, 11, 9)
Extrinsic- from tissue fator release (factor 7)
Common - factor 10
What are common Coagulation tests?
Prothrombin time (PT)- measure extrinsic pathway (prolonged = 7 defficiency)
Activated partial thromboplastin time (APTT)- measure intrinsic pathway (prolonged =8,9,11,12 one defficient)
5,10 thrombin and fibriogen common to both pathways
Thrombin clotting time
What is DIC?
Disseminated Intravascular coaguloathy
Microangiopathic haemolytic anaemia
Multiple micrthrombi formed in circulation
Consumption clotting factors and platelets
Leads to haemorrages
What causes DIC?
There is always a trigger
Eg. Malignancy, massive tissue injury, infections
What is the treatment for DIC?
Treat underlying cause
Transfusion platelets and FFP
Key features of Haemiphilia
A- lack of factor 8
- X linked recessive
- prolonged APTT, normal PT
- recombinant factor 8
B-X linked recessive
-lack factor 9
-prolonged APTT, normal PT
Recombinant factor 9
Presentation of Haemophilia
Muscle haematomas
Joint pain
Prolonged dental bleeding
Intracerebral haemorrhage
Features of Von Willebrand disease
Abnormal platelet to vessel walls
Reduced factor 8
Prolonged bleeding time, excessive bleeding from wounds, mild tendency
Thrombophilia features
Congenital or acquired haemostais defects that increase risk of thrombosis
Congenital (defficiency in natural anticoagulants, abnormal factor 5)
Aquired (antiphosphoolipod syndrome)
What are the natural anticoagulants?
Protein C - inactivates factor 5&8
Activated by thrombin binding to receptor
Protein S is cofactor
Antithrombin 3- activated by heparin, prevents clot spread by rapidly inactivating factors that are carried away from clotting site