how can infection lead to multi-organ failure
what causes intravascular activation of coagulation
loss of localisation
why uncontrolled bleeding can’t stop
- platelets consumed at faster rate than produced
what factors does vitamin K help
what do completed forms of factors ii, vii, ix, x and proteins c & s do
what are VKA monitored by
- keep blood levels within therapeutic window
what are circulating anticoagulants and what types are they split into
- lupus & factor viii antibodies
what are lupus anticoagulants
- prevent factors accumulating on phospholipid surfaces
what are factor viii anticoagulants
- same profile as haemophilia A
Defects in platelet-vessel wall interaction
Von Willebrand syndrome.
Bernard–Soulier syndrome.
Defects in platelet-platelet interaction
Glanzmann thrombasthenia.
Congenital afibrinogenemia.
Defects in platelet granules, secretion and signal transduction.
Wiskott-Aldrich Syndrome
what is haemophilia
how many cases of haemophilia are mutations
what does haemophilia result in
insufficient thrombin generation
what factor is deficient in haemophilia A
what factor is deficient in haemophilia B
what are normal levels of factors VIII & IX
what are the levels of factors VIII & IX at different stages of haemophilia
what are the consequences of haemophilia
- joint bleeding & destruction
how is clotting time restored
- replacement of VIII
what factor affect PT (prothrombin)
Factor VII
what factors affect APTT (Activated partial thermoplastin time)
what factors affect TT (thrombin time)