haemostasis Flashcards
haemostatsis is the maintenance of — system by which it works correctly w:
1- Stop blood – from – vessels
2- but also know when to stop – from becoming too big
3- contributes to – immune response
closed circulatory
escaping
injured
clot
innate
why’s it important:
1-Complications from — is the No. 1 killer in the Western world (10 million cases of VTE in US/UK annually, 0.6 million deaths)
2—- ( — ) kills more people each year than breast cancer, car crashes and AIDS combined.
3- —- is the most common cause of death in cancer patients apart from the cancer itself
4-VTE is the leading cause of — hospital death, ahead of infection and pneumonia
blood clotting
venus thrombeoblism VTE
thrombosis
preventable
progress in understanding coagulation:
Originally thought to be a consequence of blood ‘cooling’ (Hippocrates, Aristotle)
Promoters of blood coagulation - rest, ‘loss of vital force’, air - Hewson, 1773)
Understanding of role of coagulation factors and their promotion of blood clotting (1950-70s)
the balancing act of haemostatsis:
- complex balancing act between action of — and proteins that — clotting aka —
- they respond — and —
- they remain —
- enable tissue —
- stops when —
clotting proteins ( for coagulation)
inhibits (anticloagulant aka for bleeding)
- rapidly proportionally
- localised
- tissue repair
- when required
when haemostasis is desregulated we will have —
by which it affects — people / year and causes — of all hospital death
- commnerst cause of death in –
thrombosis
1 in 1000
10%
pregnancy
thrombophilia is the disorder of haemostats that – the propbality of thrombosis it can be either:
1- INHERITED (via a— defect)
2-ACQUIRED (via an – risk factor)
3-Most commonly, —
increases ( words involved: vessel wall , blood constituents , and blood flow)
genetic defect
environmental
combo of both
deep vein thrombosis DVT:
- Caused by blood –
-Clot forms in the – , normally in the –
-Associated with pain/swelling/redness, but can be –
-Extremely – if it becomes detached, enters – and becomes lodged in – (pulmonary embolism)
stasis
deep veins
legs
symptomless
dangerous
bloodstream
lungs
pulmonary embolism (PE) :
-Blockade of – by – originating from other part of the body (normally from a– )
-10-30% with DVT/PE die within month of diagnosis
pulmonary artery
clot
DVT
steps:
1- — blood vessel
2- blood vessel —
3- — formation
4- platete —
5- platelet — which prevents excessive — at the site of injury
- primary platelet plug is —
- stabilization is by — which is for coagulation cascade
normal
injury
platelet plug
adhesion
aggregation
blood loss
is not suffienct
fibrin
clot formation in vivo :
1- exposure of —
2- accumaltion of activated – at the – of injury
3- – deposition and – formation
tissue factor
platelet
site
fibrin
clot
tissue receptor is a — receptor expressed on the surface of — tissue
- not normally expressed on cells exposed to the –
- aberrant expression of TF is a major cause of —
membrane receptor
extravasculaer
blood
pathological thrombosis
— is a receptor for factor VII(a)
– binds to — with – affinity the exposed by vessel damage
- acts as the — for the blood coagulation cascade
TF
TF binds to FVIIa
high
trigger
coagulation cascade:
-In normal plasma – series of inactive clottingcfactors (protein — )
- – clotting factor is activated…
zymogen
single initial
( check slide 25)
how does thrombin generation influence clot structure:
Procoagulant serine protease:
- Activates –
-Cleaves — to –
-Feedback – (activates other coagulation factors)
-Activates —, which cross-links –
platelet
firbongen to fibrin
amplification
XIIIa
fribin
summar:
- what’s required for haemostasis is — exposure and platelet — and — in order for us to have clot formation
- starts off by normal blood vessel then platelet plug formation then coagulation cascade
tf
adhesion n activation
