Haemostasis
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- Created by: Sarah
- Created on: 29-04-17 22:41
what is normal blood volume?
4-6L
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how much percent of blood do you need to lose to go into hypovalemic shock?
30% or more
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what is hypovalemic shock?
the bloods unable to pump sufficient blood around body, blood supply to organs low -> organs fail
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what is haemostasis?
mechanism causes cessation (ending) of blood loss from damaged vessels
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what does haemostasis need?
cell-cell communication
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what are the 3 phases of haemostasis?
1) Vascular phase 2) platelet phase 3) Coagulation 4) tissue repair,clot breakdown+fibrinolysis (VPC)
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what overlies the tunica interna?
the endothelial layer- forms innermost wall of arteries
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first response of damage to capillary?
vascular phase
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what happens in vascular phase?
vascular smooth muscle contracts = vasoconstriction
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what layers contract in the vascular phase? what does this do?
endothlial cell layer, this exposes the basal lamina underneath to blood
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what do endothelial cells release in the vascular phase?
ADP, tissue factor 3 (extrinsic pathway), prostacyclin and endothelins
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why is prostacyclin released?
to reduce the spread of platelet aggregation
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why is ADP released?
for platelet aggregation
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what works against ADP?
prostacyclin- to carefully control clot formation
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what are endothelins?
peptide hormones, stimulate contraction of SM, maitain vascular phase
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a num of polymorphisms in endothelial recs ET-1 in African Americans gives what?
having polymorphism gives hypertension, inappropriate activation of endothelial rec -> inappropriate vasoconstriction
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what do endothelins do? with what property?
promote cell division as mitogenic (also stimulate contraction of SM)
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what do you see an increase of to do with endothelial cells in the vascular stage?
increased endothelial adhesion
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why do the endothelial cells stick together?
point of contact for repair,stick together in small capillaries, facilitates attachments of platelets
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what are the platelets precursors?
large cells- polyploid megakaryocte precursors
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what is the diameter of polyploid megakaryocyte precursors?
30-160um
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where are platelets formed?
bone marrow
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what is the life span of platelets?
10 days approx
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how do platelets form?
polypoid megakaryocte precurors project into marrow sinuses, pockets of cytoplasm surrounded by m pinch off, are anucleate
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diameter of platelets?
2-4um
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how many platelet fragments per microlitre of blood?
350,000
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what is the structure of the marrow sinuses?
blood rich region in the marrow, megarkaryoctes project into these and pinch off
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as platelets stick what else do they do?
activate and aggregate (promote sticking of other platelets)
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why is the platelet phase a positive feedback system?
more platelets you get sticking the more other platelets are promoted to stick
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when does platelet adhesion (platelet phase) start?
15 seconds from injury
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how is the platelet phase temp dependent?
only occurs above 32 degrees
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where do the platelets stick to?
the endothelium and basal lamina
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what is the basal lamina?
exposed collagen
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what factor is important in platelet adhesion?
von willebrands factor
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what does von willebrands factor promote?
further activation and aggregation of platelets
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events in platelet phase?
1) platelet adhesion 2) platelet activation
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how do we know platelets have become activated?
shape changes, become larger swell up, spike extension (protrusions), granulolysis
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what does granulolysis from activated platelets release?
ADP (aggregation), serotonin + thromboxane A2 (vasoconstriction) clotting factors(PF3), platelet derived growth factor (repair), calcium
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why is calcium released?
aggregation and clotting
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what is vitamin K needed for?
making clotting factors in the liver
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when does the coagulation phase happen how long?
30 seconds after injury
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2 different pathways in the coagulation phase?
1) instrinisic2) extrinsic pathway
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what is the intrisic pathway stimulated by?
exposure of collagen that activates proenzymes
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what is the extrinsic pathway started by?
tissue factor 3
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both coagulation phase pathways feed into what?
the coagulation pathway
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what pathway is activated by proenzymes activated by exposed collagen?
intrinsic pathway
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why does the exctrinsic pathway start?
consequence of damage to the tissue
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what releases calcium?
platelets
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what releases tissue factor 3 (for extrinsic)?
endothelial cells
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what comes together to form Factor 7 Tissue Factor Complex in the extrinsic pathway?
Tissue Factor 3 + calcium ions + clotting factor 7 --> factor 7 tissue complex
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what forms Factor X activator complex in the intrinsic pathway?
activated proenzymes + platelet factor 3 + calcium + clotting factors 8+9 -> Factor X Activator Complex
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what clotting factors in intrisic pathway?
8+9
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cloting factors in extrinsic pathway?
7
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what factor is the activated proenzymes in the intrisic pathway usually?
usually factor 12
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what is the final thing as a result of the coagulation cascade (both pathways)
fibrin
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what happens from factor X?
factor X-> prothrombinase catalyses prothrombin -> thrombin, thrombin catalyses fibrinogen -> fbirin
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thrombin causes positive feedback, what does it cause more relase of?
tissue factor (extrinsic) + Platelet Factor 3 (intrinsic)
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which pathway in the coagulation phase is faster?
extrinsic
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what stabilises clot + fibrin?
fibrin stablizing factor
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how long does haemostasis usually take?
1-4 minutes
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how long does platelet and clot retraction take?
30-60 minutes
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what other activated proezymes are there for the intrisic pathway?
9, 11, 12 and collagen
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why is clot restriction/retraction important?
prevent thrombus formation
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what inhibitoon effect does thrombin have?
stimulates anti thrombin?
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what does anti throbin 3 do?
minimises spread of clot, slows down coagulation,slowsclot formation
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what anticoagulants (restrict clot formation) are there?
heparin, thrombomodulin and prostacyclin
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what drugs- thrombolytics are used to stop clot formation?
warfarin and aspirin
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initial role of thrombin? long term?
positive feedback amplifies coagulation but long term supresses
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what is the clot dissolving process?
tissue plasminogen activator (TPA) + thrombonin -> plasminogen -> plasmin
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what does plasmin do?
digests fibrin strands
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what type of haemophilia are X linked recessive?
Type A + B
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what haemophilia is known as xmas disease and royal disease?
type b
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what is haemophilia type c?
autosomal recessive, AUTOSOMAL one!
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go through what factors are deficient in each type of haemophilia?
A- 8, B-9,10 C-11
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what happens in haemophilia?
haemostasis slowed-> bleed much more, bleeding under skin
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What is acquired haemophilia?
autoimmune disease destroys components needed for haemostasis
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what disorder do you get if you have an accumulation of clotting factors?
deep vein thrombosis
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what diseases give a reduction in liver function?
cirrohosis and hepatitis
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cirrohosis and hepatitis means what for clotting factors?
reduction in synthesis of clotting factors
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what will you have problems with if you're vitamin k deficient?
making clotting factors and haemostasis
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where is vitamin k from?
liver stores it, 50% by veg, 50% produced by gut bacteria
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why do newborns have a problem with haemostasis?
gut bacteria hasnt settled into pattern of producing clotting factors
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what is another version of haemophilia?
von willebrands disease
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what is von willebrands disease caused by?
deficiency in von willebrands factor
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what does vwf do?
aggregation and activation of platelets, sticks platelets to endothelium or collagen in ECM
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Other cards in this set
Card 2
Front
how much percent of blood do you need to lose to go into hypovalemic shock?
Back
30% or more
Card 3
Front
what is hypovalemic shock?
Back
Card 4
Front
what is haemostasis?
Back
Card 5
Front
what does haemostasis need?
Back
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