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Haemostasis Flashcards

(57 cards)

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1
Q

What is haemostasis

A

the cellular and biochemical processes that enables both the specific and regulated cessation of bleeding in response to vascular insult

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2
Q

What is haemostasis for?

A

to prevent blood loss from intact and injured vessels, enable tissue repair

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3
Q

describe the balance of haemostats

A

Bleeding - NORMAL HAEMOSTASIS - Thrombosis

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4
Q

what causes bleeding

A

Increase in:
Fibrinolytic factors
Anticoagulant proteins

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5
Q

what causes thrombosis

A

Increase in:
Coagulant factors
Platelets

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6
Q

outline steps in Haemostatic plug formation

A

Vessel constriction
Formation of an unstable platelet plug (platelet adhesion + platelet aggregation)
Stabilisation of plug with fibrin (blood coagulation)
Dissolution of clot and vessel repair (fibrinolysis)

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7
Q

how is the platelet plus broken down

A

fibrinolytic system

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8
Q

how are blood vessels anticoagulant

A

endothelial cells create a barrier between the blood and the procoagulant subendothelial structures

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9
Q

What component found underneath the endothelium is involved in triggering the coagulation cascade?

A

Procoagulant subendothelial structures

e.g. collagen
Tissue factor is also expressed on the surface of the cell that underlie blood vessels but it is NOT normally expressed within the circulation itself

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10
Q

what components do endothelial cells produce that are important in haemostasis

A

Prostacyclin
Thrombomodulin
Von Willebrand Factor
Plasminogen Activator

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11
Q

what cell do platelets originate from

A

megakaryocytes - mature in BM

Megakaryocytes are formed from blood stem cells

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12
Q

What process during maturation of the megakaryocytes is important for the formation of platelets?

A

Granulation

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13
Q

describe basic ultrastructure of platelet

A

OT got a nucleus but it is still a pretty active cell

storage granules

glycoprotein/thrombin receptors

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14
Q

what storage granules does the platelet contain and why are these granules important

A

ADP granules
alpha granules

storage granules for proteins including Factor V and VWF

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15
Q

what happens during platelet activation to the platelet itself (shape)

A 
conversion from passive to interactive cell
cytoskeleton change (disc shapes to pseudopod)
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16
Q

give some roles of platelets

A 
Haem/thrombosis
Cancer
Inflammation
Immunity
Atherosclerosis
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17
Q

why does VWF not normally interact with platelets in circulation

A

circulates in globular formation, binding sites hidden

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18
Q

how does collagen end up being exposed to platelets

A

endothelium damaged

sub endothelium exposed

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19
Q

Platelets can bind to the collagen in TWO ways:

A

It can bind via vWF to collagen (via the GlpIb receptor)

It can bind directly to the collagen (via the gly6 / glya2b1 receptor)

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20
Q

how do VWF sites become exposed

A

shear forces of flowing blood cause unravelling

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21
Q

under what specific conditions can platelets bind directly to collagen

A

ONLY at low shear - venous

not arteries/capillaries

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22
Q

what 2 molecules can actually cause platelet activation

A

Collagen and

thrombin( during coagulation)

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23
Q

once the platelet is bound to collagen/VWF how is it activated

Study These Flashcards
A

int.signalling causes

release the ADP from the storage granules

synthesise thromboxane

agents bind to rc on surface activate them

24
Q

What happens following the passive adhesion of platelets andengagement of receptors?

Study These Flashcards
A

The receptors signal inside the cell to release ADP from the storage granules and to synthesise thromboxane
These bind to receptors on the surface of the platelets and activate them

Once activated, GlpIIb/IIIa receptors become available, which can bind to fibrinogen and allows the platelets to aggregate

25
Which receptors on the platelets become available following activation of the platelets and what do they bind to?
glycoprotein 2b/3a receptors become available bind to fibrinogen and helps the platelets clump together AGGREGATION
26
main tests to Monitor Platelets and their Function
Platelet count - MOST IMPORTANT Bleeding time Platelet aggregation
27
normal range of platelets
Normal range: 150-400 x 109/L
28
at what point does spontaneous bleeding common
below 40 x 109/L | between 40-100 no spontaneous but bleeding but bleeding with trauma
29
what is spontaneous bleeding often caused by
autoimmune thrombocytopenia This is where autoimmune antibodies remove the platelets from the circulation
30
what are features of Auto-ITP
purpura, multiple bruises and ecchymoses
31
as platelet count continues to drop what else becomes a concern
below 10 = severe Leukaemia - Leukaemic cells populate the bone marrow so it crowds out the megakaryocytes so the platelets aren’t produced in sufficient numbers = THROMBOCYTOPENIA
32
what else can activate platelets
thrombin
33
where are clotting factors synthesised
Liver Endothelial cells Megakaryocytes
34
what are all the zymogens in the pathway
serine protease domain-containing proteins once activated cleave substrate after specific arg/lys residue
35
what is needed to trigger start of coagulation
TF bearing cells need to be exposed
36
what does TF combine with to start the coagulation cascade
TF meets factor 7 (plasma proteins) Switches enzyme on forming TF-7a complex
37
what is unique about TF
only procoagulant factor that does not require proteolytic activation
38
where is TF normally located
not exposed to blood VSMC, fibroblasts
39
where is TF expressed highly
certain organs: lungs, brain, heart, testis, uterus, placenta
40
describe the domain structure of factor 7
Serine protease domain 2X Gla domain - binds to phospholipids EGF domain - protein protein interaction
41
what is unique about gla domains
binds to phospholipid surfaces (gives ability of coagulation proteins to bind to -ve charged phospholipids) formation dependent on Vit k
42
Which factors are affected by warfarin?
2, 7, 9, 10
43
What is common to all of these factors and what is the significance of this common feature? (factors affected by warfarin)
They have a cluster of glutamic acid The glutamic acid is recognised by an enzyme in the liver and undergoes post-translational modification in the presence of vitamin K to Gamma-carboxyglutamic acid Once this extra carboxyl group is added, calcium can facilitate the binding of gamma carboxyglutamic acid to the activated platelet membrane phospholipid
44
How does warfarin actually inhibit the post-translational modification of these factors?
Warfarin inhibits vitamin K epoxide reductase thus inhibiting the gamma carboxylation of factors 2, 7, 9 and 10 This means that it stops the ability of the clotting factors to bind to the surface of the platelets ultimately reduces thrombin production
45
What factors do megakaryocytes produce?
Factor V | Von Willebrand Factor
46
what are the 2 jobs of the TF-7a complex
proteolyse FX - FXa proteolyse F1X - F1Xa
47
Tissue factor activates the clotting cascade in 2 ways but what is the difference in these 2 pathways
9 to 9a – slower but produces more thrombin | 10 to 10a – faster (but inefficient)
48
what do both factors 9a/10a do
convert prothrombin (2) to thrombin (2a)
49
State two accelerating factors. What are they activated by?
Factor VIII - precursor for 9 Factor V They are activated by trace amounts of thrombin
50
besides further propagating coagulation what does thrombin do
catalyses cleavage of fibrinogen into fibrin
51
what does TFPI do
TFPI binds and forms complex with 10a this binds and inactivates TF-7a via a Kunitz domain therefore no 10a production
52
why can TFPI not stop coagulation alone
very low conc in blood
53
Describe the function of the Protein C anticoagulant pathway.
Thrombin also has a role in anticoagulation It binds to thrombomodulin on the surface of endothelial cells and by binding to thrombomodulin it activates protein C, Protein C along with co-factor protein S INACTIVATES FACTOR Va and FACTOR VIIIa
54
what factors regulate coagulation and where in the cascade do they act
TFPI regulates initiation off coagulation Protein C/S regulates propagation phase of coagulation Anti thrombin - prevents thrombin acting away from site of damage
55
what does antithrombin do
Anti-thrombin has a reactive loop that irreversibly inhibits the active site on the clotting factors So anti-thrombin acts as a scavenger in mopping up free serine proteases that escape damage site
56
What two proteins assemble on the surface of a clot to allow fibrinolysis to take place? Where are these proteins made?
Plasminogen converted to plasmin by Tissue Plasminogen Activator (tPA) Plasminogen is a plasma protein tPA is produced by endothelial cells
57
State three laboratory tests for blood coagulation.
Activated Partial Thromboplastin Time (APTT) Prothrombin Time (PT) Thrombin Clotting Time (TCT)

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