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Cardiovascular System > 13. Haemostasis 1 > Flashcards

13. Haemostasis 1 Flashcards

1
Q

What is the role of Coagulation factors?

A

Help form clots to plug holes in vasculature

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2
Q

What is the role of Regulatory factors in haemostasis?

A

Stop coagulation system firing off prematurely

which would cause thrombosis

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3
Q

What prevents coagulation factors being triggered unnecessarily?

A

Triggers are outside the circulation in the sub endothelial tissue (Collagen and Tissue factor)

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4
Q

What is Von Willebrand Factor (vWF)?

A

A giant adhesive plasma protein

Has multiple binding sites for platelets, collagen and factor 8

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5
Q

How is Von Willebrand Factor found in blood normally?

A

In a rolled up form

Many of its binding sites are hidden

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6
Q

What happens when vWF binds to collagen?

A

Blood flow pushes it along and stretches it

vWF becomes long and thin

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7
Q

Describe platelets

A 
Fragments of megakaryocytes
Much smaller than RBCs
No nucleus
Granular
Half life ~10 days
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8
Q

List 3 stimulatory receptors on platelets and what they bind to

A

P receptors: bind ADP
Thromboxane receptors: bind thromboxane
PGI2: binds prostacyclin

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9
Q

List 2 adhesive receptors on platelets and what they bind to

A

Integrin alpha-II-b-beta-3
GPIb-alpha
Both bind to vWF

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10
Q

What is exposed when the endothelial layer is damaged?

A

Collagen and tissue factor

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11
Q

What is required in primary haemostasis?

A

Collagen
Platelets
Von Willebrand Factor
(+ fibrin in larger vessels for stabilisation)

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12
Q

Describe the formation of a platelet plug in primary haemostasis

A 
Rolled up vWF binds to exposed collagen and gets stretched out
Exposes vWF binding sites for platelets
Platelets bind as they flow by
Platelets become activated
Granules discharge, release more vWF
vWF captures more platelets
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13
Q

What do platelets bind to other platelets in a platelet plug with?

A

Fibrinogen

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14
Q

What is platelet activation?

A

Conversion from a passive to an interactive cell

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15
Q

How are activated platelets different?

A

Change shape
Expose phospholipid
Present new or activated proteins on their surface

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16
Q

What happens inside platelets when they’re activated?

A

Ca2+ flux causes granules to degranulate
Release ADP, Fibrinogen and vWF
Takes phospholipid from its surface and makes thromboxane

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17
Q

What is coagulation?

A

Formation of a fibrin mesh (occurs in secondary haemostasis)

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18
Q

List the Sites of Synthesis of Clotting Factors, Fibrinolytic Factors and Inhibitors

A

Liver (primarily)
Endothelial cells (Factor VIII and vWF)
Megakaryocytes (to platelets) (vWF and factor V)

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19
Q

What is the co-factor needed to activate factor VII?

A

Tissue factor

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20
Q

When factor VII and tissue factor form a complex what happens?

A 
Becomes activated (VIIa)
Turns inactive proteins (factors IX and X) into active forms (IXa and Xa)
21
Q

What is the dampening mechanism that turns off coagulation almost immediately?

A

TFPI

Binds to FVIIa and FXa

22
Q

What can FXa make before the coagulation process is dampened by TFPI?

A

Thrombin

23
Q

What does thrombin do if there is enough made before the dampening process?

A

Forms 2 complexes:
IXa enzyme, VIIIa cofactor, PL (phospholipid that platelets are providing)
+
Xa enzyme, Va cofactor on surface of PL with Ca2+
These make a lot more thrombin

24
Q

What extra feedback can make more FIX if needed?

A

XI activated to XIa

Converted to IX

25
Q

What does thrombin do haemostatically?

A

Thrombin cleaves fibrinogen (soluble, in blood) to form fibrin (insoluble, forms a mesh)

26
Q

Rate of thrombin production

A

Lag while becoming activated

Then lots of thrombin produced in a burst

27
Q

What does a thrombin burst generate?

A

A stronger, denser clot which is more resistant to fibrinolysis

28
Q

What effect does thrombin have on factor XIII?

A

Thrombin activates factor XIII

Factor XIII cross links fibrin and inhibits fibrinolysis

29
Q

What inhibitor does thrombin activate?

A

TAFI

An inhibitor of fibrinolysis

30
Q

What does deficiency of coagulation factors cause?

A

Bleeding disorders due to failure of a thrombin burst

31
Q

Why does blood not clot completely whenever clotting is initiated by vessel injury?

A

Coagulation inhibitory mechanisms prevent this

32
Q

List 3 proteins on the surface of endothelial cells that prevent platelet activation and unnecessary clotting

A

Heparans/ Heparin
EPCR
TM

33
Q

List 2 antiplatelet agents produced by the endothelium

A

PGI2

NO

34
Q

What does ADPase on the surface of endothelial cells do to platelets?

A

Degrades platelets

35
Q

What are the 2 direct inhibitory mechanisms for coagulation?

A

Antithrombin (AKA antithrombin III): an inhibitor of thrombin and other clotting proteinases, deals with enzymes
TFPI: in the initiation phase

36
Q

What is the indirect inhibitory mechanism for coagulation?

A

Inhibition of thrombin generation by the protein C anticoagulant pathway, deals with cofactors

37
Q

Describe the action of antithrombin (AT)

A

AT binds complexes with thrombin (IIa) and neutralises it

38
Q

Describe the effect of heparin on the action of antithrombin (AT)

A

Heparin makes AT molecule more reactive and bridges AT and IIa

39
Q

Abbreviation for thrombin

A

IIa

40
Q

Which enzymes can antithrombin inactivate?

A

IXa
Xa
XIa

41
Q

Describe the protein C pathway that down regulates thrombin generation

A

Thrombomodulin (TM) binds free thrombin
TM redirects thrombin activity from fibrinogen to protein C
Activated Protein C + cofactor protein S down-regulates thrombin generation by degrading factor Va and VIIIa

42
Q

What do free thrombins bind to? (in termination of coagulation)

A

Free thrombin binds to antithrombin, which binds to heparans on the surface of epithelium

43
Q

Fibrinolysis

A

Breaking a clot down

clots are temporary

44
Q

Describe the process of fibrinolysis

A

When fibrin is formed, tissue plasminogen activator (tPA) and Plasminogen (Pgn) form a complex
tPA turns Pgn into Plasmin
Fibrin is the target of Plasmin
Plasmin breaks down fibrin, forming fibrin degradation products
Antiplasmin regulates this: stops plasmin degrading other healthy things (process is localised)

45
Q

What happens when Coagulation Inhibitory Mechanisms Fail?

A

Inappropriate clot formation (thrombosis)

46
Q

List 3 deficiencies increasing risk of thrombosis

A

Antithrombin deficiency
Protein C deficiency
Protein S deficiency

47
Q

What imbalances of haemostasis cause bleeding?

A

If not enough pro-coagulant factors
Or
There is too much anticoagulant activity

48
Q

What imbalances of haemostasis cause thrombosis?

A

If there is too much FVIII (pro-coagulant factor)
or
Not enough antithrombin (anticoagulant)

Cardiovascular System (16 decks)

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