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Blood and defence > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

Cessation of bleeding after injury to minimise blood loss

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2
Q

What is the sequence of events involved in haemostasis?

A 
Vascular Injury 
Vasoconstriction
Platelet plug formation 
Coagulation (blood clotting)
Stabilisation of the clot
Fibrinolysis (removal of clots)
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3
Q

Why does haemostasis need to be carefully regulated?

A

Inability to clot can result in extreme hemorrhage.

Propensity to clot can result in thrombosis, which can mobilise (embolism).

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4
Q

What are platelets derived from?

A

Fragments of megakaryocytes. (large bone marrow cell)

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5
Q

How many platelets are in the blood, and what is their lifespan?

A

4x10^8, 8-10 days

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6
Q

What do platelets consist of?

A

No nuclei, most normal organelles

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7
Q

How to platelets adhere to the endothelium?

A

Bind to vWF (von willebrand factor) present on the basement membrane.

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8
Q

How do platelets aggregate to eachother?

A

Fibrinogen bridges, binding to GPIIb and GPIIa integrin receptors.

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9
Q

What causes vessel smooth muscle to contract (vascular spasm)?

A

Initially, local sympathetic pain receptor reflex.

Endothelium derived factors and platelet released factors (thromboxane A2, serotonina and ADP)

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10
Q

What is a platelet plug?

A

Platelets adhere to damaged endothelium to form a platelet plug.

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11
Q

How does a platelet plug form?

A

Von Willebrand factor (vWF), secreted which causes platelet adherence to endothelium.

Express glycoprotein receptors (GPII) that interact with other platelets, via fibrinogen bridges that stabilise platelet aggregates.

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12
Q

How do platelets promote further clotting after initial plug?

A

Platelets release cytoplasmic granules such as adenosine diphosphate (ADP), serotonin and thromboxane. Attracts more platelets to the affected area, vasoconstrict and assist in platelet aggregation.

Continuing the process in a positive feedback loop.

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13
Q

What is the coagulation cascade and what is its final reaction?

A

Clotting factors (inactive plasma serine proteases) are activated in a sequence of events known as ‘coagulation cascade’ which leads to the formation of Fibrin from inactive fibrinogen plasma protein (zymogen).

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14
Q

How does fibrin produce a clot?

A

Fibrin mesh produced that traps blood cells and causes hardening of primary plug.

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15
Q

What are the two pathways of of haemostasis and what stimulates each?

A

Intrinsic - activation of factor XII by certain negatively charged surfaces, such as collagen.

Extrinsic - trauma leading to release of tissue factor activating VII to VIIa

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16
Q

Why is the intrinsic pathway a problem clinically?

A

Can lead to coagulation following heart valve replacement

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17
Q

What is the common clotting cascade (shared by both pathways)?

A

Conversion of factor X to active Xa which catalyses the conversion of inactive prothrombin (factor II) to active thrombin (factor IIa) which polymerises soluble fibrinogen (factor I) into insoluble fibrin (factor I a) strands.

Fibrin strands form mesh around platlet plug to trap other blood cells

Fibrin cross linked - stabilised by factor XIIIa (fibrin stabilising factor)

18
Q

How does soluble fibrinogen get converted into insoluble fibrin?

A

Removal of negatively charged fibrinopeptides

19
Q

What is the independent extrinsic cascade?

A

Trauma converts VII to VIIa which along with TF catalyses the formation of Xa from X

20
Q

What is the independent intrinsic cascade?

A

Surface leads to conversion of XII to XIIa, which converts XI to XIa which converts IX to IXa. Along with VIIIa, IXa converts X to Xa.

21
Q

What does factor XIII do?

A

Factor XIII, which forms covalent bonds that stabilise and crosslink the fibrin polymers.

22
Q

Where does the cascade occur?

A

On the platelet surface

23
Q

Which factors are localised to the platelet surface?

A

Va and Xa

24
Q

How is there a feed-forward loop in haemostasis?

A

Thrombin converts factor X to Xa, this along with factor V can convert prothrombin to thrombin

25
Q

What happens in haemophilia?

A

X-linked recessive disorder: Factor VIII deficiency or factor IX deficiency (haemophilia A and B respectively)

26
Q

What are thrombins substrates?

A

Fibrinogen, factor XIII, factor XI, factor VIII, factor V

27
Q

Why are calcium and phospholipid (in platelet membrane) required for the cascade?

A

Calcium mediates the binding of the complexes via the terminal gamma-carboxy residues on FXa and FIXa to the phospholipid surfaces of platelets.

28
Q

Why is vitamin K required for clotting?

A

Adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z. In adding the carboxyl group to glutamate residues on the immature clotting factors it activates them

29
Q

What happens vitamin K when it activates factors? How is it made active again?

A

Vitamin K is oxidized

Enzyme, Vitamin K epoxide reductase (VKORC), reduces vitamin K back to its active form.

30
Q

What does warfarin do?

A

Block VKORC, deficiency of reduced vit K

31
Q

How does endothelial lining of blood vessels prevent thrombosis in undamaged vessels?

A

Physical barrier (separate platelet and coagulation factors in blood from stimulatory collagen in subendothelial layer)

Secretes heparan sulphate (activates antithrombin) which is a serine protease inhibitor and degrades clotting factors.

Releases plasminogen activators e.g. tPA

Releases extrinsic pathway inhibtor TFPI

32
Q

What does antithrombin (ATIII) do

A

Serine protease inhibitor (SERPIN) Binds to active site of factors in coagulation cascade inhibiting their action, and degrades.

33
Q

What is TFPI, what does it do?

A

Tissue factor pathway inhibitor (TFPI) limits the action of tissue factor (TF). It also inhibits excessive TF-mediated activation of FVII and FX.

34
Q

Where is antithrombin made?

A

Endothelial cells and liver

35
Q

What is activated protein C and how does it regulate?

A

Anticoagulant. It is a vitamin K-dependent serine protease enzyme that is activated by thrombin into activated protein C (APC). The activated form, along with protein S and a phospholipid as cofactors, degrades FVa and FVIIIa.

36
Q

What is fibrinolysis?

A

Prevents blood clots from growing, fibrin is degraded by plasmin

37
Q

How does plasmin arise?

A

Inactive plasminogen in circulation with fibrin in clots as its substrate. Plasminogen activators activate plasminogen and generate plasmin

38
Q

What do plasminogen and plasminogen activator both do, why?

A

Bind to fibrin which localises them

Plasmin then removes fibrin clot

39
Q

What is required for synthesis of prothrombin?

A

Vitamin K

40
Q

What do activated platelets release?

A

Serotonin, Thromboxane AE and ADP

Blood and defence (5 decks)

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