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2.2 Haematology > Haemostasis 1 > Flashcards

Haemostasis 1 Flashcards

1
Q

What is haemostasis and thrombosis?

A

The control of the clotting and coagulation pathways in blood in normal and disease states, respectively

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2
Q

What does haemostasis involve?
(4)

A

Constriction of blood vessels

Adhesion and aggregation of platelets

Formation of a fibrin mesh by coagulation cascade

Followed, ultimately, by dissolution of the clot in a process called thrombolysis or fibrinolysis

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3
Q

Define thrombosis

A

A pathological state within the vascular system which results in inappropriate activation of the normal haemostatic process

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4
Q

What is a thrombus?

A

A blood clot

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5
Q

What does thrombus formation cause?

A

The blockage of blood flow to vital areas

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6
Q

Why do we need haemostasis
(3)

A

To ensure the maintenance of blood flow under normal physiological conditions

To maintain the integrity of the vasculature

Haemostasis has tight control over the initiation and termination of coagulation, localised to the are of vessel injury

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7
Q

What is haemostasis coordinated with?

A

Inflammatory and immune responses

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8
Q

How are clots removed?

A

The clot is removed as part of vascular remodeling

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9
Q

What does the haemostatic response do?
(3)

A

Prevents the loss of blood into the tissues and maintains vascular integrity

It localises the damage to the site of injury

Repairs and re-establishes blood flow through the repaired blood vessels

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10
Q

The haemostatic response is said to be in dynamic balance, what does this mean?

A

There is balance between activation and inhibition of the pathways involved e.g. clot formation and clot dissolution

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11
Q

What happens when there is a congenital or acquired deficiency in the haemostatic response?

A

The patient presents with haemorrhage

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12
Q

What happens when there is uncontrolled activation of the pro-coagulants?
(2)

A

This may result in excessive clotting or persistence of clot

Patients may present with thrombosis or blockages

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13
Q

What does the haemostatic balance favour?

A

Naturally favours anti-coagulant e.g. no clots unless needed

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14
Q

What would happen without haemostatic balance

A

Excessive bleeding or vaso-occlusion

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15
Q

What is vaso-occlusion
(2)

A

Uncontrolled formation of thrombin in vascular system

These occlude vessels and deprive organs of blood and therefore oxygen

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16
Q

Define thrombus formation

A

Inappropriate formation of a blood clot in an intact blood vessel

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17
Q

Define an embolus

A

A floating clot that has dislodged from the position where it was formed

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18
Q

Comment on the dynamics of haemostasis balance

A

The formation and dissolution of thrombi is maintained in a delicate balance (naturally anti-coagulant)

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19
Q

Briefly describe how haemostasis responds to vessel injury
(5)

A

Severed vessel - Vasoconstriction
Platelets adhere/agglutinate and become sticky, forming a plug
Fibrin appears
Fibrin clot forms
Clot retraction occurs

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20
Q

How is thrombin formed (briefly)?
(2)

A

Prothrombin is converted to thrombin

Thrombin converts fibrinogen to fibrin

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21
Q

What happens when there is vessel injury?
(3)

A

Vasoconstriction
Release of tissue factor
Collagen becomes exposed

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22
Q

What does vasoconstriction do to repair blood vessels?

A

This reduced blood flow and therefore reduces blood loss

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23
Q

Why is collagen exposure important?

A

This allows for platelet adhesion at the site of injury

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24
Q

What exactly is meant by platelet activation?

A

Platelets change shape, secrete their granules and activate GPIIb/IIIa

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25
Q

What does platelet activation bring about?

A

Release of serotonin

Thromboxane A2, ADP

Platelet Phospholipid

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26
Q

What does serotonin do?

A

brings about vasoconstriction

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27
Q

What does thromboxane A2, ADP do?

A

Brings about vasoconstriction

Brings about platelet aggregation

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28
Q

What does platelet phospholipid do?

A

Part of the blood coagulation cascade

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29
Q

What activates the blood coagulation cascade?

A

Tissue factor

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30
Q

What does platelet aggregation do?

A

Forms the primary haemostatic plug

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31
Q

What is needed to form a stable haemostatic plug
(2)

A

Primary haemostatic plug of aggregated platelets

With the addition of fibrin from the coagulation cascade

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32
Q

List the four components of haemostasis

A

Vascular endothelium
Platelets
Coagulation pathways (pro-coagulants and anti-coagulants)
Fibrinolysis

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33
Q

How many stages are there to the haemostatic response?

A

Three stages

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34
Q

What is the primary haemostatic response?
(2)

A

Rapid response to seal the injured vessel

Components include the endothelium, sub-endothelium, VWF and platelets

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35
Q

What is the secondary haemostatic response?

A

Formation and stabilisation of the platelet plug

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36
Q

What is the tertiary haemostatic response?

A

Fibrinolysis, degradation of fibrin clot

37
Q

What is primary haemostasis

A

The initial response after vessel injury is mediated by interactions between the vessel wall and circulating platelets to begin the formation of the clot

Main players: blood vessels, VWF, platelets

38
Q

How does the blood vessel wall respond to trauma?
(4)

A

Platelets adhere to subendothelium and form platelet plug

Vasoconstriction occurs in response to localised release of vasoactive amines from activated platelets

Tissue factor is released from the endothelium which activates coagulation

vWF is also released which acts as a glue to stick platelets to the wall

39
Q

What brings about vasoconstriction and what produces them?

A

Vasoactive amines released from activated platelets

40
Q

What activates coagulation and where is it released?

A

Tissue factor, released from the endothelium

41
Q

What acts as the glue to hold the platelets together

A

Von Willebrand Factor

42
Q

Describe the role of blood vessels in haemostasis
(6)

A

Higher blood flow rate is seen in the centre of the lumen, lower flow near endothelium surface

As a result, larger RBCs are more concentrated in the centre of the blood vessel and smaller platelets are found nearer the vessel wall

Under normal conditions the endothelial layer of intima is antithrombotic (prostaglandin I2)

Upon vessel injury the endothelial cells become prothrombotic

Post injury, endothelin-1 (strong vasoconstrictor) is released to minimise blood lost

The adventitia expresses tissue factor which is crucial for initiation of the secondary response

43
Q

What gives endothelial intima it’s antithrombotic effect

A

Prostaglandin I2

44
Q

What is the strong vasoconstrictor released post injury in endothelial cells

A

Endothelin-1

45
Q

Where is tissue factor expressed from?

A

Adventitia

46
Q

What inhibits fibrin formation?

A

Heparan sulphate

47
Q

What act as vasodilators in blood vessels?

A

Prostacyclin and Nitric oxide

48
Q

List the anti-coagulant properties of endothelium (healthy)
(4)

A

Thrombomodulin/Tissue Factor Pathway Inhibitor: controls coagulation

Heparan Sulphate: inhibits fibrin formation

Prostacyclin and nitric oxide: vasodilators

Enzymes inhibit platelet function

49
Q

How does the subendothelium respond to vascular injury
(5)

A

The basement membrane and extracellular matrix becomes exposed

Collagen, VWF and fibronectin promote platelet adhesion

The endothelium vasoconstricts and becomes pro-thrombotic

Tissue factor is expressed which initiates coagulation cascade

Plasminogen activator inhibitor (PAI-1) inhibits the activation of fibrinolytic system

50
Q

What is PAI-1 and what does it do?

A

Plasminogen activator inhibitor

It prevents fibrinolysis -> breakdown of fibrin i.e. fibrin accumulates

51
Q

What is von Willebrand Factor

A

A large adhesive glycoprotein produced in endothelial cells and in the megakaryocytes

52
Q

What does vWF bind to?
(4)

A

Subendothelium collagen

GPIb on surface of non-activated platelets

GPIIbIIa on surface of activated platelets

FVIII protecting it from proteolytic degradation

53
Q

Describe in your own words how the platelet plug is formed
(5)

A

Collagen is exposed
Platelets express collagen receptors
VWF tethers the platelets to the endothelial cells by binding to GPIba
Platelets roll along endothelium which activates aIIbB3 on platelets
Platelets then bind to collagen using collagen receptors

(Need to research this more)

54
Q

What are the four steps of vasoconstriction

A

Collagen becomes exposed, platelets bind to this collagen

This brings about the release of platelet factors

This attracts more platelets

Platelets aggregate into a platelet plug

55
Q

What are platelets?
(5)

A

Anucleate cells
Discoid shape
Life span of 10 days
Critical role in haemostasis and thrombosis
Rapidly activated when vessel wall is damaged

56
Q

What facilitates platelet activation

A

Signalling proteins and surface receptors

57
Q

What facilitates platelet activation

A

Signalling proteins and surface receptors

58
Q

What does defective platelets lead to?

A

Serious bleeding

59
Q

What does activation of platelets in diseases blood vessels lead to?

A

Arterial thrombosis i.e. stroke or myocardial infarction

60
Q

What is found in the granules (a-granules) of platelets?

A

Adhesive proteins and coagulation factors

61
Q

What is attached to the surface of platelets?
(2)

A

GPIb (+ VWF + Collagen fibres)

GPIIbIIa (+ fibrinogen)

62
Q

What are the seven functions of platelets?

A

Interact with VWF to seal damaged blood vessels

Platelet-platelet interactions (primary response to form primary plug)

Negative charged surface to support coagulation complex formation (secondary response)

Deliver haemostatically active molecules locally

Localise clot fomration

Promote vasoconstriction

Promote vessel repar

63
Q

What are the three main platelet functions in haemostasis?

A

Adhesion (first three seconds)

Aggregation (10 seconds)

Coagulation (5 minutes)

64
Q

What happens in the adhesion step, first 3 seconds of clot formation?
(3)

A

Platelet-endothelial cell interactions

Platelet shape change

Release reactions

65
Q

What happens in the aggregation step of clot formation?
(3)

A

Platelet-platelet interactions

Formation of primary platelet plug

Secretion of alpha granules and dense bodies from platelets

66
Q

What happens in the coagulation step of clot formation

A

Fibrin formation

67
Q

How do platelets tether to collagen?
(3)

A

VWF anchors exposed to collagen

Blood flow facilitates the unravelling of VWF to exposue the GPib-binding site

Platelets circulating at the edge of the vessel are then captured and tethered by VWF via binding to the constitutively expressed GPIb

68
Q

Explain what is meant by platelet rolling
(2)

A

Once platelets are tethered to endothelium via VWF-GPIb interactions, the blood flow forces the platelet to roll over from the tethering point

This promotes further VWF-GPIb interactions i.e. more tethering can take place

69
Q

How does the stable adhesion of platelets take place
(3)

A

Binding to glycoproteins additional to GPIb occurs

GPIa and GPVI binds directly to collagen and GPIIbIIa binds to VWF

This brings about the stabilisation of platelet adhesion

70
Q

Define secondary haemostasis

A

Reinforcement of the platelet plug through the generation of a meshwork of insoluble fibrin

Tightly regulated pathways of caogulation factors, cofactors and inhibitos (pro-coagulation proteins and anti-coagulant proteins)

71
Q

What is the coagulation cascade?

A

A series of reactions, in which an inactive enzyme precursor is activated to cleave the next component in the cascade, ultimately resulting in the formation of cross-linked fibrin

71
Q

What are the components of the coagulation cascade?

A

Enzymes
Specifically proteases

71
Q

What is required for the coagulation cascade?

A

Calcium ions and phospholipid

71
Q

What are the two pathways of the coagulation cascde

A

Intrinsic system
Extrinsic system

72
Q

What indicates an activated coagulation factor

A

Lowercase a

e.g. Factor Xa

73
Q

What are the vitamin K dependent factors?
(6)

A

II
VII
IX
X
Protein C
Protein S

74
Q

What are the non vitamin K dependent factors

A

XII and XI

75
Q

What factors make up the intrinsic pathway?
(4)

A

XII -> XIIa

XIIa converts XI to XIa

XIa converts IX to IXa (needs Ca2+)

IXa + VIIIa converts X to Xa (needs Ca2+)

76
Q

What factors are involved in the extrinsic pathway?

A

Tissue factor converts VII to VIIa

VIIa converts X to Xa (needs Ca2+)

77
Q

What is the common pathway?
(3)

A

Xa with V converts prothrombin to thrombin (needs Ca2+)

Thrombin converts fibrinogen to fibrin and XIII to XIIIa

XIIa converts fibrin to a stable fibrin clot

78
Q

What is TFPRI

A

Tissue factor pathway inhibitor

79
Q

What does TFPI do?

A

It limits the action of tissue factor

80
Q

What is protein C

A

A major physiological anticoagulant

81
Q

What does thrombomodulin do?

A

Activates protein C

82
Q

What does activated protein C do?

A

Activated protein C along with protein S and phospholipid cofactors, degrades FVa and FVIIIa

83
Q

What does anti-thrombin II do?

A

Its a plasma protease inhibitor

It inhibits other proteases such as thrombin, IXa, Xa, XIa and XIIa

84
Q

Deficiencies of what factors cause thrombosis
(5)

A

Antithrombin
Protein C
Protein S
TFPI
Fibrinolysis

85
Q

What are the functions of fibrinolysis/tertiary haemostasis?
(4)

A

Defends against vascular occlusion preventing excess fibrin formation

Removes fibrin clot as part of vascular remodelling

Active enzyme is plasmin produced from plasminogen

Occurs once coagulation is initiated

2.2 Haematology (38 decks)

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