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2.2 Haematology > Haemostasis 1 > Flashcards

Haemostasis 1 Flashcards

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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
What does platelet activation bring about?
Release of serotonin Thromboxane A2, ADP Platelet Phospholipid
26
What does serotonin do?
brings about vasoconstriction
27
What does thromboxane A2, ADP do?
Brings about vasoconstriction Brings about platelet aggregation
28
What does platelet phospholipid do?
Part of the blood coagulation cascade
29
What activates the blood coagulation cascade?
Tissue factor
30
What does platelet aggregation do?
Forms the primary haemostatic plug
31
What is needed to form a stable haemostatic plug (2)
Primary haemostatic plug of aggregated platelets With the addition of fibrin from the coagulation cascade
32
List the four components of haemostasis
Vascular endothelium Platelets Coagulation pathways (pro-coagulants and anti-coagulants) Fibrinolysis
33
How many stages are there to the haemostatic response?
Three stages
34
What is the primary haemostatic response? (2)
Rapid response to seal the injured vessel Components include the endothelium, sub-endothelium, VWF and platelets
35
What is the secondary haemostatic response?
Formation and stabilisation of the platelet plug
36
What is the tertiary haemostatic response?
Fibrinolysis, degradation of fibrin clot
37
What is primary haemostasis
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
How does the blood vessel wall respond to trauma? (4)
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
What brings about vasoconstriction and what produces them?
Vasoactive amines released from activated platelets
40
What activates coagulation and where is it released?
Tissue factor, released from the endothelium
41
What acts as the glue to hold the platelets together
Von Willebrand Factor
42
Describe the role of blood vessels in haemostasis (6)
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
What gives endothelial intima it's antithrombotic effect
Prostaglandin I2
44
What is the strong vasoconstrictor released post injury in endothelial cells
Endothelin-1
45
Where is tissue factor expressed from?
Adventitia
46
What inhibits fibrin formation?
Heparan sulphate
47
What act as vasodilators in blood vessels?
Prostacyclin and Nitric oxide
48
List the anti-coagulant properties of endothelium (healthy) (4)
Thrombomodulin/Tissue Factor Pathway Inhibitor: controls coagulation Heparan Sulphate: inhibits fibrin formation Prostacyclin and nitric oxide: vasodilators Enzymes inhibit platelet function
49
How does the subendothelium respond to vascular injury (5)
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
What is PAI-1 and what does it do?
Plasminogen activator inhibitor It prevents fibrinolysis -> breakdown of fibrin i.e. fibrin accumulates
51
What is von Willebrand Factor
A large adhesive glycoprotein produced in endothelial cells and in the megakaryocytes
52
What does vWF bind to? (4)
Subendothelium collagen GPIb on surface of non-activated platelets GPIIbIIa on surface of activated platelets FVIII protecting it from proteolytic degradation
53
Describe in your own words how the platelet plug is formed (5)
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
What are the four steps of vasoconstriction
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
What are platelets? (5)
Anucleate cells Discoid shape Life span of 10 days Critical role in haemostasis and thrombosis Rapidly activated when vessel wall is damaged
56
What facilitates platelet activation
Signalling proteins and surface receptors
57
What facilitates platelet activation
Signalling proteins and surface receptors
58
What does defective platelets lead to?
Serious bleeding
59
What does activation of platelets in diseases blood vessels lead to?
Arterial thrombosis i.e. stroke or myocardial infarction
60
What is found in the granules (a-granules) of platelets?
Adhesive proteins and coagulation factors
61
What is attached to the surface of platelets? (2)
GPIb (+ VWF + Collagen fibres) GPIIbIIa (+ fibrinogen)
62
What are the seven functions of platelets?
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
What are the three main platelet functions in haemostasis?
Adhesion (first three seconds) Aggregation (10 seconds) Coagulation (5 minutes)
64
What happens in the adhesion step, first 3 seconds of clot formation? (3)
Platelet-endothelial cell interactions Platelet shape change Release reactions
65
What happens in the aggregation step of clot formation? (3)
Platelet-platelet interactions Formation of primary platelet plug Secretion of alpha granules and dense bodies from platelets
66
What happens in the coagulation step of clot formation
Fibrin formation
67
How do platelets tether to collagen? (3)
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
Explain what is meant by platelet rolling (2)
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
How does the stable adhesion of platelets take place (3)
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
Define secondary haemostasis
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
What is the coagulation cascade?
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
What are the components of the coagulation cascade?
Enzymes Specifically proteases
71
What is required for the coagulation cascade?
Calcium ions and phospholipid
71
What are the two pathways of the coagulation cascde
Intrinsic system Extrinsic system
72
What indicates an activated coagulation factor
Lowercase a e.g. Factor Xa
73
What are the vitamin K dependent factors? (6)
II VII IX X Protein C Protein S
74
What are the non vitamin K dependent factors
XII and XI
75
What factors make up the intrinsic pathway? (4)
XII -> XIIa XIIa converts XI to XIa XIa converts IX to IXa (needs Ca2+) IXa + VIIIa converts X to Xa (needs Ca2+)
76
What factors are involved in the extrinsic pathway?
Tissue factor converts VII to VIIa VIIa converts X to Xa (needs Ca2+)
77
What is the common pathway? (3)
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
What is TFPRI
Tissue factor pathway inhibitor
79
What does TFPI do?
It limits the action of tissue factor
80
What is protein C
A major physiological anticoagulant
81
What does thrombomodulin do?
Activates protein C
82
What does activated protein C do?
Activated protein C along with protein S and phospholipid cofactors, degrades FVa and FVIIIa
83
What does anti-thrombin II do?
Its a plasma protease inhibitor It inhibits other proteases such as thrombin, IXa, Xa, XIa and XIIa
84
Deficiencies of what factors cause thrombosis (5)
Antithrombin Protein C Protein S TFPI Fibrinolysis
85
What are the functions of fibrinolysis/tertiary haemostasis? (4)
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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