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BMS10 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

Arrest of blood loss from damaged vessels

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2
Q

Describe platelets during haemostasis

A

Non-adhesive

Circulate singly

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3
Q

What happens to platelets during vessel injury?

A

Aggregate, become stabilised by fibrin and arrest bleeding

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4
Q

What may abnormal haemostasis lead to?

A

Thrombosis

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5
Q

What can thrombosis lead to?

A

Myocardial infarction

Ischaemic stroke

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6
Q

What ensures that platelets do not activate during haemostasis?

A

Suppressive mediators and proteins produced by platelets and endothelial cells

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7
Q

Give examples of suppressive mediators

A

Nitric oxide - stops platelet activation

Prostacyclin (prostanoids) - stops platelet activation

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8
Q

What do suppressive mediators produced by endothelial cells do?

A

Prevent inappropriate smooth muscle contraction and hyperplasia

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9
Q

Describe the process of primary haemostasis

A
  1. Damage to blood vessel
  2. Exposure of platelets to collagen and vWF in extracellular/subendothelial matrix and later exposure to thrombin
  3. Platelets adhere and activate
  4. Release of mediators = positive feedback on step 3
  5. Vasoconstriction and aggregation of platelets
  6. Formation of soft platelet plug
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10
Q

What is PGI2?

A

Prostacyclin

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11
Q

How else can you write prostacyclin? (2)

A

PGI2

I2

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12
Q

What is vWF?

A

von Willebrand factor

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13
Q

Where is the extracellular/subendothelial matrix?

A

Beneath endothelial lining of vessel

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14
Q

Why does vasoconstriction occur when a vessel is damaged?

A

Decrease blood flow through this area to reduce blood loss

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15
Q

What does the extracellular/subendothelial matrix contain which is important in haemostasis?

A

vWF

Collagen

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16
Q

What allows platelets to adhere to substances in the extracellular/subendothelial matrix?

A

Adhesion molecules

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17
Q

What adhesion molecules adhere to vWF and collagen?

A

GP1b/G-protein 1b = vWF

GPVI and integrin α2β1 = collagen

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18
Q

What happens to platelets on adhesion?

A

Activation

Some adhesion causes thrombin production by platelets

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19
Q

What is COX?

A

Cyclooxygenase

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20
Q

What does COX do?

A

Produces various prostanoids

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21
Q

What does thromboxane do?

A

Further activation of platelets and vasoconstriction

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22
Q

How else can you write thromboxane?

A

TXA2

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23
Q

What is TXA2?

A

Thromboxane

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24
Q

What is 5-HT?

A

5-hydroxytryptamine

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25
Q

What does 5-hydroxytryptamine do?

A

Vasoconstriction

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26
Q

How else can you write 5-hydroxytryptamine?

A

5-HT

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27
Q

What is ADP?

A

Adenosine diphosphate

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28
Q

What does ADP do?

A

Further activation of adjacent platelets accumulating at site of injury via P2Y12 receptors

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29
Q

What receptors does ADP use?

A

P2Y12

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30
Q

What is GPIIb/IIIa?

A

Fibrinogen receptor

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31
Q

How else can the fibrinogen receptor be represented?

A

GPIIb/IIIa

αIIbβ3

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32
Q

What do fibrinogen receptors do?

A

Cross-link adjacent platelets together by fibrinogen bridges to form a soft platelet plug

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33
Q

What are the two steps of the clotting pathway?

A

Initiation/extrinsic pathway

Amplification and propagation/intrinsic pathway

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34
Q

Why is it called the extrinsic pathway?

A

Activated by factors which are usually extrinsic to blood

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35
Q

Is tissue factor intrinsic or extrinsic to blood?

A

Extrinsic

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36
Q

Where does the initiation/extrinsic pathway take place?

A

On tissue factor-expressing cells in tissue after blood leaks out of blood vessel

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37
Q

What happens in the initiation/extrinsic pathway? (reactions)

A

TF + FVII –> FVIIa

FVIIa:TF used in activation of FX (–> FXa)

FXa cleaves FII (–> FIIa)

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38
Q

What is FVII called?

A

Serine protease clotting factor (proteins with enzymatic activity)

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39
Q

What is FII?

A

Prothrombin

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40
Q

What is FIIa?

A

Thrombin

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41
Q

How else can you write prothrombin?

A

FII

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42
Q

How else can you write thrombin?

A

FIIa

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43
Q

Where is prothrombin found?

A

Surface of platelets

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44
Q

Describe the intrinsic pathway (4)

A

Initiated by thrombin

Involves activation of many factors including FV, FVIII, FIX, FX

Takes place on activated platelets

FVa complexes with FXa to accelerate thrombin production

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45
Q

What does thrombin do?

A

Cleaves fibrinogen on platelet surface to form fibrin

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46
Q

What does fibrin do?

A

Meshes together to form a stable platelet clot

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47
Q

What does FIXa do?

A

Also involved in activation of FX

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48
Q

Why are arterial clots called ‘white clots’?

A

Large platelet component appears white under microscope

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49
Q

Why are venous clots called ‘red clots’?

A

Red blood cell component appears red under microscope

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50
Q

What are arterial clots usually associated with?

A

Atherosclerosis

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51
Q

Where do white clots form?

A

Site of vascular injury/disturbed blood flow

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52
Q

What do you use to treat arterial clots?

A

Anti-platelet drugs

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53
Q

What are arterial clots a major cause of?

A

Myocardial infarction

(80% of) strokes

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54
Q

What are venous clots usually associated with? (3)

A

Stasis or turbulent flow of blood (activates components in clotting cascade)

Vascular injury following surgery or trauma

Hypercoagulability disorders

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55
Q

What makes up red clots?

A

Platelets

Fibrin

Red blood cells

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56
Q

How do you treat venous clots?

A

Anti-coagulants

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57
Q

What can venous clots cause?

A

Cardiovascular-associated death

Pulmonary emboli

58
Q

What is thrombosis?

A

Inappropriate formation of clots

59
Q

What conditions are forms of thrombosis? (4)

A

DVT

Acute coronary syndrome

Stroke

Disseminated intravascular coagulation (DIC)

60
Q

What is Virchow’s triad?

A

3 factors that contribute to thrombosis

  1. Endothelial/vascular damage
  2. Low blood flow –> stasis
  3. Hypercoagulability
61
Q

Why must we be careful when treating inappropriate clot formation?

A

Treatment increases risk of haemorrhage

62
Q

What types of drugs can be used to treat thrombosis?

A

Anti-platelet

Anti-coagulant

Fibrinolytic

63
Q

What anti-platelet drugs do generally?

A

Inhibit platelet aggregation

Limit growth/decrease risk of arterial thrombi

64
Q

What are the three types of anti-platelet drugs?

A

Aspirin

P2Y12 antagonists

GPIIb/IIIa antagonists

65
Q

What does aspirin do?

A

Inhibits COX therefore inhibiting TXA2 production (arachidonic acid –> prostaglandin H2 –> TXA2)

66
Q

What does NSAID stand for?

A

Non-steroidal anti-inflammatory drug

67
Q

What is the only irreversible NSAID?

A

Aspirin

68
Q

Why does aspirin not affect the production of PGI2?

A

PGI2 synthesised in endothelial cells

Nucleus allows more COX 2 synthesis to produce more PGI2

69
Q

Why does aspirin stop TXA2 production?

A

No nucleus in platelets

No compensation of inhibited COX 1

70
Q

Where are TXA2 and PGI2 produced?

A

TXA2 = platelets

PGI2 = endothelial cells

71
Q

Why does aspirin have an anti-platelet effect?

A

Stops TXA2 production but does not inhibit PGI2

PGI2 action predominates

No further activation of platelets by TXA2 and PGI2 stops activation

72
Q

What type of receptor is P2Y12?

A

GPCR

73
Q

What happens when P2Y12 is activated?

A

Full platelet aggregation and irreversible clot formation (amplifies)

74
Q

What are the irreversible P2Y12 antagonists? (2)

A

Clopidogrel

Prasugrel

75
Q

What are the reversible P2Y12 antagonists? (2)

A

Ticagrelor

Cangrelor

76
Q

Which irreversible P2Y12 antagonist usually has higher efficacy and why?

A

Prasugrel

Not affected by CYP450 mutations

77
Q

Which irreversible P2Y12 antagonist has a faster onset and why?

A

Prasugrel

Increased rate of conversion to active metabolite (1 step whereas clopidogrel has 2 steps)

78
Q

Why might clopidogrel vary in effect?

A

Genetic polymorphisms in CYP450 and CYP2C19

Important liver enzymes involved in conversion to active metabolite are not active

79
Q

How is ticagrelor administered?

A

Orally

80
Q

How is cangrelor administered?

A

Intravenously

81
Q

How long does the effect of cangrelor last?

A

20 mins

82
Q

What do GPIIb/IIIa antagonists do?

A

Inhibit fibrinogen bridges so no soft platelet plug formed

83
Q

What are the two classes of GPIIb/IIIa inhibitors?

A

Fab fragments (part of antibodies)

Small molecule inhibitors

84
Q

What procedure are GPIIb/IIIa inhibitors used after and why?

A

Block immediate restenosis after coronary angioplasty

85
Q

What are examples of fab fragments?

A

Abciximab/abcixifiban

Tirofiban

86
Q

What is an example of a small molecule inhibitor?

A

Eptifibatide

87
Q

What is the major side effect of GPIIb/IIIa inhibitors?

A

Major thrombocytopaenia (not for long-term use) - decreased number of platelets

88
Q

What are anti-platelet drugs used for? (3)

A

Secondary prevention (after past episodes)

Block restenosis following angioplasty = GPIIb/IIIa and P2Y12 antagonists

Dual anti-platelet therapy = more efficacy

89
Q

Give an example of dual anti-platelet therapy

A

Aspirin and clopidogrel

90
Q

Why does dual anti-platelet therapy result in higher efficacy?

A

Multiple pathways able to activate platelets

Incomplete efficacy of just one drug on entire process

91
Q

What do anti-coagulant drugs do generally?

A

Inhibit coagulation cascade (prevent propagation but do not dissolve thrombus)

92
Q

What type of drugs are used to remove thrombi?

A

Thrombolytics

93
Q

What prevents inappropriate clot formation (anti-coagulant substances)? (3)

A

Tissue factor pathway inhibitor (TFPI)

Active protein C (APC) with cofactor protein S

Antithrombin III

94
Q

What does TFPI do?

A

Complexes with FXa to inactivate

Inactivates membrane-bound TF-VIIa complex

95
Q

What produces TFPI?

A

Endothelial and other cells

96
Q

Describe the action of APC

A

Activated by thrombin-thrombomodulin

Works with protein S to inactivate FVa and FVIIIa

97
Q

*Describe the action of antithrombin III (2)

A

Activated by heparans (on endothelial cells) and heparin

Inactivates thrombin and factors IXa, Xa, XIa, XIIa when not in clot/combined with prothrombinase

98
Q

What does heparin do?

A

Activates antithrombin III

99
Q

*What is LMWH? (3)

A

Low molecular weight heparin

More predictable in effects that unfractionated heparin

*More effective on FXa than thrombin

100
Q

What is fondaparinux?

A

Synthetic polysaccharide that acts like LMWH to activate antithrombin III

101
Q

What type of molecule is warfarin?

A

Vitamin K antagonist

102
Q

What does warfarin do?

A

Inhibits vitamin K reductase in liver

So no γ-carboxylation of FII/prothrombin, FVII, FIX or FX

103
Q

What is an example of a FX inhibitor? (3)

A

Rivaroxaban

Apixaban

Edoxaban

104
Q

Why are FX inhibitors easier to use? (2)

A

Favourable safety

Do not require frequent blood monitoring

105
Q

What does DTI stand for?

A

Direct thrombin inhibitor

106
Q

Which site do DTIs inhibit?

A

Coagulation factor binding site on clot-bound and free thrombin

107
Q

Which DTIs are administered intravenously?

A

Hirudin

Lepirudin

Desirudin

108
Q

What DTI is given orally?

A

Dabigatran

109
Q

What do traditional anti-coagulants require?

A

Monthly blood tests

Dietary considerations

110
Q

What are the two types of DOAC drugs?

A

FXa and FIIa inhibitors

111
Q

Why are DOACs better than traditional anti-coagulants? (3)

A

Highly effective and faster onset

Require less monitoring of INR ratio

May reduce risk of brain bleeding when taken for stroke prevention

112
Q

Which DOAC has an antidote?

A

Dabigatran

113
Q

How are fibrinolytics administered?

A

Intravenously

114
Q

What do fibrinolytics do?

A

Activate plasminogen –> plasmin

Remove/lyse arterial thrombi

115
Q

Give two examples of fibrinolytic drugs

A

Streptokinase

Alteplase

116
Q

What does streptokinase do?

A

Binds and activates plasminogen –> plasmin

117
Q

What is streptokinase?

A

Non-enzyme protein from Streptococci

118
Q

What is a side effect of streptokinase?

A

Allergenic if used more than once

119
Q

What is r-tPA?

A

Alteplase

120
Q

Why is alteplase a good fibrinolytic drug?

A

Non-allergenic

Clot-selective = binds to plasminogen bound to fibrin in thrombi => decreased risk of haemorrhage

121
Q

What is used to treat severe haemorrhage?

A

Transexamic acid (inhibits activation of plasminogen)

122
Q

What are some conditions associated with defects in haemostasis? (5)

A

Haemophilia

Vitamin K deficiency

Antiphospholipid syndrome

von Willebrand disease

FV Leiden

123
Q

What is haemophilia? (4)

A

Recessive, X-linked

Prolonged clotting time

A = lacks FVIII

B = lacks FIX

124
Q

Which type of haemophilia is more common?

A

Haemophilia A

125
Q

What is X-mas disease?

A

Haemophilia B

126
Q

How does vitamin K deficiency affect haemostasis?

A

Vitamin K required for γ-carboxylation of FII, FVII, FIX, FX during synthesis in liver

127
Q

What can cause vitamin K deficiency? (3)

A

Poor vitamin K absorption in gut (or lack in diet)

Bile duct obstruction

Coeliac or Crohn’s disease

128
Q

What is antiphospholipid syndrome?

A

Autoimmune disease

Causes recurrent thrombosis

Antibodies for lipid-binding proteins (eg cardiolipin, Lupus anticoagulant) may inhibit Protein C or S or facilitate cleavage of prothrombin

129
Q

What is von Willebrand disease?

A

Deficient vWF (type 1/3) or defective vWF (type 2)

Leads to defective platelet binding and FVIII deficiency if severe

130
Q

What is FV Leiden?

A

Mutant FV cannot be inactivated by APC

131
Q

What are the two blood group classifications?

A

ABO

Rhesus

132
Q

Describe the ABO blood groups

A

A and B = codominant

O = recessive

A = A antigens on cells; B antibodies in blood

B = B antigens; A antibodies

AB = A and B antigens; no antibodies

O = no antigens; A and B antibodies

133
Q

What blood group is the universal donor?

A

O

134
Q

What blood group is the universal recipient?

A

AB

135
Q

Describe the Rhesus blood groups

A

Rh+ = D antigen (dominant D gene)

Rh- = no antigens

136
Q

Why may exposure to the D antigen in Rh- people be dangerous?

A

Transfusion or when an Rh- mother has an Rh+ child

Haemolytic disease in next child

137
Q

What are the possible complications of blood transfusions? (5)

A

Blood type incompatibility

Infection transmission (hepatitis, HIV, prions, malaria)

Iron overload (multiple transfusions)

Fever (transferred white blood cells)

Impaired clotting (massive transfusions with stored blood)

138
Q

Why is blood type compatibility important in transfusions?

A

Significant A/B/anti-D antibodies will cause donor cells expressing the respective antigens to agglutinate and haemolyse

139
Q

Why are donor antibodies not normally a problem in transfusions?

A

Diluted/removed

140
Q

What may large accumulations of bilirubin cause? (2)

A

Haemolytic jaundice

Renal failure

141
Q

What is bilirubin?

A

Orange-yellow substance produced during breakdown of red blood cells

BMS10 (13 decks)

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