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Haemostasis Flashcards

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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
What does 5-hydroxytryptamine do?
Vasoconstriction
26
How else can you write 5-hydroxytryptamine?
5-HT
27
What is ADP?
Adenosine diphosphate
28
What does ADP do?
Further activation of adjacent platelets accumulating at site of injury via P2Y12 receptors
29
What receptors does ADP use?
P2Y12
30
What is GPIIb/IIIa?
Fibrinogen receptor
31
How else can the fibrinogen receptor be represented?
GPIIb/IIIa αIIbβ3
32
What do fibrinogen receptors do?
Cross-link adjacent platelets together by fibrinogen bridges to form a soft platelet plug
33
What are the two steps of the clotting pathway?
Initiation/extrinsic pathway Amplification and propagation/intrinsic pathway
34
Why is it called the extrinsic pathway?
Activated by factors which are usually extrinsic to blood
35
Is tissue factor intrinsic or extrinsic to blood?
Extrinsic
36
Where does the initiation/extrinsic pathway take place?
On tissue factor-expressing cells in tissue after blood leaks out of blood vessel
37
What happens in the initiation/extrinsic pathway? (reactions)
TF + FVII --> FVIIa FVIIa:TF used in activation of FX (--> FXa) FXa cleaves FII (--> FIIa)
38
What is FVII called?
Serine protease clotting factor (proteins with enzymatic activity)
39
What is FII?
Prothrombin
40
What is FIIa?
Thrombin
41
How else can you write prothrombin?
FII
42
How else can you write thrombin?
FIIa
43
Where is prothrombin found?
Surface of platelets
44
Describe the intrinsic pathway (4)
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
45
What does thrombin do?
Cleaves fibrinogen on platelet surface to form fibrin
46
What does fibrin do?
Meshes together to form a stable platelet clot
47
What does FIXa do?
Also involved in activation of FX
48
Why are arterial clots called 'white clots'?
Large platelet component appears white under microscope
49
Why are venous clots called 'red clots'?
Red blood cell component appears red under microscope
50
What are arterial clots usually associated with?
Atherosclerosis
51
Where do white clots form?
Site of vascular injury/disturbed blood flow
52
What do you use to treat arterial clots?
Anti-platelet drugs
53
What are arterial clots a major cause of?
Myocardial infarction (80% of) strokes
54
What are venous clots usually associated with? (3)
Stasis or turbulent flow of blood (activates components in clotting cascade) Vascular injury following surgery or trauma Hypercoagulability disorders
55
What makes up red clots?
Platelets Fibrin Red blood cells
56
How do you treat venous clots?
Anti-coagulants
57
What can venous clots cause?
Cardiovascular-associated death Pulmonary emboli
58
What is thrombosis?
Inappropriate formation of clots
59
What conditions are forms of thrombosis? (4)
DVT Acute coronary syndrome Stroke Disseminated intravascular coagulation (DIC)
60
What is Virchow's triad?
3 factors that contribute to thrombosis 1. Endothelial/vascular damage 2. Low blood flow --> stasis 3. Hypercoagulability
61
Why must we be careful when treating inappropriate clot formation?
Treatment increases risk of haemorrhage
62
What types of drugs can be used to treat thrombosis?
Anti-platelet Anti-coagulant Fibrinolytic
63
What anti-platelet drugs do generally?
Inhibit platelet aggregation Limit growth/decrease risk of arterial thrombi
64
What are the three types of anti-platelet drugs?
Aspirin P2Y12 antagonists GPIIb/IIIa antagonists
65
What does aspirin do?
Inhibits COX therefore inhibiting TXA2 production (arachidonic acid --> prostaglandin H2 --> TXA2)
66
What does NSAID stand for?
Non-steroidal anti-inflammatory drug
67
What is the only irreversible NSAID?
Aspirin
68
Why does aspirin not affect the production of PGI2?
PGI2 synthesised in endothelial cells Nucleus allows more COX 2 synthesis to produce more PGI2
69
Why does aspirin stop TXA2 production?
No nucleus in platelets No compensation of inhibited COX 1
70
Where are TXA2 and PGI2 produced?
TXA2 = platelets PGI2 = endothelial cells
71
Why does aspirin have an anti-platelet effect?
Stops TXA2 production but does not inhibit PGI2 PGI2 action predominates No further activation of platelets by TXA2 and PGI2 stops activation
72
What type of receptor is P2Y12?
GPCR
73
What happens when P2Y12 is activated?
Full platelet aggregation and irreversible clot formation (amplifies)
74
What are the irreversible P2Y12 antagonists? (2)
Clopidogrel Prasugrel
75
What are the reversible P2Y12 antagonists? (2)
Ticagrelor Cangrelor
76
Which irreversible P2Y12 antagonist usually has higher efficacy and why?
Prasugrel Not affected by CYP450 mutations
77
Which irreversible P2Y12 antagonist has a faster onset and why?
Prasugrel Increased rate of conversion to active metabolite (1 step whereas clopidogrel has 2 steps)
78
Why might clopidogrel vary in effect?
Genetic polymorphisms in CYP450 and CYP2C19 Important liver enzymes involved in conversion to active metabolite are not active
79
How is ticagrelor administered?
Orally
80
How is cangrelor administered?
Intravenously
81
How long does the effect of cangrelor last?
20 mins
82
What do GPIIb/IIIa antagonists do?
Inhibit fibrinogen bridges so no soft platelet plug formed
83
What are the two classes of GPIIb/IIIa inhibitors?
Fab fragments (part of antibodies) Small molecule inhibitors
84
What procedure are GPIIb/IIIa inhibitors used after and why?
Block immediate restenosis after coronary angioplasty
85
What are examples of fab fragments?
Abciximab/abcixifiban Tirofiban
86
What is an example of a small molecule inhibitor?
Eptifibatide
87
What is the major side effect of GPIIb/IIIa inhibitors?
Major thrombocytopaenia (not for long-term use) - decreased number of platelets
88
What are anti-platelet drugs used for? (3)
Secondary prevention (after past episodes) Block restenosis following angioplasty = GPIIb/IIIa and P2Y12 antagonists Dual anti-platelet therapy = more efficacy
89
Give an example of dual anti-platelet therapy
Aspirin and clopidogrel
90
Why does dual anti-platelet therapy result in higher efficacy?
Multiple pathways able to activate platelets Incomplete efficacy of just one drug on entire process
91
What do anti-coagulant drugs do generally?
Inhibit coagulation cascade (prevent propagation but do not dissolve thrombus)
92
What type of drugs are used to remove thrombi?
Thrombolytics
93
What prevents inappropriate clot formation (anti-coagulant substances)? (3)
Tissue factor pathway inhibitor (TFPI) Active protein C (APC) with cofactor protein S Antithrombin III
94
What does TFPI do?
Complexes with FXa to inactivate Inactivates membrane-bound TF-VIIa complex
95
What produces TFPI?
Endothelial and other cells
96
Describe the action of APC
Activated by thrombin-thrombomodulin Works with protein S to inactivate FVa and FVIIIa
97
*Describe the action of antithrombin III (2)
Activated by heparans (on endothelial cells) and heparin Inactivates thrombin and factors IXa, Xa, XIa, XIIa when not in clot/combined with prothrombinase
98
What does heparin do?
Activates antithrombin III
99
*What is LMWH? (3)
Low molecular weight heparin More predictable in effects that unfractionated heparin *More effective on FXa than thrombin
100
What is fondaparinux?
Synthetic polysaccharide that acts like LMWH to activate antithrombin III
101
What type of molecule is warfarin?
Vitamin K antagonist
102
What does warfarin do?
Inhibits vitamin K reductase in liver So no γ-carboxylation of FII/prothrombin, FVII, FIX or FX
103
What is an example of a FX inhibitor? (3)
Rivaroxaban Apixaban Edoxaban
104
Why are FX inhibitors easier to use? (2)
Favourable safety Do not require frequent blood monitoring
105
What does DTI stand for?
Direct thrombin inhibitor
106
Which site do DTIs inhibit?
Coagulation factor binding site on clot-bound and free thrombin
107
Which DTIs are administered intravenously?
Hirudin Lepirudin Desirudin
108
What DTI is given orally?
Dabigatran
109
What do traditional anti-coagulants require?
Monthly blood tests Dietary considerations
110
What are the two types of DOAC drugs?
FXa and FIIa inhibitors
111
Why are DOACs better than traditional anti-coagulants? (3)
Highly effective and faster onset Require less monitoring of INR ratio May reduce risk of brain bleeding when taken for stroke prevention
112
Which DOAC has an antidote?
Dabigatran
113
How are fibrinolytics administered?
Intravenously
114
What do fibrinolytics do?
Activate plasminogen --> plasmin Remove/lyse arterial thrombi
115
Give two examples of fibrinolytic drugs
Streptokinase Alteplase
116
What does streptokinase do?
Binds and activates plasminogen --> plasmin
117
What is streptokinase?
Non-enzyme protein from Streptococci
118
What is a side effect of streptokinase?
Allergenic if used more than once
119
What is r-tPA?
Alteplase
120
Why is alteplase a good fibrinolytic drug?
Non-allergenic Clot-selective = binds to plasminogen bound to fibrin in thrombi => decreased risk of haemorrhage
121
What is used to treat severe haemorrhage?
Transexamic acid (inhibits activation of plasminogen)
122
What are some conditions associated with defects in haemostasis? (5)
Haemophilia Vitamin K deficiency Antiphospholipid syndrome von Willebrand disease FV Leiden
123
What is haemophilia? (4)
Recessive, X-linked Prolonged clotting time A = lacks FVIII B = lacks FIX
124
Which type of haemophilia is more common?
Haemophilia A
125
What is X-mas disease?
Haemophilia B
126
How does vitamin K deficiency affect haemostasis?
Vitamin K required for γ-carboxylation of FII, FVII, FIX, FX during synthesis in liver
127
What can cause vitamin K deficiency? (3)
Poor vitamin K absorption in gut (or lack in diet) Bile duct obstruction Coeliac or Crohn's disease
128
What is antiphospholipid syndrome?
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
What is von Willebrand disease?
Deficient vWF (type 1/3) or defective vWF (type 2) Leads to defective platelet binding and FVIII deficiency if severe
130
What is FV Leiden?
Mutant FV cannot be inactivated by APC
131
What are the two blood group classifications?
ABO Rhesus
132
Describe the ABO blood groups
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
What blood group is the universal donor?
O
134
What blood group is the universal recipient?
AB
135
Describe the Rhesus blood groups
Rh+ = D antigen (dominant D gene) Rh- = no antigens
136
Why may exposure to the D antigen in Rh- people be dangerous?
Transfusion or when an Rh- mother has an Rh+ child Haemolytic disease in next child
137
What are the possible complications of blood transfusions? (5)
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
Why is blood type compatibility important in transfusions?
Significant A/B/anti-D antibodies will cause donor cells expressing the respective antigens to agglutinate and haemolyse
139
Why are donor antibodies not normally a problem in transfusions?
Diluted/removed
140
What may large accumulations of bilirubin cause? (2)
Haemolytic jaundice Renal failure
141
What is bilirubin?
Orange-yellow substance produced during breakdown of red blood cells

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