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X Pharmacological Treatment Of Disease > Haemostasis/Anti-platelets > Flashcards

Haemostasis/Anti-platelets Flashcards

1
Q

what is haemostasis?

A

the arrest of bleeding from damaged blood vessels

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2
Q

how many stages of haemostasis are there?

A

3

unofficially 4

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3
Q

what are the stages of haemostasis?

A
  1. Blood vessel constriction
  2. Formation of a platelet plug
  3. Formation of a clot
    (4) . Remodelling clot
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4
Q

how do the main stages of haemostasis work?

A

endothelial damage causes vascular spasm
platelet aggregation causes platelet plug formation
coagulation cascade causes clot formation

vascular spasm also leads platelet aggregation which leads to clot formation

endothelial damage can lead to platelet aggregation which leads to coagulation cascade, or to coagulation cascade directly.

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5
Q

what is the anatomy of a blood clot?

A

thrombus: platelets in fibrin thread, erythrocytes in mesh

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6
Q

what is the aim of the coagulation phase?

A

make fibrin

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7
Q

a severed blood vessel- what is the first response? why?

A

contraction of smooth muscle - vasoconstrict

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8
Q

how does a severed blood vessel constrict?

A

release of Thromboxane A2 from platelets

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9
Q

what does TXA2 stand for?

A

Thromboxane A2

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10
Q

what is Thromboxane A2?

A

potent vasoconstrictor

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11
Q

what 3 things does Thromboxane A2 do?

A
  1. slows blood flow
  2. reduces pressure
  3. brings cut surfaces together (only permanent closure in small blood vessels)
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12
Q

in the platelet plug formation, what do platelets adhere to?

A

collagen

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13
Q

how do platelets adhere to collagen?

A

by binding to

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14
Q

where is von Willebrand’s factor secreted?

A

platelets and endothelium

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15
Q

what 3 granules do activated platelets release?

A

ADP
5-HT
TXA2

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16
Q

what does ADP stand for?

A

adenosine diphosphate

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17
Q

what does 5-HT stand for?

A

serotonin

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18
Q

what do the granules secreted by activated platelets do?

A

cause more platelets to come to increase aggregation

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19
Q

what is the change in platelets in platelet aggregation?

A

discoid platelets -> activated platelets

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20
Q

how is the loose platelet plug reinforced?

A

by fibrin meshwork which traps the blood cells

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21
Q

how is the fibrin formed?

A

fibrinogen →→(thombin)→→ fibrin

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22
Q

what are coagulation factors?

A

INACTIVE proenzymes which are synthesised from the liver

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23
Q

what are the 2 pathways that coagulation factors are activated?

A
  1. intrinsic pathway

2. extrinsic pathway

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24
Q

what is the intrinsic pathway?

A

Components are contained within the blood

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25
Q

what is the extrinsic pathway?

A

Component needed for initiation (tissue

factor) comes from outside the blood.

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26
Q

how is the intrinsic pathway initiated?

A

blood trauma

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27
Q

how is the extrinsic pathway initiated?

A

tissue trauma

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28
Q

how long does the intrinsic pathway take?

A

minutes

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29
Q

how long does the extrinsic pathway take?

A

seconds

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30
Q

what kind of ‘blood trauma’ initiates the intrinsic pathway?

A

Blood exposure to glass
Blood exposure to collagen
Platelet exposure to damaged cells

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31
Q

what is released when the extrinsic pathway is initiated?

A

tissue factor

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32
Q

what happens when the clotting factors from the intrinsic and extrinsic pathways are activated?

A

they activate the production of thrombin from prothrombin

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33
Q

what happens when thrombin is activated from the coagulation cascade?

A

fibrinogen is converted to fibrin which forms the clot

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34
Q

which factor is missing from the coagulation cascade?

A

factor VI

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35
Q

what is fibrinolysis?

A

dissolving of a clot once repair begins

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36
Q

what system(s) cause fibrinolysis?

A

fibrinolytic or thrombolytic

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37
Q

what breaks down fibrin?

38
Q

how is plasmin formed?

A

plasminogen →→→ plasmin

via plasminogen activators

39
Q

give an example of a plasminogen activator

A

tissue plasminogen activator (tPA)

40
Q

what does plasmin do?

A

Plasmin remodels the thrombus and limits the extent of thrombosis by breaking down the fibrin

41
Q

what is thrombosis?

A

the normal haemostatic processes are activated inappropriately which results in the formation of a clot (thrombus) which may cause block the blood vessels or the heart

42
Q

what predisposes thrombus formation?

A

Virchow’s triad

43
Q

what is Virchow’s triad?

A
  1. endothelial injury
  2. abnormal blood flow
  3. hypercoagulability
44
Q

what are the consequences of arterial occlusion?

A

myocardial infarction
stroke
peripheral ischaemia

45
Q

what are the causes of arterial occlusion?

A

endothelial injury due to underlying

arterial wall pathology, e.g. atherosclerosis

46
Q

what does arterial thrombi mainly consist of?

47
Q

what are the consequences of venous occlusion?

A

deep venous thrombosis and pulmonary embolism

48
Q

what are the causes of venous occlusion?

A

blood stasis, allowing build-up of platelets and

fibrin.

49
Q

what does venous thrombi mainly consist of?

50
Q

what is the primary trigger of arterial thrombosis?

A

atherosclerotic plaque ruptire

51
Q

how does an atherosclerotic plaque rupture?

A

disruption of the endothelium and release of constituents

of the plaque

52
Q

how does a venous thrombi form?

A

Endothelium remains intact but converted from a

surface with anticoagulant properties to one with procoagulant properties

53
Q

what do antiplatelet drugs do?

A

inhibit platelet aggregation

54
Q

5 examples of antiplatelet drugs

A 
Aspirin
Clopidogrel
Abciximab
Eptifibatide
Tirofiban
55
Q

what do anticoagulant drugs do?

A

inhibit coagulation cascade

56
Q

give 2 examples of anticoagulant drugs

A

heparin, warfarin

57
Q

what do fibrinolytic drugs do?

A

dissolve the clot once formed

58
Q

at the receptor level, how does platelet aggregation actually occur?

A
  1. fibrinogen crosslinks platelets to one another by binding to GPIIb-IIIa receptors on their membranes
  2. ADP and TXA2 are released from platelets that are attached to the collagen
  3. further platelets are recruited to the platelet plug and cause them to aggregate by activating their GPIIb-IIIa receptors
59
Q

how does aspirin prevent platelet aggregation?

A

blocks platelet TXA2 synthesis

60
Q

how does clopidogrel prevent platelet aggregation?

A

blocks platelet ADP receptors

61
Q

how do Abciximab, Eptifibatide and Tirofiban prevent platelet aggregation?

A

block platelet GPIIb/IIIa receptors

62
Q

how does heparin inhibit clotting factors?

A

inhibits clotting factors directly

63
Q

how was warfarin inhibit clotting factors?

A

inhibit synthesis of clotting factors in the liver

64
Q
  • Effective immediately
  • Effective in external circuits, cannulae and blood specimen containers

Heparin or Warfarin?

65
Q

what does heparin inactivate?

A

thrombin and factors XIIa, XIa, Xa, IXa

66
Q

what is Antithrombin III?

A

is part of the coagulation cascade system that regulates clotting

67
Q

how does heparin inhibit the coagulation cascade?

A

accelerates the actions of antithrombin

III - inhibiting coagulation

68
Q

how does heparin accelerate antithrombin III?

A

Antithrombin III forms a 1:1 complex with

thrombin - Heparin increases the rate at which the complex forms 100-fold

69
Q

what is a low molecular weight heparin?

A

mixture of large mucopolysaccharide molecules - fragments of heparin

70
Q

give an example of a low molecular weight heparin

A

Enoxaparin (Clexane)

71
Q

how are the effects of LMW heparin different to heparin?

A

A more predictable doseeffect
relationship
Longer duration of action

72
Q

how does warfarin act indirectly on the coagulation cascade?

A

Inhibits synthesis of vitamin K-dependent

clotting factors in the liver

73
Q

• in vivo
• when circulating clotting
factors have been
sufficiently depleted

Heparin or Warfarin?

74
Q

what is vitamin K?

A

co-factor for the production of four clotting factors in the liver

75
Q

how does warfarin inhibit the synthesis of vitamin K-dependent clotting factors in the liver?

A

warfarin is similar to part of vitamin K molecule

warfarin inhibits vitamin K epoxide reductas

76
Q

what does vitamin K epoxide reductase do?

A

normally reduces inactive vitamin K to its active form

77
Q

does warfarin have a small therapeutic window or a large therapeutic window?

78
Q

what is the biggest predictor of warfarin dose?

A

VKORC1* polymorphisms

79
Q

what drug interactions does warfarin have?

80
Q

heparin and warfarin time of onset?

A

heparin - immediately (i.v.)

warfarin - 1-3 days

81
Q

what is the clinical use of heparin?

A

Treatment of deep vein thrombosis and pulmonary
embolism

Prevention of postoperative thromboses and MI

Rapid anti-coagulation until warfarin becomes effective

82
Q

what is the clinical use of warfarin?

A

Prevention and treatment of thromboembolytic disease

Prevention of systematic embolism

83
Q

– Lepirudin
– Desirudin
– Argatroban (USA)

what are these drugs?

A

Direct Thrombin Inhibitors

84
Q

– Fondaparinux
– Idraparinux

what are these drugs?

A

Selective Factor Xa Inhibitors

85
Q

– Ximelagatran (withdrawn – toxicity)
– Dabigatran – (BNF)

what are these drugs?

A

Direct Thrombin Inhibitors

86
Q

– Rivaroxaban – (BNF)

what is this drug?

A

Selective Factor Xa Inhibitors

87
Q

what is streptokinase?

A

Bacterial protein from beta-haemolytic streptococci

88
Q

what does streptokinase do?

A

increases production of plasmin from circulating plasminogen

89
Q

what are the adverse effects of streptokinase?

A

A full allergic response

90
Q

why do you often need to give a high dose of streptokinase?

A

Antibodies against it are often present in the patient’s blood

91
Q

give and example of a Tissue Plasminogen Activators (t-PA)

92
Q

what is Alteplase used for?

A

non-antigenic substitution for streptokinase with less side effects

X Pharmacological Treatment Of Disease (9 decks)

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