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The Patient - pharmacology (Y2-1) > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is coagulation?

A

Solidification of blood to form a gel

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2
Q

What is platelet aggregation?

A

Stimulated shape change and activation of fibrinogen; platelets form clumps linked by fibrinogen

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3
Q

Inactive clotting factors need to be carboxylated and for this which vitamin is needed?

A

Vitamin K

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4
Q

Which pathway (intrinsic/extrinsic) initiates coagulation?

A

Extrinsic

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5
Q

Which pathway (intrinsic/extrinsic) sustains coagulation?

A

Intrinsic

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6
Q

Which factors are modified by carboxylation and so require vitamin K?

A

2 (prothrombin), 7, 9, 10

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7
Q

Haemophilia A is due to a loss of which factor?

A

8

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8
Q

Haemophilia B is due to loss of which factor?

A

9

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9
Q

Vitamin K deficiency can lead to coagulation problems. Why?

A

Because vitamin K is needed for carboxylation of factor 7,9, 10 and prothrombin (2)

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10
Q

Platelet aggregation is mediated by a fibrinogen receptor. What is it called?

A

GPIIb/IIIa

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11
Q

Describe the platelet activation process.

A

Prostacyclin in vessel walls suppresses the activation of platelets - leading to an increase in cAMP
Presence of thrombin activates platelets leading to a change in their shape
Platelets synthesise thromboxane A2, adrenaline, ADP
On activation, these are released from vesicles
Platelet aggregation is mediated by a fibrinogen receptor called GPIIb/IIIa and creates links between platelets
Fibrinogen is cleaved to fibrin which causes platelets to contract and tighten the plug
Exposure of platelets to acidic phospholipids promotes coagulation

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12
Q

How can atherosclerosis promote platelet activation?

A

Damage to vessel wall will disrupt prostacyclin production and so prostacyclin will not be able to suppress activation of platelets and so this promotes inappropriate activation

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13
Q

Venous pooling is a risk factor for thrombosis. True or false?

A

True

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14
Q

Is targeting coagulation, in the prevention of thrombosis more effective in venous or arterial thrombosis?

A

Venous

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15
Q

Is targeting platelet activation, in the prevention of thrombosis more effective in venous or arterial thrombosis?

A

Arterial

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16
Q

Heparins occur naturally in the body. True or false?

A

True

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17
Q

Heparins are oral anti-coagulants. True or false?

A

False - parenteral

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18
Q

How do heparins work?

A

They act via binding antithrombin III - they increase the rate of ATIII formation by 1000 fold

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19
Q

Unfractionated heparins are the most commonly used heparins. True or false?

A

False - less commonly used - mainly used with patients with renal failure

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20
Q

Which factor do low molecular weight heparins work on?

A

Factor X

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21
Q

Low molecular weight heparins affect thrombin. True or false?

A

False - only factor Xa

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22
Q

Enoxaparin, tinzaparin and dalteparin are examples of which type of anti-coagulant?

A

Low molecular weight low molecular weight heparins

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23
Q

Low molecular weight heparins have a longer duration of action and better bioavailability than unfractionated heparins. True or false?

A

True

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24
Q

Which factor does fondaparinux effect?

A

Factor Xa

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25
Q

Heparins pose a risk of haemorrhage. True or false?

A

True

26
Q

What is protamine used for?

A

As heparins are associated with risk of haemorrhage, protamine is used to inactivate heparins if haemorrhage is severe

27
Q

What is type I heparin-induced thrombocytopaenia?

A

Transient decrease in platelet number. This has no clinical consequence

28
Q

What is type II heparin-induced thrombocytopaenia?

A

Heparin induces formation of antibodies that activate platelets - may cause life threatening thrombo-emboli

29
Q

What can HIT be treated with?

A

Danaparoid

30
Q

Hirudins are a group of oral anti-coagulants. True or false?

A

False - parenteral

31
Q

How do hirudins work?

A

Inhibit thrombin

32
Q

Hirudin is present in saliva and leech and is used as an anti-coagulant. True or false?

A

False - synthetic version bivalirudin is used

33
Q

What type of anti-coagulant is argatroban and how does it work?

A

Hirudin - works by inhibiting thrombin

34
Q

Warfarin is an oral anti-platelet drug. True or false?

A

False - oral anti-coagulant

35
Q

Warfarin competitively inhibits vitamin K reductase. How does this have an anti-coagulation effect?

A

Thrombin, factor 7, 9 and 10 require carboxylation and vitamin K is needed for this. It is oxidised, but in order for it to have a continued function, it needs to be reduced. This cannot happen if warfarin is inhibiting the enzyme and so maturation of clotting factors is reduced -> anti-coagulant effect

36
Q

If severe haemorrhage is caused by warfarin, how is this stopped?

A

Give vitamin K

37
Q

Warfarin should be avoided in pregnancy. True or false?

A

True

38
Q

Warfarin is mainly given in DVT and AF. True or false?

A

True

39
Q

How can antibiotics have an effect on warfarin?

A

Microorganisms in the gut produce vitamin K so if they are killed, there is a reduction in vitamin K which will enhance the effects of warfarin

40
Q

What type of anti-coagulant is dabigatran?

A

Thrombin inhibitor

41
Q

What type of anti-coagulant is rivaroxaban?

A

Factor Xa inhibitor

42
Q

What is the aim of anti-platelet therapy?

A

Blocking production of thromboxane

43
Q

What is aspirins mechanism of action as an anti-platelet?

A

It blocks the action of COX enzymes which convert arachidonic acid to PG endoperoxides. This means that aspirin will block the production of thromboxane and prostacyclin

44
Q

Aspirin blocks the action of prostacylcin. Why is this bad?

A

Because it won’t be able to suppress platelet activation

45
Q

Can platelets synthesise new COX enzymes?

A

No - because they have no nuclei

46
Q

Can endothelial cells synthesise new COX?

A

Yes

47
Q

Low doses of aspirin affect platelets only, whereas high doses affect prostacyclin production. True or false?

A

True

48
Q

Epoprostenol is a prostacyclin antagonist. True or false?

A

False - agonist

49
Q

How does dipyridamole work?

A

Blocks PDE - so increases levels of cAMP

50
Q

Unfractionated heparins bind to thrombin but not factor Xa. True or false?

A

True

51
Q

How do P2Y receptor antagonists work as anti-platelets?

A

Activated platelets release stores of ADP and these act on P2Y receptors.
By blocking P2Y receptors, ADP cannot bind and so platelets will not be activated and hence prevents aggregation

52
Q

Fibrinolytic drugs are given IV. True or false?

A

True

53
Q

Abciximab, tirofiban and eptifibatide are which class of anti-platelets?

A

GPIIb/IIIa antagonists

54
Q

Clopidogrel and prasugrel are which type of antiplatelets?

A

P2Y irreversible antagonists

55
Q

Cangrelor and ticagrelor are which type of antiplatelets?

A

P2Y reversible antagonists

56
Q

What is tranexamic acid and how does it work?

A

Anti-fibrinolytic drug - blocks activation of plasminogen to plasmin

57
Q

What activates plasminogen?

A

tissue plasminogen activator which is released by damaged blood vessels and accumulates in the fibrin mesh of blood clot when it forms

58
Q

Plasmin breaks down the fibrin mesh of a blood clot, preventing it from becoming too large. What is this process called?

A

Fibrinolysis

59
Q

How do fibrinolytic drugs work?

A

Mimic the action of tissue plasminogen activator and so promote cleavage of plasminogen into plasmin leading to fibrinolysis

60
Q

Tranexamic acid is used to reduce bleeding. True or false?

A

True

61
Q

Alteplase, reteplase and tenecteplase are what kind of drugs?

A

fibrinolytic drugs

The Patient - pharmacology (Y2-1) (18 decks)

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