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Anticoagulants, antiplatelets & Thrombolytics > Anticoagulants, Antiplatelets & Thrombolytics > Flashcards

Anticoagulants, Antiplatelets & Thrombolytics Flashcards

1
Q

Haemostasis

A

to stop bleeding in haemorrhage

Involves: local vasoconstriction, platelet aggregation and coagulation

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2
Q

Thrombosis

A

pathological, coagulation in the absence of bleeding

Involves: Virchow’s triad

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3
Q

Virchow’s triad

A

increase coagulation, vessel damage and abnormal blood flow

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4
Q

Arterial thrombus

A

white, platelet aggregation, embolus tends to cause stroke

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5
Q

Venous thrombus

A

red, white head, red-jelly tail, fibrin rich, embolus tends to lodge in lung: PE

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6
Q

Platelets in coagulation cascade

A

endothelial damage –> platelet aggregation–> mediator (pre-existing (ADP) and newly formed (TXA2)) release, further platelet aggregation

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7
Q

Fibrin in coagulation cascade

A

endothelial damage –> clotting factor release –> X activated (Xa) –> prothrombin –> thrombin (converts fibrinogen to fibrin (forms a fibrin mesh)

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8
Q

Fibrin clot formation

A

Platelet aggregation + blood coagulation

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9
Q

Thrombin

A

fibrinogen to fibrin

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10
Q

Platelet function

A

brings clotting factors closer together for activation

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11
Q

Activation of clotting factors

A

gamma-carboxylation

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12
Q

gamma carboxylation enzyme

A

carboxylase

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13
Q

Essential requirement of carboxylase?

A

vitamin K - therefore is required for coagulation

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14
Q

Warfarin target?

A

blocks vitamin K reductase - stopping vitamin K from binding to it (preventing gamma carboxylation and coagulation)

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15
Q

Anticoagulant function?

A

prevention/ treatment of venous thrombosis/ embolism

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16
Q

Caution with anticoagulants?

A

risk of haemorrhage

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17
Q

Which clotting factors does warfarin block?

A

II, VII, IX & X

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18
Q

How is warfarin standardly taken?

A

orally

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19
Q

Fast or slow action?

A

slow (2-3 days)

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20
Q

Half life?

A

long (40 hrs)

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21
Q

Warfarin warnings?

A

difficulty of balancing anticoagulance with haemorrhage risk - low therapeutic index

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22
Q

Factors that increase haemorrhage risk when on warfarin?

A 
liver disease (less clotting factors)
fast metabolism (fast clotting factor clearance)
drug interaction: agents that inhibit hepatic metabolism of warfarin
drugs that inhibit platelet function (aspirin and NSAIDS)
drugs that inhibit reduction or availability of vitamin K
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23
Q

Factors that inhibit warfarin action (increase thrombosis risk)?

A

physiological state: pregnancy (higher clotting factor synthesis), hypothyroidism (less degradation of clotting factors), vitamin K consumption, drugs that increase the metabolism of warfarin

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24
Q

warfarin overdose treatment?

A

vitamin K or concentrate of clotting factors

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25
Q

Antithrombin III main function?

A

important inhibitor of coagulation

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26
Q

Action of antithrombin III?

A

neutralises serine protease factors (II, VII, IX, X) in coagulation cascade

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27
Q

Heparin mechanism?

A

binds to antithrombin III, increasing its affinity for serine protease factors, increasing the rate of clotting factor inactivation

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28
Q

What does heparin need to bind to to inhibit IIa (thrombin)?

A

Antithrombin III and IIa

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29
Q

What does heparin need to bind to to inhibit Xa

A

Antithrombin III

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30
Q

Examples of LMWHs?

A

enoxaparin, dalteparin

31
Q

What do LMWHs inhibit?

A

factor Xa but not IIa (thrombin)

32
Q

Heparin administration?

A

IV - immediate action

Subcutaneous - 1hr delay

33
Q

How are LMWHs excreted?

A

Renal excretion

34
Q

Adverse affects of heparin and LMWHs?

A

haemorrhage
osteoperosis (long term treatment)
hypoaldosteronism
hypersensetivity reactions

35
Q

How to reverse heparin effects?

A

protamine sulphate

36
Q

Orally active inhibitor action?

A

directly inhibits thrombin or Xa, to prevent venous thrombosis

37
Q

Example of orally active inhibitor?

A

dabigatran etexillate

38
Q

Advantages of orally active inhibitors?

A

administration convenience

predictable degree of anticoagulation

39
Q

Disadvantages of orally active inhibitors?

A

No agent to reverse haemorrhage in overdose

40
Q

Anti platelets act on which type of thrombosis?

A

arterial thrombosis

41
Q

Anti coagulants act on which type of thrombosis?

A

Venous thrombosis

42
Q

How to platelets attach to damaged vessels?

A

via surface glycoproteins and von williebrand factor (acts as a bridge)

43
Q

Aggregation occurs due to which molecules?

A 
ADP
5-hydrotrytamine (5-HT)
Thromboxane A2 (TXA2) via COX enzyme

These all cause cell surface receptors of platelets to express glycoprotein IIb/ IIIa

44
Q

How do glycoproteins cross link platelets in platelet aggregation?

A

via fibrinogen

45
Q

Acidic phospholipid exposure on platelet surface promotes the formation of?

A

Thrombin IIa - which stimulates further platelet aggregation

46
Q

how is the mass of platelets stabilised?

A

Through the conversion of fibrinogen to fibrin

47
Q

What is the role of ADP in platelet aggregation?

A

attracts more platelets

48
Q

Role of TXA2 in platelet aggregation?

A

promotes platelet aggregation, degranulation and vasoconstriction

49
Q

What is released when platelets degranulate due to TXA2?

A

more ADP and TXA2

50
Q

Platelet aggregation mainly occurs in which form of clot formation?

A

haemostasis

51
Q

What is the main anti platelet drug in use?

52
Q

how does aspirin work as an anti platelet?

A

blocks COX and prevents TXA2 synthesis

inhibits prostaglandin I2 production (TXA2 precursor)

53
Q

side effects of aspirin?

A

GI bleeding and ulceration

54
Q

Clopidogrel function?

A

links to P2Y12 receptor - irreversible inhibition

55
Q

When is clopidogrel normally used?

A

when a patient is intolerant of aspirin

56
Q

Aspirin administration?

A

normally oral

57
Q

Clopidogrel administration?

58
Q

Tirofiban used when?

A

MI prophylaxis in high risk CV patients with unstable angina

59
Q

Tirofiban short or long term drug?

A

short term

60
Q

Tirofiban administration?

61
Q

plasminogen and fibrinolytic drugs act against what?

A

the coagulation cascade

62
Q

What is the role of plasmin?

A

dissolves fibrin converting it into fibrin filaments

63
Q

Plasminogen and fibrinolytic drugs act to do what?

A

reopen occluded arteries in acute MI or stroke

64
Q

Administration of plasminogen and fibrinolytic drugs?

65
Q

What is preferred to the use of plasminogen and fibrinolytic drugs?

A

PCI if prompt

66
Q

What does PCI entail?

A

non-surgical widening of coronary artery with stent placement after dilatation

67
Q

What drug should be administered alongside PCI?

68
Q

Adverse effects of streptokinase?

A

Antibodies block action after 4 days

can cause allergies

69
Q

When is streptokinase contraindicated?

A

In recent strep infection patients

70
Q

What is alteplase (and duteplase)?

A

recombinant tissue plasminogen activator (rt-PA)

71
Q

Benefits of alte/ duteplase?

A

no allergies

72
Q

Administration of Alte/ duteplase?

A

short half life so IV infusion

73
Q

MAJOR fibrinolytic adverse side effect?

A

haemorrhage

74
Q

Control of haemorrhage due to fibrinolytic?

A

tranexamic acid - inhibits plasminogen activation

Anticoagulants, antiplatelets & Thrombolytics (1 decks)

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