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Cardiology > Anticoagulant, anti platlet and anti thrombotic drugs > Flashcards

Anticoagulant, anti platlet and anti thrombotic drugs Flashcards

1
Q

What is haemostasis?

A

arrest of blood loss from a damaged vessel

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2
Q

What are the sequence of events in haemostasis?

A
  • endothelial damage
  • platelet plug
  • fibrin clot formation
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3
Q

What occurs in the production of the platelet plug?

A
  • Platelets aggregate at the site of injury.
  • Activated platelets release a number of factors that cause more platelets to come to scene.
  • Platelets stick together which stems the loss of blood.
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4
Q

How does the fibrin clot form?

A
  • Through the blood clotting cascade, liquid blood is turned into a solid and stable clot.
  • The clot is caused by the transformation of fibrinogen to fibrin.
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5
Q

What is the role of pseudopodia in primary haemostasis?

A

helps platelets stick together

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6
Q

What do activated platelets do?

A
  • extend pseudopodia

- synthesise and release thromboxane A2 (TXA2)

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7
Q

What does TXA2 bind to?

A

-TXA2 receptor which causes the release of 5-HT and ADP

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8
Q

What is 5-HT?

A

Serotonin

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9
Q

what is the effect of TXA2 on smooth muscle?

A
  • When TXA2 binds to the TXA2 receptorr it causes vasoconstriction.
  • serotonin released binds to 5-HT receptors and also causes vasoconstriction
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10
Q

What is the role of ADP in primary haemostasis?

A

ADP binds to platelet GPCR purine recetors (P2Y12)

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11
Q

What does the activation of P2Y12 do?

A
  • activates more platelet
  • aggregate platelets into a soft plug at site of injury
  • expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation
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12
Q

How does P2Y12 aggregate platelets into a soft plug at site of injury?

A

[via increased expression of platelet glycoprotein (GP) receptors that bind fibrinogen]. TXA2 acts similarly

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13
Q

What is the role of GPIIb/IIIa receptor?

A

Allows plasma fibrinogen to bind to receptors which causes a physical bridge between platelets. Augmented by TXA2

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14
Q

What are the sequence of events in the coagulation cascade?

A
  • inactive factor 10 is converted into active factor 10a by tenase
  • inactive factor 2 is converted to active factor 2 by prothrombinase
  • fibrinogen is converted to a fibrin by thrombin (factor 2)
  • a solid clot is formed
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15
Q

What is the other name for factor 2a?

A

thrombin

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16
Q

What is the name for the inactive factor 2?

A

prothrombin

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17
Q

What is thrombosis?

A

pathological haemostasis

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18
Q

What predisposes you to thrombosis?

A

Virchow’s triad

  • endothelial damage
  • abnormal blood flow
  • increased coagubility of the blood
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19
Q

What is an arterial thrombus?

A

white thrombus: mainly platelets in a fibrin mesh

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20
Q

Where do emboli travel to in an arterial thrombus?

A

the brain or other organ

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21
Q

What drug treats arterial thrombi?

A

antiplatelet

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22
Q

What is a venous thrombus?

A

red thrombus: white head, jelly like red tail, fibrin rich

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23
Q

Where do emboli travel to in a venous thrombus?

A

lungs usually

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24
Q

What drug treats venous thrombi?

A

anticoagulants

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25
Q

What does warfarin do?

A

blocks a modification of factors X and II essential for their function

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26
Q

What does rivaroxiban do?

A

Directly inhibits factor Xa

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27
Q

What does heparin, LMWHs and fondaparinux do?

A

inactivate factor Xa via antithrombin III

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28
Q

What does dabigatran do?

A

directly inhibits factor IIa

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29
Q

What else does heparin do?

A

Inactivates factor IIa via antithrombin III

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30
Q

How d pre cursers produce active factors?

A

They are post transationally modified for example by gamma carboxylation of glutamate residues

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31
Q

Where deos Vit K come in?

A

The carboxylase enzyme that mediates carboxylation requires vitamin K

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32
Q

What is the oxidised form or Vit K called?

33
Q

What is the reduced form of Vit K called?

A

hydroquinone

34
Q

Which form of Vit K is important in gamma carboxylation?

A

reduced Vit K

35
Q

How does warfarin act upon Vit K?

A

Warfarin inhibits Vit K thereby stopping the action of the clotting factors 2,7,9 and 10

36
Q

When are anticoagulants used?

A
  • deep vein thrombosis (DVT)
  • prevention of post-operative thrombosis
  • patients with artificial heart valves
  • atrial fibrillation
37
Q

Whats the major risk of anticoagulants?

A

haemorrhage

38
Q

How is warfarin administered?

39
Q

What is the absorption of warfarin like?

40
Q

What is the onset of action of warfarin?

A

slow (2-3) days. whilst inactive factors replace active gamma carboxylated factors that are slowly cleared from the plasma

41
Q

How does warfarin compete with Vit K?

A

It compeetess with it to prevent conversion of Vit K to reduced Vit K to stop gamma carboxylation

42
Q

How is the degradation of warfarin?

A

takes ages to leave body

43
Q

Why is heparin used over warfarin in life threatening situations?

A

Warfarin takes too long to become activated

44
Q

How long do you have to wait after stopping warfarin until an operation can be done?

A

4-5 days as it takes five half lives for an agent to be cleared from the body

45
Q

What are the warnings for warfarin?

A
  • low therapeutic index
  • warfarin must be monitored on a regular basis
  • overdose can be treated by Vit K administration
  • overdose can also be treated by plasma clotting factors
46
Q

What factors potentiate warfarin action and thereby increase the risk of haemorrhage?

A
  • liver disease – decreased clotting factors
  • high metabolic rate – increased clearance of clotting factors
  • drug interactions
47
Q

What factors lessen warfarin action and thereby increase risk of thrombosis?

A
  • psychological state (pregnancy)
  • vit K consumption
  • drug interactions
48
Q

What is antithrombin III?

A

an important inhibitor of coagulation

49
Q

What does antithrombin III do?

A

neutralises all serine protease factors in the coagulation cascade by binding to their active site in a 1 to 1 ratio

50
Q

How do heparin and antithrombin III work together?

A

When antithrombin bind to heparin, it increased the rate of deactivation of active factor 2 and 10. Reduced conversion of fibrinogen to fibrin so no clot.

51
Q

How is factor 2 inactivated?

A

heparin binds to antithrombin III and factor II simultaneously

52
Q

How is factor X inactivated?

A

Heparin needs to bind to antithrombin The acceleration of the inactivation is aided by LMWHs.

53
Q

Give two examples of LMWHs

A

enoxaparin and dalteparin

54
Q

When are LMWHs not used?

A

renal failure

55
Q

What is the admistration route of heparin and LMWHs?

A

heparin - IV or SC

LMWH- SC

56
Q

What is the elimination order of heparin and LMWHs?

A

heparin- zero order

LMWH - first order

57
Q

What are the adverse effects of heparin and LMWHs?

A
  • haemorrhage
  • osteoporosis
  • hypersensitivity reactions
58
Q

What are examples of newer olly active agents that inhibit thrombin or factor 10?

A

rivaroxiban and dabiatran

59
Q

Why are the newer drugs so good?

A
  • convenience of administration

- predictable degree of anticoagulation

60
Q

What does aspirin do?

A

irreversibly blocks cycloxygenase (COX) in platelets, preventing TXA2 synthesis, but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)

61
Q

when and how is aspirin used?

A

Used orally, mainly for thromboprophylaxis in patients at high cardiovascular risk

62
Q

What is the main adverse effect of aspirin?

A

gastrointestinal bleed and ulceration

63
Q

How dies clopidogrel work?

A

Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition

64
Q

When is clopidogrel used?

A

when patients are intolerant to aspirin

65
Q

How is clopidogrel administered?

66
Q

What re the effects of combining aspirin and clopidogrel?

A

synergistic effect - work well to enhance action

67
Q

When is tirofiban used?

A

Given IV in short term treatment to prevent myocardial infarction in high risk patients with unstable angina (with aspirin and heparin)

68
Q

When are fibrinolytics used?

A

Fibrinolytics are used principally to reopen occluded arteries in acute myocardial infarction (M.I.), or stroke – less frequently life-threatening venous thrombosis or pulmonary embolism

69
Q

How are fibrinolytics administered?

70
Q

What is a better treatment than fibrinolytics?

A

percutaneous coronary intervention

71
Q

What drug do fibrinolytics work well with?

72
Q

What is streptokinase?

A

Not an enzyme, but a protein extracted from cultures of streptococci

73
Q

What does streptokinase do?

A

Reduces mortality in acute M.I. (given IV, or intracoronary) but action blocked after 4 days by the generation of antibodies. Further doses not to be given after this time

74
Q

What are the disadvantages of streptokinases?

A

May cause allergic reactions (not be given to patients with recent streptococcal infections)

75
Q

What are Alteplase and duteplase

A

Are recombinant tissue plasminogen activator (rt-PA)

76
Q

What do Alteplase and duteplase do?

A

Are more effective on fibrin bound plasminogen than plasma plasminogen and show selectivity for clots

77
Q

Do Alteplase and duteplase cause allergic reactions?

78
Q

What is the major adverse effect of fibrinolytics?

A

The major adverse effect of fibrinolytics is haemorrhage that may be controlled by oral tranexamic acid which inhibits plasminogen activation

Cardiology (32 decks)

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