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Cardiovascular > Anticoagulant's and Anti-platelet's > Flashcards

Anticoagulant's and Anti-platelet's Flashcards

1
Q

What is haemostasis?

A

The arrest of blood loss from a damaged vessel

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2
Q

What are the steps to hemostasis?

A

Vascualr wall damage exposing collagen and tissue factor (TF, thromboplastin)
Primary haemostasis (vasoconstriction, platelet adhesion, activation and aggregation by fibrinogen)
Activation of blood clotting and the formation of a stable clot (by fibrin enmeshing platelets)

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3
Q

What is formed by primary haemostasis?

A

Soft plug

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4
Q

What is formed by coagulation?

A

A solid clot

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5
Q

What will platelets send out once activated at the site of injury?

A

Cytoplasmic extensions (pseudopodia)

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6
Q

What is the function of pseudopodia?

A

They help platelets to stick together

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7
Q

What chemicals do platelets release once activated?

A

Thromboxane A2 which will bind to specific thromboxane receptors on the platelets which causes the release of serotonin and ADP

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8
Q

What does serotonin do?

A

Causes vasocontriction and serotonin will also bind to other receptors that also cause vasocontriction

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9
Q

What does ADP do in primary haemostasis?

A

It bind to platelet GPCR purine receptors that:
Act locally to activate futher platelets
Aggregate platelets into a soft plug via platelet glycoprotein receptors that bind to fibrinogen
Expose acidic phospholipids on platelet surface that initiate coagulation of blood

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10
Q

What increases the expression of platelet glycoproteins on the surface of platelets?

A

ADP and TXA2

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11
Q

What is tenasae?

A

Active factor 8 and 9

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12
Q

How does X become Xa?

A

Via tenase

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13
Q

What is prothombinase?

A

Xa and Va

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14
Q

What does prothombinase do?

A

It converts prothrombin (2) to thrombin (2a)

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15
Q

What does thrombin (2a) do?

A

Converts fibrinogen to fibrin which will then turn the soft plug into a solid clot

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16
Q

What are the targets in the coagulation cascade for drugs?

A

To inhibit the action of Xa (prothrombinase and therefore prevent prothrombin being converted to thrombin)
Inhibit the action of thrombin (prevent the conversion of fibrinogen to fibrin)

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17
Q

What is thrombosis?

A

Pathological haemostasis (a haematological plug in the absence of bleeding)

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18
Q

What is an arterial thrombus?

A

White - mainly platelets in a fibrin mesh. If the thrombus detaches from the injured wall it then becomes an embolus

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19
Q

What class of drugs are used to treat arterial thrombus?

A

Anti-platelets

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20
Q

What is a venous thrombus?

A

Red - white head, jelly-like red tail and is fibrin rich

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21
Q

What do anti-platelets do?

A

Block the aggregation and activation of platelets

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22
Q

What class of drugs are used to treat venous thrombus?

A

Anticoagulants

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23
Q

What are examples of anticoagualants?

A

Wafarin, rivaroxaban, heparin, fondaparinux, dabigatran

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24
Q

What is the action do ribaroxiban?

A

It directly inhibits factor Xa (thrombinase)

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25
Q

What does heparin, LMWHs and fondaparinux inactivate?

A

They indirectly inactivate factor Xa via the activation of antithrombin 3
Heparin also inactivated factor 2a (thrombin) via the activation of antithrombin 3

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26
Q

What does dabigatran do?

A

Directly inhibits factor 2a (thrombin)

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27
Q

What is the action of warfarin?

A

Blocks a modification of factors X and 2 which are essential for their function

28
Q

What clotting factors rely on vitamin K?

A

2, 7, 9 and 10 are all glycoprotein precursors of their active self that act as serine proteases that require modification to produce their active factors

29
Q

What is the action of vitamin K?

A

In its reduced form, it is an essential cofactor of the carboxylase enzyme that is needed to mediate gamma-carboxylation which is needed to modify the clotting factors making them acitve

30
Q

What does warfarin do to vitamin K?

A

It blocks vitamin K reductase that is needed to reduce vitamin K and therefore stops the activation of factor 2, 7, 9 and 10 making warfarin a potent anticoagulant

31
Q

When are anticoagulants used?

A 
To prevent and treat DVT and embolism: 
DVT
Prevention of post-op thrombosis
Patients with artifical heart valves 
AF
32
Q

What is the name of the reduced and active vitamin K?

A

Hydroquinone

33
Q

How is warfarin administered?

A

Orally

34
Q

What is the onset of action of warfarin?

A

Slow onset (2/3 days) whilst inactive factors replace active gamma-carboxylated factors that are slowly cleared from the plasma

35
Q

What is the half-life of warfarin?

A

About 40 hours

36
Q

How can the levels of warfarin be monitored?

A

By INR levels

37
Q

How can an overdose of warfarin be treated?

A

Via the administration of vitamin K (phytomenadione)

38
Q

What are factors that can potentiate warfarin action (risk of haemorrhage increased)?

A

Liver disease - decreased clotting factors
High metabolic rate - increased clearance of clotting factors
Drug interactions (aspirin, NSAIDS)

39
Q

What are factors that lessen warfarin action (risk of thrombosis increased)?

A

Physiological state - pregnancy (increased clotting factor synthesis)
Hypothyrodism
Vitamin K consumption
Drug interactions

40
Q

What is antithrombin 3?

A

An important inhibitor of coagulation which neutralises all serine protease factors in the coagulation cascade by binding to their active sites.

41
Q

What does heparin do to antithrombin 3?

A

It binds to antithrombin 3 increasing its affinity for serine protease clotting factors (particularly Xa and 2a) to greatly increase their rate of inactivation. Ultimately it reduces the change of fibrinogen to fibrin

42
Q

What is the difference between the way heparin will bind to 2a and Xa?

A

Heparin binds to AT3 and 2a bringing them together and accelerates the inactivation of thrombin
To inactivate Xa, heparin only needs to bind to AT3

43
Q

What do LMWHs do?

A

They inhibit factor Xa but not thrombin

44
Q

How is heparin and LMWHs administered?

A 
Heparin = IV or SC
LMWHs = SC
45
Q

What is the difference in the excretion of LMWHs and heparin?

A

LMWHs are excreted via renal

Hepain is alternative pathways and therefore heparin is preferred in renal failure

46
Q

What is the difference in elimination of heparin an LMWHs?

A

Heparin is zero order

LMWHs are first order

47
Q

What are examples of LMWHs?

A

Enoxaparin and dalterparin

48
Q

What are adverse effects of heparin and LMWHs?

A

Haemorrhage (can administer protamine sulfate which inactivates heparin)
Oseoporosis
Hypooaldosteronism
Hypersensitivity

49
Q

What are examples of orally active drugs that are direct inhibitors of thrombin?

A

Dabigartran etexilate

50
Q

What are examples of orally active drugs that are direct inhibitors of Xa?

A

Rivaroxaban

51
Q

When are anti-platelet drugs used?

A

Arterial thrombosis

52
Q

What is the action of aspirin?

A

It irreversibly blocks cycloxygenase (COX) in platelets which prevents the TXA2 synthesis and production of antithrombotic prostaglandin !2 (PGI2)

53
Q

What are the steps in TXA2 synthesis?

A

Aranchiodonic acid generation which is converted to cyclic endoperoxides by COX
Cyclic endoperoxides are then converted to TXA2 by thromboxane synthase

54
Q

When is aspirin prescribed?

A

Thromboprophylaxis in patients at high CV risk

55
Q

What is the main adverse effect of aspirin?

A

GI bleeding

Ulceration

56
Q

What is the action of clopidogrel?

A

It is a prodrug that requires hepatic metabolism

Links to GPCR purine receptors (ADP receptors) by a disulphide bond producing an irreversible inhibition

57
Q

When is clopidogrel prescribed?

A

Given in combo with aspirin post-MI

Administered orally

58
Q

When is tirofiban prescribed?

A

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

59
Q

What is the fibrinolytic cascade?

A

It exists endogenously to oppose the coagulation cascade

60
Q

What occurs during the fibrinolytic cascade?

A

Plasminogen is converted to plasmin via tPA which will then convert fibrin to fibrin fragments breaking up clots

61
Q

When are fibrinolytics used?

A

To reopen occluded arteries in acute MI or stroke

62
Q

What are examples of fibrinolytic drugs?

A

Streptokinase
Alteplase
Duteplase
All of these activate plasminogen

63
Q

What is streptokinase?

A

NOT an enzyme but a protein extracted from cultures of streptococci which reduces mortality in acute MIs but action blocked after 4 days due to the production of antibodies

64
Q

What type of drugs are alteplase and duteplase?

A

Recombinant tissue plasminogen actvators (rt-PA)

More effective on fibrin bound plasminogen than plasma plasminogen

65
Q

What is the adverse effect of fibniolytics?

A

Haemorrhage, but this can be controlled by oral tranexamic acid which inhibits plasminogen activation

Cardiovascular (27 decks)

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