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IBSc PHEM Applied Science > Clotting Drugs > Flashcards

Clotting Drugs Flashcards

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1
Q

5 stages of coagulation

A

Vasospasm
Primary haemostasis- platelet plug and anteplatelets
Secondary haemostasis- clotting cascade and anticoagulants
Clot retraction
Fibrinolysis

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2
Q

What stages of coagulation do anti platelets and anticoagulants act in

A

Antiplatelets - primary haemostasis
Anticoagulants - secondary haemostasis

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3
Q

What substances are released by damaged cells in response to injury

A

Endothelin
Thromboxane A2
Serotonin
Noradrenaline
Direct monocyte contraction also occurs

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4
Q

3 stages of platelet plug formation

A

Adhesion
Activation
Aggregation

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5
Q

What happens in the adhesion phase of platelet plug formation

A

Smooth endothelium disrupted -> turbulence and adherence
VWF sticks to exposed collagen, platelets attach to GP1A receptors on vWF

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6
Q

What substances are released in the activation phase of platelet plug formation

A

ADP (P2Y12)
Thromboxane a2
Collagen thrombin

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7
Q

What receptor becomes available when platelets are activated

A

GIIb/IIIa receptor

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8
Q

What happens in aggregation phase of platelet plug formation

A

Fibrinogen links between GIIb/IIIa receptors on activated platelets

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9
Q

What mediation targets thromboxane A2

A

Aspirin

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10
Q

What medications target ADP ( act as P2Y12 receptor antagonists)

A

Clopidogrel
Prasugrel
Ticagrelor

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11
Q

What medications antagonise GPIIB/IIIa receptors

A

Abciximab

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12
Q

Aspirin MOA

A

Irreversible COX 1+2 inhibitor
Prevents formation of thromboxane A2 by blocking conversion of Arachidonic acid to PGH2 -> decr circ TXA2
Also anti platelet effect

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13
Q

Irreversible antiplatelets

A

Aspirin (COX1)
Ticlopinide (ADP)
Clopidogrel (ADP)
Prasugrel (ADP)
Abxicimab (GP IIB/iiia)

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14
Q

Reversible antiplatelets

A

Cangrelor (ADP)
Ticagrelor (ADP)
Tirocinanti (GO IIB/IIIa)
Eprifibatide (GO IIA/IIIB)

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15
Q

Why is clopidogrel used more than prasugrel, cangrelor, ticlopidine and ticagrelor

A

P - more Haemorrhagic complications and cost
C - less effective
To - more side effects
Tg - more Haemorrhagic complications and side effects

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16
Q

Clopidogrel limitations

A

Inter patient variability
Slow onset and offset of action

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17
Q

Which antiplatelets are given IV

A

Cangrelor
Abciximab
Tirofiban
Eptifibatide

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18
Q

Indications for antiplatelets

A

Athersclerosis
Stents
CVA

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19
Q

Which receptor on ADP do some antiplatelets target

A

P2Y12

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20
Q

What does reduction in thromboxane A2 by aspirin prevent

A

Vasospasm and platelet activation

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21
Q

Which phase of primary haemostasis is targeted by aspirin clopidogrel and Abciximab

A

Aspirin - activation TXA2
Clopidogrel - activation ADP
Abciximab - aggregation GPIIB/IIIA

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22
Q

Which clotting factors are in the extrinsic pathway

A

3
7

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23
Q

Which clotting factors are in the intrinsic pathway

A

12
11
9
8

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24
Q

Which clotting factors are in the common pathway

A

1
2
4
5
10
13

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25
Q

What does prothrombin time measure

A

External and common pathways
Formation of fibrin by thromboplastin

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26
Q

Clotting blood tests

A

Prothrombin time
International normalised ratio
Activated partial thromboplastin time
Fibrinogen

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27
Q

What does INR measure

A

External and common pathways

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28
Q

Which drug is INR used to monitor

A

Warfarin

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29
Q

What does aPTT measure

A

Fibrin formation when partial thromboplastin added to plasma
Internal and common pathways

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30
Q

What does Fibrogen blood test measure

A

Quantative test of amount of fibrinogen

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31
Q

What conditions may have a low fibrinogen test result

A

Liver failure
DIC

32
Q

Which blood clotting test measures the internal pathway

A

aPTT

33
Q

Which blood clotting tests measure the external pathway

A

PT
INR

34
Q

What factors are effected in haemophilia

A

A - VIII
B - IX
Both disrupt intrinsic pathway

35
Q

What clotting factors does Antithrombin III act on

A

Thrombin (II)
9
10
11
12

36
Q

What clotting factors do protein c and s act on

A

5
8

37
Q

Antithrombin III MOI

A

Binds thrombin and factors 9 10 11 12

38
Q

What clotting factors does unfractionated heparin work on

A

9
10a
11
12

39
Q

What factor does LMWH work on

A

Xa

40
Q

What is the reversal agent for unfrac heparin and LMWH

A

Protamine

41
Q

Warfarin MOI and which clotting factors effected

A

Vitamin K antagonist
2 7 9 10 (1972)
Also impacts protein c and s

42
Q

Warfarin reversal

A

Vitamin K
Prothrombin complex
Factors 10 9 7 2

43
Q

Apixaban rivaroxaban edoxaban MOA

A

Direct Xa inhibitors

44
Q

Apixaban rivaroxaban edoxaban MOA

A

Direct Xa inhibitors

45
Q

Direct Xa inhibitors reversal

A

Adexanet alpha

46
Q

What endogenous substances control the clotting cascade

A

Anti thrombin iii
Protein c
Protein s

47
Q

Dabigatran MOA

A

direct thrombin inhibitor

48
Q

Dabigatran reversal

A

Idarucizumab

49
Q

Indications for anticoagulants

A

DVT
PE
AF
Prophylaxis

50
Q

What triggers the intrinsic extrinsic and common clotting pathways

A

Intrinsic - exposed subendothelial collagen
Extrinsic - tissue factor
Common - factor X

51
Q

Infrac heparin MOA

A

Potentiates Antithrombin

52
Q

DOACS

A

Direct Xa inhibitors (ixabans)
Direct thrombin (IIa) inhibitors - Dabigatran

53
Q

Stages of clot breakdown

A

Clot retraction
Fibrinolysis

54
Q

What enzyme causes fibrinolysis

A

Plasmin

55
Q

How is plasmin formed

A

Plasminogen activated to plasmin by tPA produced by injured endothelium

56
Q

What are the products of fibronolysis

A

Fibrinogen breakdown - fibrinogen degradation products
Fibrin breakdown - fibrin degradation products
Stabilised fibrin breakdown - d dimer
Additional breakdown - plasma proteins, V, VIII, complements, VWF

57
Q

What substance is broken down into D dimer

A

Stabilised fibrin

58
Q

TXA MOA

A

Antifibrinolytics
Competitive inhibitor of binding sites on plasminogen stopping tPA binding (prevents plasminogen binding to fibrin)

59
Q

Thrombolytic drugs

A

Streptokinase
Urokinase
Anistreplase
Alteplase
Reteplase
Tenectaplase

60
Q

Fibronolysis processes

A

Tissue plasminogen activator (tPA) released from damaged endothelial cell a few days after injury -> plasminogen to plasmin -> plasmin breaks down fibrinogen, fibrin, and stabilised fibrin

61
Q

Fibronolysis processes

A

Tissue plasminogen activator (tPA) released from damaged endothelial cell a few days after injury -> plasminogen to plasmin -> plasmin breaks down fibrinogen, fibrin, and stabilised fibrin

62
Q

Thrombolytic drug MOA

A

Analogues of tissue plasminogen activator tPA leading to rapid fibrinolysis

63
Q

What prevents blood from clotting normally

A

Endothelial cells very smooth preventing adhesion
NO dilates blood vessels maintaining laminar flow
Heparin sulphate secretes heparin and heparin like subapstances into blood
Protein C and S control clotting when it occurs

64
Q

What causes Vasospasm in response to injury

A

Damage to muscle -> calcium release -> direct muscle contraction

65
Q

What causes Vasospasm in response to injury

A

Damage to muscle -> calcium release -> direct muscle contraction

66
Q

Antithrombin III route, half life, monitoring

A

Given as infusion
Very short half life
Needs monitoring

67
Q

Heparin route

A

Infusion

68
Q

Complications of heparin

A

Heparin induced coagulopathy
Development of antibodies

69
Q

LMWH MOA

A

Converts Xa back to X

70
Q

Is protamine more effective at reversing unfrac heparin or LMWH

A

Unfrac

71
Q

How does warfarin effect coagulation in the first couple of days

A

Coagulation increased for a few days, then overall effect becomes anticoagulant

72
Q

What anticoagulant is broken down by P450

A

Warfarin

73
Q

How does Adexanet alpha work

A

Directly competes with direct Xa inhibitors

74
Q

DOAC monitoring

A

No monitoring needed

75
Q

Why are thrombolytics high risk drugs

A

Degrade all clots in body so can cause bleeding from other minor injuries, cannula sites, etc
Only used in haemodynamically unstable pts due to risks

76
Q

What is ROTEM

A

POC test to assess blood coagulation

77
Q

How are antiplatelets drugs reversed

A

Usually don’t need reversal - just wait for half life to pass usually 24-48hrs
In emergency/high risk procedure - give more platelets

IBSc PHEM Applied Science (21 decks)

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