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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
What does prothrombin time measure
External and common pathways Formation of fibrin by thromboplastin
26
Clotting blood tests
Prothrombin time International normalised ratio Activated partial thromboplastin time Fibrinogen
27
What does INR measure
External and common pathways
28
Which drug is INR used to monitor
Warfarin
29
What does aPTT measure
Fibrin formation when partial thromboplastin added to plasma Internal and common pathways
30
What does Fibrogen blood test measure
Quantative test of amount of fibrinogen
31
What conditions may have a low fibrinogen test result
Liver failure DIC
32
Which blood clotting test measures the internal pathway
aPTT
33
Which blood clotting tests measure the external pathway
PT INR
34
What factors are effected in haemophilia
A - VIII B - IX Both disrupt intrinsic pathway
35
What clotting factors does Antithrombin III act on
Thrombin (II) 9 10 11 12
36
What clotting factors do protein c and s act on
5 8
37
Antithrombin III MOI
Binds thrombin and factors 9 10 11 12
38
What clotting factors does unfractionated heparin work on
9 10a 11 12
39
What factor does LMWH work on
Xa
40
What is the reversal agent for unfrac heparin and LMWH
Protamine
41
Warfarin MOI and which clotting factors effected
Vitamin K antagonist 2 7 9 10 (1972) Also impacts protein c and s
42
Warfarin reversal
Vitamin K Prothrombin complex Factors 10 9 7 2
43
Apixaban rivaroxaban edoxaban MOA
Direct Xa inhibitors
44
Apixaban rivaroxaban edoxaban MOA
Direct Xa inhibitors
45
Direct Xa inhibitors reversal
Adexanet alpha
46
What endogenous substances control the clotting cascade
Anti thrombin iii Protein c Protein s
47
Dabigatran MOA
direct thrombin inhibitor
48
Dabigatran reversal
Idarucizumab
49
Indications for anticoagulants
DVT PE AF Prophylaxis
50
What triggers the intrinsic extrinsic and common clotting pathways
Intrinsic - exposed subendothelial collagen Extrinsic - tissue factor Common - factor X
51
Infrac heparin MOA
Potentiates Antithrombin
52
DOACS
Direct Xa inhibitors (ixabans) Direct thrombin (IIa) inhibitors - Dabigatran
53
Stages of clot breakdown
Clot retraction Fibrinolysis
54
What enzyme causes fibrinolysis
Plasmin
55
How is plasmin formed
Plasminogen activated to plasmin by tPA produced by injured endothelium
56
What are the products of fibronolysis
Fibrinogen breakdown - fibrinogen degradation products Fibrin breakdown - fibrin degradation products Stabilised fibrin breakdown - d dimer Additional breakdown - plasma proteins, V, VIII, complements, VWF
57
What substance is broken down into D dimer
Stabilised fibrin
58
TXA MOA
Antifibrinolytics Competitive inhibitor of binding sites on plasminogen stopping tPA binding (prevents plasminogen binding to fibrin)
59
Thrombolytic drugs
Streptokinase Urokinase Anistreplase Alteplase Reteplase Tenectaplase
60
Fibronolysis processes
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
Fibronolysis processes
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
Thrombolytic drug MOA
Analogues of tissue plasminogen activator tPA leading to rapid fibrinolysis
63
What prevents blood from clotting normally
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
What causes Vasospasm in response to injury
Damage to muscle -> calcium release -> direct muscle contraction
65
What causes Vasospasm in response to injury
Damage to muscle -> calcium release -> direct muscle contraction
66
Antithrombin III route, half life, monitoring
Given as infusion Very short half life Needs monitoring
67
Heparin route
Infusion
68
Complications of heparin
Heparin induced coagulopathy Development of antibodies
69
LMWH MOA
Converts Xa back to X
70
Is protamine more effective at reversing unfrac heparin or LMWH
Unfrac
71
How does warfarin effect coagulation in the first couple of days
Coagulation increased for a few days, then overall effect becomes anticoagulant
72
What anticoagulant is broken down by P450
Warfarin
73
How does Adexanet alpha work
Directly competes with direct Xa inhibitors
74
DOAC monitoring
No monitoring needed
75
Why are thrombolytics high risk drugs
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
What is ROTEM
POC test to assess blood coagulation
77
How are antiplatelets drugs reversed
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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