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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
Antithrombin III main function?
important inhibitor of coagulation
26
Action of antithrombin III?
neutralises serine protease factors (II, VII, IX, X) in coagulation cascade
27
Heparin mechanism?
binds to antithrombin III, increasing its affinity for serine protease factors, increasing the rate of clotting factor inactivation
28
What does heparin need to bind to to inhibit IIa (thrombin)?
Antithrombin III and IIa
29
What does heparin need to bind to to inhibit Xa
Antithrombin III
30
Examples of LMWHs?
enoxaparin, dalteparin
31
What do LMWHs inhibit?
factor Xa but not IIa (thrombin)
32
Heparin administration?
IV - immediate action | Subcutaneous - 1hr delay
33
How are LMWHs excreted?
Renal excretion
34
Adverse affects of heparin and LMWHs?
haemorrhage osteoperosis (long term treatment) hypoaldosteronism hypersensetivity reactions
35
How to reverse heparin effects?
protamine sulphate
36
Orally active inhibitor action?
directly inhibits thrombin or Xa, to prevent venous thrombosis
37
Example of orally active inhibitor?
dabigatran etexillate
38
Advantages of orally active inhibitors?
administration convenience | predictable degree of anticoagulation
39
Disadvantages of orally active inhibitors?
No agent to reverse haemorrhage in overdose
40
Anti platelets act on which type of thrombosis?
arterial thrombosis
41
Anti coagulants act on which type of thrombosis?
Venous thrombosis
42
How to platelets attach to damaged vessels?
via surface glycoproteins and von williebrand factor (acts as a bridge)
43
Aggregation occurs due to which molecules?
``` 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
How do glycoproteins cross link platelets in platelet aggregation?
via fibrinogen
45
Acidic phospholipid exposure on platelet surface promotes the formation of?
Thrombin IIa - which stimulates further platelet aggregation
46
how is the mass of platelets stabilised?
Through the conversion of fibrinogen to fibrin
47
What is the role of ADP in platelet aggregation?
attracts more platelets
48
Role of TXA2 in platelet aggregation?
promotes platelet aggregation, degranulation and vasoconstriction
49
What is released when platelets degranulate due to TXA2?
more ADP and TXA2
50
Platelet aggregation mainly occurs in which form of clot formation?
haemostasis
51
What is the main anti platelet drug in use?
aspirin
52
how does aspirin work as an anti platelet?
blocks COX and prevents TXA2 synthesis | inhibits prostaglandin I2 production (TXA2 precursor)
53
side effects of aspirin?
GI bleeding and ulceration
54
Clopidogrel function?
links to P2Y12 receptor - irreversible inhibition
55
When is clopidogrel normally used?
when a patient is intolerant of aspirin
56
Aspirin administration?
normally oral
57
Clopidogrel administration?
oral
58
Tirofiban used when?
MI prophylaxis in high risk CV patients with unstable angina
59
Tirofiban short or long term drug?
short term
60
Tirofiban administration?
IV
61
plasminogen and fibrinolytic drugs act against what?
the coagulation cascade
62
What is the role of plasmin?
dissolves fibrin converting it into fibrin filaments
63
Plasminogen and fibrinolytic drugs act to do what?
reopen occluded arteries in acute MI or stroke
64
Administration of plasminogen and fibrinolytic drugs?
IV asap
65
What is preferred to the use of plasminogen and fibrinolytic drugs?
PCI if prompt
66
What does PCI entail?
non-surgical widening of coronary artery with stent placement after dilatation
67
What drug should be administered alongside PCI?
aspirin
68
Adverse effects of streptokinase?
Antibodies block action after 4 days | can cause allergies
69
When is streptokinase contraindicated?
In recent strep infection patients
70
What is alteplase (and duteplase)?
recombinant tissue plasminogen activator (rt-PA)
71
Benefits of alte/ duteplase?
no allergies
72
Administration of Alte/ duteplase?
short half life so IV infusion
73
MAJOR fibrinolytic adverse side effect?
haemorrhage
74
Control of haemorrhage due to fibrinolytic?
tranexamic acid - inhibits plasminogen activation

Anticoagulants, antiplatelets & Thrombolytics (1 decks)

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