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ESA 5 - Pharmacology > Anti-Platelet Agents and Anticoagulants > Flashcards

Anti-Platelet Agents and Anticoagulants Flashcards

1
Q

What can abnormal haemostasis lead to?

A
  • Thrombosis
  • Embolism
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2
Q

What kind of clots form in the arterial system?

A

White clots

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3
Q

What might arterial clots lead to?

A
  • MI
  • CVA
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4
Q

How are arterial clots treated?

A
  • Antiplatelets
  • Thrombolysis
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5
Q

What kind of clots form in the venous system?

A

Red clots

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6
Q

What might venous clots lead to?

A
  • DVT
  • PE
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7
Q

How are venous clots treated?

A

Anti-coagulation

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8
Q

What are the components of Vircow’s Triad?

A
  • Hypercoagulability
  • Endothelial damage
  • Stasis
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9
Q

What are the categories of causes of hypercoaguability?

A
  • Genetic
  • Aquired
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10
Q

What are the genetic causes of hypercoaguability?

A
  • Protein C and S deficiency
  • Factor V Leiden
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11
Q

What are the acquired causes of hypercoaguability?

A
  • Antiphospholipid syndromes
  • Oral contraceptive pill
  • Smoking
  • Malignancy
  • Prosthetic heart valves
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12
Q

What can cause endothelial damage?

A
  • Atheroma
  • Hypertension
  • Toxins
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13
Q

Give two examples of toxins that could lead to endothelial damage

A
  • Cigarettes
  • Homocysteine
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14
Q

What can cause stasis?

A
  • Immobility
  • Cardiac abnormality
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15
Q

Give three things that might cause immobility

A
  • Ill-health
  • Post-op
  • Flights
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16
Q

Give 4 things that might cause cardiac abnormality

A
  • Atrial fibrillation
  • Congestive heart failure
  • Mitral valve disease
  • Post MI
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17
Q

What class of drug if warfarin?

A

Coumarin

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18
Q

What is the mechanism of action of warfarin?

A

It stops the conversion of vitamin K to its active reduced form, and therefore inhibits the production of vitamin K dependant clotting factors

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19
Q

What clotting factors are affected by warfarin?

A
  • II (prothrombin)
  • VII
  • IX
  • X
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20
Q

Precisely what enzymes does warfarin act on?

A
  • Vitamin K epoxide reductase
  • Vitamin K reductase
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21
Q

What effect does warfarin have on the enzymes it acts on?

A

They are competitive inhibitors

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22
Q

What is the clinical relevance of warfarin being a competitive inhibitor?

A

It means you can overcome the action of warfarin by increasing vitamin K

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23
Q

How long does the onset of action of warfarin take?

A

Days

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24
Q

Why does the onset of action of warfarin take days?

A

Due to the slow turnover of clotitng factors, resulting from their long half life - warfarin can only act on newly produced clotting factors, not already active clotting factors in the blood, and so it doesn’t have an effect until these clotting factors have been broken down

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25
Q

Where is warfarin absorbed?

A

In the GI tract

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26
Q

What does the level of reduction in vitamin K dependant factors depend on?

A

The dose

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27
Q

How is warfarin metabolised?

A

Hepatically

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28
Q

What is the result of the good GI absorption of warfarin?

A

It can be given orally, and therefore is the preferred choice for long term anti-coagulation

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29
Q

What is the result of the slow onset of action of warfarin?

A

It needs heparin to cover initially

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30
Q

What is the half life of warfarin?

A

48 hours, but variable

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31
Q

What is the result of the slow offset of warfarin?

A

Need to stop about 3 days before surgery, as need time to synthesise new clotting factors to mitigate against the possibility of bleeding

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32
Q

What is the clinical relevance of warfarin being heavily protein bound?

A

You must exercise caution with drugs that displace it

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33
Q

What enzymes are involved in the metabolism of warfarin?

A

The cytochrome P450 system

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34
Q

What caution should be taken due to the metabolism of warfarin?

A
  • Caution in liver disease
  • Caution if used with drugs that affect P450 system
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35
Q

Why should warfarin not be given in pregnancy?

A

It crosses the placenta and is teratogenic in the 1st trimester, and causes brain haemorrhage during delivery in the 3rd trimester

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36
Q

How is warfarin monitored?

A
  • Monitor extrinsic pathway factors
  • Measure prothrombin time
  • Monitor the international normalised ratio
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37
Q

What is prothrombin time?

A

Citrated plasma clotting time after adding calcium and thromboplastins

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38
Q

What does the INR allow for?

A

A standard value between labs

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39
Q

What is the INR corrected for?

A

Different lab thromboplastins reagants

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40
Q

What are the categories of drugs that interact to increase warfarins action?

A
  • Drugs that inhibit hepatic metabolism
  • Drugs that inhibit platelet function
  • Drugs that reduce vitamin K from gut bacteria

Albumin displacement and drugs that decrease GI absorption of vitamin K have a lesser effect

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41
Q

Give 5 drugs that inhibit hepatic metabolism

A
  • Amiodarone
  • Quinolone
  • Metronidazole
  • Cimetidine
  • Alcohol
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42
Q

Give a drug that inhibits platelet function

A

Aspirin

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43
Q

Give a drug that reduces vitamin K from gut bateria

A

Cephalosporin antibiotics

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44
Q

Give a class of drugs that cause albumin displacement of warfarin

A

NSAIDs

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45
Q

Give three examples of drugs that inhibit warfarin

A
  • Antiepileptics, except Na valproate
  • Rifampicin
  • St Johns Wort
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46
Q

How do most drugs inhibiting warfarin act?

A

By inducing hepatic enzymes thereby increasing the metabolism of warfarin

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47
Q

What are the indiciations for warfarin?

A
  • Deep vein thrombosis
  • Pulmonary embolism
  • Atrial fibrillation
  • Mechanical prosthetic valves
  • Patients with recurrent thromboses on warfarin
  • Thrombosis associated with inherited thrombophilia conditions
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48
Q

How long should warfarin treatment be given for after DVT?

A

3-6 months

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49
Q

How long should warfarin treatment be given for after a PE?

A

6 months

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50
Q

How long should warfarin treatment be given with atrial fibrillation?

A

Until risk > benefit

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51
Q

What INR range should be aimed for with DVT, PE, and atrial fibrillation?

A

2.0-3.0

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52
Q

What INR range should be aimed for in patients with mechanical prosthetic valves, recurrent thromboses on warfarin, and thrombosis associated with inherited thrombophilia conditions?

A

2.5-4.5

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53
Q

What are the adverse effects of warfarin?

A
  • Teratogenic
  • Bleeding/bruising
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54
Q

What sites might there be bleeding or bruising as an adverse effect of warfarin?

A
  • Intracranial
  • Epistaxis
  • Injection
  • GI loss
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55
Q

How can warfarin therapy be reversed?

A
  • Parenteral vitamin K
  • Fresh frozen plasma
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56
Q

What are the steps in prescribing warfarin?

A
  1. Indication for need
  2. PMH, e.g. PUD, SAH, bleeding disorder
  3. Medication interactions
  4. Age, mobility, falls risk score
  5. Review blood tests
  6. Consider loading dose and heparin cover
  7. Prescribe
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57
Q

Why do you need to establish a falls risk score before prescribing warfarin?

A

Because the risk of bleeding from falls is greater than the condition treated by warfarin

58
Q

What do you need to consider regarding blood tests before prescribing warfarin?

A
  • LFTs
  • Plt
  • INR
59
Q

Why do you need to check INR before starting warfarin?

A

Have to make sure you’re starting at 1

60
Q

What things need to be discussed with the patient prior to starting warfarin?

A
  • Side effects
  • Interactions
  • INR monitoring
  • Give patient anticoagulant card
61
Q

What should be discussed with the patient regarding side effects of warfarin?

A
  • The risk of bleeding, and when to consult a doctor
  • The teratogenic effects, if the patient is young and female
62
Q

What needs to be discussed with the patients regarding interactions with warfarin?

A
  • Other medications - may have to start or stop
  • May interact with over the counter drugs
  • May interact with alcohol and cranberry/grapefruit juice
63
Q

How often is a patients INR monitored on warfarin?

A

Every 1-4 weeks

64
Q

When might warfarin treatment reversal be required?

A
  • Overdose
  • Complications
  • High INR
65
Q

What should be considered when thinking about initiating warfarin reversal?

A
  • Bleeding
  • INR
  • Indication
  • If the patient has a mechanical valve, call cardiologist for advice
66
Q

What agents are used in warfarin reversal?

A
  • IV vitamin K
  • Prothrombin complex concentrate
  • Fresh frozen plasma
67
Q

How long does IV vitamin K affect re-warfarinisation?

A

6 weeks

68
Q

Why is fresh frozen plasma helpful in warfarin reversal?

A

It contains active clotting factors

69
Q

What should be done when the INR is >3.0 and <6.0 if the target is 2.5, or >4.0 and <6.0 if the target is 3.5, and there is no bleeding?

A
  • Reduce the warfarin dose, or stop
  • Restart warfrin when INR <5.0
70
Q

What should be done when INR >6.0 and <8.0, and there is no bleeding or minor bleeding?

A

Stop warfarin, and restart when INR <5.0

71
Q

What should be done when the INR is <8.0, and there is no bleeding or minor bleeding?

A
  • Stop warfarin
  • Restart warfarin when INR <5.0
  • If there is other risk factors for bleeding, give 0.5-2.5mg of vitamin K (oral)
72
Q

What should be done if there is major bleeding on warfarin?

A
  • Stop warfarin
  • Give prothrombin complex - concentrate 50 units/kg or FFP 15ml/kg (if complex not available)
  • Give 5mg of vitamin K (oral or IV)
73
Q

Describe the structure of heparins

A

They are glycosaminoglycans, with a glucose backbone, and one of 5 different groups on each glucose, some with sulphate

74
Q

What are heparins produced by?

A

Mast cells

75
Q

What is the mechanism of action of heparins?

A

They activate anti-thrombin III via a unique pentasaccharide sequence, which deactivates factor Xa and IIa mainly, and also IXa

76
Q

What are the types of heparin molecules?

A
  • Unfractionated heparin
  • Low molecular weight heparins
77
Q

How are unfractionated heparins administered?

A
  • Intravenously (continuously)
  • Occasionally, subcutaneous
78
Q

When is unfractionated heparin given subcutaneously?

A

Prophylaxis

79
Q

How are low molecular weight heparins administered?

A

Subcutaneous

80
Q

What is the molecular weight of low molecular weight heparins?

A

3-4kDa

81
Q

What is the molecular weight of unfractionated heparin?

A

Variable - 12-15kDa

82
Q

What is unfractionated heparin composed of?

A

A mix of variable long length heparin chains

83
Q

What is the mechanism of action of unfractionated heparin?

A

It has a unique pentasaccharide sequence which binds to anti-thrombin III. This causes a conformational change and increased AT III activity. AT III inactivates thrombin and factor Xa

84
Q

How do unfractionated heparin and low MW heparin differ in their mechanism of action?

A

To catalyse inhibition of IIa by AT III, heparin needs to bind simultaneously to IIa and AT III. Unfractionated heparin is large enough to do this, but low MW heparin is too small.

85
Q

What do the mechanisms of action of unfractionated heparin and low MW heparin have in common?

A

Both produce Xa inhibition by AT III, as this mechanism only needs heparin to bind to AT III

86
Q

How many saccharide units are there in low molecular weight heparin?

A

<18, usually about 15

87
Q

Describe the pharmacokinetics of low molecular weight heparin

A
  • Absorbed more uniformly
  • High bioavailability - <90%
  • Long biological half life
  • More predictable dose response
88
Q

Why do low molecular weight heparins have a more predictable dose response?

A

Because they do not bind to macrophages, endothelial cells, or plasma proteins

89
Q

What is the result of the more predictable dose response of low molecular weight heparins?

A

Means that you can prescribe using patients weight, and don’t have to monitor using blood tests

90
Q

What is the mechanism of action of low molecular weight heparin?

A

It has a unique sequence that binds to anti-thrombin III which affects factor Xa specifically

91
Q

How is low molecular weight heparin cleared?

A

By the kidneys

92
Q

What is the result of low molecular weight heparin being cleared by the kidneys?

A

Have to take care in renal failure

93
Q

Is unfractionated or low molecular weight heparin more likely to cause thrombocytopenia?

A

Unfractionated

94
Q

Give 5 examples of selective factor Xa inhibitors

A
  • Fondaparinux
  • Idaparinux
  • Rivaroxaban
  • Apixaban
  • Edoxaban
95
Q

What effect do selective factor Xa inhibitors have on thrombin?

A

None

96
Q

How do selective factor Xa inhibitors achieve their action?

A

They bind to antithrombin III via pentasaccharide, which is sufficient to inactive Xa

97
Q

Give 5 examples of direct thrombin inhibitors

A
  • Bivalirudin
  • Desirudin
  • Lepirudin
  • Argatroban
  • Dabigatran
98
Q

What effect to direct thrombin inhibitors have on factor Xa?

A

None

99
Q

Why are selective factor Xa inhibitors and direct thrombin inhibitors being used increasingly?

A
  • Less side effects
  • Don’t need as much monitoring
100
Q

Why must heparin be administered parenterally?

A

Poor GI absorption

101
Q

What are the advantages of low molecular weight heparin over unfractionated heparin?

A
  • Predictable dose response
  • Predictable bioavailability
102
Q

Why is the bioavailability of unfractionated heparin variable?

A

Due to unpredictable binding to cells and proteins

103
Q

How is unfractionated heparin adminstered?

A

IV

104
Q

How is low molecular weight heparin administered?

A

SC

105
Q

How is unfractionated heparin initiated?

A

Bolus and then intravenous infusion

106
Q

How is low molecular weight heparin initiated?

A

OD/BD

107
Q

Why is unfractionated heparin often chosen over low molecular weight heparin?

A

As it can be monitored using the APTT test - LMWH has little effect on APTT

108
Q

What is used for peri-operative prevention of thromboembolism?

A

Low dose of LMWH

109
Q

Why is heparin used to cover warfarin to cover the risk of thrombosis around times of operation?

A

Because it’s quick offset time allows for its cessation if bleeding

110
Q

How is warfarin used in the treatment of DVT, PE, and AF?

A

It is administered prior to warfarin to provide quick onset, to cover the patient whilst the warfarin loading is achieved

111
Q

What type of heparin is used in the treatment of DVT, PE, and AF?

A

LMWH, unless fine control is required, then use unfractionated and monitoring

112
Q

What acute coronary syndromes might heparin be used in the treatment of?

A
  • MI
  • Unstable angina
113
Q

What is the aim of heparin treatment in acute coronary syndromes?

A

Reduces recurrence/extension of coronary artery thrombosis

114
Q

What kind of heparin is used in acute coronary syndromes?

A

Usually LMWH

115
Q

Describe the use of heparin in pregnancy

A

Can be used cautiously in pregnancy in the place of warfarin

116
Q

What are the adverse effects of heparin?

A
  • Bruising/bleeding
  • Thrombocytopenia
  • Osteoporosis
117
Q

What are the potential bruising/bleeding sites in heparin use?

A
  • Intracranial
  • Injection sites
  • Gastrointestinal loss
  • Epistaxis
118
Q

What kind of condition is thrombocytopenia?

A

Autoimmune

119
Q

What could result from thrombocytopenia?

A

Bleeding or serious thrombosis

120
Q

What is the pathological process of thrombocytopenia?

A

Heparin and PF4 on the platelets surface are immunogenic. Immune complexes activate more platelets, release more PF4, forms more IgG and complexes, and leads to depletion of platelets and thrombosis

121
Q

What is the platelet count in thrombocytopenia?

A

<100, or a 50% reduction

122
Q

What action should be taken when a patient presents with thrombocytopenia?

A
  • Lab assay for the antibodies
  • Stop heparin, add hirudin
123
Q

How is heparin therapy reversed?

A

Protamine sulphate

124
Q

What is the mechanism of action of protamine sulphate in reversal of heparin therapy?

A

Dissociation of heparin from anti-thrombin III by irreversibly binding to heparin

125
Q

Why might heparin therapy need to be reversed?

A

Allergy/anaphylaxis

126
Q

Give 4 anti-platelet drugs

A
  • Aspirin
  • Dipyridamole
  • Clopidogrel
  • Glycoprotein IIb/IIIa inhibitors
127
Q

What are the stages in thrombotic occlusion caused by platelets?

A
  1. Plaque fissure/rupture
  2. Platelet adhesion
  3. Platelet activation
  4. Platelet aggregation
  5. Thrombotic occlusion
128
Q

What stages in the development of a thrombotic occlusion due to platelets do anti-platelet drugs act?

A
  • Platelet adhesion
  • Platelet activation
  • Platelet aggregation
129
Q

How does aspirin act as an anti-platelet drug?

A

It inhibits COX1 by covalent acetylation of serine

130
Q

What is the result of the irreversible inhibition of COX1 by aspirin in platelet therapy?

A

You need to generate new platelets for them to start working again

131
Q

Give three examples of Gp IIb/IIIa inhibitors

A
  • Abciximab
  • Tirofiban
  • Epitifibatide
132
Q

How do Gp IIb/IIIa inhibitors act as anti-platelet therapy?

A

It decreases platelet crosslinking by fibrinogen

133
Q

What are the uses of glycoprotein IIb/IIIa receptors?

A
  • High risk ACS
  • Post PCI
134
Q

What are the advantages of using glycoprotein IIb/IIIa receptors post PCI?

A

Decreases acute thrombosis and re-stenosis

135
Q

What are the disadvantages of using glycoprotein IIb/IIIa receptor antagonists post PCI?

A

Increase bleeding complications

136
Q

What is the mechanism of action of clopidogrel, prasugrel, and ticagrelor?

A

They block P2Y12, which reduces P2Y12 receptor mediated decrase in cAMP, therefore reducing aggregation

137
Q

What is ticlodipine no longer used?

A

Due to adverse effects, e.g. on the bone marrow

138
Q

What are the cardiac indications for clopidogrel, prasugrel, and ticagrelor?

A
  • Acute coronary syndrome
  • Percutaneous intervention
139
Q

What is the mechansim of action of dipyridamole?

A

Probably phosphodiesterase inhibitor

140
Q

What are the adverse effects of dipyridamole?

A
  • Flushes
  • Headaches
141
Q

Why does dipyridamole cause flushes and headaches?

A

Because it is a positive ionotrope and vasodilatory

142
Q

What is dipyridamole used for?

A

Secondary prevention of stroke

ESA 5 - Pharmacology (28 decks)

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