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Pharma > Drugs Used In Coagulation Disorders I: Antiplatelet Agents > Flashcards

Drugs Used In Coagulation Disorders I: Antiplatelet Agents Flashcards

1
Q

What are the adverse effects of Aspirin?

A

Peptic ulcer

Bleeding

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2
Q

Does aspirin have good or bad oral absorption?

A

Good

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3
Q

How is aspirin administered?

A

Orally

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4
Q

Does aspirin have high or low plasma protein binding?

A

High

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5
Q

What does the 1st pass metabolism result in?

A

The formation of salicylic acid which is a reversible inhibitor

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6
Q

What is the dose of Aspirin when used for platelet aggregation?

A

50-200mg

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7
Q

What is the dose of aspirin when used for analgesic and antipyretic usages?

A

500mg

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8
Q

What are the clinical indications of Aspirin?

A

Pain, fever, inflammation
Primary or secondary prophylaxis of arterial thromboembolic diseases
Acute cases - unstable angina, MI, coronary angioplasty, stroke

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9
Q

What us dual anti platelet therapy?

A

ASA and P2Y12 receptor antagonist

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10
Q

What is the mechanism of action of aspirin?

A

Irreversible inhibition of COX in PLT
Resulting in decreased TXA2 and PGI2 synthesis
No platelet activation

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11
Q

What is the action of the COX enzyme?

A

Converts AA to TXA2

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12
Q

What are the activators of platelets?

A 
ADP
TXA2
Collagen
5-HT
Thrombin
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13
Q

Name the thienopyridines

A 
Ticlopidine 
Clopidogrel
Prasugrel
Ticagrelor
Cangrelor
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14
Q

What is the mechanism of action of thienopyridines?

A

They are P2Y12 receptor non-competitive antagonists at the ADP receptor on platelets - they Decrease platelet aggregation

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15
Q

What are the clinical uses of the thienopyridines?

A

Cardio and cerebrovascular circulatory problems (TIA, stroke)
Dual anti platelet therapy: ASA +
P2Y12 receptor antagonist - decrease risk of
ACS and prevent coronary stent
thrombosis

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16
Q

What are the adverse effects of thienopyridines?

A

GI problems
Minor bleeding
Rarely Leuko and thrombocytopenia (especially Ticlopidine)

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17
Q

Which thienopyridines are most likely to cause thrombocytopenia and leukopenia?

A

Ticlopidine

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18
Q

Where are the thienopyridines activated?

A

In the liver

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19
Q

Are thienopyridines prodrugs?

A

Yes

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20
Q

Do thienopyridines have good or bad absorption?

A

Good

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21
Q

How are thienopyridines eliminated?

A

Renal and fecal elimination

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22
Q

Do thienopyridines have low or high protein binding?

A

High

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23
Q

What are the CYP2C19 inhibitors?

A

Omeprazol
Fluoxetine
Fluconazole

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24
Q

What is Clopidogrel inhibited by?

A

CYP2C19

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25
Q

What is the mechanism of action of Vorapaxar?

A

PAR-1 antagonist (antagonist of the thrombin receptor)

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26
Q

What is the clinical use of Vorapaxar?

A

MI (secondary prophylaxis)

Peripheral artery thrombosis (combination with aspirin)

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27
Q

Where is Vorapaxar metabolised?

A

The liver

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28
Q

What enzyme metabolised Vorapazar?

A

CYP3A

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29
Q

How is Vorapaxar administered?

A

Orally

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30
Q

What are the contraindications of Vorapaxar?

A

Bleeding
TIA
Stroke

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31
Q

What are the side effects of Vorapaxar?

A

Bleeding

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32
Q

What are the side effects of Abciximab?

A 
Bleeding
Thrombocytopenia
Hypotension
Bradycardia
Nausea
Vomiting
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33
Q

How is Abciximab administered?

A

IV

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34
Q

What is the metabolic half life of Abciximab?

A

Short - 30mins

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35
Q

What is the biological half life/duration of action of Abciximab?

36
Q

What are the clinical indications of Abciximab?

A

PCI in coronary syndrome

37
Q

What is the mechanism of action of Abciximab?

A

GP IIb/IIIa receptor antagonist decreasing platelet aggregation
Monoclonal antibody
Irreversible antagonist

38
Q

What is the mechanism of action of Eptifibatide and Tirofiban?

A

GPIIb/IIIa receptor antagonist decreasing platelet aggregation
Synthetic competitive inhibitor

39
Q

What is the clinical use of Eptifibatide?

A

PCI in coronary syndrome

40
Q

How are Eptifibatide and Tirofiban administered?

A

Continuous IV infusion due to their very short half life

41
Q

What is the duration of action of Eptifibatide and Tirofiban?

42
Q

What is the mechanism of action of Dipyridamole and Cilostazol?

A

PDE inhibition (or adenosine uptake inhibition) leading to increased cAMP levels leading to activation of PKA

  • vasodilation
  • inhibition of platelet function
43
Q

How are Dipyridamole and Cilostazol administered?

44
Q

What is the clinical indications of Dipyridamole and Cilostazol?

A

In combination with Warfarin as primary prophylaxis of thromboembolism in patients with prosthetic valves

45
Q

What is the adverse effects of Dipyridamole and Cilostazol?

A

High does can lead to risk of coronary steal effect

46
Q

When are anti-platelet drugs effective?

A

Only in arterial thrombosis

47
Q

How do we measure PLT function?

A

Using bleeding time (not very accurate)

48
Q

What does endothelial damage result in?

A

The exposure of sub-endothelial collagen and vWF

49
Q

Where is Gp1b receptor located?

50
Q

What does Gp1b receptor on platelets bind to?

51
Q

What is the result of Gp1b adherence to vWF?

A

Platelet activation

52
Q

What are released from platelet granules?

A

ADP, 5HT, TXA2

53
Q

What does ADP bind to?

A

P2Y12 receptors resulting in platelet aggregation

54
Q

What is the result of 5HT?

A

Locally as a platelet aggregator and vasoconstrictor

55
Q

What is the result of TXA2?

A

It causes platelets to change shape, causing activation and aggregation

56
Q

Is COX2 always activated?

A

No, it is preferentially activated and expressed at sights of inflammation

57
Q

What is the result of TXA2?

A

Vasoconstriction

58
Q

What is the action of aspirin?

A

Irreversible covalent acetylation of cox

Irreversible inhibition of platelet production of TXA2 the entire life of the platelet

59
Q

How should aspirin be administered in acute MI?

A

Aspirin should be chewed or crushed so that you achieve high blood concentrations quickly

60
Q

What is the mechanism of action of thienopyridines?

A

Irreversibly blocking the ADP receptor (P2Y12) on platelets

61
Q

What is a pseudo allergy?

A

Symptoms of allergies which are not IgE mediated

62
Q

Which anti-platelet drug results in pseudo allergy?

63
Q

When is pseudo allergy more likely?

A

In patients with a history of allergies

64
Q

What is the cause of he aspirin induced pseudo Allergy?

A

Block of cox leading to increased leukotrienes

65
Q

When do we use dual anti platelet therapy

A
  1. To reduce the risk of ACS and prevent coronary stent thrombosis
  2. To reduce the long term risk of cardiovascular events in patients with peripheral artery disease
  3. Acute ST elevation MI to prevent coronary artery thrombosis
  4. Prevention of Ischemic stroke in patients with atherosclerosis and known cerebrovascular disease
66
Q

What is a side effect of ticlopidine?

A

Neutropenia and granuloytopenia

67
Q

What should you do before putting a patient on ticlopidine and after the initiation of therapy?

68
Q

What does GpIIb/IIIa bind to?

A

Fibrinogen

69
Q

What is the result of GPIIb/IIIa and fibrinogen binding?

A

Activation and cross linking of platelets leading to the formation of the platelet plug

70
Q

What type of antibody is Abciximab?

A

Monoclonal IgG

71
Q

What is a major SE of GPIIb/IIIa inhibitors?

A

Drug induced thrombocytopenia

72
Q

What should be monitored frequently in platelets using GPIIb/IIIa inhibitors?

A

Platelet count

73
Q

What I the effect of anti platelet drugs on bleeding time

A

Prolonged bleeding time

74
Q

What is the clinical significance of bleeding time?

A

Patients on anti platelet drugs

vWF disease

75
Q

What does bleeding time measure?

A

Platelet function

76
Q

What can be used as symtomatic tx of intermittent claudication?

A

Cilostazol due to its vasodilatory effects

77
Q

Is there an antidote for Thienopyridines?

78
Q

What is P2Y12?

A

It is a chemoreceptor for ADP
Gi coupled
Involved in platelet aggregation

79
Q

What is PAR1?

A

Protease activated receptor

80
Q

How is PAR1 activated?

A

Via serine proteases such as thrombin

81
Q

Which coagulation factors are vitamin K dependent?

A

Factors II, VII, IX, X, proteins C and S.

82
Q

What are the endogenous platelet activators?

A 
TxA2 
ADP
Collagen
5HT
Thrombin
83
Q

Name the type of anti platelet drugs?

A 
COX inhibitors 
P2Y12 Receptor antagonists-Thienopyridines
GPIIb/IIIa receptor antagonists
PDE inhibitors
PAR-1 antagonists
84
Q

Name the GPIIb/IIIa receptor antagonists

A

Abciximab
Eptifibatide
Tirofiban

85
Q

Name the P2Y12 receptor antagonists

A 
Ticlopidine
Clopidogrel
Prasugrel
Cangreler
Ticagrelor
86
Q

Name the PAR1 antagonist

87
Q

Name the PDE inhibitors

A

Dipyridamole

Cilostazole

Pharma (23 decks)

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