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DEN 2026 - Pharmacology > Antiplatelet Agents > Flashcards

Antiplatelet Agents Flashcards

1
Q

What is haemostasis?

A

Arrest of haemorrhage

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2
Q

What is thrombosis?

A

Pathological formation of a haemostatic plug within the vasculature in the absence of bleeding

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3
Q

Name 3 processes involved in haemostasis

A
  1. Vessel wall constriction
  2. Platelet adhesion to sub-endothelial collagen, degranulation, aggregation and plug formation
  3. Blood coagulation
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4
Q

What is Virchow’s Triad?

A

Three broad categories of factors that contribute to thrombosis

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5
Q

What are the 3 categories which make up Virchow’s Tried?

A
  1. Stasis of blood flow
  2. Endothelial injury
  3. Hypercoagulability
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6
Q

Name 3 types of anti-platelet agents

A
  1. Cyclo-oxygenase inhibitors
  2. ADP receptor pathway inhibitors
  3. Phosphodiesterase inhibitors
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7
Q

What is the function of anti-platelet drugs?

A

Decrease platelet aggregation and inhibit thrombus formation in the arterial circulation

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8
Q

What do anti-platelet drugs work on the arterial circulation?

A

In fast-flowing vessels thrombi are composed of platelets with little fibrin

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9
Q

What 3 substances released by platelets promote aggregation?

A
  1. ADP
  2. Thromboxane A2 (TXA2)
  3. Serotonin (5-HT)
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10
Q

What substance released by the endothelium inhibits platelet aggregation?

A

Prostaglandin I2 (PGI2)

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11
Q

Name the 3 pathways of coagulation?

A
  1. Extrinsic
  2. Intrinsic
  3. Common
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12
Q

How is the formation of PGH2 catalysed?

A

COX-1 and COX-2 enzymes

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13
Q

What happens to PGH2 in the blood vessel walls?

A

Converted to PGI2 in wall

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14
Q

What happens to PGH2 in platelets?

A

Converted to TXA2

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15
Q

What is the mechanism of action of aspirin as an anti-platelet?

A

Selective and irreversible inactivation of COX-1 enzymes by acetylation of serine residue

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16
Q

Why is it desirable for aspirin to inactivate COX-1 enzymes?

A

COX-1 enzymes catalyse production of PGH2 from arachidonic acid so TXA2 cannot form to cause aggregation

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17
Q

What dose of aspirin is used to provide anti-platelet function?

A

75mg

18
Q

Why does platelet function recover if aspirin is stopped, even though it is non-reversible?

A
  • Platelet lifespan is 7-10 days
  • New platelets are released often
  • New platelets are not inactivated
19
Q

Why can inhibited platelets not regenerate new COX-1 enzymes?

A

There is no nuclei present in platelet cells

20
Q

Describe 5 clinical indications for prescribing aspirin at low doses as secondary prevention measures

A
  1. Ischaemic stroke
  2. Acute coronary syndrome
  3. Post myocardial infarction
  4. Angina pectoris
  5. Atrial fibrillation
21
Q

Name 3 adverse effects of aspirin

A
  1. GI irritation
  2. Hypersensitivity reactions
  3. Reye’s syndrome in children
22
Q

How may gastric irritation be reduced in a patient taking aspirin?

A

Co-administration of acid suppressant drugs

23
Q

Name 4 interactions of aspirin

A
  1. NSAIDs
  2. Corticosteroids
  3. Anticoagulants
  4. Other anti-platelet agents
24
Q

How does ADP influence platelet function?

A
  • ADP binds to purinergic P2Y12 receptors on platelets
  • Unmasks glycoprotein GPIIb/IIIa receptors
  • Exposed to fibrinogen
  • Enhanced aggregation
25
Q

Give the main type of ADP receptor pathway inhibitors drug and two examples of this type

A

Thienopyridines (clopidogrel and prasugrel)

26
Q

How do thienopyridines function?

A

Selectively and irreversibly inhibit ADP-mediated platelet activation and aggregation

27
Q

Describe the mechanism of action of clopidogrel

A
  • Pro-drug administered orally
  • 85% hydrolysed by esterases after absorption
  • 15% undergoes 2-step oxidation in liver by CYP2C19 enzymes
  • Active metabolite selective and irreversible inhibitor of ADP-dependent platelet activation
28
Q

What are 2 clinical indications for clopidogrel?

A
  1. Secondary prevention in patients intolerant of aspirin
  2. With aspirin for 3-12 months after acute coronary syndrome and following procedures to coronary arteries to prevent thrombosis
29
Q

Name 3 adverse affects of clopidogrel

A
  1. GI irritation and bleeding
  2. Dyspepsia
  3. Hypersensitivity reactions
30
Q

When may clopidogrel cause the most GI irritation and bleeding?

A

When being co-administered with clopidogrel

31
Q

What are 4 potential drawbacks of clopidogrel?

A
  • Pro-drug means there is delayed onset of action
  • Genetic variation of liver enzymes responsible for metabolism so response varies between patient
  • Drug-drug interactions
  • Irreversible inhibition of P2Y12 receptor
32
Q

Name a drug-drug interaction of clopidogrel

A

Proton pump inhibitors influence liver enzymes which metabolise clopidogrel

33
Q

Why does prasugrel tend to be more potent and predictable than clopidogrel?

A
  • There is less dependence on enzymes in the liver to form the active metabolite as the oxidation is a one-step process
  • Metabolites form in a more consistent fashion, in higher concentrations
34
Q

When is prasugrel used?

A

Acute coronary syndrome in short term as there is a greatly increased risk of bleeding

35
Q

How does ticagrelor inhibit ADP receptor pathways?

A
  • Inhibitory allosteric modulator of P2Y12 receptor

- Inhibits G-protein signalling

36
Q

What are 3 mechanisms of dipyridamole?

A
  • Thromboxane synthase inhibitor [THA2 decreases]
  • Phosphodiesterase inhibitor [cAMP increases]
  • Inhibition of reuptake and metabolism of adenosine
37
Q

What is the use of increasing cAMP concentration?

A

Less platelets are active

38
Q

What is the use of decreasing reuptake and metabolism of adenosine?

A

Adenosine has a vasodilatory effect and inhibits platelet activity so reduced uptake reduces clearance rate

39
Q

What are 2 clinical indications of dipyridamole?

A
  1. Co-administration with aspirin for secondary prevention of ischaemic stroke
  2. Co-administration with oral anticoagulants for prevention of thromboembolism in patients with prosthetic heart valves
40
Q

Name 3 adverse effects of dipyridamole

A
  1. GI irritation and bleeding
  2. Dizziness / flushing
  3. Hypersensitivity reactions

DEN 2026 - Pharmacology (22 decks)

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