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CPT > Antiplatelets and Fibrinolytics > Flashcards

Antiplatelets and Fibrinolytics Flashcards

1
Q

Compare arterial and venous thrombi in terms of fibrin and platelet count

A

Arterial (at site of atherosclerotic plaque);

  • Low fibrin content
  • High platelet content

Venous (stasis of blood);

  • High fibrin content (and RBC)
  • Low platelet content
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2
Q

Describe what happens at a healthy endothelium with regards to platelet aggregation

A
  • PGI2/ Prostacyclin produced by endothelial cells
  • PGI2 binds to platelet receptors causing an increase in cAMP
  • cAMP inhibits the release of sequestered Ca into platelet’s cytosol, thus reducing platelet aggregation
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3
Q

How does PGI2 affect GP IIb/ IIIa receptors?

A

Stabilises them

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4
Q

Platelet adhesion-> platelet activation-> platelet aggregation-> platelet plug

What causes platelet adhesion

A

Exposure of blood to sub-endothelial factors (Collagen, VWF)

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5
Q

Describe platelet activation and aggregation

A
  • Platelets adhere to each other, activate and change shape causing the release of granules (ADP, Thromboxane A2, Thrombin, Platelet Activation factor)
  • These act via their respective receptors to increase cytosolic Ca and promote further granule release
  • Granules also activate GPIIb/IIIa receptors using fibrinogen, forming bonds between platelets
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6
Q

What drugs are used to treat;

  • Platelet rich arterial thrombi
  • Low platelet venous thrombi
A

Arterial- Antiplatelet and Fibrinolytic drugs
Venous- Anticoagulants (parental and oral)

(Can use a combination e.g in secondary prevention)

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7
Q

What colour are arterial and venous thrombi?

A

Arterial- White

Venous- Red

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8
Q

What is the most potent platelet aggregator factor?

A

Thromboxane A2 (TXA2)

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9
Q

List 4 antiplatelet drug classes

A
  • Cyclo-oxygenase inhibitors
  • ADP receptor antagonists
  • Phosphodiesterase inhibitors
  • GPIIb/IIIa inhibitors
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12
Q

Is aspirin reversible?

Do we use low or high doses for antiplatelet effects?

A

No

Low doses (High for analgesic effects)

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13
Q

Higher doses of Aspirin inhibit endothelial PGI2

Describe its absorption and metabolism

A

Absorbed by passive diffusion, metabolised in liver into Salicylic acid

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14
Q

List 4 ADRs of Aspirin

A
  • GI Irritation
  • GI Bleeding (peptic ulcer)
  • Haemorrhage (stroke)
  • Hypersensitivity
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15
Q

List 3 contraindications of Aspirin

A
  • Reye’s Syndrome (can cause liver and brain damage)
  • Hypersensitivity
  • Trimester 3 pregnancy (premature DA closure)
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16
Q

List important DDIs of aspirin

A

Caution with other antiplatelets and anticoagulants

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17
Q

Why may aspirin have a lack of efficacy in some patients?

A

Due to COX1 polymorphism in individuals

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18
Q

Why does Aspirin not completely inhibit platelet aggregation?

Why does aspirin’s antiplatelet effects last for the entire lifespan of the platelet? (7-10 days)

A
  • Half life of only 20 min, rapidly metabolised-> Salicylic acid (no effect on COX)
  • Platelets cannot generate new COX
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19
Q

What aspirin course would you give to patients;

  • With a STEMI/ NSTEMI
  • With acute ischaemic stroke
A

NSTEMI/ STEMI: One loading dose of 300mg

Acute ischaemic stroke: 300mg daily for 2 weeks

20
Q

Why can Aspirin irritate the stomach?

How is this covered against when prescribing long term use of aspirin?

A
  • Inhibit COX1 in gastric mucosa-> Reduced prostaglandin production
  • Provide gastric protection (e.g a Proton pump inhibitor)
21
Q

Clopidogrel, Prasugrel and Ticagrelor are all a member of what class of drugs?

How do these work?

A
  • ADP receptor antagonists

- Inhibit ADP binding to P2Y12 receptor-> Inhibit activation of GPIIb/IIIa receptors-> Inhibit platelet aggregation

22
Q

List 2 common features of Clopidogrel and Prasugrel

A
  • Are both Prodrugs

- Are both irreversible P2Y12 inhibitors

23
Q

Compare Clopidogrel, Prasugrel and Ticagrelor with regards to onset of action

A

Clopidogrel- Slow onset of action, unless initial loading dose given

Prasugrel & Ticagelor- Rapid onset of action

24
Q

List 2 features of Ticagrelor that are distinguish it from Clopidogrel and Prasugrel

A
  • Is active itself AND has active metabolites

- Reversible action (at a different site to Clopidogrel)

25
Q

List 3 ADRs of ADP Receptor Antagonists

State 3 contraindications of these drugs

A
  • GI bleeding
  • GI Upset (Dyspepsia + diarrhoea)
  • Rarely, thrombocytopenia

Caution in patients;

  • at high risk of bleeding
  • with renal and hepatic impairment
  • using other antiplatelets/ anticoagulants
26
Q

List important DDIs of ADP receptor antagonists

A

Clopidogrel;
- Avoid drugs that inhibit the CYP enzymes needed to activate (Erythromycin, some SSRIs, Omeprazole, Ciprofloxacilin)

Ticagrelor;
- Interacts with CYP inducers & inhibitors

27
Q

How many days prior to surgery should Aspirin, Clopidogrel and Prasugrel be stopped?

Why?

A

7-10 days

Due to their effects being irreversible, can lead to bleeding during surgery

28
Q

Clopidogrel can be used as a monotherapy, where aspirin is contraindicated.

Suggest courses for NSTEMI and STEMI patients

A

NSTEMI: up to 3 months
STEMI: up to 4 weeks

29
Q

Suggest 2 drugs that can be taken with Aspirin in a patient who had an MI, for upto 12 months

A

Prasugrel and Ticagrelor

30
Q

What class of drug is Dipyridamole?

In what 2 ways does this drug work?

A
  • Phosphodiesterase inhibitors
  • Inhibits cellular reuptake of Adenosine, so increased [plasma adenosine]-> Platelet aggregation inhibited via adenosine A2 receptors
  • Inhibits phosphodiesterase, leading to reduced cAMP degradation. Thus inhibits activation of GPIIb/IIIa receptors
31
Q

List 2 ADRs and DDIs of Dipyridamole

A
  • Vomiting + diarrhoea
  • Dizziness
  • Use of other antiplatelets/ anticoagulants
  • Adenosine
32
Q

Suggest 2 uses of Dipyridamole

A
  • Secondary prevention of ischaemic stroke/ TIAs

- Adjunct for prophylaxis of thromboembolism following valve replacement

33
Q

What class of drug is Abciximab?

How does it work?

A
  • GPIIb/IIIa inhibitor

- Blocks binding of Fibrinogen and VWF (more complete as it targets final part of aggregation pathway)

34
Q

Describe the administration and use of abciximab

A
  • Administered IV

- Used only in very specific circumstances (Percutaneous Transluminal Coronary Angioplasty)

35
Q

What class of drugs are Streptokinase and Alteplase?

How do they work?

A
  • Fibrinolytic agents/ ‘Clot busters’

- Promote activation of Plasminogen to Plasmin, which breaks down Fibrin

36
Q

Describe the use of Alteplase and Steptokinase

A

Steptokinase- Can only be used once as antibodies develop

Alteplase;

  • In acute ischaemic stroke <4.5 hours from when symptoms start
  • Acutely following a STEMI diagnosis (vs a Primary PCI)
37
Q

List an ADR and DDI of Fibrinolytic agents

A
  • Bleeding

- Caution with use of other antiplatelets/ anticoagulants

38
Q

How does Tranexamic acid work?

Suggest 2 uses

A
  • Inhibits Fibrinolysis, thus stopping bleeding
  • Nosebleeds
  • Heavy, persistent period bleeding
39
Q

What is Primary PCI (Percutaneous Coronary Intervention)?

A

Insertion of a Catheter via Femoral artery, though Aorta to reach occluded coronary vessel, where a stent can be placed to leave it patent

40
Q

When should Primary PCI be used instead of a Fibrinolytic?

Primary PCI saves more muscle tissue

A

If;
- Presentation is within 2 hours of symptom onset
AND
- Primary PCI can be done within 120 mins of the time where a Fibrinolytic could’ve been given

41
Q

What do you offer to all patients post MI once haemodynamically stable?

A

ACE inhibitors

42
Q

List an ADR and a DDI for abciximab

A
  • Bleeding (dose adjusted for body weight)

- Caution with use of other antiplatelets/ anticoagulants

43
Q

Name a Cyclo-oxygenase inhibitor

How do these work as antiplatelets?

A
  • Aspirin

- Inhibit COX1, which produces TXA2 from Arachidonic acid (thus reduced platelet aggregation)

CPT (19 decks)

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