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Antiplatelet and fibrinolytic drugs Flashcards

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1
Q

Give an overview of thromboembolic diseases

A
  • Thromboembolic diseases are common
  • E.g. deep vein thrombosis and pulmonary embolism
  • Consequence of AF
  • Can result in TIAs, ischaemic stroke, MI
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2
Q

What is the difference between a thrombus and an embolus?

A
  • A thrombus is a clot adhered to a vessel wall
  • An embolus is an intravascular clot distal to the site of origin
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3
Q

What is venous thrombosis associated with?

A
  • Stasis of blood
  • Damage to veins
  • Less likely to see endothelial damage
  • High red blood cell and fibrin content
  • Low platelet content, evenly distributed
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4
Q

Outline arterial thrombosis

A
  • Usually forms at site of atherosclerosis following plaque rupture
  • Lower fibrin content and much higher platelet content
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5
Q

What is Virchow’s triad?

A
  • Reduced blood flow
  • Increased coagulability
  • Blood vessel injury
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6
Q

What can cause reduced blood flow?

A
  • Atrial fibrillation
  • Long distance travel
  • Varicose veins
  • Venous obstruction
  • Immobility
  • Ventricular/venous insufficiency
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7
Q

What can cause blood vessel injury?

A
  • Trauma
  • Orthopaedic or major surgery
  • Hypertension
  • Invasive procedures
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8
Q

What can cause increased coagulability?

A
  • Sepsis
  • Smoking
  • Coagulation disorders
  • Malignancy
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9
Q

Outline platelet activity in healthy endothelium

A
  • Prostacyclin (PGI2) produced and released by endothelial cells
  • Inhibits platelet aggregation
  • PGI2 binds to platelet receptors
  • Increases cAMP concentration in platelets
  • Causes decreased Ca2+
  • Prevents platelet aggregatory agents
  • Stabilises inactive GP IIb/IIIa receptors
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10
Q

What is the average lifespan of a platelet?

A
  • 8-10 days
  • 10% replaced each day
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11
Q

Outline how a thrombus is formed

A
  • Atherogenic pathway
  • Fibrous cap
  • Plaque rupture
  • Thrombus formation
  • Platelet adhesion at damaged endothelium
  • Extensive cascade of signalling molecules
  • Recruitment of more platelets
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12
Q

How are platelets activated?

A
  • Release of platelet granules
  • GPIIb/IIIa receptors and fibrinogen
  • Increases Ca2+ and decreases cAMP in platelets
  • Cascade and amplification from platelet to platelet
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13
Q

What are some examples of platelet granules?

A
  • ADP
  • Thromboxane A2
  • Serotonin
  • Platelet activation factor
  • Thrombin
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14
Q

What drugs do we use to target platelet-rich, white arterial thrombi?

A
  • Antiplatelet
  • Fibrinolytic drugs
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15
Q

What drugs do we use to target red venous thrombi?

A
  • Parenteral anticoagulants
  • Oral anticoagulants
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16
Q

Give examples of cyclo-oxygenase inhibitors

A
  • Aspirin
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17
Q

Outline thromboxane A2

A
  • Potent platelet aggregating agent
  • Formed from arachidonic acid by COX 1
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18
Q

What is the mechanism of action of cyclo-oxygenase inhibitors such as aspirin?

A
  • Inhibits COX-1 mediated production of thromboxane A2
  • Reduces platelet aggregation
  • Irreversible
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19
Q

Why does aspirin not completely inhibit platelet aggregation?

A
  • Other aggravating factors
  • Doesn’t irreversibly inhibit COX 1 in every patient
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20
Q

What is the low non-analgesic dose of aspirin?

A
  • 75 mg
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21
Q

What is the loading dose of aspirin used in acute coronary syndromes?

A
  • 300 mg
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22
Q

Which other part of clotting is affected by higher doses of aspirin?

A
  • Inhibits endothelial prostacyclin
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23
Q

How is aspirin absorbed into the body?

Study These Flashcards
A
  • Absorbed by passive diffusion
  • Hepatic hydrolysis to salicylic acid
24
Q

What are the adverse side effects of aspirin?

Study These Flashcards
A
  • Gastrointestinal irritation
  • GI bleeding (peptic ulcer)
  • Haemorrhage (stroke)
  • Hypersensitivity
25
What are the contraindications of aspirin?
- Reye's syndrome - avoid until <16 years - Hypersensitivity - 3rd trimester (leads to premature closure of ductus arteriosus) - Caution with other antiplatelets/anticoagulants
26
What causes a lack of efficacy of aspirin in some people?
- COX-1 polymorphisms - People produce different quantities of COX-1
27
Why does the antiplatelet effect of aspirin only last 7-10 days?
- 7-10 days is lifespan of a platelet - Platelets don't have nuclei - So they can't make more COX-1 to replace the COX-1 that is irreversible bound to aspirin
28
What are some aspirin indications?
- Some AF patients after stroke - Secondary prevention of stroke and TIA - Secondary prevention of acute coronary syndromes - NSTEMI/STEMI - initial 300 mg loading dose (chewable) - Often co-prescribed with other anti-platelet agents
29
What else needs to be prescribed for patients using aspirin in the long term?
- Gastric protection e.g. PPIs
30
Give some examples of ADP receptor antagonists
- Clopidogrel - Prasugrel - Ticagrelor
31
What is the mechanism of action of ADP receptor antagonists?
- Inhibit binding of ADP to P2Y12 receptors - Inhibit activation of GPIIb/IIIa receptors - Independent of COX pathway
32
Outline the differences between clopidogrel, prasugrel and ticagrelor
- Clopidogrel and prasugrel are irreversible inhibitors of P2Y12 - Ticagrelor acts reversibly at a different site - Clopidogrel and prasugrel are pro drugs (have active hepatic metabolites) - Ticagrelor has active metabolites - Clopidogrel has slow onset of action without a loading dose - Ticagrelor and prasugrel have a more rapid onset of action
33
What are the adverse side effects of the ADP receptor antagonists?
- Bleeding - GI upset - dyspepsia and diarrhoea - Thrombocytopenia (rare)
34
What are the contraindications of ADP receptor antagonists?
- Caution in high bleed risk patients with renal and/or hepatic impairment
35
What are the DDIs of clopidogrel?
- Requires CYPs for activation - CYP inhibitors e.g. omeprazole, ciprofloxacin, erythromycin, some SSRIs
36
What are the DDIs of ticagrelor?
- Can interact with CYP inhibitors and inducers
37
What do we need to be cautious about when prescribing any of the ADP receptor antagonists?
- When prescribing any of these drugs alongside other antiplatelet and anticoagulant agents or NSAIDs - Due to increased bleeding risk - Also need to stop up to 7 days prior to surgery
38
What are some ADP receptor antagonist indications?
- Second agent in dual antiplatelet therapy - Ischaemic stroke (when aspirin is contraindicated) - NSTEMI/STEMI - taken for up to 12 months
39
What factors dictate which ADP receptor antagonists should be used?
- Pt's age, coronary anatomy and bleed risk - Need to consider risk of cardiovascular events vs bleeding risk when prescribing
40
Give some examples of phosphodiesterase inhibitors
- Dipyridamole
41
What is the mechanism of action of phosphodiesterase inhibitors?
- Dipyridamole inhibits cellular reuptake of adenosine - Increased adenosine concentration inhibits platelet aggregation via adenosine (A2) receptors - Also prevents cAMP degradation - Inhibits expression of GPIIb/IIIa
42
What are the adverse side effects of phosphodiesterase inhibitors?
- Vomiting and diarrhoea - Dizziness
43
What are some DDIs of phosphodiesterase inhibitors?
- Antiplatelets - Anticoagulants - Adenosine
44
What are some indications of phosphodiesterase inhibitors?
- Secondary prevention of ischaemic strokes and TIAs - Adjunct for prophylaxis of thromboembolism following valve replacement - Stroke
45
Give some examples of glycoprotein IIb/IIIa inhibitors
- Abciximab
46
What is the mechanism of action of glycoprotein IIb/IIIa inhibitors?
- Blocks binding of fibrinogen and von Willebrand factor - Target final common pathway - Abciximab is an antibody that blocks GPIIb/IIIa inhibitors - Administered IV
47
What are the adverse side effects of abciximab?
- Bleeding - Dose adjustment for body weight
48
What are the DDIs of abciximab?
- Caution with other antiplatelet and anticoagulant agents
49
What are the indications of abciximab?
- Specialist use in high risk percutaneous transluminal coronary angioplasty patients with other drugs
50
Give some example of clot busters
- Streptokinase - Alteplase
51
Outline the mechanism of action of clot busters
- Fibrinolytics dissolve the fibrin meshwork of a thrombus - Prevent conversion of plasminogen to plasmin
52
What are the indications for clot busters?
- Alteplase in acute ischaemic stroke <4.5 hours from symptoms - Following STEMI diagnosis acutely - Streptokinase can only be used once as antibodies develop
53
What are the adverse side effects of clot busters?
- Bleeding
54
What are the DDIs of clot busters?
- Antiplatelets - Anticoagulants
55
When do we give primary PCI (stent)?
- Following acute STEMI - Reperfusion is essential - Offer primary PCI injury if indicated (this is the preferred coronary reperfusion strategy) - Reperfusion injury is a negative consequence of PCI - NSTEMI patients may also be candidates
56
What are the criteria for primary PCI?
- Presentation is within 12 hours of onset of symptoms - Primary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given

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