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CPT > Antiplatelet and fibrinolytic drugs > Flashcards

Antiplatelet and fibrinolytic drugs Flashcards

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?

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

What are the adverse side effects of aspirin?

A
  • Gastrointestinal irritation
  • GI bleeding (peptic ulcer)
  • Haemorrhage (stroke)
  • Hypersensitivity
25
Q

What are the contraindications of aspirin?

A
  • Reye’s syndrome - avoid until <16 years
  • Hypersensitivity
  • 3rd trimester (leads to premature closure of ductus arteriosus)
  • Caution with other antiplatelets/anticoagulants
26
Q

What causes a lack of efficacy of aspirin in some people?

A
  • COX-1 polymorphisms
  • People produce different quantities of COX-1
27
Q

Why does the antiplatelet effect of aspirin only last 7-10 days?

A
  • 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
Q

What are some aspirin indications?

A
  • 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
Q

What else needs to be prescribed for patients using aspirin in the long term?

A
  • Gastric protection e.g. PPIs
30
Q

Give some examples of ADP receptor antagonists

A
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
31
Q

What is the mechanism of action of ADP receptor antagonists?

A
  • Inhibit binding of ADP to P2Y12 receptors
  • Inhibit activation of GPIIb/IIIa receptors
  • Independent of COX pathway
32
Q

Outline the differences between clopidogrel, prasugrel and ticagrelor

A
  • 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
Q

What are the adverse side effects of the ADP receptor antagonists?

A
  • Bleeding
  • GI upset - dyspepsia and diarrhoea
  • Thrombocytopenia (rare)
34
Q

What are the contraindications of ADP receptor antagonists?

A
  • Caution in high bleed risk patients with renal and/or hepatic impairment
35
Q

What are the DDIs of clopidogrel?

A
  • Requires CYPs for activation
  • CYP inhibitors e.g. omeprazole, ciprofloxacin, erythromycin, some SSRIs
36
Q

What are the DDIs of ticagrelor?

A
  • Can interact with CYP inhibitors and inducers
37
Q

What do we need to be cautious about when prescribing any of the ADP receptor antagonists?

A
  • 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
Q

What are some ADP receptor antagonist indications?

A
  • Second agent in dual antiplatelet therapy
  • Ischaemic stroke (when aspirin is contraindicated)
  • NSTEMI/STEMI - taken for up to 12 months
39
Q

What factors dictate which ADP receptor antagonists should be used?

A
  • Pt’s age, coronary anatomy and bleed risk
  • Need to consider risk of cardiovascular events vs bleeding risk when prescribing
40
Q

Give some examples of phosphodiesterase inhibitors

A
  • Dipyridamole
41
Q

What is the mechanism of action of phosphodiesterase inhibitors?

A
  • 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
Q

What are the adverse side effects of phosphodiesterase inhibitors?

A
  • Vomiting and diarrhoea
  • Dizziness
43
Q

What are some DDIs of phosphodiesterase inhibitors?

A
  • Antiplatelets
  • Anticoagulants
  • Adenosine
44
Q

What are some indications of phosphodiesterase inhibitors?

A
  • Secondary prevention of ischaemic strokes and TIAs
  • Adjunct for prophylaxis of thromboembolism following valve replacement
  • Stroke
45
Q

Give some examples of glycoprotein IIb/IIIa inhibitors

A
  • Abciximab
46
Q

What is the mechanism of action of glycoprotein IIb/IIIa inhibitors?

A
  • Blocks binding of fibrinogen and von Willebrand factor
  • Target final common pathway
  • Abciximab is an antibody that blocks GPIIb/IIIa inhibitors
  • Administered IV
47
Q

What are the adverse side effects of abciximab?

A
  • Bleeding
  • Dose adjustment for body weight
48
Q

What are the DDIs of abciximab?

A
  • Caution with other antiplatelet and anticoagulant agents
49
Q

What are the indications of abciximab?

A
  • Specialist use in high risk percutaneous transluminal coronary angioplasty patients with other drugs
50
Q

Give some example of clot busters

A
  • Streptokinase
  • Alteplase
51
Q

Outline the mechanism of action of clot busters

A
  • Fibrinolytics dissolve the fibrin meshwork of a thrombus
  • Prevent conversion of plasminogen to plasmin
52
Q

What are the indications for clot busters?

A
  • Alteplase in acute ischaemic stroke <4.5 hours from symptoms
  • Following STEMI diagnosis acutely
  • Streptokinase can only be used once as antibodies develop
53
Q

What are the adverse side effects of clot busters?

A
  • Bleeding
54
Q

What are the DDIs of clot busters?

A
  • Antiplatelets
  • Anticoagulants
55
Q

When do we give primary PCI (stent)?

A
  • 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
Q

What are the criteria for primary PCI?

A
  • 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

CPT (22 decks)

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