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Clinical Pharmacology > Antiplatelet and Fibrinolytic drugs > Flashcards

Antiplatelet and Fibrinolytic drugs Flashcards

1
Q

What is the difference between a thrombus and an embolus?

A

Thrombus- clot adhered to vessel wall

Embolus - intravascular clot distal to the site of origin

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2
Q

What is the difference between the formation of venous thrombosis and arterial thrombosis?

A

Venous thrombosis - associated with stasis of blood +/ damage to veins. Less likely to see endothelial damage

Arterial thrombosis - usually form at the site of aatherosclerosis following plque rupture

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3
Q

How do venous thrombosis and arterial thrombosis differ microscopically?

A

Venous thrombosis - high red cell count and fibrin content, low platelet count

Arterial thrombosis - lower fibrin count, high platelet count

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4
Q

What is the action of prostocyclin in maintaining a healthy endothelium

A
  • Prostocyclin released from endothelial cells inhibits platelet aggregation
  • PGI2 binds to platelet receptors, increasing cAMP
  • increased cAMP decreases calcium preventing platelet aggregation
  • Stabilises GPIIb / IIIa receptors on platelets making them inactive
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5
Q

What factors are released by activated platelets that further activate platelets?

A
  • Thromboxane A2
  • ADP
  • Serotonin
  • PAF (Platelet activating factor)

Activate platelets by activating GPIIb/ IIIb receptors that cause aggregation by binding vWF and fibrin

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6
Q

What class of drugs do you give for platelet rich, arterial thrombi?

A

Antiplatelets and Fibrinolytic drugs

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7
Q

What class of drugs do you give for low platelet countent, ‘red’ venous thrombi?

A

Parenteral anticoagulants e.g. heparin

Oral anticoagulants e.g. warfarin

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8
Q

What is the MoA of aspirin?

A

Inhibitits COX-1 irreversibly, to limit production of Thromboxane A2 from arachidonic acid

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9
Q

How is aspirin absorbed and metabolised?

A

Absorbed by passive diffusion

Hydrolysed hepatically to salicylic acid

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10
Q

What are some of the side effects of aspirin?

A
  • Prolonged bleeding time - haemorrhagic stroke, GI bleeding (peptic ulcer)
  • Reye’s syndrome (hepatic issues) - avoid giving in <16 years
  • Hypersensitivity
  • Do not use in 3rd trimester pregnancy as closes premature closure of the ductus arteriosus of the fetus
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11
Q

Why does inhibition of platelet aggregation last the lifespan of a platelet (7-10 days)?

A

Due to irreversible inhibition of COX-1 , platelets lack nuclei so have to wait for new platelets to be made

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12
Q

In what situations would you prescribe aspirin?

A
  • Secondary prevention of stroke and TIA
  • Secondary prevention of acute coronary syndromes
  • Post PCI and stent procedures to reduce ischemic complications
  • Secondary prevention of MI in stable angina/ peripheral vascular disease
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13
Q

What should you give alongside aspirin when it is given long term?

A

Give PPI for gastric protection

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14
Q

How do ADP receptor antagonists work?

A

Inhibit binding of ADP to P2Y12 receptors → inhibits activation of GPIIb/ IIIa receptors

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15
Q

Name 3 ADP receptor antagonists

A
  • Clopidogrel
  • Prasugrel
  • Tricagrelor
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16
Q

Describe the pharmacokinetics of ADP receptor antagonists

A
  • Clopidogrel and prasugrel are irreversible inhibitors of P2Y12 and are pro-drugs
  • Clopidogrel needs a loading dose otherwise has slow onset action
  • Tricagrelor and prasugrel have more rapid onset
  • Tricagrelor acts reversibly at different sites to clopidogrel
17
Q

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

A
  • Bleeding, GI upset - dyspepsia and diarrhoea
  • Risk of thrombocytopenia (low platelet count)
  • Use with caution if renally/ hepatically impaired
18
Q

When should you give ADP receptor antagonists with caution?

A
  • Clopidogrel requires CYP2C19 for activation
    • Omperazole, Ciprofloxacin, erythromycine and some SSRIs inhibit CYP2C19
  • Tricagrelor can interact with CYP inhibitors and inducers
  • Caution when co prescribed with other antiplatelets and anticoagulants → bleeding
19
Q

When do you need to stop taking clopidogrel/ tricagrelor before surgery?

A

Clopidogrel - stopping 7 days prior to surgery

Tricagrelor - stopping 5 days prior to surgery

20
Q

When are use of ADP receptor antagonists indicated?

A
  • Clopidogrel - monotherapy when aspirin contra-indicated
  • NSTEMI patients for up to 12 months
  • STEMI with stent for up to 12 months
  • Secondary prevention of ischemic stroke/ TIA
21
Q

What is the only formal way to prescribe tricagrelor?

A

Tricagrelor + Aspirin

(Liscenced for prevention of atherothrombotic events for up to 12 months)

22
Q

Explain the mechanism of action of glycoprotein IIb/ IIIa inhibitors

A
  • Inhibits IIb/ IIIa receptors
  • Prevents binding of fibrinogen and von Willebrand factors
  • Targets the final common pathway → more complete inhibition of platelet aggregation
23
Q

Name a glycoprotein IIb/ IIIb inhibitor?

A

Abciximab

24
Q

How is abciximab administered?

A

Intravenous injection with bolus dose

25
Q

What are some of the side effects of abciximab?

A
  • Bleeding - dose adjustment needed for body weight
  • Thrombocytopenia
  • Hypotension
  • Bradycardia
26
Q

When should abciximab be prescribed with caution?

A
  • Other antiplatelet/ anticoagulants
  • Prescribed by a specialised in high risk percutameous transluminal coronary angioplasty
27
Q

What is the mechanism of action of phosphodiesterase inhibitors?

A
  • Inhibits cellular reuptake of adenosine therefore plasma adenosine is increased
  • Adenosine acts on A2 receptor to inhibit platelet aggregation
  • Also acts on phosphodiesterase inhibitors which prevent cAMP degredation → inhibit expression of GP IIb/ IIIb
28
Q

Name a phosphodiesterase inhibitor

A

Dipyridamole

29
Q

What are side effects of dipyradamole?

A
  • Flushing
  • Headache
  • Hypersensitivity
30
Q

When would you prescribe dipyradimole?

A
  • Secondary prevention of ischemic stroke and TIA
  • Adjunct for prophylaxis of thromboembolsim following valve replacement
31
Q

What is the mechanism of action of fibrinolytic agents

A

Dissolve the fibrin meshwork of thrombus by activating plasminogen activators

32
Q

Name some fibrinolytic agents

A
  • Streptokinase
  • Alteplase
  • Tranexamic acid
33
Q

When are fibrinolytics used?

A
  • Alteplase used in acute ischemic stroke <4.5 hrs
  • Following AMI diagnosis vs primary PCI
34
Q

Why can streptokinase only be used once?

A

Strepokinase is developed from streptococci

antibodies will develop onced used → will cause reaction (intra cranial haemorrhage will need ruling out)

35
Q

What should be given to all patients post MI, once haemodynamically stable?

A

ACEi

Clinical Pharmacology (25 decks)

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