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ANTIPLATELETES AGENTS

ANTIPLATELETES AGENTS. BY :DR. ISRAA OMAR. The role of platelets. Platelets play a critical role in thromboembolic disease like ischemic heart disease and stroke Platelets adhere to the diseased or damaged areas and become activated , exposing phospholipids and GPIIb/IIIa receptors.

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ANTIPLATELETES AGENTS

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  1. ANTIPLATELETES AGENTS BY :DR. ISRAA OMAR

  2. The role of platelets • Platelets play a critical role in thromboembolic disease like ischemic heart disease and stroke • Platelets adhere to the diseased or damaged areas and become activated , exposing phospholipids andGPIIb/IIIa receptors. • Platelet change their shape to stellate form • Activate platelets also synthesize and release mediators like TXA2 and ADP, which stimulate other platelets to aggregate and eventually fibrin formation and thrombosis. • Platelet aggregation is inhibited by prostaglandin I2 • TXA2 production is reduced by cAMP

  3. Aspirin( Acetylsalicylic acid ) • Aspirin inhibits COX-1 irreversibly, this will lead to inhibition of synthesis of thromboxane A2 which in turn lead to inhibition of platelet activation and aggregation.

  4. Aspirin (Acetylsalicylic acid) – mechanism of action

  5. Acetylsalicylic acid – (Aspirin)mechanism of action

  6. (Acetylsalicylic acid – (Aspirinmechanism of action

  7. (Aspirin )Acetylsalicylic acid – mechanism of action

  8. (Aspirin) Acetylsalicylic acid – mechanism of action

  9. Acetylsalicylic acid (aspirin)– pharmacokinetics • Rapid absorption of aspirin occurs in the stomach and upper intestine, with the peak plasma concentration being achieved 15-20 minutes after administration • The peak inhibitory effect on platelet aggregation is apparent approximately one hour post-administration • Aspirin produces the irreversible inhibition of the enzyme cyclooxygenase and therefore causes irreversible inhibition of platelets for the rest of their lifespan (7 days)

  10. Acetylsalicylic acid – major use • Secondary prevention of transient ischaemic attack (TIA), ischaemic stroke and myocardial infarction • Prevention of ischaemic events in patients with angina pectoris • Prevention of coronary artery bypass graft (CABG) occlusion

  11. (Aspirin )Acetylsalicylic acid – major drawbacks • Risk of gastrointestinal adverse events (ulceration and bleeding) • Allergic reactions • Is not a very effective antithrombotic drug but is widely used because of its ease of use • Lack of response in some patients (aspirin resistance) • The irreversible platelet inhibition

  12. Clopidogrel and Ticlodipine (Thienopyridines ) • It inhibits platelets aggregation by irreversibly binding for ADP receptors on the surface of platelets. • This will lead to reduce mobilization of calcium from intracellular stores and reduces the expression of glycoprotein receptors on the platelets surface

  13. ADP-receptor antagonists – mechanism of action

  14. ADP-receptor antagonists – mechanism of action

  15. ADP-receptor antagonists – mechanism of action

  16. ADP-receptor antagonists – mechanism of action

  17. ADP-receptor antagonists – pharmacokinetics • Both currently available ADP-receptor antagonists are thienopyridines that can be administered orally, and absorption is approximately 80-90% • Thienopyridines are pro-drugs that must be activated in the liver

  18. ADP-receptor antagonists– major use • Secondary prevention of ischaemic complications after myocardial infarction, ischaemic stroke and established peripheral arterial disease • Secondary prevention of ischaemic complications in patients with acute coronary syndrome (ACS) without ST-segment elevation

  19. ADP-receptor antagonists – major drawbacks • Clopidogrel is only slightly more effective than aspirin • As with aspirin, clopidogrel binds irreversibly to platelets • In some patients there is resistance to clopidogrel treatment

  20. GPIIb/IIIa-receptor antagonists • Abciximab is a monoclonal antibody with Fc region removed to prevent immunogenicity . • It bind irreversibly to GPIIb/IIIa receptors and prevent its binding to fibrinogen . • It can reduce the platelets aggregation by more than 90% .

  21. Antibody

  22. GPIIb/IIIa-receptor antagonists – mechanism of action

  23. GPIIb/IIIa-receptor antagonists – mechanism of action

  24. GPIIb/IIIa-receptor antagonists – mechanism of action

  25. GPIIb/IIIa-receptor antagonists – mechanism of action

  26. GPIIb/IIIa-receptor antagonists – mechanism of action

  27. GPIIb/IIIa-receptor antagonists– major use • Prevention of ischaemic cardiac complications in patients with acute coronary syndrome (ACS) without ST-elevation and during percutaneous coronary interventions (PCI), in combination with aspirin and heparin

  28. Dipyramole • It is a phosphodiaestrase inhibitor . • It increases intracellular cyclic AMP ,thus reducing TXA2 synthesizes and also potentiate the prostacyclin effect on platelets making them less sticky and therefore making them less adhesive to thrombogenic surface . • It is ineffective when used alone ;should be used with aspirin • it reduces the risk of stroke . • Unlike aspirin it does not increase the risk of bleeding

  29. Thank you

  30. Referrences: • Lippincottes pharmacology • Rang and dale pharmacology

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