1 / 29

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.

niles
Download Presentation

ANTIPLATELETES AGENTS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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. • Activate platelets also synthesize and release mediators like TXA2 and ADP, which stimulate other platelets to aggregate and eventually fibrin formation and thrombosis.

  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. GPIIb/IIIa-receptor antagonists – mechanism of action

  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– 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

  27. Dipyramole • It is a phosphodiaestrase inhibitor . • It is ineffective when used alone ;should be used with aspirin . • 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 reduces the risk of stroke . • Unlike aspirin it does not increase the risk of bleeding

  28. Thank you

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

More Related