antiplatelet agent

1. TOPIC: ANTIPLATELET AGENTS
PRESENTED BY:
Omkar Kumar Kuwar
Department of Pharmacology
ISF College of Pharmacy, MOGA
omkar.official.955@gmail.com
GUIDED BY:
Dr. Arti Singh
Associate Professor
Department of Pharmacology
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2. CONTENTS
• INTRODUCTION
• Platelet mechanism
• Drugs classification
• Site of action
• Uses
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3. INTRODUCTION
Antiplatelet are the drugs that inhibits the
platelet aggregation and thrombus formation are
called antiplatelet drugs.
Antiplatelet are group of medicines that stops
blood cell (platelets) from sticking together &
forming blood clots.
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Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

4. PLATELET MECHANISM
 cAMP plays a key role in platelet mechanism ( Aggregatory or
Anti-aggregatory).
 High concentration of cAMP inhibit Adhesion and low Conc. Having
opposite action.
 cAMP is formed by Adenyl cyclase Activation & Degraded by
phosphodiesterase.
 TXA-2 and ADP inhibit Adenyl cyclase. Thus Decrease camp than Platelet
aggregation & Adhesion.
 Prostacyclin, PGI2 stimulate Adenyl cyclase than increase cAMP Conc.
They show Anti-aggregatory effect.
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

5. Fig.01; Platelet adhesion and aggregation. GPVI and GPIb are platelet receptors that bind to collagen and vWF, causing platelets
to adhere to the sub endothelium of a damaged blood vessel. PAR-1 and PAR-4 are PARs that respond to thrombin (IIa); P2Y1
and P2Y12 are receptors for ADP; when stimulated by agonists, these receptors activate the fibrinogen-binding protein
GPIIb/IIIa and COX-1 to promote platelet aggregation and secretion. TxA2 is the major product of COX-1 involved in platelet
activation. Prostacyclin (PGI2), synthesized by endothelial cells, inhibits platelet activation.
Smooth muscle cells /macrophages
PLATELETMECHANISM
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

6. DRUGS CLASSIFICATION
1. TXA-2 synthesis inhibitors:- Aspirin
2. Platelet cAMP enhancer :- Dipyridamole
3. P2y12 Receptor blockers: -Ticlopidine, Clopidogrel, Prasugrel,
4. GPIIb/IIIa Antagonist : Abciximab, Eptifibatide, Tirofiban,
5. PGI2 Analogues: Epoprostenol.
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

7. Site of Action of Antiplatelet drugs
Reference: Goodman & Gilman’s the pharmacological
basis of Therapeutics 13th edition page no 585-602.

8. USES OF ANTIPLATELET DRUGS
Unstable Angina.
Acute myocardial infraction.
Cerebrovascular disease.
Coronary Bypass implants.
Venous Thromboembolism.
Peripheral vascular Disease.
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

9. ASPIRIN
• Aspirin is a NSAIDs drug. Which blocks the production of TXA-2 by acetylation a
serine residue near the Active site of platelet cox-1.
• Anti thrombotic effect achieved at low Dose (<100mg daily)
Uses :
 Acute myocardial infraction or acute ischemic stroke.
 Secondary prevention in patient with stroke, coronary artery disease, or
peripheral artery disease.
Contraindications :
Aspirin Warfarin : may increase the risk of excessive Bleeding,
Adverse effect: Abdominal or Stomach pain, Bloody or cloudy urine
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

10. DIPYRIDAMOLE
• It is an antiplatelet drug that interferes with platelet function by
increasing the intracellular Conc. Of cAMP. By activation of Adenyl
cyclase and inhibition of phosphodiesterase or by blocking reuptake
of Adenosine.
• Available as a fix dose combination tablet with Aspirin.
Uses :
 Secondary prevention of stroke when combined with Aspirin.
Adverse effect: Feeling or Being Sick, Headaches and Diarrhea,
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

11. CLOPIDOGREL
• Clopidogrel is thienopyridine prodrug that inhibits the P2Y-12 receptor
irreversibly.
Uses :
 Acute coronary syndrome.
 Secondary prevention in patients with myocardial infraction, stroke or
peripheral artery disease.
Drug interactions: Not given with PPIs ( omeprazole, pantoprazole )
because they inhibit the CYP219 enzyme,
Adverse effect: Rashes. itching. uncontrolled bleeding,
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

12. PRASUGREL
• It is the newest member of Thienopyridine class,
• It is a pro-drug that requires metabolic activation in liver.
• It is irreversibly inhibit the P2Y-12 receptors.
Uses :
 For Acute coronary symptoms.
Contraindicated in patients with cerebrovascular disease, prior intracranial bleed,
or > 75years of age.
Drug interactions: with anticoagulant or NSAIDs drugs. Due to increase risk of
bleeding.
Adverse effect: Chest pain, Rash, Itching, Swelling of the face, Trouble with
Swallowing or Breathing
Reference: Goodman & Gilman’s the pharmacological basis of Therapeutics 13th edition page no 585-602

13. Reference
• Reference: Goodman & Gilman’s the pharmacological basis of
Therapeutics 13th edition page no 585-602.
• KD.Tripathi essential of medical pharmacology, seventh edition,
• Rang and Dale’s pharmacology 9th edition, page no: 319-330

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