SN7 SHORT NOTE 5M ★ High-yield

Classify antiplatelet drugs. Describe the mechanism, uses and adverse effects of aspirin and clopidogrel.

Pharmacology · 2nd Professional — Para-Clinical

Definition

Antiplatelet drugs inhibit platelet activation or aggregation, and are the mainstay of preventing and treating arterial thrombosis.

Classification and Mechanisms

Class	Drug	Mechanism	Onset and duration
COX inhibitor	Aspirin	Irreversible acetylation of platelet COX-1, abolishing thromboxane A2	Within an hour if chewed; lasts the platelet lifespan of 7–10 days
P2Y12 blockers	Clopidogrel, prasugrel	Irreversibly block the ADP receptor; both are prodrugs	Clopidogrel needs CYP2C19 activation, so effect is variable; 5–7 days to wear off
P2Y12 — reversible	Ticagrelor	Reversible; not a prodrug, so faster and more consistent	Effect wears off in 3–5 days; causes dyspnoea in some
GPIIb/IIIa inhibitors	Abciximab, eptifibatide, tirofiban	Block the final common pathway — fibrinogen cross-linking	Intravenous only, around angioplasty
Phosphodiesterase inhibitors	Dipyridamole, cilostazol	Raise platelet cAMP	Adjunctive

CLINICAL PEARL

Low-dose aspirin works because the platelet has no nucleus. A single small dose irreversibly acetylates COX-1 in every platelet it meets, and the platelet cannot make new enzyme, so the effect lasts its whole lifespan. Endothelial cells can resynthesise COX and continue producing protective prostacyclin. That asymmetry is why 75 mg daily is antithrombotic while higher doses are merely more ulcerogenic.

Uses

Acute coronary syndrome — aspirin chewed immediately, plus ticagrelor or clopidogrel; the single most valuable early drug
After percutaneous coronary intervention — dual antiplatelet therapy for a defined period to prevent stent thrombosis, then aspirin alone
Secondary prevention after infarction, ischaemic stroke or transient ischaemic attack, and in peripheral arterial disease
Primary prevention is NO longer routine — in people without established disease the bleeding risk broadly offsets the benefit

Adverse Effects and Practical Points

Bleeding — gastrointestinal above all; risk multiplies when antiplatelets are combined with each other, with anticoagulants, or with NSAIDs and steroids
Aspirin — dyspepsia and peptic ulceration, bronchospasm in aspirin-sensitive asthma, and REYE syndrome in children with viral illness, which is why it is avoided under 16
Add a proton pump inhibitor for patients at high gastrointestinal risk; omeprazole may reduce clopidogrel activation through CYP2C19, so pantoprazole is preferred
Stopping dual therapy early after a stent risks stent thrombosis, which is frequently fatal; any planned surgery must be discussed with the cardiologist rather than the drugs simply stopped
NSAIDs taken before aspirin can block its antiplatelet effect by competing for the COX-1 site — a common and unrecognised cause of apparent aspirin failure

Applied Aspects

Aspirin must be chewed in suspected infarction, not swallowed whole, so that it is absorbed within minutes
Ask specifically about over-the-counter NSAIDs and traditional remedies, which patients do not regard as drugs and which add materially to bleeding risk
Aspirin is cheap, universally available and one of the highest-value drugs in medicine — its correct use in acute coronary syndrome saves more lives per rupee than almost anything else available
Do not stop aspirin for minor procedures such as dental extraction or cataract surgery; the thrombotic risk of stopping usually exceeds the bleeding risk of continuing
Reserve dual antiplatelet therapy for defined indications and periods; continuing it indefinitely without reason multiplies bleeding without further benefit

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