| Class | Antiplatelet agent |
|---|---|
| Chemistry |
Aromatic acetate |
| Routes of administration |
Oral |
| Absorption |
Oral bioavailability 50% due to first pass effect(but, well absorbed) |
| Solubility |
pKa 2.97; only slighly water-soluble |
| Distribution |
VOD=0.1-0.2 L/kg; 58% protein-bound |
| Metabolism |
80% is metabolised in the liver; active metabolite (salicylic acid) is responsible for much of the analgesic and antiinflammatory effect, but has little antiplatelet activity. |
| Elimination |
Salicylic acid is eliminated in the urine; renal clearance of aspirin itself becomes more important with overdose |
| Time course of action |
Aspirin half life is only 20 minutes; half-life of salicylic acid can range from 2 to 12 hours, depending on the dose. |
| Target receptor |
COX-1 and COX-2 isoforms of the cycloxygenase enzyme |
| Mechanism of action |
By inhibiting the activity of COX-1 isoenzyme, aspirin decreases the synthesis of trhomboxane-A2, which is a potent platelet activator. The result is a decrease in platelet activation and aggregation. This inhibition is irreversible (acetylation) |
| Clinical effects |
COX-1 inhibitor and nonselective NSAID side effects: |
| Literature reference |
Nagelschmitz et al, 2014 |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology |
Antiplatelet agents; not to be confused with the heavily abrdiged A brief summary of antiplatelet agents from the Second Part Exam. Also Salicylate toxicity, and specifically the lactate rise associated with salicylate overdose. |
| Related SAQs |
Question 12 from the second paper of 2017 (aspirin vs. clopidogrel) Question 20 from the second paper of 2015 (aspirin vs. clopidogrel) Question 3 from thw second paper of 2013 (mechanism, and also aspirin) Question 5 from the second paper of 2010 (mechanism) |