Classification

Non-steroidal anti-inflammatory drugs (NSAIDs) may be classified by chemical group or by mode of action.

Chemical groups

1. (a) Salicylic acids

2. — Acetylated (e.g. acetylsalicylic acid (aspirin)).

3. — Non-acetylated (e.g. diflunisal).

4. (b) Acetic acids

5. — Indoleacetic acids (e.g. indomethacin, sulindac).

6. — Phenylacetic acids (e.g. diclofenac).

7. — Pyrroleacetic acids (e.g. ketorolac).

8. (c) Coxibs (e.g. celecoxib, parecoxib, etoricoxib).

9. (d) Fenamates (e.g. mefenamic acid).

10. (e) Oxicams (e.g. piroxicam, meloxicam).

11. (f) Phenazones (e.g. dipyrone).

12. (g) Propionic acids (e.g. ibuprofen, naproxen).

13. (h) Pyrazolones (e.g. phenylbutazone).

14. (i) Others (e.g. paracetamol (acetaminophen)).

Mechanisms of action of anti-inflammatory analgesics

The enzyme cyclo-oxygenase (COX) catalyses the production of prostaglandins (PGs) and thromboxanes from arachidonic acid. COX exists in at least two isoforms, with a wide range of physiological activity as simplified in the Table 41.1.

When tissues are traumatised by surgery, there is a release of pro-inflammatory mediators that induce COX-2. Increased levels of the PGs formed can induce peripheral sensitisation of nociceptors, but also secondary sensitisation in the dorsal horn by blockade of the inhibitory action of glycine. This action, by induction of the gene for COX-2 protein is described further below. The role of COX-2 in the nervous system is therefore not only peripheral but also central, with COX-2 inhibitors that cross the blood—brain barrier potentially reducing central sensitisation.