Pharmacology for Anaesthesia and Intensive Care

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Section IICoredrugs in anaesthetic practice

Table 9.5.Classification of NSAIDs.

Group Class Drug

Non-specific COX inhibitors salicylates

acetic acid derivatives

anthralinic acids

pyrazolones

proprionic acids

para-aminophenols

oxicams

aspirin

diclofenac, ketorolac, indomethacin

mefanamic acid

phenylbutazone,

ibuprofen, naproxen

paracetamol

tenoxicam, piroxicam

Preferential COX-2 inhibitors oxicams meloxicam

Specific COX-2 inhibitors pyrazole

methylsulphone

phenylacetic acid

derivative

parecoxib, celecoxib, rofecoxib

etoricoxib

lumaricoxib

of cyclic endoperoxidases and thromboxane A 2 prevents platelet aggregation and

vasoconstriction and, therefore, inhibits the haemostatic process. The effects of

aspirin on platelets last for the life span of the platelet for two reasons: platelets are

unable to generate new cyclo-oxygenase and the enzyme inhibition is irreversible.

Upto 14 days are required to generate new platelets. COX-2 inhibition has no effect

on platelet function even at high doses.


Drug interactions – caution should be exercised when NSAIDs are administered

with anticoagulants such as heparin or warfarin, especially as the latter may be dis-

placed from its plasma protein-binding sites, increasing its effects. Serum lithium

may be increased when administered with NSAIDs and its levels should, therefore,

be monitored.


Hepatotoxicity – this is normally observed following prolonged or excessive use of

NSAIDs. Up to 15% of patients may experience a rise in serum transaminase levels,

even following short courses.

O

OH

Paracetamol

N—C—CH 3

H— ——

Aspirin

C— OH

——

O

H 3 C— C — O

——

O

Figure 9.4.Structures of aspirin and paracetamol.