NSAIDs

Question 1

Example of NSAID

Answer 1

Diclofenac

Question 2

Elimination of NSAIDs

Answer 2

Approximately 65% of the dose is excreted in the urine and approximately 35% in the bile as conjugates of unchanged diclofenac plus metabolites.

Question 3

Indications

Answer 3

Pain and inflammation

Question 4

Mechanism of action

Answer 4

NSAIDs inhibit synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase (COX).

COX-1 is the constitutive form. It stimulates prostaglandin synthesis that is essential to preserve integrity of the gastric mucosa; maintain renal perfusion (by dilating afferent glomerular arterioles); and inhibit thrombus formation at the vascular endothelium.

COX-2 is the inducible form, expressed in response to inflammatory stimuli. It stimulates production of prostaglandins that cause inflammation and pain.

Question 5

Contraindications

Answer 5

GI toxicity - indigestion, renal impairment, liver failure, heart failure

Question 6

Side effects

Answer 6

GI toxicity - indigestion, renal impairment, increased cardiovascular risk

Question 7

Interactions

Answer 7

Ulceration: aspirin, steroids
Bleeding: anticoagulants, SSRIs
renal impairment: ACE inhibitors, diuretics

Question 8

Patient information

Answer 8

Explain you are recommending an anti-inflammatory drug to help improve symptoms of pain, swelling and/or fever.

Oral NSAIDs should be taken with food to minimise GI upset.

Warn patients that the most common side effect is indigestion and advise them to stop treatment and seek medical advice if this occurs.

For patients with acute pain, explain that long-term use, e.g. beyond 10 days, is not recommended due to the risk of side effects.