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7 SBAs on opioids and analgesics
Viva
4 viva questions
Why does giving 50 µg of intrathecal fentanyl instead of 20 µg not improve the block?
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Because the spinal µ-receptor pool in the substantia gelatinosa is finite and is already close to saturated at 20 µg. Fentanyl is highly lipid-soluble, so the additional drug does not remain in cerebrospinal fluid to find more receptors — it is taken up into cord, epidural fat and the systemic circulation, where it produces side effects. The analgesic curve has plateaued; the side-effect curve has not.
A patient with atypical plasma cholinesterase needs a remifentanil infusion. Any concern?
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None on that account. Remifentanil is hydrolysed by non-specific plasma and tissue esterases, which are a different enzyme system from plasma cholinesterase. Its clearance is unaffected. The concern in that patient is suxamethonium, not remifentanil.
You stop a three-hour remifentanil infusion at the end of surgery. What must already have happened?
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A longer-acting analgesic must already be established and working. Remifentanil offset is 3 to 4 minutes and leaves no residual analgesia at all, so the patient goes from profound opioid effect to none within a few minutes — and acute tolerance or hyperalgesia may mean their requirement is higher than baseline, not lower.
Why does a patient on fluoxetine get no relief from codeine?
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Codeine is a prodrug requiring CYP2D6 to demethylate it to morphine, and fluoxetine is a potent CYP2D6 inhibitor. Without conversion there is essentially no active drug. The same mechanism explains the absence of effect in genetic poor metabolisers, and the toxicity risk in ultra-rapid ones.