Primary Examination SAQs

Study notes for the ANZCA Primary Examination SAQs


with 5 comments

2011a(6)99a(10) Write a brief outline of the pharmacology of remifentanil

2011a(2)07a(5) Classify non-opioid drugs used in the treatment of neuropathic pain and indicate proposed mechanisms of analgesic action and potential adverse effects

2009a(5)04a(4)01b(12)Outline the effects of an opioid injected in the intrathecal space

2008b(4) Briefly outline the pharmacology of ketamine with reference to its use as an analgesic agent in the post-operative period

2007b(3): Outline the important pharmacological considerations concerning choice of opioid and dosage when converting from IV morphine to oral opioid analgesia in the post operative period

2006b(8)03b(5)00a(10)95b(12)Describe the pathogenesis and management of paracetamol toxicity

2006b(5)Briefly explain the mechanisms responsible for NSAID-induced SE. Outline the adv, dis of selective COX2 inhibitors

2006a(7)97b(15)Briefly outline the pharmacology of naloxone

2005a(2)98b(11)Outline the acute adverse effects of opioid receptor agonists. Describe the mech of the acute adverse effects of opioid recpetor agonists

2004b(4)Write short notes on tramadol

2003a(6)00b(12)Explain how differences in pharmacokinetics of alfentanil and fentanyl influence the way they are given IV

2002b(6)Write brief notes on tolerance and dependence in relation to opioid analgesics

2002a(12)Outline potential mechanisms of action of NSAIDs and potential adverse effects

2000a(15)Describe the effects of opioids on the respiratory system

1996b(9)Explain factors which determine duration of effect of IV administered bolus doses of fentanyl

1996a(11)Describe briefly the pharmacokinetics of pethidine

MAKEUP: Write short notes on the pharmacology of parecoxib




Written by primarysaqs

December 29, 2009 at 1:52 pm

5 Responses

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  1. 1999(10)remifentanil MoA: incr intra cellular ca and incr k influx. should it be Inc k efflux, and dec intracellular ca?


    July 6, 2010 at 6:58 pm

    • Iza, you are partially correct. Mu receptor activation reduce neuronal excitability by an increase in K conductance (resulting in cell hyperpolarisation), but also inhibits Ca entry leading to a decrease in intracellular Ca. Rang & Dale have a good summary of the cellular actions of opioids.


      July 6, 2010 at 7:27 pm

  2. Amanda, Norpethidine is hydrolysed to norpethidinic acid, not pethidinic acid as in 1996a(11): Describe briefly the pharmacokinetics of pethidine. Cheers…


    June 8, 2011 at 12:58 pm

    • Hi Damien
      I disagree with your above comment as it has skipped a few steps.
      Pethidine is actually metabolised by multiple pathways:
      1. liver cytochrome oxidases to norpethidine (which is neurotoxic)
      – Norpethidine is metabolised either to minor metabolites for excretion via kidneys, by liver carboxyesterase to norpethidinic acid (which is inactive), or conjugated directly for renal excretion
      – Norpethidinic acid is conjugated with glucoronic acid for renal excretion
      2. Liver carboxyesterase to pethidinic acid (which is inactive)
      – Metabolised to either norpethidinic acid or directly conjugated for excretion by kidneys
      3. Metabolised to minor metabolites which are excreted in urine



      June 16, 2011 at 2:32 pm

  3. Amanda, Apologies for the brevity of my original post. I was certainly not trying to explain the entire metabolism pathway, just one minor aspect. To that end, what I have stated is the same as you have pointed out in pathway #1. That is, that norpethidine is hydrolysed (via caboxyesterase) to norpethidinic acid. I hope you agree that the correction is valid. Cheers, Damien…


    June 17, 2011 at 3:37 pm

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