BT_GS 1.47 Discuss the indications for muscle relaxation in anaesthesia

This LO really is more directly applicable to the final exam. However, it certainly won’t hurt to think about this LO in the context of your pharmacology study. Just don’t expect this material to turn up in a primary MCQ.

T/F face mask ventilation almost always improves after the onset of neuromuscular blockade (Ref 1)

T/F ensuring complete / optimal paralysis is an important step during a difficult or failed intubation (Ref 2)

T/F Intraoperative nerve monitoring is inhibited by neuromuscular blockade (e.g. recurrent laryngeal nerve during thyroidectomy; facial nerve during parotidectomy). It will be necessary to ensure that the muscle relaxant has worn off by the time monitoring is needed. Using rocuronium means that a small dose of sugammadex can be used if required. (Ref 3)

T/F in an intubated patient with severe bronchospasm, maintaining neuromuscular blockade will help with ventilation by directly relaxing bronchial smooth muscle (Ref 4)

T/F Suxamethonium 0.5 mg/kg is usually used for ECT. This produces partial neuromuscular blockade, so that some seizure activity can be observed, but without any risk of injury to the patient. (Ref 5)


  1. Warters etal. The effect of neuromuscular blockade on mask ventilation. Anaesthesia, 2011; 66: 163-7
  2. Difficult Airway Society. Management of unanticipated difficult intubation in adults (Flowchart), 2015.
  3. Empis de Vendin etal. Recurrent laryngeal nerve monitoring and rocuronium: a selective sugammadex reversal protocol. World J Surg, 2017; 41: 2298-2303
  4. Kam & Power 3rd edition, page 29-30.
  5. Mirzakhani etal. Neuromuscular blocking agents for electroconvulsive therapy: a systematic review. Acta Anaesth Scand, 2012; 56: 3-16.

BT_PM 1.21 Describe the pharmacology of opioid antagonists

T/F  naloxone is a competitive opioid antagonist, which binds covalently to opioid receptors

T/F  in the presence of an agonist, a competitive antagonist has the effect of making the agonist less potent

T/F  the structure of naloxone is almost identical to morphine

T/F  naloxone has zero efficacy, and low receptor affinity

T/F  using small titrated doses of naloxone, it is possible to reverse respiratory depression without reversing analgesia

T/F  especially at high doses, the partial agonist buprenorphine can act as an antagonist to other opioids

T/F  Suboxone™ contains a mixture of buprenorphine and naloxone, and is used in the management of opioid abuse (can you explain why the naloxone is added?)


  • any decent pharmacology book will contain the answers to the above
  • general information about agonists and antagonists would be found in the chapter(s) on pharmacodynamics

BT_GS 1.15 Define tachyphylaxis, tolerance, addiction, dependence and idiosyncrasy and describe mechanisms of tolerance

T/F  tolerance is the diminished response to a drug, which occurs due to repeated exposure

T/F  tachyphylaxis is a form of tolerance that occurs rapidly (often within a few doses), usually due to depletion of neurotransmitter

T/F  ephedrine and metaraminol are equally likely to produce tachyphylaxis

T/F  mechanisms of opioid tolerance can include: receptor downregulation; metabolic enzyme induction; and alterations to second messenger systems

T/F  patients who develop tolerance to the analgesic and sedative effects of opioids, will still exhibit miosis even to small doses

T/F  physical drug dependence occurs when continued administration of a drug is required for normal function and/or to prevent a withdrawal syndrome

T/F  drug dependence and drug addiction are the same thing

1. Goodman & Gillman 13th edition, Chapter 24 and 20

2018.2 SAQ 7 – dose response curves for opioids

Using opioids as examples, describe and illustrate with graphs, what you understand by the terms “potency”, “efficacy”, “partial agonist”, “competitive antagonist” and “therapeutic index”

The above terms are staples of pharmacodynamics and enable us to describe the effects of drugs on the body. This question asks you to apply your knowledge of these terms to a group of drugs we use on a daily basis.

To answer this question well you would need to have a good working knowledge of both graded and quantal dose response curves.

There are some previous posts on dose response curves here,  here and here. They might help get you in the mood…

BT_GS 1.3 Define and explain dose-effect relationships of drugs with reference to:

· Graded and quantal response

· Therapeutic index

· Potency and efficacy

· Competitive and non-competitive antagonists

· Partial agonists, mixed agonist-antagonists and inverse agonists

· Additive and synergistic effects of drug combinations

BT_PM 1.22 Describe the pharmacodynamics of individual opioids and evaluate their clinical applications

The analgesic potency of fentanyl is about 10 times more than morphine T/F

Therapeutic index is defined as ED50/TD50 T/F

Both naloxone and naltrexone are competitive antagonists at mu opioid receptors T/F

The dose response curve for an antagonist always shows the effect of the antagonist in the presence of an agonist, as the antagonist itself has no intrinsic activity T/F

Buprenorphine is a partial agonist at the mu opioid receptor but is still a potent analgesic. T/F

The relative analgesic potency of fentanyl and alfentanil could be determined on both a graded and quantal dose response curve. T/F

The therapeutic index for morphine with respect to itch is likely to be smaller than the therapeutic index for respiratory depression T/F

Morphine, alfentanil and fentanyl have equal analgesic efficacy T/F

BT_GS 1.19 Describe the mechanisms of drug interaction

Mechanisms of drug interaction can be classified as: pharmacodynamic, pharmacokinetic, and pharmaceutic.

T/F  the interaction between nitrous oxide and sevoflurane is an example of synergism because the combined effect is greater than would be predicted by simple addition

T/F  the interaction between propofol and remifentanil can be represented by a linear isobologram

T/F  in a patient using buprenorphine patches, morphine can have a reduced effect because buprenorphine is a partial antagonist

T/F  in a patient who has been reversed with neostigmine, but then needs to be urgently reintubated, suxamethonium would have a significantly reduced effect

T/F  cigarette smoking inhibits many of the cytochrome P450 enzymes, thereby slowing the metabolism of many drugs

T/F  competition for plasma protein binding sites between drugs, is a common reason for adverse drug effects in anaesthesia

T/F  if suxamethonium is injected into an IV port immediately after thiopentone, a precipitate will form in the line


Hemmings & Hopkins, Chapter 9 (Anesthetic drug interactions)


BT_GS 1.5 Explain the law of mass action and describe affinity and dissociation constants

The law of mass action states that the rate of a reaction is proportional to the concentration of the reacting substrates     T/F

The affinity constant (Ka) is a measure strength of drug-receptor binding    T/F

The dissociation constant (Kd) is a measure of the the tendency for the drug-receptor complex to split    T/F

Ka is the molar concentration of the drug at which 50% of receptors are bound at equilibrium     T/F

Kd is the molar concentration of the drug at which 50% of receptors are bound at equilibrium    T/F


BT_GS 1.1 Explain the concept of drug action with respect to: Receptor theory, Enzyme interactions, Physico-chemical interactions

All drug receptors are proteins         T/F

In general, drugs binding to receptors cause a conformational change     T/F

Physiologic response is directly proportional to the number of receptors bound by drug   T/F

An enzyme is a biological catalyst  that increases the speed of a reaction without being consumed in the reaction itself   T/F

A zero-order reaction is one whose rate is independent of the concentration of the reacting components and is, therefore, constant     T/F

The Michaelis-Menten equation can model the velocity of both zero-order and first order reactions   T/F


The following is an (incomplete) list of a few ‘types’ of receptors I could think of or find in a few textbooks I perused.  I am sure you can add to this list.
Stretch receptors
Metabotropic receptors
Ionotropic receptors
Drug receptors
Hormonal receptors
Neurotransmitter receptors
Sensory receptors
Can you provide a definition of a ‘receptor’ that covers the list above?
Which of these would not fit with the usual idea of a ligand/receptor interaction?
There was a time when the concept of a receptor did not exist but now we use the word almost every day.
How did we get from then to now, i.e. what is the evidence for the existence of receptors?
There are six LO’s relevant to receptor theory.  A number have been covered before and there are two that will be covered is the next two posts.
BT_GS 1.1 Explain the concept of drug action with respect to: Receptor theory, Enzyme interactions, Physico-chemical interactions
BT_GS 1.5 Explain the law of mass action and describe affinity and dissociation constants
I know BT_GS 1.21 does not mention receptors but it is related to the main question of this post. Can you explain how?
These two eBooks on the ANZCA Library website have comprehensive sections on receptor theory:
Rang & Dale’s Pharmacology 8e Ch 2 How drugs act: general principles. (Probably the better of the two)
Goodman & Gilman The Pharmacological Basis of Therapeutics 13e Ch 3
This historical article may help with the ‘evidence’ question above: The receptor concept: pharmacology’s big idea
This website has a useful summary on the ‘Receptor Theory of Drug Action’ page.  On this  website, you will also find a link to the 2017 CICM Primary Syllabus.
If you think the CICM syllabus seems similar to the ANZCA Primary Exam LO’s (Appendix Two) – you would be right – the CICM syllabus was created from the old ANZCA Primary Exam Syllabus.
Which one do you prefer?