It is quite possible to spend the entire ten minutes writing an answer to a SAQ and score zero. To avoid this, your SAQ (and viva) should consist of verifiable facts which are specific to the question asked.
Let us consider how we could achieve a zero score in the hypothetical question: “Write short notes on novifentanil”
We could start with a definition:
- Drug: a medicine or other substance which has a physiological effect when ingested or otherwise introduced into the body.
Now we can segue into some value judgements:
- Novifentanil is a useful drug.
- I recommend it
- It is cheap and readily available. (An answer often given in vivas: So are THC, crack and ice)
- Novifentanil is potent
We will now conclude with some statements which are worthless because they could be applied to (almost) any drug.
- The intravenous preparation is a sterile clear colourless solution
- When given intravenously it has 100% bioavailability
- When given orally it is absorbed in the gut and undergoes first pass metabolism
- It is metabolised in the liver
- Metabolites are excreted in the kidneys
- It acts on receptors
- Side effects include nausea, vomiting rash and rarely anaphylaxis
- Contraindications include allergic reaction
We could alternatively score high marks by covering the same issues:
- potent: Compare the potency with other drugs in this class. Does the potency have any other implications, such as altering time to peak effect?
- useful: What is it particularly useful for compared with other drugs in the same class?
- clear colourless solution: Why is it clear?
- Is it intrinsically water soluble, is it an ionisable acid or base, is it dissolved in an additive such as propylene glycol?
- What problems might the additives cause?
- Is it safe to give it neuraxially?
- Will it exhibit ion-trapping?
- first pass metabolism: Does this imply anything about whether or not the drug is effective orally?
- metabolism: It is very easy to get lost in the metabolic pathways. Some of the important things to figure out are:
- are there any active metabolites
- is there any genetic / drug interaction consequences of the pathways which are used? What will this imply in patients with liver disease? If it is metabolised by an enzyme such as CYP3A4 where you probably won’t see many interactions this is also important. (There are some exceptions to this such as St John’s Wort.)
- excreted renally: Does it have active metabolites? Is it excreted unchanged renally? Is it reabsorbed or secreted? If none of these, how is it affected by renal failure?
- receptors: state which ones and what effects these cause
- Side effects:
- are they different or the same as other drugs in the same class?
- are there any specific side effects which you need to mention?
- are there any class specific side effects that this drug does not exhibit?
- I recommend it: are there any specific indications for which it is recommended?
BT_GS 1.36 Describe the pharmacokinetics of neuromuscular blocking agents
BT_GS 1.37 Describe the pharmacological differences between neuromuscular blocking agents, and the clinical significance of these differences
Another “core” SAQ! The level of detail needed to answer this question is understandably high, as you would expect in a specialist anaesthetics exam.
The best reference is Miller.
T / F the ED95 for suxamethonium is 1 mg/kg, and for rocuronium is 0.6 mg/kg
T / F train of four can be used to assess the depth of block produced by both suxamethonium and rocuronium
T / F suxamethonium can trigger MH, but rocuronium does not
T / F patients with myasthenia gravis are resistant to suxamethonium, but very sensitive to rocuronium
T / F Suxamethonium is metabolised by plasma cholinesterase, to succinyl monocholine and choline. Rocuronium is metabolised in the liver – the main metabolite is 17, desacetyl-rocuronium, which is mainly excreted in the bile.
T / F the duration of paralysis with suxamethonium is 5-10 minutes. This increases to 1-2 hours in people who are homozygous atypical for the plasma cholinesterase gene
T / F Suxamethonium has some affinity for muscarinic ACh receptors, which can cause bradycardia. Rocuronium has no affinity for MAChR’s.
T / F (taken from NAP 6 Report, page 4) suxamethonium was almost twice as likely to cause anaphylaxis as any other NMBA, with a rate of 11.1 per 100,000 administrations
BT_GS 1.25 Describe the effects of the inhalational agents on the cardiovascular, respiratory, and central nervous systems
Another core SAQ! The reference is Miller.
T / F a patient anaesthetised with sevoflurane as the sole agent would have a decreased tidal volume, and an increased respiratory rate
T / F apnoea can be produced with sevoflurane
T / F sevoflurane decreases the slope of the CO2 response curve, and shifts it to the right
T / F 0.1 MAC is enough to significantly blunt the increase in ventilation normally seen with hypoxaemia
T / F sevoflurane is a bronchodilator
T / F at > 1 MAC, sevoflurane inhibits hypoxic pulmonary vasoconstriction, making it unsuitable during one lung ventilation
T / F sevoflurane impairs the function of cilia on the respiratory endothelium
Discuss the factors that affect oxygen transport from the alveoli to the tissues
No prizes for guessing why this is an important topic…
I have previously posted on the oxygen cascade and included a reference at that post which you may like to refer to. This topic is well covered in both of the respiratory physiology textbooks on the reading list.
BT_PO 1.23 Oxygen cascade
BT_PO1.24 Describe the alveolar exchange of oxygen and carbon dioxide
BT_PO 1.25 Discuss diffusion capacity and its measurement
BT_PO 1.31 Discuss the carriage of oxygen in blood, etc.
The first 4 of these are reasonably easy, as are the ones in my other post on this topic.
There is a linear relationship between PaO2 and oxygen content of arterial blood T/F
It is normal for the A-a gradient of oxygen to increase with increasing age T/F
Breathing a hypoxic mixture will generally result in hyperventilation, in an attempt to return alveolar oxygen levels to normal T/F
A patient breathing room air with a Hb of 15g/dL will have the same oxygen carrying capacity as a patient with a Hb of 10g/dL breathing 100% O2 T/F
A person with an oxygen consumption of 200ml/min, breathing room air, will require an alveolar ventilation rate of at least 1L/min to prevent alveolar PO2 reaching zero T/F (the answer to this one can be found in a very interesting graph in Nunn’s Chapter on Oxygen)
Briefly describe the principles (50%) and sources of error (50%) in the measurement of arterial blood pressure using an automated oscillometric non-invasive monitor
This is a piece of equipment we use multiple times each day so pretty reasonable that we should know how it works and what makes it not work so well.
This topic will be covered in any equipment textbook, but here is a nice little article from BJA Education.
All of the statements below are core.
BT_SQ 1.6 Describe the methods of measurement applicable to anaesthesia, including clinical utility, complications and sources of error in particular Blood pressure measurement
Systolic BP is taken as the point at which the oscillations suddenly increase T/F
Modern oscillometric BP machines have one cuff that both occludes the artery and senses the oscillations T/F
The pressure drop in the cuff may be continuous or stepped T/T
Calcified arteries may cause inaccurate readings as the vessels cannot be compressed T/F
External pressure on the cuff does not affect readings T/F
The readings are equally accurate across the full spectrum of blood pressure T/F
I love these photos by Korean artist Myoung Ho Lin where a white drop sheet is placed behind a tree in its natural environment. Viewed at NGV (sorry about the reflection of the lights)
It has been a busy week for the current Primary Exam candidates, with the vivas running from Monday until today. I hope the exam went well for those of you sitting today.
Many of the contributors to this blog have also been very busy, examining.
I have been taking my own advice and have been on a, somewhat unfortunately timed, holiday 😬
I think that everyone deserves, and benefits from, taking some time off periodically.
There will be no posts for the rest of this week, but we will be back on Monday with posts from the recent SAQ questions.
See you then and I hope you find some time to relax and recharge.
Sunset last night, Hamilton Island
This is the LO number that the work of breathing post from yesterday was given by mistake, so surfactant fell through the gaps…
I am sure you would find the answers to these in either West or Nunn’s (Lumb) books. I used Nunn because I am still on holidays.
Surface tension in the alveoli is reduced by the presence of surfactant T/F
BT_PO 1.10 Surfactant properties and role in respiratory mechanics
Surfactant ensures that surface tension is equal throughout the lung T/F
Surfactant release is stimulated by high volume lung inflation T/F
Surfactant plays a role in keeping the alveoli free from transudate T/F
Surfactant has an important immunological function in the lung T/F
Why is surfactant important in preventing collapse of small alveoli? Which physical law determines pressure within a sphere? If you do a little mathematical equation looking an pressure within an alveolus with a 0.1mm sphere and one with a 0.2mm sphere assuming equal surface tension, you will be able to work out the answer to the second statement.
Again my best wishes for those of you with vivas today
Tasmanian temperate rainforest -divine…
This was being listed as one of the LO’s we hadn’t covered which surprised me!
A bit of investigative work uncovered a nice post by transpendantic acid well over a year ago. It had a typo giving it the wrong LO number, which I have corrected.
PS. I hope the vivas go well for those of you sitting today 😊
Three Cape track, Tasmania
Next week the viva exams will again be held in Melbourne. My very best wishes to all of you who are sitting. The majority of you will be delighted at the end of the day, but for some of you the outcome will not be what you hoped.
I have previously posted some words for those of you who are unsuccessful on this attempt and my sentiments from that post hold true.
It is easy to see lack of success in the exam purely at its face value – a failure.
If you find yourself in this position, I challenge you to look further. As anaesthetists we should be on a lifelong journey of self education. We strive to become more knowledgeable each year, so that our patients receive our best possible care.
As you sit the Primary Exam, you are relatively close to the start of the path. Failing the exam gives you a rare opportunity to become a better version of your future self. Speaking with multiple registrars who have been required to sit the exam more than once, they all feel more knowledgeable for the experience. This is likely to be the only time where you dedicate yourselves to the basic sciences underpinning anaesthesia. Embrace the opportunity to be better.
It is long path over the lifetime of a career, a small amount of time at this extra step needn’t be viewed in the negative . Enjoy the journey…..
In my books, this is not a very exciting topic….
I have only included what I would consider reasonably core statements here so I think it would be reasonable that you knew them all
BT_PO 1.74 Outline the constituents and functions of plasma
Plasma accounts for approximately 60-70% of blood volume T/F
Albumin is almost exclusively confined to the plasma in normal physiological states T/F
The negative charge of albumin results in a higher concentration of cations in the plasma compared with interstitial fluid, due to the Donnan effect T/F
Plasma proteins hold fluid and electrolytes within the capillaries, resulting in little exchange of substances between the plasma and interstitial fluid T/F
Antibodies against red blood cell antigens are present in the plasma of all individuals T/F
AB+ patients make universal plasma donors T/F ( the answer to this will give you the answer to the previous statement)