ANZCA Part 1 SAQs: Recent Episodes
Vibhushan Manchanda
My personal collection of my model answers for a bunch of SAQs for the ANZCA part one exam. Only recorded after I’ve managed to write an 8-10 min answer rather than including long explanations. Derived from various textbooks and model answers (propofol dreams, ketamine nightmares, adrenaline memories). This is not medical advice for individuals, nor is it clinical advice for healthcare professionals.
Hit the headings and use loads of examples with some detail about the examples (as per examiners report)
Draw compartment model. PK/PD structure. PK needs to include accumulation and elimination.
More than just a valsalva but similar principles. Don’t forget frank starling graph and indirect effects.
Protective: RID (reservoir, immunological, drugs). Regulatory: SEAMS (storage, endocrine, acid base, metabolic, synthesis)
Weirdly not put into a section of its own in Nunn’s or West’s. Ended up using deranged physiology for most of it. Use a graph for FRC and CC.
Brandis very good again. Do a graph at the end with arterial and venous lines showing Haldane effect.
Maternal (uterine artery) O2 = 105mmHg, CO2 = 30mmHg. Foetal (umbilical artery) O2 = 20mmHg, CO2 = 50mmHg.
Not been asked for a while, much easier to approach and understand this question once you have a good grasp of viscosity/density and laminar/turbulent flow
Lots of different terminology for the states of VDNaC and the gates. Voltage = M gate (outer gate). Time = H gate (inner gate). Resting = closed M open H. Active = both open. Inactive = open M closed H.
Adrenaline memories answer very good. I changed some of the headings to simplify it with how I understand it. The key is understanding the difference in venodilation and vasodilation.
A hard one to do in 10 mins but thankfully examiners report says Doppler and CO measurement are “extra marks” rather than pass marks.
Povidine iodine and alcoholic chlorhexidine. This is a 2-3/5 answer. Apart from knowing that I shouldn’t inject chlorhex into someone’s spinal cord I’m not sure how this makes me a better anaesthetist.
This is a good starting point and probably a pass as per examiners reports, but if you get time then add more detail (e.g. baroreceptor reflexes to volume changes, CVS effects of potential hyperkalaemia)
Na+ transport passive as per Power and Kam. Doesn’t make sense to me but it’s a recommended text so going to run with it 👍🏽
Graph from ketamine nightmares is elite for understanding but not sure I would have time to draw three graphs. Could do the full table for VQ at dead space/apex/ideal alveolar gas/base/shunt with O2 and CO2 values if you get time.
Makeup question by ex chair of examiners. Answer based off a friend’s answer (Matt Avery) that she gave a 5/5 to!
Graph very important. TEG probably simpler but I chose ROTEM because it’s what they actually use at work and this exam is all about becoming a better anaesthetist!
Has been asked both as a written SAQ and with a booklet containing images and shorter questions
Serotonergic, COX3, endogenous cannabinoids. Management of toxicity to be covered in another episode.
At the start I think it’s worth putting abbreviations to denote A for anterior, P for posterior, M for medial, L for lateral
Look up a diagram. Best one I could find was Ketamine Nightmares (had both on same axes and content rather than saturation %). Also correction that bicarbonate carriage is by combination with water via carbonic anhydrase, not by “combination with bicarbonate”.
Minor error where I said Cl content increases the strong ion difference but actually it decreases it… my bad (Stewart approach 🤦♂️). But still the point stands that it causes a minor hyperchloraemic acidosis with the alkalosis of H+ being consumed by cori cycle for metabolism of lactate as the dominant process from CSL infusion.
An annoyingly broad question that asked for the onset and offset, also didn’t specify topical or subcutaneous or nerve block. A narrower scope would make for an easier question.
Numbers for equilibration of compartments refer to 3 time constants (not half lives) and are from Hemmings and Egan. Sevo 2 min FRC, 9 min VRG, 7 hrs MG, 5 days FG. Des 2 min FRC, 8 min VRG, 5 hrs MG, 3 days FG.
Nail your definitions, graph, table, and learn the numbers for effect site concentrations
Everyone use TIVA so that this is out of the syllabus ASAP or at least only given as much importance as knowing that ether has a BGPC of 12
A really hard one to get done in 10 mins especially if you include graphs. Focus on answering the question.
Re alloimmunisation it’s worth adding possible future transfusion reactions as well as haemolytic disease of the newborn
Kudos to all the TIVA divas, imagine in 20 years time if pharmacokinetics of volatiles isn’t in the syllabus 🤯
A hard one to do in 10 mins. Breadth over depth. Look up an oxygen cascade diagram for the intro if you don’t have one in your head.
Why do I need to know this?
A) because patients think we put them to sleep so we should know what sleep is
B) because we need to pass the exam and it's in the curriculum
I think the answer is B
If you don't set your airway pressures to multiples of five or even numbers, we cannot be friends.
Not sure if A2 agonist/opioids actually speed up onset of block, I couldn't find a source to confirm or deny...
So small and so cute but being a nose breather and having tiny nostrils is a bit silly (I would absolutely do the same to constantly feed though)
Attenuated with training, such as cycling for anaesthetists (also a great way to procrastinate study)
Is it really a circle or is it more like a polygon? Look up/make sure you can draw a diagram for this one.
Ouch. Thanks to Lauren Foster for suggesting this answer should include opioids increasing chronic pain by NMDA agonism, increased spinal dysnorphins, down regulation of opioid receptor number and sensitivity