For those of you who have chosen to sit the ANZCA primary exam this month, my very best wishes for you with the written component on Tuesday.
I hope those of you sitting have been able to maintain the focus on your studies amid the very unsettled world we find ourselves living in.
Perhaps today and tomorrow are a time to do something solely for you. What is possible will obviously differ depending on where in Australasia you live, but something enjoyable and relaxing doesn’t need to be done far from home.
I have previously written a post on the benefits of taking a short break before the exam It seems as though that post was written in a different world, but the message still holds true.
I will be thinking of you all on Tuesday – best wishes.
We are living in a very topsy turvey world at the moment and I really feel for those of you preparing for the exam. We as human beings are poorly equipped to deal with uncertainty and yet that is what we a faced with constantly at the moment.
Today I thought I would give you links to some study tips I have posted in the past. Many of them relate to our own behaviours and habits, which are things which we still have control over.
Please remember that if you need extra help at this time, ANZCA provides access to free psychological support. Do not hesitate to access this service if you think it will benefit you in the run up to the exam.
Study tip – avoid getting too much of a good thing… – this post talks about the double edged sword of stress. In the current climate, I think that we all need to be consciously addressing our stress levels in order to maintain ourselves in a constructive zone.
The Primary Exam in just one step on a lifelong path The words of this post, although initially intended for those who had been unsuccessful in the exam, may provide solace for those of you who feel stuck in limbo this year and had your exams and/or training plans disrupted.
I hope that all of you are able to find some moments of joy in your lives this weekend. Please know that you are all in my thoughts…
Discuss the effects of ageing on the respiratory system.
Increasingly, we are having to anaesthetise older and extremely old patients. It is important to know how their physiology differs from younger patients in order to deliver the best possible care.
BT_PO 1.37 Discuss the effect of ageing on ventilation
There is another post on this topic here and as I mentioned in that post, I think that Nunn’s Applied Respiratory Physiology is the best for this subject (unfortunately the references are dotted throughout the book)
PaCO2 levels rise as a part of normal ageing due to a reduced capacity for diffusion T/F
PaO2 levels fall gradually as part of the normal ageing process T/F
The ventilatory response to hyercapnoea is blunted with ageing T/F
Compliance of the chest wall decreases with ageing due to decreased mobility of the costochondral joints T/F
FRC decreases as part of the normal process of ageing T/F
Static compliance of the lungs falls with advancing age T/F
Another drug we use on a daily basis (at least where I work as sugammadex is deemed too expensive for routine reversal).
Over 15 yrs ago, (but still seared on my brain) I made one of the 3 drug errors I know of. I gave a baby a 5x excess dose of neostigmine having mistakenly drawn up my calculated volume from the adult rather than baby sized ampoule. One side effect was prominent. What do you think it would have been? It responded very quickly to atropine, which I assumed I had forgotten to give. It was only on inspection of my ampoules once the situation had resolved that I discovered my mistake…
You will find decent information on this topic in any pharmacology text.
BT_GS 1.40 Describe the adverse effects of anticholinesterase agents
Neostigmine will slow the breakdown of ACh throughout the body T/F
Neostigmine will produce weakness via actions at the NMJ regardless of the dose used T/F
Bradycardia is main effect of neostigmine on the cardiovascular system T/F
Neostigmine is highly lipid soluble, so seizures are likely to occur when large doses are given T/F
Neostigmine may cause diarrhoea T/F
Patents taking neostigmine have an increased risk of acute angle glaucoma T/F
There is another post on this material here if you want some more practice.
Describe the time course between an intravenous injection of a general anaesthetic agent to loss of consciousness. Explain the delay using pharmacokinetic principles.
This is core business for us. You need to understand this material really well. It is also excellent material for the vivas (but bear in mind that there will not be overlap between material examined in an SAQ paper and the corresponding series of vivas)
For such a core area, the textbook coverage of this is not great. I suggest Ch 2 in Hemmings and Egan Pharmacologyand Physiology for Anaesthesia.
BT_GS 1.12 Explain and describe the clinical application of concepts related to intravenous and infusion kinetics including: Effect-site and effect-site equilibration time Concept of context sensitive half time Calculation of loading and maintenance dosage regime
BT_GS 1.30 Describe and compare the pharmacokinetics of intravenous induction and sedative agents
Loss of consciousness (LOC) requires the effect site concentration of the agent to reach certain ‘threshold’ concentration T/F
Drug must transfer from the central compartment to the effect site in order for LOC to occur T/F
In general the longer the t1/2keo the faster the onset of LOC T/F
The time taken for loss of consciousness is equal to the time to peak effect T/F
Giving a larger dose of the drug will speed LOC by shortening the time to peak effect T/F
A low cardiac output state will slow time to loss of consciousness as delivery of drug to the effect site is slowed T/F
If you want to have a play around with some PK parameters and see how they alter plasma and effect site concentration then have a look at this site developed by PrimaryLOs
Describe the ionic basis of automaticity in the pacemaker cells of the sino-atrial node
Some pretty core CVS physiology here.
On somewhat related material, I have written a post on slow response action potentials previously. The last statement in that post seems particularly apt for this question…
Pappano and Wier Cardiovascular Physiology would be my go to for this topic.
BT_PO 1.43 Discuss the physiological basis of electrical activity and its relationship to mechanical events including the ionic basis of automaticity the normal and abnormal processes of cardiac excitation
The cells of the sino-atrial node form the natural pacemaker as they have the fastest intrinsic depolarisation rate T/F
Pacemaker cells in the SA node do not have a fixed resting membrane potential T/F
During phase 4 of the SA nodal AP calcium moves into the cell via L-type Ca2+ channels T/F
There is an outward flux of K+ in nodal cells which decreases thoroughout phase 4 F/T
Activation of the vagus nerve will cause the SA nodal cell membrane to be more negative at the start of phase 4 T/F
An inward sodium current (the funny current) is triggered when the membrane potential of the nodal cell becomes more negative than about -60mV T/F