Yesterday was the anniversary of Michelangelo’s death (1564). Michelangelo was a very keen observer of humans and created a body of anatomically correct drawings. He had apparently hoped to publish a volume of anatomy for the artist, but it appears that this dream was never realised.
You may enjoy reading this article where the “delivery” of Adam in the Sistine Chapel is viewed from an anatomical perspective ( quite amazing – but I couldn’t find a suitable LO!)
It appears that he also had an interest in renal anatomy and the functions of the kidney, so let’s go with that theme for today.
BT_PO 1.61 Describe the functional anatomy of the kidneys and urinary tract
On Tuesday this week, I conducted a webinar discussing some tips for the primary exam.
If you are interested, the slides and a recording of the majority of the talk, are available on Networks.
There was a question I was unable to answer on the evening which I said I would answer here today. I also thought I would highlight a couple of useful resources that I mentioned during the talk
The question related to the MCQ paper and what writing implement it is to be answered with. The answer is pencil! All stationery requirements for the MCQ paper are supplied by the College. However, you need to bring your own (pens) for the SAQ.
You can find all the details you should need regarding what to bring, here in the “Useful information” section.
I mentioned some resources which have been discussed on this podcast before, which are likely to be helpful to those who are earlier in their exam preparation. Below are the links to the posts which discuss them:
I mentioned that there have been posts on antiarrythmics in the past, but not one on these agents as far as I could see. They do appear in the tocolytic section of syllabus too, so you might find a few statements on them there.
I am going to focus on verapamil today as an agent with significant cardiac effects. It is not a benign drug, especially when other drugs are given with it.
BT_PO 1.57 Describe the pharmacology of antiarrhythmic agents and their clinical applications including calcium antagonists
Verapamil produces both bradycardia and negative ionotropy T/F
Verapamil is a good adjuvant to dantrolene in the treatment of MH as a means to control tachycardia T/F
The use of an intra-operative esmolol infusion, as part of a balanced anaesthetic, in a patient on verapamil may produce profound bradycardia T/F
Calcium channel antagonists enhance recovery from non-depolarising neuromuscular blockade T/F
*High dose insulin therapy can be used in the management of verapamil overdose T/F
*this one is not core, but quite interesting I thought
I had a look at the antiarrythmics page yesterday, when writing my post and saw specific mention of a drug I confess to never having heard of. Are you in the same boat?
How could this drug have escaped my attention? It seems to have become available around the time I finished medical school, so no real excuse there. Perhaps it is due to its specific indication for use…
I thought it was a good opportunity to learn something new and share it with you. All the statements below are true and are what I thought most noteworthy about this previously unknown (to me) drug…
BT_PO 1.57 Describe the pharmacology of antiarrhythmic agents and their clinical applications including ibutilide
Ibutilide is used for pharmacological cardioversion of atrial fibrillation and atrial flutter (but is more effective for the treatment of flutter)
It is a class III antiarrythmic which activates the late inward sodium current
It is administered by intravenous infusion
Over 80% of the dose excreted unchanged by the kidneys
It is more effective than sotalol at terminating the arrythmia
The main adverse effect is triggering of polymorphic VT which occurred in about 1.5% of trial patients
The risk of Torsades is dose dependent so tends to occur towards the end of the infusion but the risk is short lived due to the short t1/2 (3 hrs)
If you want further information, there are a few good review articles but they are all behind a paywall ( I find that very annoying, especially when over 20 yrs old…).
This is another of the “left over” LOs. There have actually been plenty of posts on anti arrhythmic drugs, you just need to search them individually.
The classic way of thinking of these drugs is using the Vaughan Williams classification. Miles Vaughan Williams died in 2016, just short of his 98th birthday. He is not to be confused with the other famous Vaughan Williams, Ralph, the composer, who was his father’s cousin. Perhaps you can put this rendition of The Lark Ascending on in the background whilst reading this post.
The Vaughan Williams classification has stood the test of time. A recent article published in Circulation helps place new drugs and understanding of electrophysiology in the context of the original classification (you do not need to know anywhere near this level of detail)
The answer to these statements should be found in most pharmacology texts
BT_PO 1.56 Describe the physiological and pharmacological basis of antiarrhythmic therapy including classification based on electro-physiological activity and mechanism of action
Individual antiarrythmic drugs work via a single class action T/F
Class Ib antiarrythmics reduce the peak Na+ current and shorten the action potential durationT/F
Class III antiarrythmics enhance potassium conductance in the heart T/F
Sotolol, as a beta blocker, has exclusively class II action T/F
Adenosine fits neatly within the Vaughan Williams classification *T/F
*you may change your mind on the answer to this one if you read the Circulation article
Today we have a post from a guest blogger – a previous chair of the ANZCA Primary Exam. He has made a couple of appearances on the blog previously (here and here)
Stewart Adams died recently. He discovered ibuprofen, and knew that he had discovered a great drug when he took it and it cured his hangover. I’m sure all ANZCA trainees drink alcohol sensibly, but if you do over imbibe after your future success in the primary, you can always remember Stewart Adams if you are considering pharmaceutical remedies.
In addition to doing copious timed SAQs, I hope you have been practising doing 1 minute answer plans. In reading time, you will have 1 minute per question to think about and write a rough plan of your intended answer.
There have been two previous posts about using reading time effectively.
It’s not that difficult to learn this material. I would strongly recommend that you read the two references below. They present the material in a straightforward, and very clinically relevant way.
T/F specificity is the ability of a diagnostic test to detect people who do NOT have a disease
T/F to calculate the sensitivity and specificity of a new diagnostic test, you would apply it to a random sample of the general population
T/F a false negative is a person who HAS the disease, but tested negative on a diagnostic test
T/F to know whether a diagnostic test will be of any clinical value, it is essential to know the prevalence of the disease being tested for
T/F positive predictive value tells us the probability that a given patient HAS the disease if the test is positive
Make sure you understand this material well enough to answer this past SAQ….
A new test called the “intubation score” has a reported 90% sensitivity and 70% specificity when used to predict difficult intubation. Describe how this information and other statistics related to this test can be used in predicting difficult intubation. How will the incidence of difficult intubation affect the performance of this test? (pass rates have previously been 29-53%)
Lalkhen A, McCluskeyA. Clinical tests: specificity and sensitivity. CEACCP 2008; 8: 221-223.
Yentis S. Predicting difficult intubation – worthwhile exercise or pointless ritual? Anaes 2002; 57: 105-109.
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)
Warters etal. The effect of neuromuscular blockade on mask ventilation. Anaesthesia, 2011; 66: 163-7
Difficult Airway Society. Management of unanticipated difficult intubation in adults (Flowchart), 2015.
Empis de Vendin etal. Recurrent laryngeal nerve monitoring and rocuronium: a selective sugammadex reversal protocol. World J Surg, 2017; 41: 2298-2303
Kam & Power 3rd edition, page 29-30.
Mirzakhani etal. Neuromuscular blocking agents for electroconvulsive therapy: a systematic review. Acta Anaesth Scand, 2012; 56: 3-16.