I would strongly recommend that you don’t apply Monday though. Today is a good day.
Some of you may have noticed that I have migrated the List of LOs over from the previous site. You can now access this LO list through the menu on the home page.
BT_PO 1.50 Describe the cardiovascular changes that occur with morbid
An increased extracellular volume may be a causative factor in hypertension in the obese TRUE/FALSE
Blood volume per kg body weight is less in the obese than in the lean TRUE/FALSE
Hyperinsulinaemia may be a causative factor in hypertension in the obese TRUE/FALSE
A cuff that is too small will over-read the blood pressure in the obese TRUE/FALSE
Fat blood flow is approximately 10 ml/min/100g TRUE/FALSE
I have taken this from Hemmings and Hopkins Chapter 71 but the material is scattered throughout the recommended texts and can also be deduced if you have a good grasp of the topic
Coming in an aesthetically pleasing little orange container, glucagon is a drug anaesthetists administer infrequently. Funnily enough the most common indication that we give glucagon for has nothing to do with hypoglycaemia. Rather it is given to treat suspected spasm of the sphincter of Oddi demonstrated on an intraoperative cholangiogram when performed during a lap chole. The second most common indication in our sphere of influence is probably the management of impacted food boluses. Both of these indications relate to the smooth muscle relaxant action of glucagon.
Glucagon is an anabolic hormone TRUE/FALSE
Glucagon is synthesized by the alpha cells of the islets of Langerhans TRUE/FALSE
Glucagon is effective in the management of beta blocker overdose because it firmly binds to adrenoceptors TRUE/FALSE
Glucagon is an inotrope and chronotrope TRUE/FALSE
Glucagon binds to a G protein coupled receptor and inhibits adenylate cyclase activity and thus reduces cAMP TRUE/FALSE
A standard Mars bar (53g) contains 30g of glucose. They used to be given to pregnant women as a component of the glucose challenge test for gestational diabetes. I don’t know if this is still the case.
The glucose transporter, GLUT-4, is ubiquitous and found in most cells in the body TRUE/FALSE
Hepatic uptake of glucose is dependent on the presence of insulin TRUE/FALSE
Glucokinase phosphorylates glucose and is a pivotal enzyme in the glycolysis pathway TRUE/ FALSE
Alterations in glucose transport occur within seconds of insulin release TRUE/FALSE
Insulin has trophic and mitogenic actions TRUE/FALSE
A bonus question- are glucose and dextrose the same thing?
Vallecula suggested that the photo from the other day (quite similar to this one) could have been the wall of the operating theatre due to platelet dysfunction. I liked that description and thought it apt for today’s topic….
Here is a link to the BJA education article on antiplatelet agents. The link above will take you to the post with an article on the physiology. Again these agents will be widely covered in the textbooks…
BT_PO 1.122 Classify and describe the pharmacology of anti-platelet drugs
Both clopidogrel and prasugrel are prodrugs and subject to inter-individual differences in activity due to genetic polymorphism of their metabolic pathways TRUE/FALSE
Both clopidogrel and prasugrel block the ADP receptor and are hence associated with the same risk of bleeding as each other TRUE/FALSE
Platelet function returns to normal approximately 7 days after ceasing abciximab TRUE/FALSE
All GP IIb-IIIa receptor antagonists can produce thrombocytopenia TRUE/FALSE
Low dose aspirin (75 100mg/day) is the only drug which selectively inhibits the COX-1 isoenzyme TRUE/FALSE
(cake via pinterest – yum!!)
It is a year ago today that Dr Primarylos authored the first ever post on this blog.
Since that time: there have been 10 contributors to the blog; we have posted 280 posts; the blog has been viewed almost 33,000 times in 69 countries, across all continents except Antarctica.
Thank you so much for your continued support of our blog. Our aim is to provide a useful resource and I hope that we are doing, and continue to do, that.
As a little bit of a one year retrospective, I have included links to the most popular posts by each of our authors (reverse alphabetical order as those guys never get to be at the top)
woundedwildebeest Examiner musings on candidacy Pt I
vallecula Study Tip – doing effective revision
transpedanticacid Preparing for the Primary
SpeakNoEvil 8 minutes….
primarylos Induction Agents BT_GS 1.57 (this is co-incidentally also the first post – that’s cool)
lantanapurpura BT_PM1.18 : neuraxial opioids
cynicalanaesthetist Cool books that should be on the ‘Recommended texts for the Primary’ list #2
I found it interesting that many these posts were not actually related to the learning outcomes, but rather study tips or encouraging words. Please do be encouraged – the ANZCA Primary Exam is an exacting one, but is is achievable and your presence here is a positive sign.
Cue the music – let’s celebrate!!
That’s the actual Ether Dome pictured above. You can visit it- I haven’t done so yet but it is on my bucket list. The picture on the back wall was commissioned after the 150th celebration of Ether Day. Although possibly not as famous as Robert Hinckley’s painting, ‘The First Operation with Ether’, it is certainly more historically accurate.
To the statements then regarding National Anaesthesia Day:
It has always been celebrated on this date in Australia. False, it has only been recently that Australia has deigned to celebrate it on the actual date.
Morton tried to patent ether calling his mystery drug ‘Letheon’. True, he and his mentor, a Professor of Chemistry named Charles Jackson, applied for and got a patent. This was withdrawn later- Morton was determined to get all the recognition (and profits) for himself. He and Jackson fought a bitter lifelong quarrel to be recognised as the sole true discoverer of anaesthesia.
Morton was running late on the momentous day setting an unfortunate precedent. True, he was having problems getting his inhaler device ready in time. Surgeons have been bemoaning ‘equipment issues’ on our part ever since.
Morton was the first person to administer ether successfully for a surgical procedure. False, we know at least one other person successfully used ether for surgery prior to October 16, 1846. A rural doctor called Crawford Long used ether in 1842. Idiot didn’t tell anyone about it and he didn’t publish his findings until 1849.
Morton killed himself by cutting his femoral artery at the age of 48 while imprisoned. He was incarcerated for throwing acid in a prostitute’s face. This is false. The details relate to the unfortunate demise of Morton’s partner, Horace Wells. He died at the age of 33, the other details are correct. He never recovered from being booed off ‘stage’ after his failed attempt to demonstrate anaesthesia with nitrous oxide. He was a victim of the pharmacokinetic properties of the agent more than a failing of the agent itself. Morton’s choice of ether, a highly soluble agent with a slower offset of action, was the key to his success. Morton died of a stroke.
Write brief notes on the pharmacology of tramadol.
A question like this is a gift because it requires little more than reproducing what is on one of your summary cards! This question requires no higher order application or integration of knowledge, but it is still important for core drugs like tramadol, to be able to recall pharmacological data in significant detail. This is what you should be doing when you draw up the drug!!
T / F tramadol is a racemic mixture of 2 enantiomers – the (-) isomer inhibits noradrenaline reuptake and the (+) isomer inhibits serotonin reuptake
T / F tramadol is metabolised by CYP2D6 to O-desmethyltramadol, which is responsible for most of the opioid effect
T / F patients who are ultra-rapid codeine metabolisers, are also ultra-rapid tramadol metabolisers
T / F tramadol is 90% renally excreted, with 30% being excreted as unchanged drug
T / F tramadol has low potential for dependence and abuse
T / F tramadol does not cause respiratory depression or constipation
T / F some anaesthetists describe tramadol as a weak analgesic that reliably causes nausea and vomiting
Describe the pharmacodynamic properties of propofol EXCLUDING its effect on the central nervous system. Describe how these influence clinical use.
Propofol is a drug which anaesthetists use every day. Candidates should not be surprised to find that the primary exam requires an in depth and intimate knowledge of this drug. Many candidates did not address the second part of this SAQ at all.
T / F propofol does not inhibit hypoxic pulmonary vasoconstriction, and is a slight bronchodilator so it is suitable to use in patients with COAD
T / F propofol reduces uterine tone, so it can increase the risk of PPH
T / F a dangerous fall in blood pressure can result from a propofol induction if the patient is hypovolaemic, because propofol is a direct vasodilator and inhibits the baroreceptor reflex
T / F propofol blunts upper airway reflexes – it was serendipitous that propofol came into clinical use at the same time as Dr Archie Brain delevloped the LMA
T / F propofol increases intraocular pressure, so it should not be used in cases of eye trauma
T / F a propofol infusion alone can reliably prevent movement during surgery in an unparalysed patient