EP19 - Special Episode | Practice Viva with Abe

Hello guys and welcome back to count to 10. My name is Arnie and today we have another practice live-over demonstration. Joining me today is Abe and I want to thank Abe for doing this Vibe. I've done a previous one with Ben just not too long ago. As you guys know doing these live practice live-over demonstrations itself is stressful enough and with a week left to go before the exam I want to thank Abe for taking time to do one of these with me. We're wishing him obviously the best of luck on the day. We're going to keep it the same format as we did last time which is a one minute perusal and two topics five minutes each. So I total of a 10 minute Vibe. Again this is different to the Vibe on the day which is going to be two minute perusal for the candidates and then a 20 minute topic repeated three times so 60 minutes overall. So let's go and dive straight into it. Hey Abe thanks for joining me. How are you feeling a week out from the Vibe? Yeah not too bad. I'm feeling a bit over-vivid at times but I'm just trying to push through that last week because you know there's a clear end point now and yeah just trying to keep the confidence levels higher. Yeah I'm sure you'll smash it on the day that Vibe particularly does start to keep creeping with especially a week to go. You just want your Vibe to be at now and you're ready to go probably. Look I think you'll be do really well and we're going to just keep it really simple today you've done Vibe is with me in the past so it's going to one minute perusal, a 10 minute Vibe, two topics if you're ready to get straight into it. I'll start my one minute perusal now and your opening question is how is general anesthesia different from sleep? I'm just going to repeat that. How is general anesthesia different from sleep? So you have roughly 45 seconds left. So hello there candidate. My name is Arnie. Do you understand the opening question? Yes. Right. Can you tell me how is general anesthesia different from sleep? So they're both reversible forms of loss of consciousness however general anesthetic will you will not be able to be roused by the verbal or tactile stimulation and also anesthesia is drug induced. Yeah good. Tell me do you know of different types of sleep? Yeah so you have non-rem and REM? Yeah and what is the difference between non-rem and non-rem sleep? So non-rem occurs first in the sleep cycle followed by REM and REM is they both have different sort of physiological changes that occur in the body and different restoration sort of purposes. Yeah good. You mentioned a sleep cycle. How long is a normal sleep cycle? For non-rem it's broken up into different stages. The overall would be I think about 30 to 120 minutes where REM is about 15 to 90 minutes I believe. Sure probably less. Yep go on. Yeah. How much of our sleep out of that is REM and non-rem. So if you have to break in down to percentages how much is REM and non-rem? I always say the majority would be non-rem. Long duration however yeah. So you mentioned some stages of non-rem sleep. What stages are you well? There's four stages in non-rem. So it occurs chronologically as I say stage one to stage four as you get deeper into the sleep cycle. So the stage one is associated with differences in terms of if you were to monitor the electrical activity in the brain with EEG you get different waveforms that occur as you progress down the stages. Yeah so what waveforms would you see going from stage one to stage four say if I attached an EEG to your brain as you went to sleep? So stage one you would have theta waves present and then stage two you'd have theta waves with sleep spindles potentially. Stage three would be delta waves with sleep spindles and then finally stage four would be majority would just be delta waves. Are you sure you see theta waves in stage one? It's probably beginning to see them. You would have a larger proportion of alpha waves as well compared to an awake putt. What frequency are alpha waves compared to theta waves? Alpha waves are a lower frequency they're between so beta waves are greater than 20 hertz I believe and alpha waves or I'm going to say 12 to 20 hertz. Yeah good and theta waves. Theta waves would be 8 to 12. Good okay and so moving on from the non-rem stages of sleep do you know if any different stages in REM sleep? I believe there's two phases. Yeah what are those? I'm not exactly sure which one goes first but I believe there's a tonic in a phasic phase. Yeah good. Say I took off an EEG monitor and I wanted to see if you were sleeping using clinical signs. What signs could I use to see if you were sleeping? Clinical signs in terms of like attaching monitoring like say heart rate or yeah so in REM you have an irregular respiratory pattern potentially with an increased respiratory rate. You would also have increased heart rate and other clinical signs would be that you could actually potentially see the eye moving and REM sleep. Yeah good. So now I attached the EEG monitor back onto you but this time you're now under a general anesthetic. How do I tell the difference in EEG between someone that's under a GA versus someone that's sleeping? So in a general anesthetic you'll have other waveforms that you might not have sleeping such as burst suppression. If the anesthetic is too deep potentially you won't have sleep spindles I believe in a general anesthetic. Sleep spindles to my knowledge are high frequency waveforms that are part of the normal sleep cycle in terms of inhibition of inhibitory neurons I believe. I'm going to stop you there. We're going to talk about a different topic now. What is the normal blood glucose in a fasting patient? 3.5 to 5.5 million miles per liter. Okay sure. Say we give this fasting patient a bolus of food. How does their blood glucose go back to that normal range? So you have two particular hormones that are important in this regulation of blood glucose that's insulin and glucose gone. So as you have a yeah after an ingestion of food you'll have an increase to your blood glucose levels as you've absorbed into the systemic circulation. This will then be sensed in the pancreas specifically by the beta cells. This will release insulin to allow the glucose levels to fall to a more normal or normal range. You mentioned some sensors being the pancreas. Are there any other sensors of glucose in our body? Another pancreas is the majority. I'd say the liver but I'm not exactly sure. Good. Anything else in the brain? I'm not sure. That's okay. I'm on a point. So as insulin is released from the pancreas, where is insulin stored within the pancreas? It's stored in the beta cells in the islet of lanyl hands. Good. And what is the mechanism of its release? In terms of the cellular mechanism. Yes. So you have trying to remember now. I think it's de-polarization essentially which results in exorcite traces of the insulin through the vesicles. So you have to have an increased intercellular calcium to achieve this. And this is, I believe, de-polarization of the cell. I can't remember the exact mechanism. I'm going to have to say, yeah. That's okay. Mine a point. You mentioned that insulin, we said that insulin would be increased when glucose levels are increased. What other stimuli do you know of that cause insulin release apart from blood glucose? I believe you also have... I'm not sure. I think cortisol probably wouldn't be one. Are you sure about that? Yeah. I'm just trying to think. Black stress response would increase insulin. So I guess yeah, cortisol could, yeah, it would potentially to increase insulin. ACT8, I'm going to... that's basically cortisol. Catecholamines as well. Yeah. What about types of food? What would they do to insulin? Types of food in terms of carbohydrates? Yeah. What other types of food do you know of? Proteins, lipids? Good. What do you think they would do to insulin? They would also increase its secretion. What inhibits insulin release? And so if you have a low blood sugar level... Good. If you have... or what would inhibit glucose gone as well. So not quite that's a minor point. What's the endogenous half-life of insulin? Endogenous half-life. It's quite short. It wouldn't be very long. I'm not exactly sure at the time. That's all right. So how does insulin increase the uptake of glucose by cells in the body? So you have insulin-dependent glucose transporters. Yeah. It can be found in the muscles and also the out-of-place tissue. So these are glucose four receptors. Good. Or transporters, I should say. So yeah, they need insulin to allow glucose to be driven into the cell. Yeah. What other type of glucose receptors do you know of? You have glute-1, which is in the brain. These are insulin-independent. And also have glute-2, which is found in the liver, again, insulin-independent. And what type of diffusion is this using the glute receptors? It is a... well, it'd be facilitated. Is it required any energy? It would. Yeah. So it's active, facilitated. Perfect. And we'll stop there. That's 10 minutes. Hmm. How do you feel? Yeah. See, I'm a bit scratching on the... It's always... I don't know. One of those topics in insulin. I've read about it so much, but I just always seem to forget it for some reason. Endocrine's always one of those ones, where a lot of the topics I just find that I can't really produce a good viber in all the time. Yeah, I always seem to forget things, but yeah, that's what it is. Yeah, I feel like Endocrine is one of those things. It's one of those where I learn bivers, unfortunately. Yeah. What's one thing that I think... what's one thing that you think you did well and what's one thing you think you could have improved on? I think... I've kind of got this in for like previously. Like, if I don't know something, you just tell them to, you know, you can either give it a quick stab if you have a rough guess, if not just say you don't know, just to move on. If it's not a critical question, like, if it's a critical question, then you should probably try and think about it, give yourself some time to take a breath and just think about it. But if it's just like a minor kind of thing that they want to know about and you don't know, then you just kind of move on quickly. Yeah, yeah. And what's one thing you think you could have improved on apart from that? I'm not sure, but you could probably tell me. Look, I think we've obviously done Vibe as previously in the past and the obvious non-technical thing that I think was pretty easy to see was the way you answered questions and you made a considered effort, whether you've done it deliberately or not, was give short sharp answers and let the example take you. And I think we've discussed this in the past. You can either have two approaches. If you're really confident, you can ramble and talk and give an answer to something, but then you go down the rabbit hole of have I given the right answer to where the Vibe is going and have I lost marks and wasted time. And I think you've chosen the other approach, which is give the answer that they're asking for. And if they want more detail, the examiner will ask for that detail. I think that's definitely a safer way to do it. And it's also a way that you can kind of be led by the examiner, which some examiner's will probably like to do with that. You need to categorise with that. And I think questions such as the endocrine Vibe, I don't really lend itself to categorization really well, but categorization is key to be led down because if you don't mention it, they can't say something for you. In terms of the actual technical Vibe, so these Vibe is there again, I have a habit of giving Vibe is that aren't really core topics, but can be linked to core topics. The example being would you get a Vibe about anesthesia and sleep and would you get a Vibe asking about cycles of sleep? Probably not. If you go by averages, it's probably a really low likelihood. Has there been questions about sleep? Certainly. And so is it fair game? Yeah, it's in the curriculum. Do I expect you to know in-depth knowledge about sleep? No, I don't. I expect you to know the basics, which is no non-REM from REM. I kind of let you off the hook a couple of times. You gave a good definition of general anesthesia, but you probably gave a sub-par definition of sleep. Which again, is opening question is not meant to be any quite marks given. It's supposed to make you feel comfortable, which I think was fine. I wanted more detail. I just asked you I didn't really because you showed that you understood what general anesthesia was and was just fine for me. It's a roughly a 90-minute cycle which is sleep. If you go into technicals and roughly 80-90% of your sleep is REM sleep and so non-REM and then the remaining is REM. And that differs between neonates, adults and elderly. The waveforms that are probably the most important. Just run me through your waveforms again in terms of how they go from most high frequency to lowest frequency. Yeah, so the highest frequency is beta waves. And you go, so they're traditionally like I think rather than 20 hertz. You also have gamma waves, which is like very very high frequency, but I think they're not always talked about when we talk about sleep and stuff. Not really that important. Beta than alpha. Alpha is like eight. Sorry, is 12 to 20 ish. Yeah, so this is where we kind of let you off the hook. Beta is divided into high beta and low beta waves. And then you refer from wave frequency, like it can be 12 to 13 hertz up to like 35 hertz. And high frequency beta or high beta is things that are above 20 and low frequency beta is like 2212. Yeah. And then you get alpha, which is 12 to 8. Then we get into theta, which is 8 to 4. And then delta is essentially 1 to 4. Yeah, we just missed the low frequency. Yeah, like in terms of the ranges, I think I was I was one off. Basically, it was known. Yeah. And again, it's a minor point, but if someone's vibing you on sleep, they're probably love the sleep topics, so they want you to know that. But that's not where this viber is really important. And I think that's the key thing to get out of this, because what the viber was important about, yeah, you knew the waveforms. Like, yes, you got it a bit wrong, but we talked about the non clinical, I mean, the clinical signs of telling someone's asleep. So you knew the heart rate changes, the respiratory changes, and you were quick to that. But I think the real key was knowing how a waveform in the EEG would look for someone who's got under general anesthesia versus someone sleeping. And there you mentioned the key things, which was a burst suppression. I don't think you mentioned isoelectric wave, but you mentioned burst suppression. You mentioned the sleep spindle, and the other things you could mention was a K complex, a K complex and sleep spindles are unique to a sleeping person. And the suppression is unique to a general anesthesia and isoelectric waves unique to a general anesthesia. And I think that was the key in this viber that I had constructed. Could you differentiate the EEGs between? And that showed that you had understanding. If we had time, we would then talk about, you know, I think the fairness of this viber is that this viber could easily skip from being about sleep to just being about waveforms and going and linking that to BIS. Yeah, of course. Yeah. And I think BIS would be a very fair equipment question, equipment viber to get. And then we talk about different kind of drugs that affect BIS. What are the factors that affect BIS? You know, when is the BIS unreliable? And how does the BIS actually work? That would be a very fair viber that would link into this. How do you feel hearing that? Yeah, that makes that makes that makes sense to everything you said. In terms of the glucose, blood glucose viber, so we talked about it at the start, but it's really a ROTELAND one and it's one of those things. You just go back and you have to just look at it because the number one question is, why are we asking any of these questions in a viber? And a good understanding of insulin can be pretty well defended by most people. They can say, as an examiner, well, we fast patients all the time. So therefore, we need to know how insulin and glucose gone work. And we know the triggers that cause insulin exactly where insulin works, exactly the type of receptors that it works on and a really good understanding of these things. And then we manipulate people by giving them insulin infusions if they got high sugars and stuff like that. So it's a drug that we commonly give as well as the fact that we're commonly making patients into a faster state. So that's the defending of why this viber was asked. In terms of your answers, you had the good answers about sensors. So hyperthalamus is the other one that be missed, but pancreas and liver, yeah, and liver being a main glucose stat. And then although you didn't know the specifics about how insulin release is gets released from the beta langahan cells, you knew that it involved calcium, you knew that it involved some kind of depolarization of the cell. And you said the keyword, which is exocytosis, which is all the main points, you know, the specifics is, yeah, glucose goes into the cell, it gets made into ATP, ATP blocks potassium ATP channels, causes the depolarizing of the cells, the calcium influxes, calcium abundance to vesicles that have stored insulin. And that causes exocytosis of insulin. The triggers of insulin release are a bit tricky, but they're things like amino acids, fatty acids, glucose gone is actually a trigger, and that's a trick question. So glucose gone is a trigger for insulin release, because it's again, yeah, but you should have good understanding because you show like it's a stress hormone like cortisol in stress, we have increased insulin release. So cortisol will be a trigger as well. And what inhibits it is yeah, low BSL and exercise. And then other drugs like some other substances like somatostatin. Yeah, insulin is not very long half-life because we have to recreate it all the time. So it's like a couple of minutes in terms of endogenous half-life. And then we talked about glue receptors. And again, we could have gone and talked about different types of diffusion. So your active processes versus your passive processes being passive, not requiring energy. So simple diffusion, facilitated diffusion, and active requiring energy. And they can be very co-transport and other things like exone and dosytosis. So that's kind of the gist of that. And again, it's a pretty dry viable. I think I've at all the main points, but your technique of answering quickly and having short, sharp answers, I think was a key to get through the viable really well. Do you have any takeaways now that you had some feedback? No, I think I agree with all your points. Like you said, I think just trying to be short snappy, just answer the question really. I've had, and when I was doing viable early on, I was rambling a lot, and you know, I could see that he can kind of sense a bit of a loss of confidence with the examiners when you do that. So you just want to just be short snappy and so what they've actually asked and just leave it like that and direct you where they want to go. Yeah. And I think your comfortability in this setting and also will bowed well on the day when it's a different environment, and it's a bit more stressful. So I want to thank you for doing this because I know it's not the easiest doing a live practice fiber demonstration. It's something that I'd be very nervous doing as well. So I want to thank you for doing that. Oh, good. And I wish you all the best of luck in your viable next week. Yeah. Good luck next week. And thanks to everyone listening. I hope you guys get something non-technical and technical out of this. And again, good luck to your Abe next week. And I know you'll smash it and get the result that you want. Cheers, mate. [Music]