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Nerve Structure and Action Potential for Orthopaedic Exams
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Nerve Structure and Action Potential for Orthopaedic Exams
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Language: EN.
Segment:0 .
Good evening, everyone, welcome again. This week's the teaching session delivered by our first guest mentor group, just to introduce ourselves we have for us, I'd been facilitating the session tonight. We have chosen he will be the presenter and we have Ramesh. She will be supporting him.
We also have word and David from the mentor group. Sean is going to present very important and very hard topic. Very few people are there to talk about it, so this is kindly prepared. It is about nerve anatomy, physiology and must neurophysiology and how to draw a nerve. So there'll be two parts of this presentation, first part about how to draw a nerve and how to discuss and talk about action potential.
And after a small break, there will be another discussion about neuromuscular junction and the function of muscle cells. Please use the chat option to ask any questions next to your name. You will find raise hand option also to raise your hand and please stay alert. We randomly pick one of the candidates to answer questions that Shawn feel are appropriate.
So over to Shawn without any further delay. Thanks thank you for asking. First of all, congratulations. I know you guys are about to see the exam again, but congratulations to the guys who have passed and anyone who hasn't passed. Stick with us. We will help you. Don't worry along those lines.
The first thing to say about nerves is everyone panics about these things. There is nothing to worry about. So if you ask to draw a nerve, the first thing to do is to draw three circles. So just three quick circles. To we and then draw lines connecting these circles, so.
And again, my lack of artistry is showing that up very nicely. So what you then have is you say this is a nerve, this is a cross-section of the earth, which you then get is your nerve covered by an epimysium museum. Your middle layer, which is a bunch of nerve, which is a bunch of nerve cells, which is a bunch of nerve fibers which are bonded together by Perry.
And finally, your end of year, which then has individual nerve cell fibers. OK, axons together now the reason why that's important is it's part of the understanding that this is the cross section. But understanding that the blood supply to these nerve cells are actually twofold. There's extrinsic and intrinsic blood supply. The extrinsic blood supply enters through the epi and the.
So you can do that through the app and then attaches onto a pari pari arterial, which essentially is just on the outside of the Perry. OK that's the extrinsic blood supply. The intrinsic blood supply virtually drops down through that, and then individual nerve cells nerve axons with the blood supply, individual capacitance of the nerve.
OK, so what that means, then, is when you mobilize nurse nerve, like when you're doing an ulnar nerve transfer what you do ulnar nerve release and transfer what you're doing is your device realising that nerve by disconnecting it from its expensive blood supply. However, the intrinsic muscles supply is still preserved because there's communication all the way along the end zone. And what that that clinical application is, if you're doing your transfer and make sure you don't put tension on your nerve because if you put a little bit of tension on the nerve, you're actually stopping the blood supply.
And the more tension you do, the higher the more likelihood you lose the blood supply to the to the intrinsic blood supply. You're going to lose the extrinsic anyway because you mobilize it away from its vessels. However, the communication of the intrinsic is still preserved, so this is an important clinical aspect of this knowledge. OK that's when you have to go a nerve cross section. Now we're going to again excuse the very bad drawing, but this is not an artistic competition, we're going to draw a nerve cell.
This is what they're going to ask you to do. So what I do is just draw a large, very poorly drawn circle and then going on down the line with dendrite coming in this way, I say that it's a new created cell. What is a nerve cell? What is nerve? It's a highly specialized connective tissue, which is a form of communication and from the nerve to the rest of the body, from the brain to the rest of the body.
And it's quite important to show that there is a mound here. This area? The x-amount. And then what you need to do is demonstrate that you understand that there are schwann cells which create myelin chiefs. And I'm refer to these as, you know, the grumpier between the mining chiefs.
OK why is that important? Because the mining chiefs essentially are insulation around nerves, the nerve axon. They prevent the communication of sodium and potassium moving through that to the axon in that area. So it's like a big copper wire with the conduction plastic on it, with small little gaps into it. The this is important because this is what the term that you need to use is sultry, sultry conduction sultry conduction.
A couple of other things you need to talk about when you're drawing. This is to say that the the intracellular intracellular the sodium is in low concentration or potassium is high concentration. Extracellular potassium is low concentration. Sodium is high concentration. How would you remember that? Well, what your normal blood tests your potassium is a low number six one.
Lower sodium is 122. That's blood that's outside your cells. This is important because this is all about nerve production. So I then describe the the conduction in this situation. I say that there's a synopsis on dendrites where nerve stimuli come in or other stimuli come in, for example, stretch receptors and muscle as part of your reflex pathway. So if your stimuli are coming in, they hit the deck, right?
They then go through the cell body. And the cell body has an effect on the action potential that does come, the action potential slot can dissipate or magnify in the cell body, depending on the function of that cell body. Once it reaches the mound, it then reaches it, then reaches an all or nothing threshold. If it passes that threshold, it will continue to conduct down.
So we will drop this diagram for now and come back to action potentials. We talked about thresholds you need to then draw. At this point, you need to draw an action potential graph. Everyone has a tendency to do this. I think that's just setting you up for having to explain something a little bit more difficult to explain by making a graph a little bit more difficult to do.
So what I would suggest instead is putting your y-axis much higher. The reason why is you can then demonstrate straightaway that this access is a negative. You start off in your negative area and you can go up to a positive or. So you draw your own, your y-axis, make sure you do show that you're talking about milliseconds.
OK, because all of this is quite important in describing how the action potential comes, I remember we talked about the threshold so you can get multiple stimuli hitting the dendrite multiple action potentials, trying to reach the amount of the action if if you get a small hit. Which doesn't reach a threshold.
It'll go back down again if you get multiple hits or one large hit. It eventually reaches the threshold, which is usually around minus 55. And once that happens, the actual potential propagates. Now what you then get is about one millisecond of action potential and then you go down to hyper minus level. And this area is what we call the refractory period from here to about.
Here is the refractory period. So what's happening in this situation? Everyone knows how to draw this diagram, but they can't explain what is happening. So once action potential reaches the mound, once it reaches a threshold, sodium channels a voltage gated sodium channels start to open. These sodium channels allow diffusion of sodium across the cosmology gradient into the cell.
So you've got high concentration sodium outside the body, outside the cell body. Now you're getting the sodium diffusing into the axon because the voltage gate is open. Once the voltage gate is open, it stays open only for one millisecond. So as much sodium can get in as quickly as it can. This creates a second voltage gated channel, the potassium one to open.
This is again a diffusion type channel. This allows potassium to move from a low concentrated area to a high concentrated area. So if I just change the colors of the diagram, which is going to show you what the what's happening with the sodium gated channel is about here doing the same thing and they're closing at this point. Potassium gated channels.
Are here and the only start to open here. And then close down here once. Once we reach the threshold level where we've got to to negative charge the action potential. Sorry, the charge within the action is negative, then the ATP pump ATP pump sodium potassium exchange pump, which is ATP controlled, is then activated.
This redresses the balance until the balances come back to normal again, with sodium leaving the cell in exchange for potassium coming into the cell. There can be no activation of these nerve cells, so that's that prevents multiple rapid signals coming down that axon. Therefore, it's in motion, for example, that actually prevents hyper stimuli of the neuro or the motor units.
OK why is this important to understand in terms of our clinical application? So first of all, we talked about solitary conduction. There is another form of corruption without myelin sheath where you can get just the diffuse conduction as there's one group of sodium channels open, the next one's open. That's a slower conduction than the substrate conduction. So if you lose your schwann cells, if you lose your myelin sheath, you lose the ability to treat conduction so your reflexes are slower, your ability to respond to one much slower but more important in our everyday applications.
We use local anesthetic. We use it for every block. We give local anesthetic topically. We give it into arthroplasty interventions. The effect the way the local anesthetic works, its sodium channel blocker, it binds reversibly to the sodium channels. So once they're opened the voltage gate. Once the voltage gated sodium channels are opened, the local anesthetic binds to them and prevents them from closing by preventing them from closing.
They prevent the the whole process from occurring. They block the channel completely, so therefore no sodium can get in. Therefore, no action potential can propagate. Does that make sense? That's the clinical application there. If we talk about. The pathway down the axon, the you can appreciate the voltage gated channels are not energy dependent, however, the sodium potassium pump is energy dependent.
ATP dependent on ATP requires oxygenation. Again, this is the reason why it's important to know the blood supply and to protect the blood supply when you're doing a transfer. OK for us, can I anyone got any questions so far? I haven't received any particular questions yet. But do you feel you have a question to ask? Let me know. So can I ask?
Anyone can tell me about why they're why it's so important to know about the threshold for conduction. Is there any clinical application to that threshold? Anyone wants to answer. I will look. I will pick someone randomly. So excuse me, guys, will our big fires. I know he's a good guy.
If I ask you to answer one question, please. Trying to work to make. So, yes, we can hear you. Yeah OK. Sorry, I've missed the last part there. A lot of question and what not, but pretty sure, to be honest. OK, so during the conversation, during my presentation, I mentioned that there's a threshold level that's required for propagation of the actual potential is there.
Can you think of a reason as to why that has clinical applications in our everyday life? I think it's because when the threshold is reached, the representative propagates and the strength doesn't matter if it's not reached. OK so for example, in your I mentioned earlier on that your reflex pathway is is action potential control, but also specifically how many sensors activate and send the signal up to the spinal cord.
So if you were doing a patellar reflex on a patient who you get, if you press on your patella now, press lightly on it. What what happens is you don't get to quads, kick back. You don't get to kick the patella reflex reflex correct pressing lightly. It's really hard, really fast. That creates hyper stimuli of multiple receptors, which are being actioned by quick movement, but also by high force.
They send the signal up. There's no time for the signal to go up to the brain to say, actually, I know that this is what's happening. Don't give a kick back. Instead, they go through the spinal cord and come straight down because enough stimuli, enough sensors have received and hit the dendrites. So if I draw that cell again for you just very quickly.
So if this sell sell, so this dendrite, this dendrite and this dendrite all get hit and they send their stimuli into the mound here, they're more likely to get a propagation there rather than just one dendrite sending a signal across. Does that make sense? So if you get one sensory signal coming here hitting onto that dendrite with a single pressure, not hard, fast on your patellar tendon, you're not going to get which special, but you're getting multiple hits.
Therefore, this cell is propagating multiple action potentials, which eventually all congregate in the mound, which reaches threshold they they collect together, they connect together, and then you get a reflex, then you get a signal sent to your quads from their direct. OK, I have a question. Sean, I think a common exam question when when these issues are discussed is the game theory and would you be able to cut this have been asked about the game theory in this scenario?
I don't know if that's something you see in reference to the voltage gates in reference to pain. Is that? Yes yeah. In reference to pain. I'm not familiar, but I do know that a regional sympathetic dystrophy is the loss of impedance or partly due to loss of impedance of feedback in process.
So what's happening is you're getting multiple firing of your action potentials, your multiple sensory feed into your nerves. The nerves are not getting activated. This is your cell cell body. And if you remember, I said some of the cell bodies inhibit action potential transmission depending on what their function is, while others multiply it. So for example, if you're getting a single sensory associated with pain that is more likely to go through to the axon than transmit from the dendrites across the cell body into the axon for cells that are designed to have reflexes to pain.
While the wild cells that are not designed to stop you from going into tenotomy will try to decrease, the number of it will be inhibitory to the actual potential crossing the cell body. So you need actually a lot more stimuli before the actual potential across the cell body itself. Yeah, thank you.
OK, guys. So let's. That's a good question, David, do you want to answer that one? Polio what about polio? I was just thinking that's quite common question is particularly in post-polio syndrome?
Yeah I'm sorry, I haven't thought about that. So you have no, I just remembering you had a very good explanation of it previously. That's why I was thinking about it. That's a popular question at the moment. It's gone from my mind, but we'll think about it the next time. What is the question, david? Post-polio syndrome with regards to action potential?
Why do why do you get this so polio in terms of the virus, you have the acute infection when their children, then when they're older, they have post-polio syndrome, which is a result of reduced was it reduced muscle neuro neuromuscular junction? I can't quite remember off the top of my head, but there's a common popular question and it's quite common. A good. Sorry, I'm a bit too close.
No no, no, no. Fine fine. I mean, I know it's coming to me. I'll get it now then. But yeah, I think I think that's a very good question, David. I think post-polio scenarios can come in exam. Very rare these days, obviously, but they can't come, particularly in the clinical part of the exam. Yeah, you could be faced with polio or many years ago, you know, from the 40s or 50s.
And it's important to know that post-polio present with muscle weakness, paralysis, myalgia and fatigue. But the actual neurophysiological reason behind it is something that we we need to look into. Yes, thank you. All right. I know the I've got the answer somewhere. I'll use it when I did my webinar as a little bit at the end.
Don't worry. That'd be great. Thanks, David very much. Sorry, I just I just remembered what post-polio connection to nerves. So in a patient who suffers polio, they lose a lot of their nerves, initially in the first hit of their disease. However, those patients are often the ones that do well because the initial attack polio that seem to be working well and so on there they have no problems.
What's happening with those is they get hit at a young age. So when those nerves that supply the muscles, let's say, for example, your quadriceps, muscles, the nerves that are supplying your quadriceps, muscles as they get injured in polio, our nerves grow, grow their dandruff. So if I draw this picture to you, this is actually quite a good point. Thank you very much, David.
So if in terms of a motor unit, what is the definition of motor unit? It is a single nerve and all the muscles innovated by that single motor nerve. So when a motor unit is taken out by polio, the surviving motor units try to recruit the muscles that were lost to the to the off of the first nerve. So what you get is an extra axon growing off and creating further neuromuscular function to recruit these muscles.
So I'm trying to draw muscle here, so to recruit these different capacities. So if you've got multiple accidents, each one is different to my classical. So what then happens is as you got bigger and bigger motor units, a single injury to a single motor unit, a single die off as the cells get fatigued and tired over time. As the cells die off with aging, the effect is much more pronounced at a younger age and of these patients, because for one nerve to get hit and post-polio syndrome, what's really happening is the cell is dying off and a large percentage of the muscle and the quadriceps muscle, for example, are dying are dying off.
That entire motor unit is not working. So that's the progressive weakness that you see in the patient who's getting developed post-polio syndrome. Does that make sense? Yes, it does. Thank you. Sure sure, we have another five minutes to go. Yeah so I think if there's no immediate questions, you need this and go on to neuromuscular junction and how the action potential conducts across.
Yeah, I think we will have a small break. We have a few minutes, everyone. If anyone has a question, let me know we will pass it on to members of the faculty to see if we can have any answer to your questions or if you have any questions we can put it through. No, they don't seem to be any questions at the moment.
So, Ramesh, would you like to add anything to Sean's talk about the nerve structure and physiology? I think it was a very sort of comprehensive, concise and comprehensive. Was pretty good. The only thing I want to ask is what you mentioned refractory period is that period just after the actual potential that arises or is it the whole thing?
So the once the sodium channels are activated, they can't be reactivated for two milliseconds from that moment on. So if you look at the period, it's actually over two milliseconds. Unfortunately, we always throw our action potential to cut off before the two. So my advice is make you draw your thing, right? So you don't have to explain that it's too many seconds.
OK, that's a good point. Yeah thanks. OK excellent. Excellent. Thank you. Good question. Good questions are as important as good answers. OK, guys. So we will have a small break, five minutes break for people to stretch their legs and we will restart again in five minutes with another blog talking about more about action potential, how it propagates through the neuromuscular junction and through the muscle cells.
Very important exam question and topic and very important to understand. Well, that's it's easy to score high. If you understand this concept, examiners will be very impressed. So I'll end this meeting, guys, and I will see you again in five minutes. I will post another link again. No, it's not too late.
It's not too late. But I just missed the last part because I recall because, you know, people have passed the exemption. There are phone calls coming. So regarding the questions of the and physiology, one of the common question is what happens to the nerve when it is dissected? So I think this is something which can be asked from any one of the candidates, and they can prepare because it's written quite nicely.
One of the books but there is a common question they can ask actually in what happens proximity and what happens digitally and what happens in different areas and how how it that can be a clinical scenario that you are operating and then suddenly you cut the nerve. Then what will happen? We will. We will do that. We will do that at the end of the next session as a as a hot topic hot seat session.
And you'll be the examiner for it. OK, so OK.
Segment:0 .
Good evening, everyone, welcome again. This week's the teaching session delivered by our first guest mentor group, just to introduce ourselves we have for us, I'd been facilitating the session tonight. We have chosen he will be the presenter and we have Ramesh. She will be supporting him.
We also have word and David from the mentor group. Sean is going to present very important and very hard topic. Very few people are there to talk about it, so this is kindly prepared. It is about nerve anatomy, physiology and must neurophysiology and how to draw a nerve. So there'll be two parts of this presentation, first part about how to draw a nerve and how to discuss and talk about action potential.
And after a small break, there will be another discussion about neuromuscular junction and the function of muscle cells. Please use the chat option to ask any questions next to your name. You will find raise hand option also to raise your hand and please stay alert. We randomly pick one of the candidates to answer questions that Shawn feel are appropriate.
So over to Shawn without any further delay. Thanks thank you for asking. First of all, congratulations. I know you guys are about to see the exam again, but congratulations to the guys who have passed and anyone who hasn't passed. Stick with us. We will help you. Don't worry along those lines.
The first thing to say about nerves is everyone panics about these things. There is nothing to worry about. So if you ask to draw a nerve, the first thing to do is to draw three circles. So just three quick circles. To we and then draw lines connecting these circles, so.
And again, my lack of artistry is showing that up very nicely. So what you then have is you say this is a nerve, this is a cross-section of the earth, which you then get is your nerve covered by an epimysium museum. Your middle layer, which is a bunch of nerve, which is a bunch of nerve cells, which is a bunch of nerve fibers which are bonded together by Perry.
And finally, your end of year, which then has individual nerve cell fibers. OK, axons together now the reason why that's important is it's part of the understanding that this is the cross section. But understanding that the blood supply to these nerve cells are actually twofold. There's extrinsic and intrinsic blood supply. The extrinsic blood supply enters through the epi and the.
So you can do that through the app and then attaches onto a pari pari arterial, which essentially is just on the outside of the Perry. OK that's the extrinsic blood supply. The intrinsic blood supply virtually drops down through that, and then individual nerve cells nerve axons with the blood supply, individual capacitance of the nerve.
OK, so what that means, then, is when you mobilize nurse nerve, like when you're doing an ulnar nerve transfer what you do ulnar nerve release and transfer what you're doing is your device realising that nerve by disconnecting it from its expensive blood supply. However, the intrinsic muscles supply is still preserved because there's communication all the way along the end zone. And what that that clinical application is, if you're doing your transfer and make sure you don't put tension on your nerve because if you put a little bit of tension on the nerve, you're actually stopping the blood supply.
And the more tension you do, the higher the more likelihood you lose the blood supply to the to the intrinsic blood supply. You're going to lose the extrinsic anyway because you mobilize it away from its vessels. However, the communication of the intrinsic is still preserved, so this is an important clinical aspect of this knowledge. OK that's when you have to go a nerve cross section. Now we're going to again excuse the very bad drawing, but this is not an artistic competition, we're going to draw a nerve cell.
This is what they're going to ask you to do. So what I do is just draw a large, very poorly drawn circle and then going on down the line with dendrite coming in this way, I say that it's a new created cell. What is a nerve cell? What is nerve? It's a highly specialized connective tissue, which is a form of communication and from the nerve to the rest of the body, from the brain to the rest of the body.
And it's quite important to show that there is a mound here. This area? The x-amount. And then what you need to do is demonstrate that you understand that there are schwann cells which create myelin chiefs. And I'm refer to these as, you know, the grumpier between the mining chiefs.
OK why is that important? Because the mining chiefs essentially are insulation around nerves, the nerve axon. They prevent the communication of sodium and potassium moving through that to the axon in that area. So it's like a big copper wire with the conduction plastic on it, with small little gaps into it. The this is important because this is what the term that you need to use is sultry, sultry conduction sultry conduction.
A couple of other things you need to talk about when you're drawing. This is to say that the the intracellular intracellular the sodium is in low concentration or potassium is high concentration. Extracellular potassium is low concentration. Sodium is high concentration. How would you remember that? Well, what your normal blood tests your potassium is a low number six one.
Lower sodium is 122. That's blood that's outside your cells. This is important because this is all about nerve production. So I then describe the the conduction in this situation. I say that there's a synopsis on dendrites where nerve stimuli come in or other stimuli come in, for example, stretch receptors and muscle as part of your reflex pathway. So if your stimuli are coming in, they hit the deck, right?
They then go through the cell body. And the cell body has an effect on the action potential that does come, the action potential slot can dissipate or magnify in the cell body, depending on the function of that cell body. Once it reaches the mound, it then reaches it, then reaches an all or nothing threshold. If it passes that threshold, it will continue to conduct down.
So we will drop this diagram for now and come back to action potentials. We talked about thresholds you need to then draw. At this point, you need to draw an action potential graph. Everyone has a tendency to do this. I think that's just setting you up for having to explain something a little bit more difficult to explain by making a graph a little bit more difficult to do.
So what I would suggest instead is putting your y-axis much higher. The reason why is you can then demonstrate straightaway that this access is a negative. You start off in your negative area and you can go up to a positive or. So you draw your own, your y-axis, make sure you do show that you're talking about milliseconds.
OK, because all of this is quite important in describing how the action potential comes, I remember we talked about the threshold so you can get multiple stimuli hitting the dendrite multiple action potentials, trying to reach the amount of the action if if you get a small hit. Which doesn't reach a threshold.
It'll go back down again if you get multiple hits or one large hit. It eventually reaches the threshold, which is usually around minus 55. And once that happens, the actual potential propagates. Now what you then get is about one millisecond of action potential and then you go down to hyper minus level. And this area is what we call the refractory period from here to about.
Here is the refractory period. So what's happening in this situation? Everyone knows how to draw this diagram, but they can't explain what is happening. So once action potential reaches the mound, once it reaches a threshold, sodium channels a voltage gated sodium channels start to open. These sodium channels allow diffusion of sodium across the cosmology gradient into the cell.
So you've got high concentration sodium outside the body, outside the cell body. Now you're getting the sodium diffusing into the axon because the voltage gate is open. Once the voltage gate is open, it stays open only for one millisecond. So as much sodium can get in as quickly as it can. This creates a second voltage gated channel, the potassium one to open.
This is again a diffusion type channel. This allows potassium to move from a low concentrated area to a high concentrated area. So if I just change the colors of the diagram, which is going to show you what the what's happening with the sodium gated channel is about here doing the same thing and they're closing at this point. Potassium gated channels.
Are here and the only start to open here. And then close down here once. Once we reach the threshold level where we've got to to negative charge the action potential. Sorry, the charge within the action is negative, then the ATP pump ATP pump sodium potassium exchange pump, which is ATP controlled, is then activated.
This redresses the balance until the balances come back to normal again, with sodium leaving the cell in exchange for potassium coming into the cell. There can be no activation of these nerve cells, so that's that prevents multiple rapid signals coming down that axon. Therefore, it's in motion, for example, that actually prevents hyper stimuli of the neuro or the motor units.
OK why is this important to understand in terms of our clinical application? So first of all, we talked about solitary conduction. There is another form of corruption without myelin sheath where you can get just the diffuse conduction as there's one group of sodium channels open, the next one's open. That's a slower conduction than the substrate conduction. So if you lose your schwann cells, if you lose your myelin sheath, you lose the ability to treat conduction so your reflexes are slower, your ability to respond to one much slower but more important in our everyday applications.
We use local anesthetic. We use it for every block. We give local anesthetic topically. We give it into arthroplasty interventions. The effect the way the local anesthetic works, its sodium channel blocker, it binds reversibly to the sodium channels. So once they're opened the voltage gate. Once the voltage gated sodium channels are opened, the local anesthetic binds to them and prevents them from closing by preventing them from closing.
They prevent the the whole process from occurring. They block the channel completely, so therefore no sodium can get in. Therefore, no action potential can propagate. Does that make sense? That's the clinical application there. If we talk about. The pathway down the axon, the you can appreciate the voltage gated channels are not energy dependent, however, the sodium potassium pump is energy dependent.
ATP dependent on ATP requires oxygenation. Again, this is the reason why it's important to know the blood supply and to protect the blood supply when you're doing a transfer. OK for us, can I anyone got any questions so far? I haven't received any particular questions yet. But do you feel you have a question to ask? Let me know. So can I ask?
Anyone can tell me about why they're why it's so important to know about the threshold for conduction. Is there any clinical application to that threshold? Anyone wants to answer. I will look. I will pick someone randomly. So excuse me, guys, will our big fires. I know he's a good guy.
If I ask you to answer one question, please. Trying to work to make. So, yes, we can hear you. Yeah OK. Sorry, I've missed the last part there. A lot of question and what not, but pretty sure, to be honest. OK, so during the conversation, during my presentation, I mentioned that there's a threshold level that's required for propagation of the actual potential is there.
Can you think of a reason as to why that has clinical applications in our everyday life? I think it's because when the threshold is reached, the representative propagates and the strength doesn't matter if it's not reached. OK so for example, in your I mentioned earlier on that your reflex pathway is is action potential control, but also specifically how many sensors activate and send the signal up to the spinal cord.
So if you were doing a patellar reflex on a patient who you get, if you press on your patella now, press lightly on it. What what happens is you don't get to quads, kick back. You don't get to kick the patella reflex reflex correct pressing lightly. It's really hard, really fast. That creates hyper stimuli of multiple receptors, which are being actioned by quick movement, but also by high force.
They send the signal up. There's no time for the signal to go up to the brain to say, actually, I know that this is what's happening. Don't give a kick back. Instead, they go through the spinal cord and come straight down because enough stimuli, enough sensors have received and hit the dendrites. So if I draw that cell again for you just very quickly.
So if this sell sell, so this dendrite, this dendrite and this dendrite all get hit and they send their stimuli into the mound here, they're more likely to get a propagation there rather than just one dendrite sending a signal across. Does that make sense? So if you get one sensory signal coming here hitting onto that dendrite with a single pressure, not hard, fast on your patellar tendon, you're not going to get which special, but you're getting multiple hits.
Therefore, this cell is propagating multiple action potentials, which eventually all congregate in the mound, which reaches threshold they they collect together, they connect together, and then you get a reflex, then you get a signal sent to your quads from their direct. OK, I have a question. Sean, I think a common exam question when when these issues are discussed is the game theory and would you be able to cut this have been asked about the game theory in this scenario?
I don't know if that's something you see in reference to the voltage gates in reference to pain. Is that? Yes yeah. In reference to pain. I'm not familiar, but I do know that a regional sympathetic dystrophy is the loss of impedance or partly due to loss of impedance of feedback in process.
So what's happening is you're getting multiple firing of your action potentials, your multiple sensory feed into your nerves. The nerves are not getting activated. This is your cell cell body. And if you remember, I said some of the cell bodies inhibit action potential transmission depending on what their function is, while others multiply it. So for example, if you're getting a single sensory associated with pain that is more likely to go through to the axon than transmit from the dendrites across the cell body into the axon for cells that are designed to have reflexes to pain.
While the wild cells that are not designed to stop you from going into tenotomy will try to decrease, the number of it will be inhibitory to the actual potential crossing the cell body. So you need actually a lot more stimuli before the actual potential across the cell body itself. Yeah, thank you.
OK, guys. So let's. That's a good question, David, do you want to answer that one? Polio what about polio? I was just thinking that's quite common question is particularly in post-polio syndrome?
Yeah I'm sorry, I haven't thought about that. So you have no, I just remembering you had a very good explanation of it previously. That's why I was thinking about it. That's a popular question at the moment. It's gone from my mind, but we'll think about it the next time. What is the question, david? Post-polio syndrome with regards to action potential?
Why do why do you get this so polio in terms of the virus, you have the acute infection when their children, then when they're older, they have post-polio syndrome, which is a result of reduced was it reduced muscle neuro neuromuscular junction? I can't quite remember off the top of my head, but there's a common popular question and it's quite common. A good. Sorry, I'm a bit too close.
No no, no, no. Fine fine. I mean, I know it's coming to me. I'll get it now then. But yeah, I think I think that's a very good question, David. I think post-polio scenarios can come in exam. Very rare these days, obviously, but they can't come, particularly in the clinical part of the exam. Yeah, you could be faced with polio or many years ago, you know, from the 40s or 50s.
And it's important to know that post-polio present with muscle weakness, paralysis, myalgia and fatigue. But the actual neurophysiological reason behind it is something that we we need to look into. Yes, thank you. All right. I know the I've got the answer somewhere. I'll use it when I did my webinar as a little bit at the end.
Don't worry. That'd be great. Thanks, David very much. Sorry, I just I just remembered what post-polio connection to nerves. So in a patient who suffers polio, they lose a lot of their nerves, initially in the first hit of their disease. However, those patients are often the ones that do well because the initial attack polio that seem to be working well and so on there they have no problems.
What's happening with those is they get hit at a young age. So when those nerves that supply the muscles, let's say, for example, your quadriceps, muscles, the nerves that are supplying your quadriceps, muscles as they get injured in polio, our nerves grow, grow their dandruff. So if I draw this picture to you, this is actually quite a good point. Thank you very much, David.
So if in terms of a motor unit, what is the definition of motor unit? It is a single nerve and all the muscles innovated by that single motor nerve. So when a motor unit is taken out by polio, the surviving motor units try to recruit the muscles that were lost to the to the off of the first nerve. So what you get is an extra axon growing off and creating further neuromuscular function to recruit these muscles.
So I'm trying to draw muscle here, so to recruit these different capacities. So if you've got multiple accidents, each one is different to my classical. So what then happens is as you got bigger and bigger motor units, a single injury to a single motor unit, a single die off as the cells get fatigued and tired over time. As the cells die off with aging, the effect is much more pronounced at a younger age and of these patients, because for one nerve to get hit and post-polio syndrome, what's really happening is the cell is dying off and a large percentage of the muscle and the quadriceps muscle, for example, are dying are dying off.
That entire motor unit is not working. So that's the progressive weakness that you see in the patient who's getting developed post-polio syndrome. Does that make sense? Yes, it does. Thank you. Sure sure, we have another five minutes to go. Yeah so I think if there's no immediate questions, you need this and go on to neuromuscular junction and how the action potential conducts across.
Yeah, I think we will have a small break. We have a few minutes, everyone. If anyone has a question, let me know we will pass it on to members of the faculty to see if we can have any answer to your questions or if you have any questions we can put it through. No, they don't seem to be any questions at the moment.
So, Ramesh, would you like to add anything to Sean's talk about the nerve structure and physiology? I think it was a very sort of comprehensive, concise and comprehensive. Was pretty good. The only thing I want to ask is what you mentioned refractory period is that period just after the actual potential that arises or is it the whole thing?
So the once the sodium channels are activated, they can't be reactivated for two milliseconds from that moment on. So if you look at the period, it's actually over two milliseconds. Unfortunately, we always throw our action potential to cut off before the two. So my advice is make you draw your thing, right? So you don't have to explain that it's too many seconds.
OK, that's a good point. Yeah thanks. OK excellent. Excellent. Thank you. Good question. Good questions are as important as good answers. OK, guys. So we will have a small break, five minutes break for people to stretch their legs and we will restart again in five minutes with another blog talking about more about action potential, how it propagates through the neuromuscular junction and through the muscle cells.
Very important exam question and topic and very important to understand. Well, that's it's easy to score high. If you understand this concept, examiners will be very impressed. So I'll end this meeting, guys, and I will see you again in five minutes. I will post another link again. No, it's not too late.
It's not too late. But I just missed the last part because I recall because, you know, people have passed the exemption. There are phone calls coming. So regarding the questions of the and physiology, one of the common question is what happens to the nerve when it is dissected? So I think this is something which can be asked from any one of the candidates, and they can prepare because it's written quite nicely.
One of the books but there is a common question they can ask actually in what happens proximity and what happens digitally and what happens in different areas and how how it that can be a clinical scenario that you are operating and then suddenly you cut the nerve. Then what will happen? We will. We will do that. We will do that at the end of the next session as a as a hot topic hot seat session.
And you'll be the examiner for it. OK, so OK.
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