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The Sarcomere for Orthopaedic Exams
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The Sarcomere for Orthopaedic Exams
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Segment:0 .
So welcome, everyone back. Sorry about the slight delay. We will get over all these technical difficulties very soon. Back to Sean to tell us more about malfunction, action potential and neuromuscular junction over to Sean. Thank you. So we've talked about action potential and why it's important that you talk about threshold level.
And once you reach threshold, then the action potential is on the. The reason why that's important is because once the action potential is propagating down the axon, there's nothing to take it back. And remember, some of these actions are extremely long. They reach from the neck all the way down to the fingertips or the muscles of the muscles. So there's no take back on it, a better way of saying it reaches the sign up and will cross the neuromuscular junction and will activate muscles on the other side.
So good control is quite important. So now we've got to the synapse at the very end. If we take again, this is keep your drawing simple, don't do anything too fancy and don't spend time doing art. OK, so if we draw the axon down like this, we can see and then draw simple flare of that. And then I like to draw kind of ruffled border to represent vesicle binding to the synapse. I then draw my circle, which is forming a neuromuscular junction, a synapse with the muscle.
OK, if this is muscle, this is axon. You've got your action potential coming down here. I also like to draw a little microtubules within the action. And I label them as microtubules. Welcome to why that's important. So once the action potential reaches down here, they create open up voltage gated calcium channels. This allows calcium to enter the UPS, the presynaptic side so placed on us, and this binds to vesicles, which contain acetic holding.
The seat, according comes from the cell body and is migrating all the way down from the cell block that's produced in the cell body, migrates all the way down and created a vesicles which come all the way down to the end to the neuromuscular junction. So they're essentially a storage container procedure for what's calcium binds to this, according to the sorry apologize to the vesicle, the vesicle is then able to bind to the presynaptic left once it's formed to preselect, they think.
According to the finance here, the situation crosses the junction of binds to nicotinic acetylcholine receptor. Now, the mistake everyone makes in this is they keep saying that calcium nicotine, specifically receptors and someone's got the microphone on which they could turn it off. Please thank you. The nicotinic receptors, everyone mistakes them as the main calcium to stop what happens that they actually are sodium channels.
Once the second binds to this, here the sodium come and creates a no action in this action potential then travels across the tube into of the factory to what I call what you call to action potential. Traveling this way and coming down the tubes into the muscle are sophomores. OK, we come to understand how to go then and the importance of the ability.
But remember, calcium UPS, it's not possible. That's a whole different story. It's sodium associated with co-signing to create connection, potentially in the secondary. Now can we combine applications of this is quite important. So we use watchman injections in our everyday clinical practice, but it doesn't prevent calcium coming in here. It doesn't find here. It actually binds to the vesicle and prevents calcium, which is at best, calcium can point into the vesicle.
The vessel cannot connect to the membrane to see. So when you ask this question, they usually ask you a question along the lines of where does Washington work? It's pretty synaptic free neuromuscular junction. It binds to the bicycle. It's reversible binding. So why is that important to say that? Because even botulism is temporary?
The binding is permanent. The reason why effect is temporary. Is there's a limit of how much oxygen in a cell body can produce in any one time, and it's actually quite dependent on recycling this, according which has been released into the synaptic cleft. So what you need to know about this is once the critical point here on the nicotinic receptor, it's a cleaved in half cholinesterase, which then creates two parts acetylcholine and code.
These are reabsorbed into the presynaptic and then are traveling back up where microtubules in separate vesicles to be bound together by ribosomes again in the cell body. And then, as you can see, it's a recycling process that has to be created. So what happens is when you use butchering them is that there isn't this recycling of 6 o'clock on this hospital.
So for some reason, the cell seems to think it's being injured and it creates sprouts of axons. And these axons try to find the muscles that it was originally trying to innovate for the sprouting of axons. But usually what then happens is instead the body. The cell body manages to find more control over a few years and builds up enough C to call it back in its cell body to be able to start the whole process again once the whole process starts again.
These sprouting axons disappear. Ok? so does everyone understand that? I think that's very important principle, he said about the toxin injections and how they inhibit release of start calling. And it's very it's very commonly repeatedly asked question on these days on the theory that I haven't received any questions.
But do you have any questions? Do you want to put the candidates? We have at least three people here going for April. Mm-hmm Could could you tell me in the process, I've described something that's binding. We're sorry, which is pre neuromuscular junction, any chemicals we use or anything we use, which is possibly neuromuscular junction? Yes can I put this question to them?
Would read, please just be on. All right. Oh, that's OK. So it's a postsynaptic. Is it the local anesthetic that we put in to stop the sodium channels? So yeah, you can't make that argument, but are you going to stick in the local anesthetic into muscle?
Or do you aim more to cover the axon of the nerve? One Mason the muscle, isn't it? No, I would disagree. Generally, when you're doing local anesthetic, you're trying to individually take off axons like digital block nerve blocks higher up. You need to stop that. They're more a systemic drug that is rescues.
I can't remember. In terms of general, anesthetic sucks and alkaline. Yeah, that's the muscle relaxant egawa test. Why is it a muscle relaxant? Or I don't know the mechanism of action. The clue is in its name, so I seem to recall in axilo. It's a binder to essentially the nicotinic receptor.
It binds to that it prevents proper development of action, potential post synapse in the muscle. The second email. So how does that do that? So have you ever this to agitate or to breathe. And then they stop breathing when they're using suction calling? Because what's happening is it requires the gait to be opened by acetylcholine, and then the suction fits into that and blocks it.
OK, so it needs the gait to be opened first, then it blocks it, so once it's blocked, no more action potential can come across. So if there's no more sodium coming across into the economy, then there's no action potential in this epidemic traveling down the T tubules. Therefore, there is no calcium release into the South. Therefore, the bindings of the active and Mason fibers will not occur, or the axilo Mason proteins will not occur.
So therefore, instead of binding tight, really? And then you get the relaxation for muscle. OK, OK. We have a comment from what? Go ahead, please. Yeah so going back to what Sean has said in clinical practice, where do you need muscle relaxation, commonly in our clinical practice? Should we put this question to you because he was asking, can we put this question to him?
Himanta please. I didn't quite get the question, to be honest. Can you repeat that, please? So as your son, Sean said that the NIPE Colleen, you can have muscle relaxation. So clinical scenarios, which are the conditions where you would need muscle relaxation. In fact, it is important to tell the anesthetist that you may require muscle relaxation for doing that particular procedure.
For example, when you are reducing a dislocated hip. Yes, Yes. And I think that's a clinical it's important because what I've seen commonly the anesthetists are not happy to get the relaxation. So you have to specify them and for the same reason, because then they have to take longer time for the patient to promote. So this can be a clinical scenario.
They can ask may not be very common, but as you said, if we inform the anesthetist beforehand that I would need most of the session for the same reason that it will allow me to have an easy relocation of the dislocated hip. So time is when you so so you can see why this is important in our clinical practice to understand where this muscle relaxation is important and when to use it, because the ministers don't like using it, because that means the patient is completely muscle relaxed, including the breathing, and it takes much longer for they have to maintain the breathing for that patient and take them much longer to recover.
So there are times when you need it and times when you don't need it. So as an example, in my case, in my work in the hemisphere with the large head, the tight muscles having difficulty reducing, especially if you're using a heavier capacity, which is one size fits all. Rather than risk fracturing the femur, I ask the anesthetist sometimes when I'm having difficulty reducing to give muscle relaxant, that makes a difference to reducing your hip.
Same in a total hip replacement. You can even consider it. You should consider using it in a difficult reduction of a child. But be aware so many do not like to use that in the child. OK so it's quite important to understand the basics. The basic science gives you a lot of understanding of your clinical practice and to use that in your daily practice.
OK so moving on now, guys, are you all happy with that? That's great, thank you, Sean. OK, so a couple of things to draw muscle if you said to draw a muscle again, the same principle. Just draw three circles and connect those three circles. Well, just do the same thing, epi Perry, and end up. And again, the blood supply is almost the same.
You've got an intrinsic and extrinsic blood supply. They create a plexus of blood vessels all around the fibrils, and you can see the blood supply to muscle is always very good because of that. So, OK, but the blood supply to nerves is good but delicate. You need to be aware of the difference between the two. Now, in terms of muscle, you can make a discussion a lot of things of muscle, but if you ask to draw a circle there.
Don't start doing that cross section stuff. They don't want to talk about that, they want to talk about individual muscle cells and fibroblasts, bio fibers. OK, so first thing to do. Again, nothing complicated. You are not artists. Don't complicate your picture. Just draw very quick lines.
So what I like to do is I draw one line in the middle. If I can get my tent to work, I would like them. Two deadlines and you notice I'm drawing my deadline straight. I don't do this because that just it makes it more difficult for you to draw your act into the mix and make sure you're acting for them. It's line up with each other because it doesn't look good if they don't.
Just like that and then your Mason guy. OK, next thing to do is to say, this is your band, this is your line, this is the z band. These are this is your age band. So let's draw it down here. And a. What's the difference, a is all of the Mason is only the product, which is not covered by acting.
Why is the whole length of your acting? OK so you're all happy to draw that very quickly, just discuss that because you need to show this cross section pattern, because that is important in how muscles certain work. OK, now the next thing to say about all of this, remember, we're talking about the conduction of an action potential from the brain all the way down to the muscle cell and intrinsic muscles Allen.
Why do you get contraction in the muscle cells? So we talked about the open muscular, we talked about sodium channels on the subcutaneous, which are then propagated down the abuse. Into the actual software itself, the rules for want of a better way of saying it is where the active and the Mason clinics meet up. The teacher was into space into those the certainly the membrane around the muscle graduates into the actual sarcomere itself.
Breaking this, the rules to allow sodium channel within the wheels so you're not within. As the action potential comes down, these two bills, they create voltage gated channels, which open these multiple gated channels. Sorry, they bind to these voltage channels are bound to cycle seismic reticulum mechanically channels. These channels allow calcium from the plasma reticulum, which is intracytoplasmic like a vacuum for want of a better way of saying it or a small sac inside the circuitry, they contain lots of calcium.
Once this voltage gait comes here, it opens up these calcium channels and the calcium channel floods into the salmon. The more calcium that gets into the circulation, the more the muscle contracts. And I'll show you why in a moment. But I just want to rehash what I said from the beginning all the way down. So you guys got this into your head.
I can't emphasize this enough to understand what electrons are involved in each part. So sorry, what ions are involved in each part in the axon? It's sodium and potassium in the pre sign-ups calcium binding to basically pulling into the sign-ups sea and crossing the sign-ups binding to the postsynaptic in the postsynaptic flat, which then opens up sodium channels.
The sodium channels create another action potential in the circulating air, which travels down the tube like an action potential. So the axon, which opens up the best way to describe it. It's like you've got axon free sign UPS, post synapse axon. And please sign up again, because you're then opening up the sarcoplasmic reticulum and calcium rods into the muscles, so you get it sodium, potassium, calcium, acetylcholine, sodium, calcium.
Yep OK, so now the next say is the difference between actin and myosin and why they work, so acting is a bounce to the z. This is that this is the two that this is one sarcomere. So between two sets this one start. So this is important to show. I'm going to draw it in a very microscopic way so we can see as much of it as possible. So if I draw the act in, what we then have is acting, which I'm going to do a little bit more complicated than that.
You also have a proper of Mason leaving around the acting. OK in the epimysium, you have the troponin compound. Which go in? Which actually prevent. Which are bound to the epimysium.
The reason why that's important to understand acting sells itself have a Mason binding site within the actin fiber with the indirect proteins. However, this myosin binding site is covered by epimysium, not Mason, but by epimysium. The epimysium prevents myosin the Mason that we were talking about here from binding to this actin binding site.
Who to the Mason binding site only acted once calcium comes in here with the calcium reacts with the soy binds to the troponin c, which changes the configuration of troponin I, which allows troponin T to pull the Mason away, and it causes a mismatch between the epimysium and the myosin binding site. That means now you have an exposed myosin binding site, which allows your myosin head to bind to the myosin binding site.
Remember, your Mason is made out of two heavy chains and four light chains in the body. We don't know what the full life in the human. We're not sure what the function of the light chains are, but we do know that the heavy chains S1 and S2 are involved in binding of myosin heads onto Mason binding site on active. So what then happens is once that's exposed, that means that a magnet for the myosin head Mason head binds to the actin.
If everyone can see my picture, I'll just show you myosin head mice. This is my head. My finger is Mason head. That's myosin, a protein that's acting up here. Mason head binds to the myosin binding site and then as part of the ATP, which from ATP to ATP, you get a reconfiguration of the myosin head. And as the ATP is released, you have the Mason head coming off once another ATP binds to the Mason head.
It's charges the Mason head, so it allows it to reattach. But it's this movement that's important because as you can see, this movement is pulling the act in. So if you've got if you imagine this is acting and for limits, this is my son for the image and the heads on the on, the two filaments are working against each other. You're getting the desk disks coming closer together. Does that make sense?
Yes OK, thank you. So the more calcium you have, the more myosin binding sites are exposed and therefore the more active the myosin heads become. Remember this energy isn't requiring a process or ATP is part of this process. If you take a look at ramachandran, it just shows you a lovely diagram.
It tells you straight away how ATP is involved in all this. Very easy picture to see. OK I think common questions that could be asked on this topic include types of muscle fibers, slow twitch, fast twitch and what type energy each one, you are very important to read about that. And also they could ask about different types or shapes of muscles.
And obviously, the sarcomere function that one explained here, they could ask you also, how about how different types of muscle actions and isometric isotonic either cannot take muscle actions, and this could all come into the same station? All depends on how smooth you are flowing through the topic. To be honest, the discussion of how to draw sarcoma and how it functions and its connection to action potential would take you past five minutes if they say, draw me a cross section of muscle that's potentially talking about all the other stuff.
What is concentric body centric activities and so on? OK someone was asking me. There was a question solely on the chat. How is resting potential established and maintained? I presume you're talking about within the Exxon. Mohammed, and if Mohammed could confirm that's what he's talking about within the Exxon.
OK, I'll just presume that's what he's talking about. Yes, within the action. OK, so Mohammed, remember we were talking about voltage gated channels. There's three types of channels in the axilo. First is voltage gated sodium channel, then voltage gated potassium channel. These two channels disrupt the resting potential. OK, but what maintains the resting potential is ATP potassium apologia sodium potassium exchange pump.
This is an energy dependent pump, so the body has to work to continuously maintain resting potential. It uses energy to maintain its potential. If you ask any nutritionist, they'll tell you your rest your minimum. If you're completely resting, you'll need 1800s calories to 2,500 calories, depending on your size.
That's because your body needs energy to maintain the basic functions, such as maintaining resting potential in your cells, as well as getting muscles to breathe and hard to breathe. And so on. Great we have a couple of minutes to want to analyze this topic, please. OK, so can I just go back to polio? If you don't mind just for the sake of completion, there is a portfolio.
I know. I knew. I knew this really well, and I don't know why I forgot it, but essentially just want to make sure you guys understand. So polio affects the motor neurons. It knocks them out as a child. It's a virus that gives it leaving the anterior horn cells with their own cells and wipes out axons.
What happens is selectively destroys motor nerves. OK, so a patient who has normal sensation but motor loss, be wary. That's a polio patient, not cerebral palsy. Not anything else. It's a polio patient. OK the second thing to say about that is if they survive their first attack, axilo and some patients survive and don't have any serious symptoms of polio.
But then later on in the middle age, they develop what's called post-polio syndrome. Can I just say this one? I think you were right first time. It is viral destruction of the anterior horn of the spinal cord. Yeah, that's correct. Yeah, Yeah. A wholesales.
Yeah and also it can affect the brain itself. In addition, the brain stem cells? Yeah OK. So these are one of these. So a child that survives polio without symptoms can still develop post-polio syndrome because what's happening is that the nerve cells remember, I told you when you get botulinum injections, botching injections, what happens is the axon seems to think it's injured and then tries to sprout extra synapses to create to try and recruit more muscle fibers.
So the best way to talk about this is every nerve. One nerve will supply multiple motor fibers. But those motor fibers don't lie next to each other. They're actually very separated. And so, for example, let's talk about nerve one supplying why this fiber here and this fiber here, that's nerve one skipping the one in the middle. The reason why this occurs is it's so that any nerve that stimulated will cause contraction across the whole muscle body, as opposed to 1 small part of the muscle body.
Now the bigger muscles in the body have far more muscle fibers per nerve than smaller, fine tuned muscles like the ones in the hand. So we have more nerve endings. We have more nerve endings in terms of how many muscle fibers than in the hand than we do in our quadriceps. As a child, when the nerves are damaged or destroyed, the other surviving nerves try to recruit the muscle fibers that have become generated.
So a larger portion of the muscles are now taken up by less number of motor nerves, and this is fine. So the child has a normal childhood, potentially normal childhood. They're not severely affected by their polio, do not have long term consequences. Initially seem to have recovered from their polio. But when they reach middle age, what happens is that there is a fatigue of those nerves.
They finally die out. They can't take anymore, and you get massive muscle degeneration at that point because these nerves. One theory is that these nerves overwork the situation and therefore they're tired. Other there are other theories. For example, there is a connection with the possible reactivation of latent viruses. That's one theory, and another possibility is that they get hit by another virus and enterovirus, which they are more sensitive to because they've been had polio and so on.
Do you understand that connection? It's really worthwhile getting that in because if you get a polio patient, it's nice to be able to talk about the pathophysiology associated with the possible syndrome. I would be posting these recordings later on for people to listen to again and see again so they can thinking those information more. Any comment about these topics?
Ramesh neuromuscular junction and muscle cell function. I think some birdies in the chat room desperate has done an effect. So the idea is because there is concentration difference of the sodium expert and intracellular there is a drive for sodium to come in and it continues until it reaches an equilibrium.
OK, so it's not just the Donald effect, the idea is to maintain equilibrium, which is called Donald equilibrium, and that basically, I think what he was trying to say in the Jack Muhammad. Yeah, thank you. Thank you very much for that. Thank you for the clarification. That's great. I think we are running out of time now.
We've had the hot seat question, but I think we are running out of time at this moment. Happy to do hot seat with anybody for.
Segment:0 .
So welcome, everyone back. Sorry about the slight delay. We will get over all these technical difficulties very soon. Back to Sean to tell us more about malfunction, action potential and neuromuscular junction over to Sean. Thank you. So we've talked about action potential and why it's important that you talk about threshold level.
And once you reach threshold, then the action potential is on the. The reason why that's important is because once the action potential is propagating down the axon, there's nothing to take it back. And remember, some of these actions are extremely long. They reach from the neck all the way down to the fingertips or the muscles of the muscles. So there's no take back on it, a better way of saying it reaches the sign up and will cross the neuromuscular junction and will activate muscles on the other side.
So good control is quite important. So now we've got to the synapse at the very end. If we take again, this is keep your drawing simple, don't do anything too fancy and don't spend time doing art. OK, so if we draw the axon down like this, we can see and then draw simple flare of that. And then I like to draw kind of ruffled border to represent vesicle binding to the synapse. I then draw my circle, which is forming a neuromuscular junction, a synapse with the muscle.
OK, if this is muscle, this is axon. You've got your action potential coming down here. I also like to draw a little microtubules within the action. And I label them as microtubules. Welcome to why that's important. So once the action potential reaches down here, they create open up voltage gated calcium channels. This allows calcium to enter the UPS, the presynaptic side so placed on us, and this binds to vesicles, which contain acetic holding.
The seat, according comes from the cell body and is migrating all the way down from the cell block that's produced in the cell body, migrates all the way down and created a vesicles which come all the way down to the end to the neuromuscular junction. So they're essentially a storage container procedure for what's calcium binds to this, according to the sorry apologize to the vesicle, the vesicle is then able to bind to the presynaptic left once it's formed to preselect, they think.
According to the finance here, the situation crosses the junction of binds to nicotinic acetylcholine receptor. Now, the mistake everyone makes in this is they keep saying that calcium nicotine, specifically receptors and someone's got the microphone on which they could turn it off. Please thank you. The nicotinic receptors, everyone mistakes them as the main calcium to stop what happens that they actually are sodium channels.
Once the second binds to this, here the sodium come and creates a no action in this action potential then travels across the tube into of the factory to what I call what you call to action potential. Traveling this way and coming down the tubes into the muscle are sophomores. OK, we come to understand how to go then and the importance of the ability.
But remember, calcium UPS, it's not possible. That's a whole different story. It's sodium associated with co-signing to create connection, potentially in the secondary. Now can we combine applications of this is quite important. So we use watchman injections in our everyday clinical practice, but it doesn't prevent calcium coming in here. It doesn't find here. It actually binds to the vesicle and prevents calcium, which is at best, calcium can point into the vesicle.
The vessel cannot connect to the membrane to see. So when you ask this question, they usually ask you a question along the lines of where does Washington work? It's pretty synaptic free neuromuscular junction. It binds to the bicycle. It's reversible binding. So why is that important to say that? Because even botulism is temporary?
The binding is permanent. The reason why effect is temporary. Is there's a limit of how much oxygen in a cell body can produce in any one time, and it's actually quite dependent on recycling this, according which has been released into the synaptic cleft. So what you need to know about this is once the critical point here on the nicotinic receptor, it's a cleaved in half cholinesterase, which then creates two parts acetylcholine and code.
These are reabsorbed into the presynaptic and then are traveling back up where microtubules in separate vesicles to be bound together by ribosomes again in the cell body. And then, as you can see, it's a recycling process that has to be created. So what happens is when you use butchering them is that there isn't this recycling of 6 o'clock on this hospital.
So for some reason, the cell seems to think it's being injured and it creates sprouts of axons. And these axons try to find the muscles that it was originally trying to innovate for the sprouting of axons. But usually what then happens is instead the body. The cell body manages to find more control over a few years and builds up enough C to call it back in its cell body to be able to start the whole process again once the whole process starts again.
These sprouting axons disappear. Ok? so does everyone understand that? I think that's very important principle, he said about the toxin injections and how they inhibit release of start calling. And it's very it's very commonly repeatedly asked question on these days on the theory that I haven't received any questions.
But do you have any questions? Do you want to put the candidates? We have at least three people here going for April. Mm-hmm Could could you tell me in the process, I've described something that's binding. We're sorry, which is pre neuromuscular junction, any chemicals we use or anything we use, which is possibly neuromuscular junction? Yes can I put this question to them?
Would read, please just be on. All right. Oh, that's OK. So it's a postsynaptic. Is it the local anesthetic that we put in to stop the sodium channels? So yeah, you can't make that argument, but are you going to stick in the local anesthetic into muscle?
Or do you aim more to cover the axon of the nerve? One Mason the muscle, isn't it? No, I would disagree. Generally, when you're doing local anesthetic, you're trying to individually take off axons like digital block nerve blocks higher up. You need to stop that. They're more a systemic drug that is rescues.
I can't remember. In terms of general, anesthetic sucks and alkaline. Yeah, that's the muscle relaxant egawa test. Why is it a muscle relaxant? Or I don't know the mechanism of action. The clue is in its name, so I seem to recall in axilo. It's a binder to essentially the nicotinic receptor.
It binds to that it prevents proper development of action, potential post synapse in the muscle. The second email. So how does that do that? So have you ever this to agitate or to breathe. And then they stop breathing when they're using suction calling? Because what's happening is it requires the gait to be opened by acetylcholine, and then the suction fits into that and blocks it.
OK, so it needs the gait to be opened first, then it blocks it, so once it's blocked, no more action potential can come across. So if there's no more sodium coming across into the economy, then there's no action potential in this epidemic traveling down the T tubules. Therefore, there is no calcium release into the South. Therefore, the bindings of the active and Mason fibers will not occur, or the axilo Mason proteins will not occur.
So therefore, instead of binding tight, really? And then you get the relaxation for muscle. OK, OK. We have a comment from what? Go ahead, please. Yeah so going back to what Sean has said in clinical practice, where do you need muscle relaxation, commonly in our clinical practice? Should we put this question to you because he was asking, can we put this question to him?
Himanta please. I didn't quite get the question, to be honest. Can you repeat that, please? So as your son, Sean said that the NIPE Colleen, you can have muscle relaxation. So clinical scenarios, which are the conditions where you would need muscle relaxation. In fact, it is important to tell the anesthetist that you may require muscle relaxation for doing that particular procedure.
For example, when you are reducing a dislocated hip. Yes, Yes. And I think that's a clinical it's important because what I've seen commonly the anesthetists are not happy to get the relaxation. So you have to specify them and for the same reason, because then they have to take longer time for the patient to promote. So this can be a clinical scenario.
They can ask may not be very common, but as you said, if we inform the anesthetist beforehand that I would need most of the session for the same reason that it will allow me to have an easy relocation of the dislocated hip. So time is when you so so you can see why this is important in our clinical practice to understand where this muscle relaxation is important and when to use it, because the ministers don't like using it, because that means the patient is completely muscle relaxed, including the breathing, and it takes much longer for they have to maintain the breathing for that patient and take them much longer to recover.
So there are times when you need it and times when you don't need it. So as an example, in my case, in my work in the hemisphere with the large head, the tight muscles having difficulty reducing, especially if you're using a heavier capacity, which is one size fits all. Rather than risk fracturing the femur, I ask the anesthetist sometimes when I'm having difficulty reducing to give muscle relaxant, that makes a difference to reducing your hip.
Same in a total hip replacement. You can even consider it. You should consider using it in a difficult reduction of a child. But be aware so many do not like to use that in the child. OK so it's quite important to understand the basics. The basic science gives you a lot of understanding of your clinical practice and to use that in your daily practice.
OK so moving on now, guys, are you all happy with that? That's great, thank you, Sean. OK, so a couple of things to draw muscle if you said to draw a muscle again, the same principle. Just draw three circles and connect those three circles. Well, just do the same thing, epi Perry, and end up. And again, the blood supply is almost the same.
You've got an intrinsic and extrinsic blood supply. They create a plexus of blood vessels all around the fibrils, and you can see the blood supply to muscle is always very good because of that. So, OK, but the blood supply to nerves is good but delicate. You need to be aware of the difference between the two. Now, in terms of muscle, you can make a discussion a lot of things of muscle, but if you ask to draw a circle there.
Don't start doing that cross section stuff. They don't want to talk about that, they want to talk about individual muscle cells and fibroblasts, bio fibers. OK, so first thing to do. Again, nothing complicated. You are not artists. Don't complicate your picture. Just draw very quick lines.
So what I like to do is I draw one line in the middle. If I can get my tent to work, I would like them. Two deadlines and you notice I'm drawing my deadline straight. I don't do this because that just it makes it more difficult for you to draw your act into the mix and make sure you're acting for them. It's line up with each other because it doesn't look good if they don't.
Just like that and then your Mason guy. OK, next thing to do is to say, this is your band, this is your line, this is the z band. These are this is your age band. So let's draw it down here. And a. What's the difference, a is all of the Mason is only the product, which is not covered by acting.
Why is the whole length of your acting? OK so you're all happy to draw that very quickly, just discuss that because you need to show this cross section pattern, because that is important in how muscles certain work. OK, now the next thing to say about all of this, remember, we're talking about the conduction of an action potential from the brain all the way down to the muscle cell and intrinsic muscles Allen.
Why do you get contraction in the muscle cells? So we talked about the open muscular, we talked about sodium channels on the subcutaneous, which are then propagated down the abuse. Into the actual software itself, the rules for want of a better way of saying it is where the active and the Mason clinics meet up. The teacher was into space into those the certainly the membrane around the muscle graduates into the actual sarcomere itself.
Breaking this, the rules to allow sodium channel within the wheels so you're not within. As the action potential comes down, these two bills, they create voltage gated channels, which open these multiple gated channels. Sorry, they bind to these voltage channels are bound to cycle seismic reticulum mechanically channels. These channels allow calcium from the plasma reticulum, which is intracytoplasmic like a vacuum for want of a better way of saying it or a small sac inside the circuitry, they contain lots of calcium.
Once this voltage gait comes here, it opens up these calcium channels and the calcium channel floods into the salmon. The more calcium that gets into the circulation, the more the muscle contracts. And I'll show you why in a moment. But I just want to rehash what I said from the beginning all the way down. So you guys got this into your head.
I can't emphasize this enough to understand what electrons are involved in each part. So sorry, what ions are involved in each part in the axon? It's sodium and potassium in the pre sign-ups calcium binding to basically pulling into the sign-ups sea and crossing the sign-ups binding to the postsynaptic in the postsynaptic flat, which then opens up sodium channels.
The sodium channels create another action potential in the circulating air, which travels down the tube like an action potential. So the axon, which opens up the best way to describe it. It's like you've got axon free sign UPS, post synapse axon. And please sign up again, because you're then opening up the sarcoplasmic reticulum and calcium rods into the muscles, so you get it sodium, potassium, calcium, acetylcholine, sodium, calcium.
Yep OK, so now the next say is the difference between actin and myosin and why they work, so acting is a bounce to the z. This is that this is the two that this is one sarcomere. So between two sets this one start. So this is important to show. I'm going to draw it in a very microscopic way so we can see as much of it as possible. So if I draw the act in, what we then have is acting, which I'm going to do a little bit more complicated than that.
You also have a proper of Mason leaving around the acting. OK in the epimysium, you have the troponin compound. Which go in? Which actually prevent. Which are bound to the epimysium.
The reason why that's important to understand acting sells itself have a Mason binding site within the actin fiber with the indirect proteins. However, this myosin binding site is covered by epimysium, not Mason, but by epimysium. The epimysium prevents myosin the Mason that we were talking about here from binding to this actin binding site.
Who to the Mason binding site only acted once calcium comes in here with the calcium reacts with the soy binds to the troponin c, which changes the configuration of troponin I, which allows troponin T to pull the Mason away, and it causes a mismatch between the epimysium and the myosin binding site. That means now you have an exposed myosin binding site, which allows your myosin head to bind to the myosin binding site.
Remember, your Mason is made out of two heavy chains and four light chains in the body. We don't know what the full life in the human. We're not sure what the function of the light chains are, but we do know that the heavy chains S1 and S2 are involved in binding of myosin heads onto Mason binding site on active. So what then happens is once that's exposed, that means that a magnet for the myosin head Mason head binds to the actin.
If everyone can see my picture, I'll just show you myosin head mice. This is my head. My finger is Mason head. That's myosin, a protein that's acting up here. Mason head binds to the myosin binding site and then as part of the ATP, which from ATP to ATP, you get a reconfiguration of the myosin head. And as the ATP is released, you have the Mason head coming off once another ATP binds to the Mason head.
It's charges the Mason head, so it allows it to reattach. But it's this movement that's important because as you can see, this movement is pulling the act in. So if you've got if you imagine this is acting and for limits, this is my son for the image and the heads on the on, the two filaments are working against each other. You're getting the desk disks coming closer together. Does that make sense?
Yes OK, thank you. So the more calcium you have, the more myosin binding sites are exposed and therefore the more active the myosin heads become. Remember this energy isn't requiring a process or ATP is part of this process. If you take a look at ramachandran, it just shows you a lovely diagram.
It tells you straight away how ATP is involved in all this. Very easy picture to see. OK I think common questions that could be asked on this topic include types of muscle fibers, slow twitch, fast twitch and what type energy each one, you are very important to read about that. And also they could ask about different types or shapes of muscles.
And obviously, the sarcomere function that one explained here, they could ask you also, how about how different types of muscle actions and isometric isotonic either cannot take muscle actions, and this could all come into the same station? All depends on how smooth you are flowing through the topic. To be honest, the discussion of how to draw sarcoma and how it functions and its connection to action potential would take you past five minutes if they say, draw me a cross section of muscle that's potentially talking about all the other stuff.
What is concentric body centric activities and so on? OK someone was asking me. There was a question solely on the chat. How is resting potential established and maintained? I presume you're talking about within the Exxon. Mohammed, and if Mohammed could confirm that's what he's talking about within the Exxon.
OK, I'll just presume that's what he's talking about. Yes, within the action. OK, so Mohammed, remember we were talking about voltage gated channels. There's three types of channels in the axilo. First is voltage gated sodium channel, then voltage gated potassium channel. These two channels disrupt the resting potential. OK, but what maintains the resting potential is ATP potassium apologia sodium potassium exchange pump.
This is an energy dependent pump, so the body has to work to continuously maintain resting potential. It uses energy to maintain its potential. If you ask any nutritionist, they'll tell you your rest your minimum. If you're completely resting, you'll need 1800s calories to 2,500 calories, depending on your size.
That's because your body needs energy to maintain the basic functions, such as maintaining resting potential in your cells, as well as getting muscles to breathe and hard to breathe. And so on. Great we have a couple of minutes to want to analyze this topic, please. OK, so can I just go back to polio? If you don't mind just for the sake of completion, there is a portfolio.
I know. I knew. I knew this really well, and I don't know why I forgot it, but essentially just want to make sure you guys understand. So polio affects the motor neurons. It knocks them out as a child. It's a virus that gives it leaving the anterior horn cells with their own cells and wipes out axons.
What happens is selectively destroys motor nerves. OK, so a patient who has normal sensation but motor loss, be wary. That's a polio patient, not cerebral palsy. Not anything else. It's a polio patient. OK the second thing to say about that is if they survive their first attack, axilo and some patients survive and don't have any serious symptoms of polio.
But then later on in the middle age, they develop what's called post-polio syndrome. Can I just say this one? I think you were right first time. It is viral destruction of the anterior horn of the spinal cord. Yeah, that's correct. Yeah, Yeah. A wholesales.
Yeah and also it can affect the brain itself. In addition, the brain stem cells? Yeah OK. So these are one of these. So a child that survives polio without symptoms can still develop post-polio syndrome because what's happening is that the nerve cells remember, I told you when you get botulinum injections, botching injections, what happens is the axon seems to think it's injured and then tries to sprout extra synapses to create to try and recruit more muscle fibers.
So the best way to talk about this is every nerve. One nerve will supply multiple motor fibers. But those motor fibers don't lie next to each other. They're actually very separated. And so, for example, let's talk about nerve one supplying why this fiber here and this fiber here, that's nerve one skipping the one in the middle. The reason why this occurs is it's so that any nerve that stimulated will cause contraction across the whole muscle body, as opposed to 1 small part of the muscle body.
Now the bigger muscles in the body have far more muscle fibers per nerve than smaller, fine tuned muscles like the ones in the hand. So we have more nerve endings. We have more nerve endings in terms of how many muscle fibers than in the hand than we do in our quadriceps. As a child, when the nerves are damaged or destroyed, the other surviving nerves try to recruit the muscle fibers that have become generated.
So a larger portion of the muscles are now taken up by less number of motor nerves, and this is fine. So the child has a normal childhood, potentially normal childhood. They're not severely affected by their polio, do not have long term consequences. Initially seem to have recovered from their polio. But when they reach middle age, what happens is that there is a fatigue of those nerves.
They finally die out. They can't take anymore, and you get massive muscle degeneration at that point because these nerves. One theory is that these nerves overwork the situation and therefore they're tired. Other there are other theories. For example, there is a connection with the possible reactivation of latent viruses. That's one theory, and another possibility is that they get hit by another virus and enterovirus, which they are more sensitive to because they've been had polio and so on.
Do you understand that connection? It's really worthwhile getting that in because if you get a polio patient, it's nice to be able to talk about the pathophysiology associated with the possible syndrome. I would be posting these recordings later on for people to listen to again and see again so they can thinking those information more. Any comment about these topics?
Ramesh neuromuscular junction and muscle cell function. I think some birdies in the chat room desperate has done an effect. So the idea is because there is concentration difference of the sodium expert and intracellular there is a drive for sodium to come in and it continues until it reaches an equilibrium.
OK, so it's not just the Donald effect, the idea is to maintain equilibrium, which is called Donald equilibrium, and that basically, I think what he was trying to say in the Jack Muhammad. Yeah, thank you. Thank you very much for that. Thank you for the clarification. That's great. I think we are running out of time now.
We've had the hot seat question, but I think we are running out of time at this moment. Happy to do hot seat with anybody for.
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