So this is a lecture where we are going to introduce again some basic principles that apply to a lot of pharmacology. But we're going to really focus on a very specific use of pharmacology which is inhibiting transmission at the neuromuscular junction. So by now you should have had a reasonable amount of information about what's happening there, how we're getting an action potential down a motor neuron, and how that is causing contraction of muscle that are fundamental bit of knowledge so far. I'm going to recap that because it's quite important for today's lecture. And if you've got any questions about that part, we'll have a moment or two later on. We can kind of suss out what's going on too, if need be. So purpose of today's lecture is to cover these learning outcomes.
I'll point out I'm going to mention quite a few different drugs. You don't need to memorize all of those drugs. I think an example of each class is usually pretty good, but I'll try to highlight the examples as we go through so you can see what's going on. It's much more important that you can actually talk about the mechanism of action, what's going on that's underlying and underpinning the kind of different classes and why it matters to make that distinction between the terminology we use later on between depolarizing and nondepolarizing blockers, for example. We'll also look at recovery, right? The main function of most of the drugs we're going to talk about today is to stop voluntary control of skeletal muscle, right? We don't want to do that for a long period of time. In most cases, we want to aid recovery of that post surgical intervention, for example. And we can do that by using some other pharmacology, which is really quite interesting and relates to all sorts of stuff, including international poisoning and espionage. Right. So this lecture will have it all.
Okay. We're going to cover quite a range of things now as a class of drugs. The derivative of the compounds that we're going to talk about are the neuromuscular junction blocking agents. Right. Why are these clinically used. We want to remove the ability of people to voluntarily control their muscle, and that has wide range of uses from essentially intubating someone. If you want to get an airway tube into someone, they're going to not want that to happen voluntarily. You need to basically stop that reflex control of their muscle to enable you to intubate them. So short, rapid administration of a drug that prevents that voluntary control of muscle allows you to insert the endo tracheal intubation tube during surgical procedures. You might need to relax the abdominal muscles to get access into that cavity for surgery, right? You might need to relax the muscles around a dislocated joint to relocate it, right? You can start to think of all the clinical reasons here that this would be useful.
The other things are useful here is that actually the use of these drugs can help you decrease the amount of general anaesthetic you need to use in patients. And general anesthetics come with risk, right? They're not a class of drug that are without risk to administer. So anything you can do to reduce the amount of drug you need to add in those contacts is good. And there's that kind of synergistic interaction there that helps it. If someone's in intensive care and there's a mechanical ventilation that's required, if you need to take control of that patient's breathing, then this is a way in which you can do it as well. And the other one I'd like to point out is that bottom use here during electroconvulsive therapy, because there's this kind of pop culture image that electroconvulsive therapy, which is when you apply electrodes to the side of someone's head, you administer electric shock to them to try and help them when they've got severe depression.
For example, the pop culture reference of that is often someone being restrained and biting down between something they're fully conscious. And it's a really harrowing, very kind of like tragic scene to watch where the reality is patients are undergoing electroconvulsive therapy, have got a general anaesthetic, so they're unconscious. They've got a neuromuscular junction blocking agent, they've been administered so you can't actually see any muscle spasms or change in their body when it's administered. So it's a very different clinical picture from what is represented in terms of the pop culture references.
And this is where a really interesting class of drugs comes up. Right now these were originally observed in about fifteen hundreds by Sir Walter Raleigh. Right. And the original use of these drugs, where a lot of these compounds have come from, is indigenous use in Central and South America to essentially kill prey. And this is that kind of classic example of the poison dart, right? So this would be a thick tar like substance that was made from extracts of different vegetation. Strychnos related family plant at the top there, or chondodendron down here, which is a relative of the rhododendron bush that you might find kicking around in the UK as well, but slightly less toxic in the UK. And essentially you make a slurry of this, boil it down, tip the the dart in it, and then you can shoot the prey and the prey will die. And then you can eat the prey without you dying, which is Fundamentally quite important in this process. Right. Why? Why does a dart that is injected into a prey. Mean that prey is paralyzed and dies? But you can safely eat it afterwards. What do you think's going on there? Right. A minute. What could be potential solutions to this? Why might that happen? Have a chat. You can't absorb anything. Yes. Spot on. Absolutely. For the benefit of repeating across. You can't absorb it from the gastrointestinal tract. So it's similar here. Similar kind of thing. Right. You've got an idea that the chemical properties of this drug could influence what's going on. It could be the stability of it. It could be what it binds to. Or it could be that it's so charged, such a strong electrical structure to it that it can't get absorbed through your gastrointestinal tract. So if you were to orally administer this drug, none of it would get into your bloodstream. But if you inject it directly into the bloodstream, it gets in absolutely fine. Right.
So the route of administration matters here considerably. Okay. The other options we've got are absolutely viable and could be the way in which different drugs get detoxified and might not have the same effect that you expect to see. But that's the key one here, and that's really important. And we'll come back to that again a little bit as well. This um, table here, I've given you some notes on the Galen element, which helps you understand why we need to know a few different drugs, how you might want to remember and think about the class of drugs and memorize some of the information.
But the key thing here is I just wanted to demonstrate that we've got a range of different onsets, some that are really fast acting and some that are really short acting. These give us a range of different drugs we can choose depending on what the circumstance is. If you're wanting to intubate someone, you want that to be a fast onset and you don't need it to last very long. So you might choose something like Suxamethonium, which has got fast onset and a short duration. If you're doing a prolonged surgical intervention, it might not matter that you need to get someone immobile quickly, but you might want to keep them immobile for a longer period of time.
You'd probably choose a different drug. So by having a range, we can choose. The other thing that's here is you can see there's clustering of side effects, isn't there? Right. So you don't need to remember which ones are aminosteroidal which ones are benzylisoquinoliniums. But this is just to show you that the side effects clusters by some of those chemical structures. So benzos, for example, are much more likely to cause histamine release. And histamine release causes constriction of airways, right? It can also cause a coughing kind of afterwards as well. Right. It can also cause a patient's blood pressure to drop. So if your patient's blood pressure is already low, you probably don't want to risk using something that's going to drop it even further. So having a range allows you to select the right one for the patient's situation as well. The other steroidal is up here.
The main side effects associated with them are tachycardia. So an increase in heart rate. And that's actually caused by these drugs having an effect on muscarinic acetylcholine receptors that are present on the heart. And how that happens Or talk about the autonomic nervous system lectures that are coming up later this semester. Same for Suxamethonium. Suxamethonium can also affect your heart, but it causes bradycardia, right? It slows down your heart rate again because it's acting on the same receptors, but this time to activate them, agonize them rather than inhibit them, which is what your steroidals are doing.
So many side effects associated with suxamethonium cardiac dysrhythmias because of that, potassium concentration coming out can also cause a sort of post-operative myalgia, the sense that you've been through like flu like symptoms because of those muscle fasciculations. It can also trigger malignant hyperthermia, which I know you've kind of got a guided study coming up at some point this semester about as well. That is something that is important to remember as a risk factor. These class of drugs. That's it folks. Thank you very, very much for your time and your attention this morning. And I'll see you in a couple of weeks for the autonomic nervous system.
