Tonsillopharyngitis | Clinical Medicine

[snorts] What's up ninja nerds? In this video today, we're going to be talking about tonselo ferngitis. Now, I like to really just consider this a topic on throat infections. And there's a lot that we're going to talk about within this. And it's going to be kind of like compartmentalized. We're going to talk about viral tonsitis, which is kind of like it could be a part of the common cold. You can see this with influenza and COVID. We'll talk about mono infectious monucleiosis, the good old kissing disease. We'll also talk about group A strep uh classically known as strep throat. And then we'll also sprinkle in there some some fingial dtheria. And so there is a lot of things in this topic and if you guys like it, you learn a lot, you enjoy it, support us, hit the like button, comment down the comment section, subscribe, anything, one of those things are going to make a difference and help us to continue to keep making free videos for you guys' enjoyment. So help us out in that way. Also, real quick, I know I say it, but I really believe in the products that we offer on our website. If you guys go down to the description box below, there's a link to our website. We offer things like some really high yield nodes, illustrations to follow along with, and things that are more for application based learning, quizzes, flashcards. Go check them out. Without further ado, let's get into this. When we talk about uh kind of tonsil fangitis in general, we have to have a definition of it, right? And and it's probably like, Zack, do I really need to do this? Like, I'm a med student. I'm a PA student. I'm not I'm not stupid. No, I'm not saying that. I'm just saying we should have an understanding of these definitions. I think they help us in overall just concept of the topic. And what we know about tonsillitis even though it's very very simple is it's inflammation of the tonsils. Now the twinsils there is not just one tonsil. Um even though in this diagram the most often tonsils that are affected I'd say and usually most of these types of infections um is usually the palatine tonsils which we can see right here but there is other tonsils and and I'm not going to go through all of them but I am going to mention something that we've talked about probably at least some point in um anatomy and we call it Waldy's ring. All right so I want you guys to remember this one. We're going to write it down here because it comes into play especially with uh good old mono is we call this wall dyer's ring and it's basically like a ring of tonsils. All right, there's a couple different tonsils and I'm going to kind of just show you something interesting about it. We have one tonsil that's really kind of up here in the nasal fairings. For right now, I'm gonna kind of just draw it as like a thickened area. And you're going to know that it's a tonsill or tissue. And it's called we got two names for them, right? One is we can call them the um the fingial tonsils. We also call them the addenoids. Either way, I'm going to represent that as this bluish kind of color. We only really have one of these. Then you have like a little hole that connects to your middle ear. So I'll draw this. There's like a little hole here. This is called the ustian tube, the fangotanic tube. You can you can call it whatever you want it, but it's one of those two. There's a tonsil that wraps around that one, and it's called the tubal tonsils, but you got them on both sides because you got two ears, right? So, here we're going to have a tubal tonsil here, and we're going to have a tubal tonsil there. The next thing is as we go down, you have this next one, this pink one, and it actually sits like when you look in someone's mouth, you have these arches, right? And one, they call them pillars. Here's like a posterior tonsular pillar. Here's an anterior tonsular pillar. And right in there, you can see these like little things called the palatine tonsils. Now, you got them on both sides. So, you got two of those. So, I technically have two palletine tonsils. So, I got two tubal tonsils. I got two palletine tonsils. And then I got one more. What color shall we pick? Let's go brown. So, this one is right at the base kind of like kind of at the posterior portion base of the tongue. These are called your lingual tonsils. And you only got one of them. So here is your lingual tonsils. Do you notice what this does? I bet you see it right. If I were to kind of connect these, that is a ring. And that ring is made up of these tinsils. And again, what are these tonsils again? It is the fingial or the addenoids, the tubal tonsils, the palatine tonsils and the lingual tonsils. So when someone technically gets an infectious process and it causes inflammation of those tonsils, it could be any of these. But if I told you which ones are most often affected is the case. It really depends. In infectious monucleiosis, it could be all of them. and group A strep it tends to really plague these the palatine tonsils. So that's what I want you to take away from this. So inflammation of the tonsils it could be any of these. What about fngitis? Fingitisitis is inflammation of the ferings but you know you got three layers of the ferings bro. We have in blue the nasop fernx we have in pink the oro fernx and we have in orange the luringo fernx. So technically when we say there is inflammation of the fairings it really could be any of these. It's just probably most often it's going to be the oro fairings. And so again I want you to remember that this is inflammation of the fernx. But again when we talk about the ferinx what I want you guys to know is that it could be any part of the ferings. It could be the naso could be the oro could be the lingo. But if I really wanted to be particular, it's most often that good old oro ferinx. All right. So cool. We have inflammation of the tonsils, which could be any of these, but if I told you which ones are probably most often affected, I'll put an asterisk next to them. It's the palatine tonsils, but it could be any of these, especially mono. Mono will affect all. So here let's actually make a little note a little important note is infectious monucleiosis affects all of them and that's pretty significant because the reason why is when those tonsils get super inflamed they can narrow the airway and it can cause airway obstruction either way I want you to remember for the most part palatine is the most affected or ferinx is the most affected when you get inflammation of these things what would be the way that these patients would present. Well, the first thing is I know that this is usually in the throat region. So, if it's going to be really really sore, it would cause throat pain. That's pretty straightforward, right? So, any kind of inflammation primarily in this area, and I'm going to represent this with kind of like this squiggly red line here. This is all inflammation. So, what's the primary location of this that it's going to cause pain? It's going to be the throat. So, the most common presentation, let's do it here in red, is going to be throat pain. All right? And we often can say that's a sore throat, throat pain either way. But here's the next thing I want you guys to add on to this. When a person has throat pain, it could just be pain in general at rest. But sometimes that could cause pain with swallowing. So throat pain kind of depends. It could just be pain that's just there all the time or it could really really hurt when they try to swallow. And that's something that's pretty common in any of these kinds of tonsil fangitis that we'll have is they're going to have throat pain. Now, for the most part, this infectious eeteology whenever it is happening, regardless if it's viral, bacterial, or anything else, this usually causes an inflammatory response. We know this whenever there's inflammation. So, here's the tissue damage which is causing the pain, right? But there's also going to be cytoines. This is a natural immune response. It's regardless. Now, in viral cases, it may not be as intense of an inflammatory response. In bacterial cases, it may be more, you know, significant, especially group A strep. But what you're going to know is that they're going to pump out things like interlucan one. They're going to pump out things like TNF alpha. We know this. We've already we're we're experts at this point. And interlucan 6. This is all the response of inflammation coming to the area, which we'll kind of dig into here and, you know, piece by piece and you'll kind of make sense of that. But all of these things, what they do is they kind of um they obviously alert the immune system, right? So they're going to really really activate your immune system depending upon the cells. Obviously you can have things like macrofasages and neutrfils and all of those aspects. So you're going to get a immune response, right? So you're going to definitely stimulate an immune response. All right? So you're going to stimulate a immune response. But there's one other critical thing that whenever there's enough of these cytoines present, not only are they going to activate your immune system cells to come in there and do the dang thing and fight, but it's also going to activate things like the hypothalamus. And so a part of this immune response is you can absolutely expect for the patient to develop some degree of fever. And that's usually because what we happen is this immune response. We also see that this activates the hypothalamus. And when you activate the hypothalamus, that resets your body's like thermostat. And that thermostat activation, it kind of turns the heat up, if you will. And that is going to then say, "Hey, bro, I ain't chilling around at no normal temperature anymore. I'm rocking this like fever at greater than 38 degrees C." And again, that fever is depended more on the eeology. So for example in like viral and infectious probably not like a high-grade fever for something like group A strep they can have like a pretty high fever. So so far we got a patient who has throat pain. So that's one symptom that's pretty common in this triad. So we have throat pain. The second thing is they can have a fever and this is probably due to the general inflammatory response. The more intense the immune response depends upon the pathogen. The last thing here is for most of them when you get infections of the throat, I want you to think about this. Where would it drain? There is lymphatic tissues all around these areas. So, they're going to pick up any kind of inflammatory debris and pathogens and that stuff's going to circulate, circulate, circulate. Where is it going to to drain? If you really want to think about this, you know, the cervical nodes, you have what's called the jugular digastric nodes. We're not we don't need to know that. We just need to know it's usually in the anterior part of the neck. So anter cervical lympidenopathy is often times the most common presentation of tonsilopharangitis. But either way what I want you to know is that from this infection the pathogens which we'll just for right now I'm going to represent in this greenish color here. Actually no let's do purple because I got the lymph nodes being green. We got these pathogens and inflammatory debris. Right? This is the pathogens. Any kind of inflammatory debris. Our lymphatics are supposed to clear that stuff up. But what happens is it drains into the closest lymph nodes. Where are those lymph nodes? The cervical lymph nodes. So once these things drain down into the cervical lymph nodes, they're going to get all that kind of like uh inflammatory debris. So let's again let's show the inflammatory debris moving through the lymphatics. It gets into these lymph nodes and then what happens is you get an immune reaction there because naturally this is there's going to be antigens. There's going to be all these kinds of pathogens. They're going to create this inflammatory reactive response. And so these things are going to start to get angry and they're going to start to kind of enlarge. And what is that called whenever your lymph nodes enlarge? Lymphadonopathy. So what are you going to get as a result here? You're going to get lymphenopathy. But here's what I want us to be very very particular with. I already kind of told you this. Which lymph nodes are going to be enlarged? It's most often anterior. So here you think about this. You have your external clom mastoid here and you have this kind of midline part of the neck. You have a anterior triangle. That's usually where most of those lymph nodes are going to be inflamed. But if I take the sternoccyle mastoid in the trapezius, what's this one? That's the posterior triangle. So there is two different types of lympadinopathy. And I think this is worth mentioning. I do because it comes up on the exam often is that when we talk about these there is anterior cervical lympadinopathy and then what's the other one posterior cervical. Now oftent times with posterior cervical this is usually when someone has more of a generalized lympadenopathy which means their their lymph nodes are being attacked in multiple places besides the drainage point. That's something we would see more often and we'll get into it. Our good old friend here monucleiosis whereas anterior you can see that in viral you can see that in group A strep. You can see it in fingial. But the most common one I want you guys associated with is group A strep for this one and mono due to something called EBV for the posterior cervical. So for the most part patient comes in and say man I got a sore throat. It hurts when I swallow. And then on top of that, I I feel warm. You check their temp. They got a fever. And on top of that, you go and you palpate their nodes and you're like, "Oh man, yeah, you do. You have some swelling here in your anterior or posterior cervical nodes. We start to already have a thought process that I got some kind of tonsil ferngitis possibly going on." Well, then I got to look in their mouth and I got to see what do I see? Is it multiple tonsils being inflamed? Is their throat really, really red? Is there exudate? Is there any other kind of stuff? We'll get into that as we go along, but you get the point. We have a start here. So now what I want to do is I want to go over these different types of uh tons of ferngitis if you will. So the first one is going to be your viral cases. This is pretty much the common cold, right? So you can see it as a part of the common cold. So when we think about these viruses, we obviously know that we're talking about viruses, but the question is is which viruses would I want to associate this with? Most of the time it's things like rhino, adno, those are usually your offending triggers. So I definitely would want you to think about things like rhino virus probably even like parinfluenza adno but then what's the two that I really am like uh these ones can actually cause some pretty significant problems. I would definitely want you to remember things like influenza which we'll have our own lecture on and then I'll write this down here we'll get another little connection but SARS KV2 why is SARS KV2 really important because of CO 19 right? Okay, so CO 19 has the ability to affect the upper and lower respiratory tract just like influenza can. Right? So these are two really really nasty ones. These are two really really nasty ones. And again we'll have individual lectures on this but most of the time it's probably going to be the brino adno parinfluenza. So how do they get in? It's the same concept. Somebody decides to talk to you. They're like you know maybe they're spraying a little bit more than they're actually talking. You know they say don't spray you know kind of thing. And these respiratory droplets they make their way in this way. They get their way in this way. And I told you before, we talked about this in rhinocyusitis. They they move and they don't just have to damage one particular area. They can move along the respiratory tract and damage a bunch of different areas. And so sometimes what you may notice with this patient is they may get injury here in the nasal ferings or in the nasal cavity. But the problem here is that they start to kind of induce damage here in the tonsils or they start to induce damage here in the oral fernx. And that's where we see these problems. But they're spread the way that they get in is what? Respiratory droplets. So someone is having this infection and they spray it to you. That's why we often think about these during seasonal outbreaks or kids or daycarees or you went to a hospital or you went somewhere where there was an exposure. That's usually the key thing. Now once these puppies get in here and they start wreaking some havoc, what does that look like? Let's just pretend that we're zooming in on these two tissues. That's all we're going to do is we're going to take these two tissues and we're going to really really zoom in and see what does this actually look like at the cellular level. I'm not asking for us to be molecular biologists, dudes, or immunologists. I'm just looking for us to have an understanding on the epithelium. So, here's your epithelium. Here's your epithelium, which is, you know, usually in these scenarios, it's more of like a a squamus epithelium, right? because it's mo it's meant for you exposure to hot liquids and hard foods that can cause abrasion. So, we want it to be pretty tough. But when these when these pathogens kind of expose to this area, they they have the ability to access the epithelium and they do it where's my purple marker here? They do it via these like little special receptors and they're present on all kinds of them. They're called eye cams, right? And so they they use these to kind of get into the cell. That's all they do. They use it as a transport mechanism. So what if you really wanted to know what are these things that are allowing for them to attach? Well, there's different types of them, but I, you know, probably ICAM receptors are probably going to be the biggest one. So IM receptors, but I don't think that's the key thing to know. What I do want you to know is that once they get into these cells, they undergo replication. So once the virus kind of gets infected, so let's say that this virus hops into a couple of these cells. So it hops in and then usually what happens is it under goes a replication process, pops some more of these off, pops some more of these off and they spread and they move. So here virus gets in. We'll represent with some dots. The virus is in there, it's replicating like bunnies and then it pops off going pop off and then what happens is it just spread these viruses that allow for it to go to what? To the next cell. If it goes to the next cell, it can damage this. If it goes to the next cell, it can damage this. What ends up happening as a result? You cause damage and death to these epithelial cells. Now, thank God epithelial cells can replicate. You can fix that, but you're going to damage them. So, the end result out of all of this is you get some epithelial cell injury. So, some epithelial cell injury and that's for the mucosa and that's really the problematic issue. So once you get injury, what's the natural response from tissue injury? We don't need to go through all of this crap, right? Because I don't want to it's not the reason why I don't want to go through all of this stuff is because guess what? It wouldn't really affect us in the overall grand scheme and the diagnostics of the treatment. But you're gonna have as this tissue gets injured, it's going to start secretreting certain types of inflammatory mediators, right? And so these could be different types of damage associated molecular pathogens, all that kind of stuff like that. All that's going to do is it's going to pull in immune system cells. Usually it's going to be things like macrofasages. You may get some lymphocytes that come to the area, but the whole goal is to alert. It's to kind of trigger to stimulate, if you will, an immune response. And then that's going to cause inflammation. And that inflammation is going to activate specific nerves that are in this area. What kind of nerves supply the fernx and the tonsils, the tonsils? Things like your fingial, your glossopherrenial nerve, your vagus nerve. They have those fibers that can pick it up and that's that's what causes the pain, right? So, you're going to basically kind of release these things, but we don't need to really know it because it's not going to really change anything that we need to know about the disease. It's not going to change anything about how we treat it. It's just good for us to have kind of a holistic understanding that you're going to get an immune response. And all that's going to do is it's going to take this injury and it's just going to worsen the inflammation because you need that to kind of clear this out. So you're going to get as a result inflammation, my dudes and and my and my dudetss, you know, and then because of that, what's going to happen? You're going to get the pain. So we already we already got that grasp there. So what in the heck helps me to differentiate this from any of the other ones? Well, really what it comes down to is I told you kind of back here. This this little virus doesn't just wreak havoc in one area. This may be the area that wres havoc, but it may also wreak some havoc in here. What if right this thing got here caused some damage here caused some damage here. Where else can it move? Down here. Was it down there? The larynx. And because of that, they get some injury here in the larynx. So, you get the point. This respiratory droplet, if I were to kind of take this concept here, we only focused in on these areas and how it causes damage, which causes pain. Viruses don't care if you if you only know that it only affects this one area. It affects multiple areas. So, what I want you to think about is this thing can get in here and it can wreak havoc to the actual nasal cavity. It can even move over here and cause damage here. It can get here and cause damage here. It can get here, cause damage here. It can get here and cause damage here. So what I'm trying to get essentially is what does this call when you cause inflammation of the nasal cavity which then kind of then because it's connected via osteomal complexes to the sinuses what can you get as a result if I cause some kind of injury in this area here what is this called rhinocinusitis right so you can get some kind of viral rhinocinusitis I'm not going to write that out but I want you to tell me what's the well ah stink let's let's do it We put a viral rhino sinocitis. The big thing I want you to tell me about this is what's the primary kind of like symptoms that may be present with this. [clears throat] Well, this may cause things like a runny nose, some post-nasal drip, some congestion, right? That that's the kind of stuff that we talked about before is you can get something like maybe a post nasal drip because of all the inflammation and the mucus dripping into the back of the throat. You can get some nasal discharge and what else can you get? We already said you can get some congestion. We use like a special term which I'm going to I'm going to hit it at the end. It's called kisa. Kisa is kind of like a general thing of a patient who has congestion. They have nasal discharge and post-nasal drip. It's going to come in handy. I promise. The other thing is that it not only damages here. We already see how it can cause the tonsillitis, the fngitis. That makes sense, right? We already we already did that part up here and a little bit here. But what if it causes some inflammation of the larynx and you get laryngitis. All right. So if I get some laryngitis that can cause like a horseness of the voice, right? That can definitely cause like a horseness of the voice. But what's another thing that's kind of important with laryngitis besides having the uh the horarsseness? We can definitely write that down. So let's write down maybe there's some horarsseness. But there's really a big thing that I want you to think about. the cough, right? And usually the cough is kind of like it's it's it's non-productive. It's relatively dry for the most part. So, I have something that I want you guys to see here. I told you that this technically comes as one general definition which we called what? Kisa. And then the biggest thing for the laryngitis is the cough. Right? This is the most common one. Well, there's one more and that last one is conjunctivitis. And you're like, wait, dude, what the what the heck are you talking about, bro? Adno virus especially can kind of connect the eye and you can get damage to the epithelium of the actual um the conjunctiva. And so often times we remember what's called the three C's to help you to kind of differentiate the three C's to differentiate viral from something like bacterial. So here's what I want you to know. Patient with viral tonsil fngitis can have like a low-grade fever. It can have a sore throat. It can have some anterior cervical libidenopathy. But what makes it unique for the exams is that it injures multiple other areas of your upper respiratory tract. So you may see things like kisa, you may see things like a cough. And that's really important because guess what? There's something called the centator criteria, the modified centtor criteria. And guess what's super critical to that? The presence or absence of a cough. And that's you're going to see why that comes into play. And then conjunctivitis. So having the three C's really makes you think about a viral eeology rather than a bacterial. All right. Boom. Roasted as Michael Scott would say. Let's move on to the next component here. The next component is infectious monucleiosis. All right. Now, with infectious monucleiosis, actually, let me sit down because, you know, probably easier for my my dude here, Robbo, uh, for the camera. So, let's let's kind of do this part here. With infectious monucleiosis, what is the primary ethiology? It is EBV. EBV. So, EBV is called Epstein bar virus. We're not talking about what is that guy's name? Jeffrey Epstein. Hopefully, don't don't like crucify me, but that that's not the virus that we're talking about. It's not named after him. It's a specific virus. It's the Epstein bar virus. It's it's actually sometimes associated not just with monucleiosis, but even cases of lymphoma. So, it's a pretty important virus. But what makes this one different from these? Because you're like, "Dude, this is technically a virus, Zach. Why are you including it here?" Because this virus doesn't behave like these viruses do. This virus behaves completely differently. And so, how this virus gets in is usually it's going to be saliva. So, you go out with your friend and you're, you know, a little sucky sucky with the face and stuff and you're swapping spit or, you know, you think it's cute to to share your your your Dr. Pepper with them and they got the EBVs, right? That is the carrier for this virus. And once that gets in there, guess what it likes to attack? It needs an entry point to get to your immune system. That's what makes this one different. So, you're probably like, "Zack, you're kind of saying the same dang thing. It's going to love the tonsils." Loves the tonsils. And it's not just one of those. It could be any of those. That's what I want you to remember. Remember Waldar's ring? It could affect any of them, but it's also going to hit the oro ferings. So, we're going to have kind of a similar presentation, but you're like, "Okay, Zach, you're already kind of starting off. It's just different from saliva, respiratory droplets. I got it. Okay, here's what I want us to do. I want to see how this thing technically behaves." So, I'm going to bring this one here. I'm going to bring this one here. And all we're going to do is we're going to do a little zoom in, if you will, and kind of talk about how this actually works. So, as we zoom in, we kind of know already the differences in the eeteology, which is the pathogen. We know the differences in the way that it's transmitted. We know it's targeting any of the tonsils and the oral ferings. Well, here we're going to just zoom in on the epithelium here. So, here is your epithelium. And this is usually some type of squamus epithelium like stratified EBV. Basically, it gets its way. There's different types of ways that it can get in. And I don't think that that's super relevant because we don't target EBV with specific drugs. We don't need to have all this diagnostic test. So some of the immunology isn't always that critical for us to know. But let's say that this EBV it gets its way in. Once it gets its way into the epithelium, it now has the DNA which it needs to start cooking up some more viruses. So this thing starts undergoing what we want it purple. Sorry. This thing uses it's the same kind of thing. gets its way in and this thing starts cooking, making some viruses. Once it does that, it's going to pop that cell and then it's going to spread to this one and it's going to spread to this one. So, it's going to cause what? The same exact process I talked to you guys about. It's going to undergo replication. It's going to pop this cell, spit some of these out that go to this one, spit some more out to go to this one. Either way, you're propagating this thing like a Plinko game and you're causing destruction of the epithelium. and you're going to get the same response. You're going to get an inflammatory response, right? So, what's the end result out of all of this? Well, we know that the end result of causing this damage is you're going to get some degree of epithelial cell injury. So, that's the same. No different there. All right, cool. Well, tell me where this differs, Zachary. The area that it differs is the next step. Not only can it kind of spread to the other epithelial cells and cause the epithelial cell injury, this virus then says, Watch this, bro. Hold my beer. And what it does is it gets out here. So, here's the the uh virus got replicated, causes damage. Here's the virus here. It sees B cells as like its best friend. These other viruses didn't say nothing about no dang B cells. So, here we have a B cell. And this B cell is just chilling around. He's just hanging out, not doing anything. And this B cell has a specific protein. Now again I don't want to go crazy on these but it's mentioned in the textbook so I'm going to mention it. It's called the CD21. It's a cluster differentiation protein on the surface. It is the entryway for this virus to get into the B cell which is why it really matters. So what happens is this EBV uses this as an entryway and we'll do the same thing over here gets into this B cell. So let's say again here's some of these little virus particles. That's the way that it gets in. Once it gets into this B cell, this B cell is now infected. Right? So, it got in and now what kind of difference do we have here? We have what's called a I'm going to say this is a normal B cell that all right this is a B cell that we're going to denote is infected. This is an infected B cell. Now, normally you would be like, "Oh, this dude's just going to pop these B cells open, right, bro?" No. That's what's crazy about this thing. The the virus is like kind of smart and it's kind of tricky in a way. And what it does is is I don't think you guys need to know this, but it increases like the expression of specific markers. And all it does is is in two things. Two things it does. One is it tells the B cell to proliferate and it makes it kind of like hard for the immune system to actually beat up. The second, so that's one thing. So, one thing it's going to do is this thing is going to go and it's going to go hide in areas that it loves to hide in. It's going to go hide in the lymph nodes. It's going to go hide in the liver. And it's going to go and hide in the spleen. And I'm going to do this for reference here. This is the one that we kind of get a little nervous about. And I'll explain why, but it's going to go there, and it's going to hide. And what it's going to do in here is it's going to go deposit. And I'm going to draw a bunch of these. So, what did I tell you is going to happen? One of the things that's going to happen is once this virus gets in there, it turns on specific genes and and it changes the way that the B cell behaves. And the biggest thing that I want you to know is is it under goes proliferation and deposition. All right? It's not going to court. It's not it's it's proliferating and it's going to go and deposit into particular organs. So, you're going to get a lot of proliferation. And I'm not kidding. this thing is going to replicate like bunnies. But where it's going to want to do that is in these particular tissues. So that's one thing. One thing is we're going to get lots of proliferation and deposition. So what I'll do is is I'll draw a bunch of little circles here. This is just my infected B cells. And these things are going to go and occupy a bunch of space in these organs. And then you you guys are already probably going to start to get what that will do [laughter] in this particular scenario. But there's one other thing and this is what I think is cool. The virus not only tells it to proliferate and deposit, it like I I don't I don't know how it does it, but it tells the B cell to turn into like a a poser. So, it becomes a plasma like cell. Let's just let's just say that it's a plasma-like cell. And it it's so weird that it can turn on specific genes to cause this plasma cell to produce antibodies. And I'm just going to make these antibodies random different colors. And the reason why is they're super random. We'll make maybe a couple of them. We'll make them orange. Maybe we'll make these ones pink. The whole point here is that they have no benefit whatsoever except for us as clinicians when it tells it to become a plasma-like cell and to make I'm going to call these junk antibodies because that's what they are. They don't do a dang thing. But there is one true benefit of these junk antibodies. So what happens is the virus stimulates two pathways. One is the proliferation and deposition and the other one is to turn into a plasma-like cell and then increase these junk antibbody production. So it increases this junk antibodies. These junk antibodies we can actually test. You know what these are called? These are called heteropiles. So we call them junk but we also can call them heterroile antibodies. They don't serve a purpose. We just happen to find out through some way, shape or form that when we test these against sheep and cow red blood cells, these antibodies of glutinate and it makes me think that they have an infection from EV EBV. So that EBV, this is what I want you guys to know is EBV [clears throat] basically kind of turns on specific it kind of re changes the way that the B cell behaves. So this EBV changes all the the the different kind of inherent processes of the B cell, but I'm just going to say it changes the B cell. And that's what I want you to take away from this. This EBV changes the B cell. And it changes it in what way? To turn into a plasma-like cell or to go and deposit into these particular organs. Now, you're probably like, "Okay, Zach, I get it. We're getting somewhere, right? This is We're going to talk about how why this is important a little bit later. We will. I promise. This, I'm guessing, has some significance because if I got a lot of cells, they're going to enlarge. Absolutely. But let's let's hold on for a second because here's the other thing. These EBV viruses now, normally this is a process that takes time. Did you know this? This takes a while. This isn't something like when a person gets infected, this kind of process happens like within a couple days. We're talking weeks, bro. And then on top of that, this next process even can take longer. So what happens is these EBV viruses what happens is they get exposed to different types of immune system cells. What kind of cell is this right here? What would what would you call this one? This is a macrofase. But you also have something called dendritic cells too. Right? For right now I want you to trust me that it's we're just going to call it an antigen presenting cell. That's normal, right? Antigen. Usually for the most part that's macrofasages. That's dendritic cells of some sort. But these little suckers they're smart man. They're good at sampling things. And so what happens is they undergo what's the process called when they take them inside. They have an endoome fagosome. Uh they then fuse with lysosome. Then they express a piece of that little uh pathogen on their major histoibility complex. It's called fagocytosis. Right? So this is this process here is called fagocytosis and then it's going to undergo antigen processing. Right? That's all I want you to know. Fagocytosis and then it's going to go undergo antigen processing. So who is it processing it and presenting it to? a T-C cell. So, here is a T- cell. Usually, this could be a CD4, it could be a CD8, it could be both of them. So, it could be to a CD4 positive T- cell, could be to a CD8 positive T- cell. Once this thing presents that the TE-C cell can do two things. One and this is what makes it super crazy is one is it can drive the proliferation and formation of these weird CD8 cells. So this pathway is we're going to make a ton and I mean a ton of CD8 positive T- cells and they're going to look super funky. They're proliferating like bunnies. But I'm going to write something here which is going to become important in the diagnostic section is they look weird and it's just because of the way that they're having to proliferate. They don't look normal. They're atypical appearing. That's key. But what happens in this process is that we push this. There's different cytoines. We don't need to know all that. But it pumps a lot of these in. And these now have been primed to say, "Oh, I recognize an EBV antigen." And dude, I'm really good at going into lymph nodes and finding out where these dang things are. Time to go on the hunt. And all these things do is they say, "Watch this." And they start moving in the same direction. And so what I'm going to do is for for keeping the color so we don't absolutely have this go insane is I'm going to do this. I'm going to have a box around all of these like this. a box around this. Okay? And what I want you to know is is these CD8 cells are going to go into this box and they're going to go and deposit into this area. And what I'm going to do is for color sake, I'm going to call these CDA cells. I'm going to make them just a little bit red so we can see this. So they're a little bit red. So guess what they're going to go? They're going to go into this area and they're going to fight. So now we're going to have a lot of CD8 cells. We're going to have an infected B cells all in the spleen, all in the lymph nodes, all in the liver, and these things are going to enlarge. And what you're going to get out of as a result out of this is three different things. All right? One is your lymph nodes are going to get big as a son of a gun. The second thing is your spleen is going to get big as a son of a gun. And the liver can get as big as a son of a gun. So what are the two things there? We're gonna have lymphatinopathy. Now, this is why I told you that in the tonsils, once you infect the palatine, guess what? This puppy can get into the lymphatic tissues, go all over the place. This is generalized, dude. This doesn't have to be in the anterior cervical nose. Could be the posterior, could be the axillary, could be anywhere the heck it wants. That's why it's really important. And so, I would I would call this more generalized. It just so happens to be that that one area that we see it is in the posterior cervical nodes. The second thing is so we did lymph nodes. Let's go here. Hatomegali is a pathomegaly going to do anything? It could it cause could cause like a little bump in the LFTs potentially. But the real one that we get a little bit nervous about is the spleen and that's splenomegali. And the reason why the spleen is something that we get scared about is because if this thing gets big enough and big enough and big enough, what is the risk? You run the risk. So this increases your risk of a splenic rupture especially in what types of kids who are maybe going out and doing some crazy kind of contact sports. So increased risk of splenic ruptures. So this is this is something that could actually change the outcome of a child's life and that's why this is something that we need to know. So you're probably like, okay, we we've talked about a lot. I see that this is much different from this patient. Much different. We got some weird antibodies. We got some weird CD8 cells. I got other organs that are getting all kinds of big. One other thing I want to tell you. We did this pathway. What about this pathway? We got another thing here. The other thing is we have to eventually have an ability to fight off these EBVs. And so what happens is these teac cells what they do is they kind of release different types of cytoines. And these cytoines actually what I should say is it releases cytoines. Um if I don't erase this nicely, my my cameraman is going to like have a heart attack. So hold on a second guys. Um what happens here is that this T- cell releases cytoines that drives a particular process and what is that process? It's taking a B cell and making it into a real plasma cell. So this is a B cell and this is not an infected. You see how this one this one's not infected. It's completely normal. So this is a normal B cell. Dude's fine. He turns into a real deal plasma cell. And this real deal plasma cell has all the information from this interaction to produce the correct antibodies. And these correct antibodies that it makes depends on timing. And these are the real deal. So we should actually make them a real deal color. Let's go with let's go with this bluish color here. And so it makes different antibodies. So, we're going to have these EBV antibodies, and we'll get into these a little bit later. I don't want us to get too crazy right now, but the plasma cell will actually produce EBV antibodies. And if it's IGM, what does that mean? It means it's probably more of an acute phase. If it's IGG, it probably is maybe more of a past or chronic. And there's one other one that we'll talk about called EB um EBNA, which is basically the Epstein bar nuclear antigen antibodies. Those usually indicate more of a prior or kind of like chronic type of exposure. So that's why these are important is they come into play with actually diagnosing it definitively. This is kind of one of those tests where it just says they probably have EBV. But what are you getting out of all of this that's much different from this, right? There's one other thing that I think is the most critical when you have this much immune activity going on which is absolutely insane compared to compared to here. I have just absolute insane off the charts T-C cell activity B cell activity all these things are coming into play. I have an insane immune response. What do you think that does to just your overall Oh, bro, I'm so tired. I got cells constantly fighting fatigue. I mean, I they say that that is probably one of the most common things that you're going to see here is this excessive and and severe and more chronic fatigue. So, that insane immune response that we've kind of experienced here with this patient, that is going to be the primary driver. So, what you'll notice in these patients is a couple things. You'll notice that they have the sore throat. They'll have the tonsils that are inflamed, right? And sometimes these tonsils can be big as a son of a gun because of the lympadinopathy and they can affect all of them. We already talked about that. We also noticed that they could have some EBV antibodies that are really helpful. We noticed that they can have some other antibodies that can be helpful. And we noticed that they can have organs that are affected and they get these weird I actually want to put a little box around this. They get these weird kind of like lymphocytes that are atypical appearing. So they'll have like a higher white count uh with lymphocytes predominant. But the patient who comes in with a sore throat, sore tonsils, maybe some fever, some posterior cervical lymphnopathy, insane fatigue and a really swollen spleen and some weird lymphocytes screams more EBV than it does this picture. And I hope that makes sense. And so now what I want to do is I want to move into the next component here, which is the patient who comes in with nasty nasty group A strep. So with group A strep, what's what's kind of the deal with with this one? With group A strep, this sucker is um it's just a nasty pathogen, man. It's it's a it's really a nasty pathogen. When we talk about group A strep, it's also another name for it if you guys want. So here we have this strepus, right? So it's more in a linear chain. uh strep caucus. I've been drawing these all in okay black. So here we have so we have two names. One is we can call this streptocous strepus pyagans but another name is more that group a strep. So it's a group a strepcockus beta hemolyticus type of pathogen. Right? This is the primary trigger thus the name. So what happens with this is again it's it's it's usually something where it's an exposure, right? So it's usually spread via some type of exposure. So in other words, you're around maybe a child or a daycare or something like that and this is passed on. So usually this is going to be something that is very very very contagious. All right? So it can be spread via respiratory droplets. Right? So that's one kind of nasty thing about this one is it can be spread via maybe different types of respiratory droplets. It makes it like highly contagious obviously, but once it gets in there, we talked about this this this sucker will damage the oral fairings and it'll damage the tonsils and we'll talk about how, right? So obviously that's the next step is to say okay we know that this thing is going to cause it's going to wreak some havoc but how is it going to wreak some havoc which is kind of like the important thing because we have some commonalities and we're starting to differentiate these slowly but how do I really really kind of get down to this so group a strep has got like a bunch of different stuff right so what I want you to know here is on it we first thing we got to do is this you get exposed to this thing imagine I take like something that I want to get it to stick to a wall. If I just throw like a bean bag at the wall, it's going to hit the wall and fall off. It needs something. What if I took that bean bag and I covered it in like gorilla glue or something like a paste that when I threw it at the wall, it stuck to the wall? These group A straps got something like that. And so what I want you to know is let's do here this pinkish color. They have like these little like little Velcro pieces. They have like these little Velcro pieces. All right. And I'll do two different colors of them. We'll do one here in pink and then we'll do one here in this kind of orang-ish color. So, we got to get this thing to really stick to the epithelium because this this is our epithelium, right? But what we know right now is that this is our epithelium of the tonsils, the epithelium of the oral ferings that we're trying to get this thing to stick to. And here's our group A strep. Right on its surface, it's got these two little hookers. Oh, not hookers, hooks. Holy crap. Uh, this is called F protein. So, it's called your F-Proin. And this one is called the M protein. And this is the big one. This is the This is the real real important one. The M protein is like this is the heavy hitter. This is the one that carries most of that ability and that weight, right? This one's kind of like it gets you to stick, but this one gets you to stick and then really do some damage, right? So, what these things are going to do is they're going to allow for this pathogen, the bacteria, to stick to different types of like proteins and receptors that are present on the epithelial cell surface. So, all these things do is they trigger pretty much an adhesion. So, they're really, this is the first thing that they're going to do is they're going to stimulate a really strong adhesion, right? Okay. So, they're going to connect and they're going to get ready to do some actual damage. That's what these things do is they stimulate adhesion. Once they've adhered, they got to get their way to damage. They got to start doing some stuff. And what they do is they got all these like little c all these like little kind of like pockets and vesicles that they're going to start releasing a bunch of different things. One of them is called streptoly. So it's going to release something called streptoly. Another thing it's going to release is something called hya laurana hyalo. I'm so bad at spelling. Hyaluronadase hyaluronidases. All right. The next thing is it's also going to release like this weird little thing called SP B which is kind of like a little proteaseier. So there's there's three different things that are released. streptolyin hyaluronidase and this kind of like weird exotoxin. It's like a pyrogenic exotoxin called spaf. What happens is these things basically are like the drillers. All they do is they come to this area and they say, "Bro, I'm going to put some holes in some cells. I'm going to start ripping apart the tight junctions between them." And so now what I got is I got these things burring holes in my cells. So now I got some holes in my cells and then on top of that I got it like ripping the glue between the cells. What does this create an opportunity for? For bacteria and all that stuff and toxins to get in between. So all that ends up happening as a result of these things is this triggers cell destruction or epithelial cell injury. So it causes epithelial cell injury. And it's not just the epithelial cells themselves, it's also the spaces between them. So they damage tight junctions, they put holes inside of the cell. All this creates as an opportunity for the pathogen and different types of toxins to get right in. So this first thing is adhesion. The second thing is we get the epithelial cell injury. When we do that, we create a gateway. And now all we need is for this pathogen that's just chilling out right here to say, "Oh, I created some holes in some cells or I created a big space." So let's imagine here that it did its damage. And let's say that we kind of really opened up a tight junction right here and now this pathogen can get right in. So now there's entry. So we cause adhesion with the M proteins, the F- proteins. We release different types of enzymes and proteases that kind of bur their way through the cells, create an entryway, and now this pathogen has just entered. So now we have entry. From here we we get some some rough things that basically starts to happen. The first thing here is this pathogen essentially is going to really activate it's going to cause more damage. So essentially once it gets into the area, it's going to start causing more damage. So if you really want to, it's going to get in here and you're going to start getting more tissue damage essentially, right? This thing is just a really nasty little son of a gun. And so we'll kind of show that that it's causing damage to these tissue cells. So you're going to get injury to the epithelial cells, which we did from the outside. And then these pathogens are just going to kind of continue to release more of those damaging enzymes to keep damaging epithelial tissue. When epithelial tissue is damaged, what did I tell you it does? Well, it kind of releases like different like alarmins, if you will, or like different damage associated pathogen, molecular peptides. All I want you to know is is it sends a signal. So, it's going to release different types of chemocines or cytoines. And the problem with this is is that neutrfils, they they love bacteria. They respond heavily to that. And this is going to basically go and tell the neutrfils, "Hey, bro, you've been telling me to let you know when I got something going on, I need you. Come get my back." And all it does is these chemocines, they activate neutrfils. And the neutrfils, well, they're going to really, really want to come out here and do some stuff. They're going to want to fight. And when we activate these neutrfils, they come to the area and they go here. They even come out here into this area and they start kind of releasing proteasis and reactive oxygen species. And essentially what ends up happening is we cause some damage. We're going to hit some of these. We may not dent them all, but we're going to we're going to do some damage. And what's going to happen is you're going to get all of this perent material. So a pergolent exudate. And that's really really helpful and kind of difference because neutrfils once they come in here they release all these different types of protection species. They're going to release things like proteases and they are going to cause some serious damage and they're going to try and when they do that unfortunately they hit some of our own cellular debris. So there's there's some innocent bystanders in that process. You're going to dent some of them and you're going to get some perinexate. Where is that exitate going to appear? It's going to appear in this area. So, some of this material may go through and into this mucosal lumen. And what happens is when you look at the patient's tonsils or you look at their throat, it's going to be super inflamed. All of them will be inflamed and red. But when I see a lot of exudate, that pulin appearing exudate looks like pus on the tonsils and maybe on the fairings, I start to think a little bit more possibly about group A strep. You can see it in mono, don't get me wrong. You can see this in mono, but this is the one that they like to talk about and again with that centor criteria. All right, this thing is [sighs] it's nasty though, right? So neutrfils are going to come and they're going to be the first reactive phase, but you also have to have other ways. You have to have other ways of killing pathogens besides neutrfils. And so what happens is these pathogens essentially they get taken up by who? Different antigen presenting cells. So who is this right here? This is a macrofase, but this could be a dendritic cell. This is an antigen presenting cell. What does it do to get this thing inside of him? That sounds weird, but it's called fagocytosis. So it goes under goes what's called faggoytosis. And then it also under goes antigen processing. And so it takes a piece of that antigen and puts it on its surface to interact with who? A T- cell. So this T- cell and usually this is a T- helpper cell as those over there could be both you know CD4 CD8 so T- helpper and cytotoxic cells this is a T- helpper cell for the most part this interaction is going to activate the T- cell once you have this interaction boom you activate this T- cell what the T- cell then does is it does just what we talked about over there it pushes this reaction to take a B cell to go into a plasma cell now I got B cell and I'm going to turn this into a plasma cell. And the beauty here is that this plasma cell has now been programmed to make antibodies against that specific little sucker right there. And what does he do? That's what he does. So we already talked about how these macrofasages, they come into this area and they kind of help you with this process. They undergo that fagocytosis. These plasma cells are going to start pumping out antibodies. And we have all these different types of antibodies. And these are real deal antibodies. These aren't these aren't a joke, right? These aren't little junk antibodies like we talked about mono. These are some real deal. So we have these group a strep antibodies. Now do you need to know these? Kind of. What I want you to know is is there's a couple of them. One is we make them against things like the streptoly, we make them against things like spabi, we make them against things like the M protein and all these other different things. So we have a couple. So we have for example, we have some like anti- M antibodies. We have things like anti- SP. We have things like anti- streptoly and then we have different like O antibodies and there's even another one because there's enzymes called DNAes that those are also prevalent too. The reason why I tell you all of this is there's kind of two different reasons. Some of these are diagnostic. Which ones are more for diagnostic utility? these that I'm gonna kind of do in this red color. What I mean is when a patient ends up having anti-DNAs B positive antibodies, it tells you more likely. You often don't ever think about this. At some point you or somebody you know has had strep throat. They ever test your blood for anti-DNACb antibodies? No, because you don't really have to. But if a person had like streped throat and they ended up with another infection somewhere else, for example, they ended up with a a related reaction um affecting their heart or other areas like maybe potentially their kidneys, you may test to see if they had these antibodies present because it tells you that they had a prior exposure and an infection. And so these are more for that diagnostic utility. So that's what I want you guys to remember is they have more what type of utility? Diagnostic utility. It's just we don't often use them except in certain scenarios maybe like rohematic fever and things like postpocal glomeritis. These in this bluish color we don't use them for testing but they're the reason why we have the problems that we have. [laughter] So these which we'll talk about guess what uh a little bit over there somewhere. We're going to talk about how these cause damage. So these are the ones that cause the damage. dishes. These are the ones that we use to tell if they had an infection. So, basically diagnostic utility is for infectious exposure. These I'm going to talk about these a little bit later. These are the ones that cause the damage. So, we'll talk about this later. We'll well I'll write it for right now, but we'll talk about things called post streptoco glam nephritis and we'll talk about something called roheatic fever. So, they're the ones that may trigger that process. What I want you to know is that they're supposed to just be going and damaging this pathogen. That's what they're supposed to be. But there is some benefits of these when it comes to diagnostics. So we produce these antibodies. Guess where they're going to go? So not only do we have neutrfils fighting, we have antigen presenting cells presenting this to make antibodies because guess what we want those antibodies to do? We want the antibodies to go here and click onto them, activate compliment proteins, activate more macrofasages and kill all of this. That's our goal. But they come with a potential utility and that's what's important. You're like, "All right, Zach, I I got it. So, I got a person who's pulining exodate. I got some antibodies that they'll produce. I still don't feel how this is really helping me." All right, hold on. The other thing I want you to know is that these the these strep once they get in to like you know they access your tissue or they even if they get into the bloodstream the problem with these things is that they release these different types of nasty toxins. So let's say that it releases these pyrogenic toxins. And when it releases these pyrogenic toxins, the degree and the amount that they release determines some very unique subtypes and pictures that I'll talk about. These again we're going to call them there's S Pa and S P. All I want you to know is that essentially what these things are is they are called pyrogenic toxins. So again, what are they called here? I'll write it over here. These are essentially these are called your pyrogenic toxins. They're going to go set fire to things kind of. And that's what I want you to remember. Pyrogenic that probably plays a big role in the fever response. It does. These things what they do is they act like the best way of defining them is not just a toxin but it's called a super antigen. What these things do is is they act like um a bridge. They act like a bridge. I'm going to use I'm going to use uh this pinkish color here. So I'm going to represent this spat A spat B as these like little pink dots. But I'm going to zoom in on one of them. All it's going to do is it's going to act like a handshake between these two. All right, between what two things? The MHC2 complex and the T- cell receptor. So, it's going to basically act as a bridge between the MHC2 and the T- cell receptor. Normally, what do you need for that interaction to take place? You need an antigen. Well, this dude, these dudes are the super antigens. And what they do is is they stimulate this interaction. They hyperactivate this TE-C cell. When you hyperactivate this T-C cell, uh what kind of T- cell is it again? Can you guys remember the T- helpper cell? When you activate this T helper cell, this thing just goes into like hyperactive mode and starts pumping out things like interlucan one, interlucan six, tumor necrotic factor alpha. And I'm not talking just like little drips. I'm talking like this stuff is pumping, bro. And because of that, these cytoines, what they do is is they create some systemic responses. One is they love what? They love the brain, the hypothalamus. And when they act in the hypothalamus, they do some nasty stuff. They act on your vessels and they can also act on your skin tissue. And let me explain what happens here. One is that it can act on the hypothalamus, right? So here's your hypothalamus. It's going to go ahead and stimulate that puppy. When you activate the hypothalamus, what's that going to trigger? A fever, right? And now we already talked that we know that these things have fever, but this is the one that I really, you get why I'm saying this is the one that you don't get like a little low-grade fever. They they usually get like more of a high-grade fever. And it's because of the inflammatory response, but because of these. So another thing I have to write this pyrogenic toxins but I want you to remember them as super let's actually write this down super antigens because these things will activate this response and you'll get tons of these enough of them that you're going to get a fever response because of how they activate the good old hypo phalamus. He resets that thermostat and he's getting ready to cook you go right that's one thing. The second thing is it makes your vessels dilate. Why? Why do you want to dilate vessels? Why do you want to make them leaky? Well, if I got an infectious process here, what do I want to bring to the area? Compliment proteins, white blood cells. Don't I need a bigger lumen to bring more things into the area to fight that off? Yeah. Problem is is when it gets into your systemic circulation, it can make some terrible things. The fear is that if it causes too much vasoddilation. So, let's actually write this down. It's going to act on here. It's going to cause vasoddilation. So, two effects are going to occur here. One is vasoddilation and the other one is we'll put some holes in this this vessel is capillary leakage. So two effects here. Let's write these out again. One is vasoddilation which is making the vessel bigger bigger diameter. So vasoddilation that's going to bring more blood flow to the area. The next one is you're going to make the capillaries leak. So you're going to cause capillary leak process and you're going to intensify that process. And again it's all because you want more immune system cells to come to the area. The problem is is if you have too many of these and they're getting into your systemic circulation, it's not just going to affect it at the throat. Where is it going to affect it? It's going to affect it in your systemic circulation. The fear is that if this causes this process and your systemic circulation is you can get low blood pressure, you can get hypotension. And so if I get systemic vasoddilation and capillary leak but the dilation part the fear of this is this may cause this may increase the risk of hypotension. There is a condition which can happen in group A strep if this occurs and it's called toxic shock syndrome. That's what I want you to remember. So, I want you to basically what this is doing is is if those super antigens cause enough of a problem, it can put a patient into what's called toxic shock syndrome. Not crazy common, but it's something to think about. So, if I had a person who had streped throat, all of a sudden they have a fever, hypotension, holy crap, I'm going to be scared about toxic shock syndrome. If I had another scenario where these cytoines are basically creating like an a rash type of picture and so the next thing is it creates like this weird type of rash and so you get kind of a change in the skin and this skin is you get it can occur all over the body but there's two areas which we tend to see it one is you get a kind of a scarletform oh please lord help me get this right scarletform rash which is pretty much diffuse, dude. It's all over the body. You get this thing all over the body and it's like um it's like sandpaper. That's I guess the best way to describe it. So, if you had a terminology on the exam where you had a patient who ended up having strep throat, they had a fever, and then on top of that, they have this sandpaper rash that's all over the body. That's that's a weird thing. There's one other area that it affects as well, though. And the other thing is it affects the tongue. And it's it's kind of odd. It kind of causes that similar kind of effect on the tongue. It kind of makes the tongue, it kind of rips off the kind of outer whitey covering and it causes the tongue to get bright as a strawberry and end up something with what's called a strawberry tongue. And this is all because of like skin. This is dermal changes. Obviously, this is more mucoutaneous changes. But either way, this subtype, if you will, because of the group A strep is called scarlet fever. We call this scarlet fever. So you're getting the point here for a patient to have group A strep. Here here's what I want you to take away from it. Two scenarios here. Two kind of subtypes. Besides the perlenexate, besides the high fever, the anterior cervical lympodinopathy. The big thing here is that the two potential complications from these super antigens. One is you can get something called toxic shock syndrome. The second thing is you can end up with something called scarlet fever. The differences between these is that both of them will have a fever. Both will have a fever. So what's the differences between these? This one will usually have fever and it can have a rash. So that's another thing. But the big difference here is the hypotension. This one will have a fever and this one will definitely have a rash but it will not have any kind of like hypotension. So the big thing here is you'll see maybe low blood pressure here is you should have normal hemodynamics. But the big difference here is that this could have a fever and a rash. This one can have a fever and it can have a rash as well. But the hypotension is the big thing and this is all because of the super antigens from the group A strep. So, what did I want you to take away from this? Group A strep is a very contagious infection. It's a nasty, disgusting, terrible bacteria that can wreak havoc on your tonsils and your fingial epithelium. It can cause a lot of different problems. But the big thing that I want you to know is because of the neutrifilic infiltration, a lot of the inflammatory reactions, the kind of inflammation that you'll see in the throat has more of a pervolent appearance. You'll have some antibodies that are very, very helpful. And these pyiogenic toxins, they really amplify a fever. And in some young, young young children, they can get things like scarlet fever. They could get things like toxic shock syndrome. If I had to tell you which one that you're probably going to see more likely on a vignette, it's probably going to be scarlet fever over the toxic shock syndrome picture. But again, you guys are getting an overall view here. Let us now talk about what about the patient who comes in with the dreaded absolutely feared dtheria. So dtheria is like it's obviously it shouldn't be that common but the people that you would want to think about this in is probably the people who aren't getting vaccinated. The reason why is a part of our vaccines usually for example things like the teddap right your tetanus your defaria and your ptasus kind of like vaccines we're we're trying to protect the child's immune system and make sure that if they ever become exposed they have the ability to fight that off um this kind of pathogen I I hate the way that they spell this one and I'm might get it wrong but with fendial dtheria it this may be a misnomer where people will say, "Oh, it's only on the fairings that's involving it." That's not true. It can be the tonsils. So, you can have infection and inflammation of the tonsils and the fairings. It's just we see this more often causing a weird thing on the fairings. With this one, the eeteology here is called corny. I just I just know I'm going to butcher this one, guys, but I'm going to do my best. Corny bacterium defer. All right. Corny bacterium def. Holy crap. I he gave me the knot of approval. All right. So, we we got this one. Corny bacterium dtheria. This one is obviously it's it's a it's a very nasty one. The key thing here that I want you guys to associate this one with in a clinical context in a person is that oftent times if you have been exposed that's that's that's fine but the big difference here that what causes the injury what causes the damage which causes all the problems that we're going to talk about here is that this I don't yes it can be spread via respiratory droplets all of those components but the big thing here is that you want to have an immune ability to to fight against it and so the key patient population which we see this in so that's what I want you to remember is who are at risk so the risk factors for getting something like this because this one is like it could be spread from somebody with respiratory droplets respiratory droplets kissing somebody right who has the infection how do you get this one the risk factors for this one is those who are underimmunized or not not immunized right so I want you to look for you know some degree of um lack lack of vaccination or maybe undervaccinated. So, some degree of that. So, it's lack of vaccination or maybe it's undervaccinated, right? And this is they're supposed to be getting kind of like a a vaccine that kind of gives them an ability to fight off this if they ever become exposed to it. That's why most people shouldn't have this. And so the problem here is is that yes, you can become exposed to it, but the key thing is is that you want to be able to fight against it. And so having that vaccination creates basically antibodies. And you want these antibodies that if you ever become exposed that you generated from a passive immunity, obviously the vaccine to fight against it. If you don't have that ability, you don't have this ability to stop this process. So I don't have the antibodies or I don't have enough of them. And so this process is going to occur easily. We want this to naturally stop it, but we're not going to have that ability. And so essentially what we do is we kind of allow for this infection to take place and take hold and cause some serious issues. So what does that look like? So again, coronary bacterium dtheri, you can become exposed to it through respiratory droplets through a bunch of different ways. But most people can fight against it if they have the actual immune system, the passive immunity there to do it. But if you don't have it, you're going to get an infection. What would that look like? We're going to zoom in here. This one is um it's absolutely terrifying. And I think it's important for us to kind of see the effects of that. You know, I don't want to get on like the political aspects of of of vaccination, but it this will kind of give you an appreciation of why it's really important, I think. So, when we think about how this affects the epithelium, this this this uh this pathogen right here, it has a an ability to kind of come in and stick to the epithelial cells. So, all I'm doing here is I'm taking one epithelium here. I'm taking this one epithelium and I'm going to zoom in on it. Right? So, we're really really zooming in. So, as I zoom in here, so we're going to zoom in on this cell. Let's see how it actually works. This bacteria once it becomes exposed to the epithelium, it sticks to it. So, it's like velcro kind of like the M protein, F protein. It sticks to it. All right, cool. I'm stuck. What am I going to do now? How am I going to cause damage? Once it's stuck, it releases a uh exotoxin. And this exotoxin is like a subunit. So, I'm going to draw it in two colors. What's a cool Let's do let's do pink as one version. So, I'm going to draw like a circle here as one part of it. And then let's do let's just do red. Let's do red as the other part. Actually, no, it's gonna be too much. Let's just do let's do purple. Let's do purple as the other part here. So, we're going to have two different parts of this toxin. All right. Two different parts. This one over here in the pink, we're going to call it the A subunit. So, we're going to call this one the A subunit. That's this piece. This one over here in the the purple color is the B subunit. So, you have two subunits here, right? Here's the A subunit in this pinkish color. And here's the B subunit in the purple color. The B subunit is what allows for the exotoxin to stick to the receptors on the epithelial cell. So that's the first thing. So the first thing is this toxin is going to then move and bind here. But what does it look like? It would technically look like this. So I'm going to show you here. Here's the pink I mean the purple part which is the B subunit binding to the receptor. And then here I need my pink color here that this thing is just hanging around. All right. Then what happens is this undergoes receptor mediated endoccytosis. What is that process called? Receptor mediated endoccytosis. It brings the actual membrane in into like a little vesicle that has the receptor and then on that receptor is what? The B subunit and the A subunit. The next thing we know about basic cellular biology is that it then undergoes an acidification process. What the heck does that mean? Acidification means we pump protons. So it under goes I'm just going to write here acidification. That's the first step. Well technically the second step. So second step. First one is endo cytosis. Um it's called receptor media. I don't have enough room to write all that crap though. So first step is endoccytosis. That was the first step. All right. So, we'll put one here. Second step was acidification. All that means is we pump protons into this actual vesicle. Why? When you pump protons into this vesicle, it makes the subunit change a little bit. Essentially, what it does is is it makes the A subunit get pumped out. And that's what we need it to do. So, what it does is it kind of pushes out. It's really cool. It pushes that pink little guy out of this little endoome and into the cytool. So here I have my a subunits. All right, my a subunit is then out here. What the heck do I got to do with this? Now there is something here called elongation factor 2. What happens is when this A subunit is present, it can activate cellular enzyatic processes that you're probably like, dude, do I really have to know this? I don't know. Probably not, but we're going to do it anyway because it's cool. What it does is this little guy here, this a subunit leads to a change in the reaction. What it does is it takes this EF2 from a um let's say an active state. Yeah, let's say this is an active state. so it can do what it needs to do. And all we're going to do is is we're going to turn it into a inactive enzyme, an inactive elongation factor 2. Well, the only way we can do that is that something has to happen. And that's where this a subunit comes in. The a subunit comes in here and it does something called, if you don't remember this part, that's okay. But it does something where it takes an ADP and a ribos and under goes ADP ribosilation. I know that's that's a lot. I I get it. I I do. But it basically helps to stimulate this ADP ribbos to get added on to this EF2. And so what I'll do is I'll throw like a little earring on here. Here's a little earring. It's weighing this little dude down here. And we'll represent the ADP ribos with this kind of like red color. Let's say here's the ADP ribos. It's going to weigh it down, making it inactive. If it's inactive, guess what elongation factor 2 is supposed to do? It's supposed to generate proteins. It's supposed to stimulate protein synthesis. If this isn't active, can it stimulate protein synthesis anymore? No. So now what happens is you inhibit protein synthesis. you shut this process down because you don't have the elongation factor that's supposed to be stimulating it. So now I end up with a decrease in protein synthesis. If I don't undergo protein synthesis, can cells survive? No. So then it winds up happening. Cell death eventually ensues. And whenever that occurs over multiple tissue cells, that leads to what's we what we call necrosis. And that is really a kind of a scary dang thing, man. Is that we're going to then cause the cells to die. That cell death is called necrosis. And what tissue is undergoing necrosis? The frenial tissue and the tonsular tissue. And anything anything that this toxin comes into exposure with? Because all this thing has got to do is just keep doing that. Keep releasing those nasty nasty exotoxins and it's going to keep causing damage. So what's going to end up happening here is, and this is what's really, really the problematic issue here. This necrosis is completely different from everything else that we talked about. It's kind of scary. So what I want you to understand here is it produces I'm going to I'm going to write it down, but I want you to see what actually happens. It causes a pseudo membrane to form. And that is the big difference here. All right? It's a pseudo membrane. And where on the ferinx is where we primarily see it, but it can extend into the tonsils, the tonsils. How does this happen? Okay, once you cause these cells to die, right? So here's here's these green little things. These are your these are your diffia, right? And they're causing these cells to die. So we'll represent that with the red axis. Once they die, right? And how do they do that? They release their toxins. and the toxins got in caused the cells to die. Once that happens, you get an inflammatory reaction. That inflammatory reaction, so we'll kind of pull like a little thing over here. This is going to cause once you have damage of cells, what's it going to do? It's going to cause an an inflammatory response. So, it's going to cause an inflammatory response. Who's going to come to the area who loves bacteria? Neutrfils. and it's gonna activate the neutrfils to come to the area. The neutrifils are going to move to this area. And what they're going to do is they're going to leak out. And then when they leak out, guess where they're going to go? They're going to go out here into this area and they're going to start to fight. And the problem we know about neutrfils is what they are. They don't care about anything around them. [laughter] And so they're going to start kind of releasing proteasis and right uh reactive oxygen species and it's going to try and damage these bacteria but the problem is it's going to damage everything else. The other thing is so what what kind of got drawn to the area? One was neutrfils. The other thing that gets drawn to the area is plasma proteins. But there's one specific plasma protein that we really see heavily in this and this is called fibbrin. really it's it's the fibbrinogen but eventually gets converted into fibbrin. This is going to be moving through this area. And what happens whenever you have lots of inflammation? What happens to the vessels in that area? They dilate and they become leaky. If they become leaky, guess what happens? They also flow out. And so now what I'm going to do is I'm going to show that some of this fiber in this bluish color is leaking out and then it kind of comes over this and it kind of encases in it what the neutrfils the bacteria all these dead cells and it's kind of like a hardish covering that is the pseudomembrane and that's what you would have here is you would have a pseudomem is basically dead cells or necrotic cells You'd have immune system cells like white blood cells. You'd have bacteria. And then you would have all of this fibbrin around it. And guess what this does? This makes the pathogen like really kind of scary because guess what it can keep doing unless you kill it? It can just keep releasing exotoxins and getting that. This is the scary part is that once you have the pseudo membrane, it it's kind of your immune system's way of trying to wall it off. But the this this pathogen's smart, dude. And so all it has to do is is once this pathogen actually is here and it has some dead cells, all that has to happen is that toxin which we represented in what color here? Here was the B subunit. What was the other one? It was the A subunit. This exotoxin doesn't have to just stay in the ferinx and the tonsils. This exotoxin can then do what? Circulate through the bloodstream. And when it circulates through the bloodstream, guess who it likes to go and see? It likes to see two other tissues. What are these two tissues? The one is the myioardium. And what it'll do is is it'll cause I'm going to represent it here in this this red color. That exotoxin will get down here, get into the cell, cause decreasing protein synthesis, cause these cells to die. So then what happens is I get death of myocardial cells. When you get death of myioardial cells, dude, you know what could actually happen? It could cause a lot of different problems. If you kill enough of the ventricular myioardium, you could cause the patient to go into acute heart failure. So one thing that can happen is we end up with what's called myocarditis, right? So it's technically this terminology is called myocarditis, which is inflammation of the myocardium due to this pathogen. It's an infectious process though. When you damage a good chunk of the mioardium though, one thing that could happen, especially if it's a large portion of the ventricular myioardium, is you could put a patient into acute heart failure. That is a possibility. So it could cause acute heart failure. And so obviously that looks differently depending upon the degree. So patient could end up with a decreased left ventricular ejection fraction. They can end up with dilated ventricles. They could end up with pulmonary edema. They could end up with peripheral edema. You get the point. We know that that's one complication. The other thing is that ventricular myioardium and other parts of the mioardium consist of not just the contractile portion the non-contractile portion dude and if I damage like things like the perkingi and the bundle system and other things like that what could I end up with I could end up with heart blocks and so you could end up with different types of things. So two things, one is you could end up with a conduction block, right? Which would come up on an ECG or worst case scenario, you could even cause a deadly arrhythmia. You could cause a deadly arrhythmia like what maybe Vacc Vib etc. So you get the point here. That's pretty absolutely terrifying. And why is this happening? because all it took was for that exotoxin to get systemic and go and damage these tissues. The other thing is it likes to damage neurons. So it actually causes neuropathy and the way it causes neuropathy is basically the exotoxins they damage the myelin and so they cause this myelin to kind of unfold if you will. What's that called? Whenever you kind of remove the myelin sheets what's that called? That's called demyelination. So what it does is it triggers something called demination and that demination will then cause the neuropathy. Now neuropathy obviously can look so many different ways, right? And it depends upon which nerves you're involving. But this can be reversible. It's just you have to make sure that you get to it before you cause extensive damage. And so this could be peripheral, sometimes it could be cranial nerves, you could get a lot of different nerves. So that's why it's kind of like it's not the big thing I want you to take away is like what type of nerves but you can know that this could be peripheral nerves and a lot of the times we can even see this cranial nerves. So peripheral nerves and you can even see um cranial nerves believe it or not cranial nerves can also get affected. The last thing I will tell you is that this exotoxin when it's in the ferinx this stuff like it's it's like um it's like pouring hydro like essentially what happens is it causes necrosis along its path. So you get the pseudo membrane right you can get things like myocarditis and neuropathy which is really really critical. One other thing that I would add is that this pseudo membrane it is really important but this necrosis can spread. So, not only does it cause myocarditis and neuropathy, but there's one other area that I want you guys to understand, the neck. So, it gets into your cervical lymph nodes and it gets into the soft tissue of your neck and it it I'm not kidding, just imagine it as though you're pouring just an absolute death trap of cells in the neck. And so, what happens is not only does the necrosis cause the pseuda membrane and these types of things, but one other thing that we see with this one is something called a bull neck. And all this is is it's inflamm it's basically necrosis of the tissues in the neck and lympadinopathy. The problem with this that we'll talk about a little bit later is it can obstruct the airway. And so that's one of the key things with um patients who have this type of tonsiloparangitis is you'll appreciate a bull neck. You'll see this pseudo membrane. They may have complications that they're at risk for and you know which kind of like risk factors and ways that they can become exposed. The thing I'll leave you with with this is that I spent all this time here showing you something that you probably like, do I really need to know all this stuff, Zach? Maybe not. But one thing I will tell you is that the bacteria can be there and release exotoxins and cause damage. So if you think that like with group A strep, I just treat them with antibiotics and they'll get better, you could get rid of that. But guess what? the exotoxins, if they're around, they're going to do this in all kinds of tissues. So, what is something that's absolutely needed in this that's not needed in all the other one? Something that can bind up the exotoxin, an antitoxin. And that's why I kind of spend some time talking about it in a roundabout way. But either way, we've covered all of these types of infections. I want to talk about the worst case scenario and the patients worst day of their life. What are some things that maybe make them come to the emergency department or make them really, really sick? And we have to identify that can happen with these infections. The next thing I want to talk about is whenever you have a patient who comes in, they have a sore throat. It could be something as simple as what we talked about, right? Such as a sore throat, a fever, limpopathy. Maybe they have some characteristics that really scream infectious mono, viral tonsil fangitis, root a strep, dtheria, etc. What about the patient that you're really really concerned about? This is a higher level, more acuity. This is like, oh, I actually am really nervous for this patient. That's when we have to look for a patient who comes in with like maybe they have a sore throat, maybe they have a fever, maybe they have lympadinopathy, but they have strider, they're having difficulty breathing, they're having a increased work of breathing, they're hypoxic. Those are some scary scenarios. And what kind of things would happen that way? Well, think about this. In fial dtheria, what did we say that they had? Well, we kind of used this is the example that like here we're going to have their ferinx tissue, right? And then we said on that we had some bacteria. So here's the bacteria. And then we said we brought in neutrfils, right? So we brought in some neutrfils. And then we said we brought in fibbrin. And that fibbrin kind of really covered all of this and intertwined it. And you ended up with this very very heavy heavy what we call pseudo membrane. Well, this thing is taking up space inside of your oral cavity and inside of your fairings. Right? The other nasty thing about these things, I didn't say this, but do you see how intimately connected the pseudomembrane is with your vascular system? If you try to scrape that dang thing off, you're going to bleed like crazy. So, it can bleed really easily. It's one of the nasty things. But think about this. Because of this, what does it have? It has mass effect. That mass effect is going to do what? It's going to obstruct the airway. And so that's really the problematic thing here is that with fingial dtheria, the significant issue here is that you got a patient who has what? They have a pseudo membrane that's blocking their airway. So they have a pseudo membrane that is obstructing the airway, right? Because air is supposed to flow where? Well, it's either supposed to flow through the nose or through the mouth and then through this area here of the fairings and then down into the larynx. But what do you have here? You have an obstruction. So that's the issue is that whenever you have air flowing through here and it's supposed to go through here, you got this big old honky chunky thing that is blocking that. All right, that's one scenario. The other thing here is that I told you frenial dtheria, remember I told you that they have the exotoxins, they get to the lymph nodes and they have all of this kind of like necrotic debris that occurs in the neck. they get a bull neck. Well, all of this is the same thing. They have all of this I'm just going to represent here in red. All of this kind of inflammatory lymphatinopathy, necrotic tissue all in the neck and it's going to cause so much inflammation. And what's this called? That's that bull neck. Well, the bull neck is doing what? It's compressing. It's that soft tissue that's compressing on the airway. And so again, you get the same thing here, dude. You get a bull neck that is obstructing the airway and that's that's why we would see this and so one of the big things here is when you have a patient so why why am I telling you all of this dtheria may be one of those things that they present pretty scary and so what I mean is when you see something like an airway obstruction often times this will be a person who comes in with a couple different symptoms one is they may come in with the worst case scenario which is they may be hypoxmic right so they may have some hypoxmia so low SPO2 or if they get an AG their PAO2 is going to be low but we have something like that right the second thing is that they can have a increased work of breathing so we're going to put work of breathing so in other words what could that look like they could be using accessory muscles they could be breathing really really fast they could be breathing deeply they could be having nasal flaring intercostal retractions you get the point they look like they're struggling another thing is that they could have significant tissue hypoxia that they look blue as a smurf Perf. What's that called? Cyanosis. Cyanosis. And then the last scenario here is that when you have so much of this obstruction, when air is trying to come in and you have things which obstructing air flow through the fairings or you have things compressing on the larynx, it can cause air to have to smooth through a small channel and sometimes that may cause this characteristic sign of upper airway obstruction which we call strider. So in a patient who presents with things like strider hypoxmia, work of breathing, and maybe some cyanosis, you take a look in your mouth and you say, "Oh my gosh, there's a big membrane there." Or you look at their neck and it's swollen as all crap. That is a concerning patient that you need to act on immediately. In the same way, group A strep, we didn't talk about this yet, and I need you to trust me that we're going to talk about it, okay? But in deep neck infections when you have that strep infection, when you have that strep infection, it does often times more than not just cause infection of the tonsils which we represented here in this pink color or it causes infection of the fingial tissue. And when you get injury here, you get inflammation. And what we know is that sometimes that inflammation can lead to um possibly a collected infected material that starts to wall itself off. And one of the concerns here is that you start to get a patient that can form abscesses. So let's say here I get an abscess here or in this scenario here let's say here we have this patient they had and they had fngitis tons of fngitis and all of a sudden they end up with this pocket of pus in their retrofaringial space that can be called a retrofaringial abscess. Another thing is they can cause infection of the tonsils in the peronsular space behind it and that can really bulge and push the tonsils and everything into the actual oral cavity. Either way, you're [clears throat] narrowing it's causing obstructions. So when a patient has group A strep, group A strep, yes it can cause simply tons of ferangitis and that's [clears throat] at its most simplest form. But what if that infection doesn't stop there? What if it continues and it forms an abscess? And it forms an abscess in specific deep neck spaces. So then you get a abscess formation and the most common areas is two of them and we'll get into this a little bit later that you can see this one is you can get what's called a retrofaringial abscess. Another one is called a parapharingial abscess. Another one is called a peronsular abscess. They form in the retrofaringial space. Parapharingial space, per tonsular space. You are getting the point here that this abscess forms in deep neck spaces that can have mass effect and that mass effect is going to obstruct or narrow the airway. All of these will do what? Obstruct the airway in some way, shape or form. So they will obstruct the airway and then the patient will present with what? They'll present with strider. They'll present with hypoxmia. They'll present with an increased work of breathing. They'll present with maybe some cyanosis, maybe some strider. And then you look in their mouth and you say, "Oh my gosh, there's a big bulging abscess in the back of their their throat or oh my gosh, I see the tonsils popping out." you're going to have those kinds of things that kind of queue you off to think, oh, could it have been a group A strep that caused tonsil ferngitis and then it caused a separative complication like a deep neck infection? So, that's kind of what I want you to take away from this. Now, with that being said, group A strep can have two different types of complications. I kind of already said it. Separative, which means it can cause pus pockets, and then non-superative. So again, one thing I want you to remember is if I had a patient who gets group A strep, let's say here's the group A strep. Here's your group A strep. The group A strep gets in here and it can cause something very very simple, right? So it has a couple different options. One is it can cause tonsillo fngitis, right? We kind of already discussed this. So the group A strep gets in you have some type of respiratory droplet whatever it may be gets in starts wreaking some havoc and causing some damage here right so then what ends up happening you get inflammation of the tonsils and you get inflammation of the ferings what can happen is from this when you get the infection and inflammation of those tissue spaces is it could cause a separative complication and nonsuperative so what do I mean by that one is it can cause what we're going to call a deep neck infections. This is your separative your separative meaning it's going to cause these like walled off abscesses. The other one is going to be non separative which means this is going to be more of an immune reaction and guess which ones these are? It's going to be rheumatic fever and post streptocoal glamitis which we'll talk about after we talk about the separative ones. So this is the one that we need to discuss here which is it led to an infection that got really really bad and it got into these deep neck spaces. So we have to kind of do a little bit of anatomy. I'm not going to go crazy because we're going to have a lecture on this on its own. But let's say for an example here I have a tonsil right here, right? And we know that the tonsil sits in this space. There's two different arches here is called your I'm going to put I'm going to abbreviate them the palatto glossal arch. This one back here is called the palatto feringial arch. And here is your tonsil. Whenever an infection starts here in the tonsils, it can break through the capsule and get into this space. And you see this space here? It's there's a red line which is forming that space. It's kind of breaking it up. This red line is called the superior fingial constrictor. And basically what it is is it's kind of forming it. It's it's kind of like the last part. So behind the tonsular capsule and right on this side I'm going to have all the green in there. All this green is the infection that's kind of spreading into this area here. See all this on this side in this case let's say the right side of the red line that is all the per tonsular space that is where we get a peronsular abscess. So when I talk about these what I want you to remember is a per tonsular abscess is an infection of what space? It's an infection of the peronsular space. You might be like, "Dude, this is like way too simple, Zach. Why are you talking to me like this?" I promise. I'm going to give you a little bit of things that will make it kind of come together. So, infection of the perry tonsular space, which we're going to represent. Let's do it here. Let's use this orange. The orange is going to be kind of an asterisk here. Asterisk here, asterisk here. That's your per tonsular space, right? Is all of this part right here. Orange there, orange there. All right, that is the per tonsor space. So that's an infection. So you start off a group A strep. It breaks through the tonsils and gets into that space. We'll talk about what that looks like in the deep neck infections. Oftent times it causes so much swelling it pushes the tonsils and even the uvula to the other side. Now the superior fingial constrictor is a really important landmark. The reason why is if the infection breaks through the peronsular space through the superior ferendial constrictor muscles, it moves into this other space right over here on the other side of the superendial constrictor. And now we're going to represent this in green and this is going to fill up this space. All this green is now an abscess that's kind of just spreading into this space. What is this space? That is called the parapharingial space. So that is called a parapharingial abscess. Parapharingial abscess. All this is is an infection of the parapharingial space. And then I will again mark out what those spaces are. But this is an infection of the paringial space. And again, let's use a color. Let's use pink. Let's use pink. So, I'm going to put some asterisks in here. And there is a pink there, a pink there, pink there, pink there. This is all the parapharingial space. That's where an infection is. And this is usually the something that can happen is where the infection starts at the tonsils, spreads its way to the peronsular space, spreads its way through the superior constrictor and gets to this area. >> [sighs and gasps] >> The other thing that can happen and I don't want to get too crazy but there's one other one that's just really really nasty and that's called the retro feringial abscess. When you look here, here's the mucosa right in the pink. So the mucosa of the ferinx and then the tonsils. Then right here you have this superior fingial constrictor muscle. And then the back part here we have something called the buckarangial fascia. And then there's this little space right here between it. So here I'm going to put this space in like a bluish color here. I'm going to kind of like this is the buckle ferrenial fashcia that right here that's the allar fascia and this space here in blue is called the retrofaringial space. Infections can break through this parapharingial space and in here and cause an abscess. That's one way. Another way is that infections that start off in the ferinx can travel via lymph nodes. there's lymph nodes in the retrofenzal space. So if you get infection of the ferinx, it can spread to the lymph nodes and cause separative kind of like um lympadinitis and that can cause it to break open. Either way, you get the point here is that the infection can get into the retrofaringial space. When it gets into the retrofaringial space that can bulge so when you think about this perons bulges the tonsils and the uvula paraphernials can bulge whole frenial wall and also obscure the mand this is the this is actually the mandible. It can obscure the mandible. Retrofaringial space bulges the posterior wall. You get the point. All of these things are bulging and pushing into the ferinx narrowing the airway. And that's a really nasty thing. So retrofaringial space is an infection of the retrofaringial space. And that's I mean that's obviously kind of pretty obvious but infection of retro ferrenial space and you're probably like okay well do I need to know all the different like ways that it'll present you can but guess what we're going to talk about those things when we get into the lecture on deep neck infection so I don't want to spend too much time on it I just want you to know that group A strep can cause tons fingitis and if it's not treated accordingly it can become a deep neck infection such as retrofaringial peronsular parapharingial abscesses. When these cause infections, they cause mass effect. They bulge. They push things such as the tonsils, such as the lateral fingial wall, such as the posterior fingial wall, narrowing the airway and causing airway obstruction along with their all additional specific clinical cues which we will talk about in that lecture. This is not a deep neck infection lecture. This is the tonsil fngitis lecture. I hope this gives you an appreciation of another complication that can occur here. All right. When you see a person who comes in and they got a really sore throat, you look in their oral cavity and you notice all this like tonsular swelling and bulging. You notice swelling of the the lateral fingial wall. You notice bulging or neck swelling. You notice bulging in the posterior wall and maybe some sore neck muscles that you you're having a hard time kind of extending your neck because you get infection close to those muscles. You think about abscesses or deep neck infections. All right. What about the non-superative ones? Well, this goes back to those antibodies that [laughter] I was talking about. So, with roheatic fever, do you guys remember um there was the Velcro, the hardcore Velcro uh protein on it. Do you guys remember it was the M protein. What color did we make it? We made it pink. So, we made it pink. So, here's what I'm going to do. I'm going to draw a couple pink dots on here. Here's your M protein. when your body creates kind of um antibodies against those right it's going to make some antibodies these antibodies you want it to go and attack the M protein so these are your anti-imm so what were they called these were called your anti- M antibodies and what they're supposed to do is they're supposed to go there and attack this and trigger an immune response and kill this son of a gun right that's what we want to do we want this to go and create an immune response And and essentially we want to do what? We want to destroy the bacteria, right? So we want to destroy pathogen. That's that's the goal. That's the goal of the antibodies is to help to destroy the pathogen. However, this M protein can look similar to some of the proteins and other tissues of the body. Maybe it's in the joints, maybe it's in the heart valves, maybe it's somewhere in the skin, maybe it's in the brain. And what happens is these antibodies they go and they crossreact. You develop like a type two kind of like uh hypersensitivity reaction where these antibodies they go and they deposit and they find proteins that mimic the M protein. And when they do that they deposit into these tissues and they create an immune reaction that unfortunately causes destruction of our own tissue. And so what happens is here the antibodies deposit into the joints. Here the antibodies deposit into the heart valves. Here they deposit into the subcutaneous tissue. Here they deposit into the actual dermis and the epidermis. Here they deposit into the uh the basil ganglia. And what ends up happening is you end up with a inflammatory response. And unfortunately that inflammatory response produces a disease process. And what does that disease process look like? Well, I want you to remember roheatic fever, there is something called the Jones criteria that it causes joint pain. So, it damages the joints, which we call, in this case, we're just going to put that it causes um well, here we'll just put joints. So, it causes joint damage. We'll actually do the first letter and red and then we'll cause we'll do the rest in black. So, joint injury. All right. And really all it's doing is it's it's causing arthalgis, right? But there's the J for Jones. The next one's a little bit of a of a stretch is it damages the heart. And so you can think about the heart as almost looks like an O. So O. And so you're going to get heart disease or you're going to get carditis. And so what I'm going to do here is I'm just going to write down. I'm going to put carditis. But I want you to remember that the carditis that the O kind of somewhat looks like a heart. And I'll and I'll put all this together in the end. The next thing is it causes swelling in the actual subcutaneous tissue and they produce these things called nodules. So then we're going to have something called subcutaneous nodules, right? So nodules and then it's going to cause this weird red ring of a rash. So it's so it looks like this. You have like a red ring and in the center there's clearing of it, right? So sometimes you have what's called a bullseye rash, right? Which we see in limes disease. This one is you have a ring but the center of it is that it's usually it's cleared so you don't have that bullseye type of appearance and so this one is called aryththema marginatum. So it's called aythemma marginatum. Arythemma marginum. And then the last part of the jones is the s. And when you damage the basil ganglia, it causes a korea form movement. And so we call that sidenhams korea. So what is it again? Sidenhams. Korea. So, think about how all of this looks. Now, we're going to kind of make this work where romatic fever, you use the term the Jones criteria and it helps you to remember all the damage that these antibodies that are unfortunately there's what's called molecular mimicry and they're attacking tissues that look like they have the M protein similarities to the pathogen. It is the Jones. So J for the joints, O you make it look like a heart. So carditis, N for the nodules, E for the ariththemma marginatum and S for the synite enhanced Korea. All right, this is a non-superative one. It's a auto antibbody reaction. Now a lot of the times people will ask you how do you prevent this? You treat it. Can this be prevented? Rheumatic fever. Yes, you prevent it by treating them with antibiotics. This next one we're going to talk about, it doesn't matter if you treat them with antibiotics or not. It's not necessarily preventable. It can happen regardless if you treat them or if you don't treat them. And that's really kind of interesting. This one you can prevent with treating them. This one, it can happen regardless. So, what happens here is kind of a similar concept. These plasma cells are pumping out antibodies and there's all these different types of antibodies. We talked about the anti-DNAs, the anti-steply O antibodies and those are more for diagnostic to tell you if you had an exposure but I told you the ones that are wreaking havoc are the anti-imm right that was the one here for roheatic fever. Do you guys remember? And then there's another one which is the anti-SPEB which is that kind of like it's that pyrogenic toxin the protease. And so we produce another one which is called anti- SPB antibodies. And what they tend to do is they tend to go and find the SPEB like a little free antigen. You guys remember that that's basically a toxin that this uh this group A strep releases. It releases that toxin and we'll represent this in a let's do pink. I think we did pink if I remember correctly. H we didn't really annotate it but here we'll put here that this is the toxin. And this is the SPEB, right? So there's the SPEB SP. And this antibodies that we're going to produce here, they are going to go and they're going to find that and they're going to stick to it. And when they go and they stick to it, here's the unfortunate thing. You now have an antigen antibbody complex. This one, you didn't have an antigen antibody complex. The antigen was in the actual tissue. This is the antigen antibbody complex. This antigen antibbody complex which I said like a thousand times already. I'm sorry. It can go and deposit into tissues. So let's actually draw the intermediate. Here's our antigen antibbody complex. Here is the antibbody which is the anti-SP antibodies and then the pink is the pyrogenic toxin SP. This goes and deposits into the glomemeular basement membrane. So what are we going to get? We're going to get GBM deposition. Bro, when that does that, it then causes GBM destruction. You activate compliment proteins and neutrifils. All these things start coming to this area. And when they get to this area, essentially what they're going to do is they're going to get compliment proteins, neutrfils, and they're going to start tearing this thing up. And you are going to get some holes in that GBM. And when you get holes in the GBM and you end up with this inflammation of the glomemeular basement membrane, things start leaking out. What kind of things start leaking out, my friends? Red blood cells is one. I'm going to represent that with well a red blood cell. Another thing that can leak out here besides the red blood cells is proteins. I'll represent these with these blue dots. And so what ends up going into the urine? You get protein in the urine. So you get protein ura. It's not as significant as you would get in someone who has like nefertic syndrome, but you're going to get hematia. And the hematia is really really critical here that whenever these red blood cells kind of like they get stuck in the tubules, you get a bunch of them and it forms a cast. And so we say that they have what's called RBC cast. So that that is really really helpful, but we talked about that in the renal section. So I won't go absolutely ham bone on that, but what they're going to end up having in their urine is lots of protein and they're going to have blood in their urine. And one of the key differences here is that when you have lots of protein and you have lots of red blood cells, you have the cast. The other thing here is that when you damage the GBM and you cause it to become inflamed, you affect your glomeular filtration rate that drops off. And so another thing that happens is from this injury, you affect, yes, you cause things to leak out, but you actually lose the ability to effectively filter things. And so that is called the glomemeular filtration rate. And so I'll kind of represent that bringing it kind of this way. All right. So we're going to allow things to leak out because there's holes, but we're not going to allow for the proper filtration process of plasma. And so this leads to a drop off in the GFR. And what that can do is that can cause things like an acute kidney injury and that can cause either a bump in the patient's creatinine or that can cause things like oligura, which is kind of common. But the other thing here is that whenever you drop off their glam filtration rate, you cause like retention of things like sodium and water and as a result that can cause volume overload and that can cause things like edema and that's also going to cause hypertension. So the other thing that's going to happen is that you're going to cause sodium and water to be retained which is going to cause edema and it's also going to cause the patient's blood pressure to go up. And so one of the key things that you want to think about it for a patient here is let's say that a patient came in right and you had to comp you had to differentiate here. You had a patient who came in, they had group A strep, they had strep throat sometime weeks later, they ended up with the Jones things, that's rohematic fever. This could have been prevented if you treated them with antibiotics. Post streptocock is maybe like a couple weeks, maybe one or two weeks, they ended up having streped throat. You didn't they end up getting treated. All of a sudden, they're they're pissing red Coca-Cola colored urine. They're swollen as all crap around their face. Their blood pressure is up. They got some kidney injury. And then you think about what the heck happened here. This could have been post streptoco. This could be postreptoco myrritis. They had an antigen antibbody complex that occurred here and it wouldn't have mattered if you treated them or not. They ended up just happening because of it. This right here is it's going to take this is kind of a what's called a glomemeular nephritis. It's it's a nefritic syndrome picture. You have to treat the underlying cause which is the infection if you haven't already. But on top of that, you have to treat, unfortunately, the symptoms until this kidney can heal. And that's different. Here, we actually have to treat an infection. They're going to be on antibiotics. This one, if I didn't treat it, make sure that you did. If you did treat it, all right, cool. But now, we're just dealing with the symptoms, and we're going to try to deal with that the best that we can. Oftentimes, deep neck infections are a result of not adequately treating the infection. So, you guys should get a really good glimpse of what all of this means when it comes to group A strep and how rough it can be. What I want to do now is, and you're probably like, "Anna, more dude. Come on. I want to be done. I want to go eat dinner. I want to go lift. I I know, but just hang in there with me." I want you to take some time now and say, "Let's put all of this together. Let's think about us this as clinicians. Let's have a application of this knowledge. And now let's talk about when a patient presents in this type of form and fashion, what's the test that I do? How do I know the results of that test? What's the nest test if I have to do that? Basically, how do I diagnose it? And then once I figure out the diagnosis, how do I treat it appropriately? Let's do that now. All right, let's move on to our diagnostic approach here. So, we want to think clinically. What is probably the most common chief complaint when a patient has an infection of their throat? Regardless if it's viral, uh, you know, tonsilopharangitis, regardless if it's a bacterial cause, regardless if it's mono or and dtheria or whatever, whatever it may be, it's going to be throat pain, right? So, they're going to have some type of like sore throat. Um, that could be just a sore throat in general. It could also be accompanied with like difficulty with or pain with swallowing. So, a lot of these things are going to culminate in that type of way. I think whenever you have that, I think it's always just a good thing to start to kind of stratify likely risks and overall just a patient who maybe presents with some signs that are really really scary and we call those those red flag signs. So, things that maybe tell me that this is a little bit more concerning uh than like a a basic tonsoitis. This is things like deep neck infections. This is things like epigalitis. This is things like dtheria which takes me to a really really serious bucket right. So what are those things that I would want you guys to think about? Well a tonsillop fangitis can easily you know spread um into your you know particular spaces deep neck spaces and so that's when you get worried about like deep neck infections per tonsler perhapenial abscesses also dtheria that tends to really cause a necrosis of the frenial tissue. It causes a membrane to form. It causes a lot of swelling within the fairings that can cause neck swelling, significant neck swelling. Um, and again, we'll talk about this in the lingial infection lecture, but epiglatitis, that one tends to cause a significant amount of epiglotic swelling where it can cause significant strider. It can cause a lot of things that can obstruct the airway. So that's not really related to the tonsil fngitis but again you get the point that in these scenarios when a patient has throat pain it is really really to kind of highlight is this a really scary one like dtheria epiglotitis or a deep neck infection and so what would be some of those things that would kind of scream to me any airway obstructive signs. So any kind of respiratory distress whether this is disna typnia accessory muscle use um whether it's intercostal retractions nasal flaring and the biggest one is strider because it's a usually inspiratory it's as you take a deep breath in there's so much swelling or things that are in the airway that it's obstructing the flow of air that's really concerning for like a peronsil or a parapharangial um retrofarrenial absess it also really concerns me things like you know dtheria it concerns me for things like epiglatitis tismus is a really concerning sign for kind of an infection of a deep neck, muffled voice, deep neck infection, especially even epiglotitis, drooling, inability to swallow secretions. That really, really scares me about epiglotitis and some deep neck infections. Neck swelling and pain is your deep neck infections. That's also going to be concerning for things especially like dther area that causes a really severe degree of neck swelling. Hemodynamic instability is usually concerned that this is now a patient who's become septic per se. um or they've developed so much respiratory failure that their hypoxia is starting to increase the risk of them going into cardiac arrest. Uh these are really really really high yield things to consider because if a patient has these your decision process is not guided by all right let's get some imaging all right let's do the lab let's do no no no no you secure their airway if they have enough concern and airway compromise because if you don't and it's too late they could then again develop a complete almost near total obstruction they could end up with a surgical airway as a result of that they could again go into cardiac arrest there's just a lot of things that could happen and you need to be on the ball. So really closely monitor the airway, their cardiac status and if there's any concern you need to intubate good good vascular access your basic ABCs. All right. So, if the patient has those, that's when you think about deep neck infections. You think about things like dtheria, right? That's really what I'm starting to think about. At least when it comes to the discussions that we had on the whiteboard, right? If I hear tismas, if I hear drooling, if I hear of a hot potato voice, if I hear of neck swelling, that's when I start thinking about deep neck infections. And we'll actually have a dedicated lecture to really differentiate between a per tonsler to differentiate between a paraphernial, between a retrofaringial, and even lovewigs. So these are things that are really really important and we'll get into those. Some of them are clinical diagnoses and when you look in the oral cavity and you examine the neck, some of them you need to get CT imaging of the neck. All right, the next thing is what if I have a patient who has a recent history where they are not they're not vaccinated, they're unvaccinated, right? And they present with a bull neck. That's one thing. But here's the characteristic term, the pseudo membrane. You look here and you see this kind of like area on the ferinx and the tonsils that is kind of like this weird looking plaque. And when you try to scrape at it and kind of like remove it, it can really bleed because it's super adherent and there's lots of necrosis that is involving some of the nearby blood vessels. So that really screams to me dtheria. So whenever I think dtheria, the first thing that you want to do is you want to get a throat culture and you want to do it under a specific medium because that medium is going to tell you whether or not you have the presence of that bacteria. If you have that bacteria, the next thing is to determine is does that bacteria have a gene capable of producing a dangerous exotoxin? That's when we do the PCR test. And if that comes up positive, you then need to say, okay, are they producing the exotoxin? And that's when you do the reflex toxin testing. And that will confirm the type of toxygenic dtheria, which you'll end up reporting to a lot of your, you know, CDC and things like that. But in that scenario, the patient likely has dtheria. But again, I can't stress this enough. You're not going through all of these imaging and testing until you have managed the airway first. Airway is king in these scenarios. All right, that covers that. What about the patient who doesn't really have the red flag signs? Well, then you have time. You can actually really evaluate their oral cavity, their lymph nodes, look at their vitals, maybe get labs, maybe get imaging, etc. In that scenario, that's when you have the time. So, what I would then first do is I'd take a good look. If I take a look here and I look at the fairings, it looks like it's kind of like it's definitely red. I can see some redness. I can see kind of some overall edema. Um here I can notice that there's definitely a lot of edema and redness and swelling and even in some little bit of petiki here. And in this one I notice like some exudates on the tonsils. All of these things are telling me that this could be a tonsilloparangitis, right? Especially if that's accompanied with things like fever and anterior cervical or posterior cervical lympadinopathy. that's really really tender to the touch and those are telling me that I probably got a tonsillop ferangitis. The question is is it viral? Is it bacterial? Those are really really important questions to ask. Well, oftent times viral cases especially things like parinfluenza, rhino, adno, influenza, covid 19. Those things carry with it a characteristic viral syndrome. In other words, they have a cough. Right? [laughter] That's one common feature. They have kurasa which is almost like a term for they have a culmination of symptoms like maybe they have some rhinora some nasal drainage. They have a congestion and then on top of that some of that fluid there can leak backwards uh into the the actual fairings and they can get what's called a post-nasal drip. A lot of those things really tells me that this could be again some kisa maybe some sino rhinocyitis going on. Um the other thing is conjunctivitis especially with like adno that one can really cause a kind of a watery discharge as well. So all these things really kind of make me think about a viral case and if they have that all right cool this probably is more a viral tonso ferngitis most likely right that's really really important now the question what I'd say is would I go and like swab the fairings and see if there is a particular virus only if it's a concern for influenza and covid-19 which we'll have our individual video lectures on to discuss those more in detail for example does a patient who has influenza they're going to present with a really high fever they're going to have a lot of body aches So muscle, joint aches, co 19, you'll probably look for a recent exposure and something like a nausemia or a aquezia, which is a small decreased smell, decrease in taste. Those things really suggest more of a potential COVID picture. For those, you would do a nasoparangial PCR. So you'll actually swab, you'll see what comes up from that PCR. And again, that would tell you if there's something like what? Well, particularly is there something like um you know SARS Kovv2 which would suggest a COVID 19 or is there an influenza strain that would tell you that you have influence and again we'll get into those in individual lectures but for right now oftentimes you don't test them for viruses unless they fit these particular pictures. Now let's say that they don't have any of these viral syndromes, right? In that scenario, you want to think about bacterial causes and then monucleiosis due to an EBV, which is a type of virus, but again, it's more Epstein bar virus related. In these scenarios, what you want to do is I want you to do two things. I want you to think about a suspicion for monucleiosis and also consider working them up what's called a Mentor criteria. So let's say that you think that the patient has a suspicion of monucleiosis. What's the key characteristic feature? Extreme fatigue, extreme lethargy, just generalized malaise is a very common one. Another thing here is they get spenomegaly. A large proportion probably at least 50% or more develop spinomegaly. So you're going to palpate maybe some enlargement around that left upper quadrant or fullness in that area. Um sometimes you may also have some posterior chain lymphenopathy. They can get generalized. So they can get anterior and posterior but you definitely see more posterior chain involvement because of the flow at which those lymph nodes it kind of propagates. Um, another one is if you happen to see this, it's it's not needed, but let's say that the patient gets a CBC upon along this process because of a fever, whatever else it may be, the CBC shows that they have a high white count, but it's lymphocy predominant, and you get a peripheral blood smear mentioned in the actual uh, you know, test, it may show lymphocytosis, but the blood smear may show particularly that they have these like atypical kind of reactive lymphocytes that you would kind of see here with a really large cytoplasm, pretty big guys. All right. If they have these features, you got to get a monospot. The monospot's going to be the way to go. Now, let's say that you get the monospot test and it comes back positive. What the heck does [laughter] that mean? Here's what I want you to think about. In a patient who gets infected by EBV, the EBV attacks your B cells and then again it affects your, you know, your body's ability to produce, it's going to lead to your body producing antibodies. And your body produces antibodies against the EBV virus, but it also produces these things called heterophile antibodies which we found can attack sheep and maybe even horses like red blood cells. And so we do a special test where basically we take the patient's blood which has these antibodies in them and we expose it to these sheep and you know other kind of animals red blood cells and if it leads to them clumping and aglutinating that really tells me that they have these heterophile antibodies and that presence of that really leads to a very strong suspicion of monucleiosis. Right? Here's the thing though. Even if a patient has a negative monospot, it still could mean that they have mono, especially if you got the test like a little too early, like at least less than a week of their symptom onset, that could cause a negative monospot test. So you may need to repeat it after that time frame or if they're really young, like less than 5 years of age, sometimes even in those who have other viral infections, CMV, HIV, etc. So in that scenario that they have the negative monospot, what would that mean? Well, that could mean that they again it was too early, but it also could mean that they truly don't have the infection. And so in that scenario, what that means is that means that the patient doesn't have those heterophile antibodies. So when you present it to the red cells, what's going to happen? There's not going to be any lis or glutination because they don't have the antibodies to click and interact with those red blood cell antigens. So they're not going to have any clumping. But it could mean that mean that they don't have the infection, but it also could mean that you were too early or they're just uh there's they're false negatives and again that's really common in that pediatric population. So that's when we would get an EBV corology. So again EBV corology is really important in those patients that are less than five years. You got it too early like you know a week less than a week from symptom onset or they have other viral infections. That's when I would get the EBV p corology. The reason why is this one really specifically looks at the antibodies directed against the EBV. So it's going to be one of the best tests. It's just it takes some time to to actually get done. So what you're going to want to do here is let's say that you do the EBD corology. What this does is you're you're going to look here. You have time right here. You have an antibbody tighter and we're going to look at specific antibodies determines if this is an active or acute infection or if it's a past dormant kind of infection. So the first one that's usually produced is an IGM antibbody that's produced against the viral capsids, right? So you'll see what's called the anti-VCA IGM go. And you'll also notice that they'll produce the IGG just a little bit later. And then you'll also notice that one of the antibodies that is not produced in this acute phase is called the EBNA, the anti-EBNA. That one should not be produced in it should be produced a lot later and that one will be negative. So what you'll notice is during this primary infection these will be positive. That is the key difference here. Usually as you progress forward with the actual infection then what happens is the IGM drops off and the IGG and anti-EBNA persist. And this tells me that this is more of a past or prior infection. And then eventually you can get a reactivation have kind of a similar event like we talked about, right? But that is what I want you to remember. So, we're going to really be looking for these two to be positive and this to be negative. And if that happens, we diagnose mono. All right. All right. That covers mono. What about the patient who you don't really have that suspicion of monucleiosis? That's when you do the modified centator criteria and you're going to try to get a score. What you're looking at is when you looked at their oral cavity, do they have a lot of exidate or swelling of the tonsils? If they do, they get a point. Do they have tender and swollen anterior cervical lymph nodes? If they do, they get a point. The next thing is, do they have a fever at least greater than 38 degrees CC? They do, they get a point. And the last thing that I want you guys, well actually not the last thing, we also look at do they have a cough or not. So if they have a cough, that suggests potentially more of a viral syndrome. If they don't have a cough, that suggests potentially a group A strep infection. Right? You get the point. The last thing is we look at age. This is definitely an infection that's more common in the pediatric population. So the younger they are, at least greater than three they have to be. So 3 to 14 really they get a point. As they go higher we either give no points or we take away points. So 15 to like generally 44 will probably go zero and then greater than 44 we're going to go up to that kind of negative one. Basically you kind of plug in all of these things and you say okay what's the score now? If the score is zero to one you don't really do anything. All right you're just going to go ahead and say it's unlikely that it's bacterial. It's probably viral. All right. If the score is two or greater then you need to go and test them for group A strep and you may get a culture depending upon that especially in the peds patients. All right the next one is very very controversial and a score of four plus some guidelines will say treat them empirically and others will say you still should test them. I doubt that you'll get questions on that. So stick within at least remembering the two plus range. All right? Because a lot of the guidelines are trying to really really push that even if you have that 4 plus, you should still test them with a rapid antigen detection test to at least see if it's positive and then go from there and treat them. That's the key thing here. And again, it's just trying to reduce the risk of antibiotic resistance. So let's say that you do this and that score comes up two plus. That's when you get the rapid antigen detection test. Some guidelines will even say if it's four plus. If it comes up what? Positive, it's group A strep. You're good. Done. If it comes up negative though, you can get a throat culture in only really one specific scenario if they're a ped patient. Adults, we usually just defer. All right? And we say it's unlikely that it's bacterial. It's probably more viral. All right? If that throat culture comes back positive with the group A strep, boom, you diagnosed it. So that's kind of like your backup way of just making sure that the rapid antigen detection test didn't give you that false negative. Right? Now another thing that's also kind of important here is when these throat cultures are negative you then think is this a viral cause right that's probably most of those scenarios one thing I want you to think about in those scenarios is does the patient at any point in time present with an STI history right they have inappropriate sexual activity they present with like you know vaginal discharge or maybe urethal discharge of some point from a male that is when I want you to think about this and if there is a chance of you even gone monoccoal conjunctivitis, you want to do what's called a nucleic acid amplification test from you do a swab and you'll send that out and that's going to at least help you to see if there's any things like gorrhea maybe even like a co- infection with chlamyia but ganoccoal one is a really really important one because that changes the type of antibiotic that you're going to treat them with that one's sept trioxone whereas these ones that we're going to talk about here they're primarily things like penicellin or amoxicil all right so that really covers the way that I want you guys to kind of analyze these and think about these is in a stepbystep fashion when we're kind of working up a patient who comes in with that new onset throat pain. All right. Once we've determined the underlying cause, then we treat them accordingly. So, for example, if it's viral, you do nothing. You just give supportive care. There's no antibiotics that are getting enlisted here. If it's the group A strep, you do give them oral antibiotics. And that oral antibiotic kind of comes with specific questions. Do they have a penicellin allergy? If they don't have a penicellin allergy, you'll be safe to give them penicellin or amoxicylin. So that's what I would initiate, right? Penicellin V or a moxicil. If they got a penicellin option, you got to ask the question, well, what type? Is it a type one? So they go to full-blown anaphilaxis. If it's no, you can probably get away with like an oral sephilosporn like se kellex, right? Sephillexin. If they do, you probably would want to go with something like maybe like a macroy of sort like a zithroycin chloriththramy. You're trying to really only reach for these in those scenarios because of the high resistance that we've seen with them. All right, gyneak. I kind of already alluded to it in the diagnostic approach that when you've diagnosed this one, it's usually sept trioxone. Now, if you're working a patient up and you're not sure if it's chlamydia, you can also consider giving them something like a macroy, so like a zithroyc or um sometimes even chlorithroyc to cover for the chlamydia case. But again, that would just be until it comes back and say, okay, the in nucleic acid amplification test didn't show any kind of like chlamyia and then you would kind of drop that. But generally you're going to start with sept trioxone if you're sure and you can you can consider adding on the macrolyide for the co- infection with chlamydia. Now dtheria this one if they ask you in the exam what's the first thing I want you guys to remember it's airway management not giving them you know a specific test not getting cultures and things like that it's always airway management from airway management the next important decision that comes along with that is the antitoxin. The antitoxin is probably even more important than the antibiotic. The reason why is when you give these, you're going to give an antitoxin, but you're also going to give an antibiotic like penicellin G or ariththramy. The antibiotic will eradicate the bacteria. The antitoxin will neutralize the already circulating or localized toxin. And that's really important because what this toxin is doing is essentially the the toxin is causing destruction of these cells. You want to give something that's going to neutralize that toxin to prevent it from damaging the cells even more. The reason why is dtheria. Not only does it cause a fingial involvement, but it can get into the bloodstream, spread to the myioardium, and you can get myocarditis, which can lead to cardiac arhythmias. If it's bad enough, it can cause enough damage that it can put you into an acute heart failure. So, it's really, really, really important to get these antitoxins in to prevent the continued damage and then give the antibiotic to eradicate the bacteria from even being present to produce more toxins. All right, the last thing is infectious monucleiosis. With this one, you don't do anything. Just like the viral cases, it's all supportive. In rare scenarios, you can consider steroids because there's so much tonsular hypertrophy and a lot of even sometimes the uh generalized lympadinopathy. It can cause enough neck swelling and kind of like tonsular swelling where it can obstruct the airway a little bit. You may consider steroids, but that's pretty rare. Often times more than not, it's supportive. And tell them to not go five rounds or six rounds with Mike Tyson where he's going to drill you in the spleen and give you some type of like splenic rupture. So that's why it's really really critical to avoid any kind of like aggressive contact sports for a while. All right, at least until they improve and you're going to give them a pretty decent timeline before they can go back and engage in this. All right, again taking away from this, we'll talk about these in their individual lectures. But the reason why I told you that for viral tonsil feritis, it's pretty much supportive because that covers most of your cases and can scenarios like influenza and co 19 which we'll have individual lectures and talk about those. You can give them antivirals. Those are really the only two virus infections that you can't they have to meet specific criteria for- for example we'll get into it but influenza can be treated with ocelmavir and then co 19 can be treated with things like paxlovid so there is antivirals that are utilized but it's under specific clinical criteria and it's a specific type of virus but again we'll talk about this in an individual lecture w my friends we did a lot here with throat infections and I hope that it made sense I really hope that you guys enjoyed it I hope you learned a lot and Man, I love you guys. I thank you guys. And as always, until next time.