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Is billed as a pathology and microbiology. But actually, in reality, there's just no hope um to be able to cover both in any to any relevant degree. So I've chosen to focus on pathology, I think. Yeah, especially um those of you who are UK trainees or UK medical school uh based or um I don't think pathology is very well taught for us. And so I think um for part A and for part B, you actually need a level of innate understanding of pathology, I think, um especially the basic concepts and the basic terms. So that's really what I'll go through because pathology is essentially split up into general concepts and then system based. So for example, you know, cardiology, like related pathology, you know, respiratory, et cetera, et cetera. So we won't have time to obviously go through every system. But what we can do is make sure that the basics are um as well um solidified as possible. And I think it's really important. So again, same bit of background, a little bit about me for those who are new. Um I haven't seen me. Um So um my name is I'm uh essentially on my F three, I guess. Um, I'm working as an orthopedic clinical research fellow at the Southwest London Elective orthopedic Center. Um, here as an education officer for NST S for this year. Um, just a bit of background about me. I, uh, did my medical school at UCL then did, uh, foundation training F one F two in Basildon. Um, and as head I'm on my F three. and honestly, I don't know what, where I'm going towards, I have done both part one and uh part A and part B of MRC S and um so hopefully can provide you a little bit of uh guidance for those who have it coming up. Um Good. So um these are the key learning objectives today. So I want you to be able to understand all these concepts. So that's cell adaptation, cell death, necrosis and apoptosis, neoplasia. What is staging and what is grading and the difference between them? What are the features of actually obtaining a tissue diagnosis? What is inflammation and finally, some bit more on wound healing? Now, if everyone can go on to men, same form as um for those who attended um the thoracic anatomy lecture or tutorial, uh not gonna be hopefully, you know, like didactics, call it a lecture. But yeah, if you can all open the cure, then go to men and we'll just have like basically a long, long, long um list of questions. Remember guys, this is gonna be like as useful as you make it. So the more you put in, the more you get a, 100% if you volunteer and just cos mental is all anonymous, right? Like I don't get to see who said it and whatnot. And even if you did II don't really care at all if you get the wrong answer. And I think actually when you get the wrong answer or you get an answer wrong, rather you remember it even better as well. So with that in mind, I 100% encourage you to give responses. Um And yeah, we'll ex cos when you say something wrong. For example, I have a chance to also explain why that might not be the case. OK? So with the all that in mind, um if you go on the mentum, we'll get started. OK, good. So first things first and by the way, I do have some summary like flow charts that I've made to explain some of these more like uh you know, difficult concepts and how they all link together and that's the key to see the bigger picture. OK? In uh pathology. So cell adaptations, well, what does anyone know like the different types of cell adaptations? Um So just start typing on, I mean, a few of them obviously are listed on here. There are a couple that are not listed on the slides. So hopefully you'll pick those up. But yeah, anyone wants to um type out the uh different types of cell adaptations. So for example, you have a cell at rest and nothing happens to it, but you put a certain type of stress on it and it has to adapt to it. Um And how are the diff what are the different ways in which it can adapt? So, someone's volunteered. So, hyperplasia, dysplasia, metaplasia. Fantastic. Exactly. Good. So, yeah, hyperplasia. Good. Um We've got another one obviously on the slide here. That's hypertrophy. Um Can anyone suggest anyones that I might not be on the, on the sl on the screen? So, yeah, absolutely. Yeah, dysplasia, metaplasia. Very good. Yeah. Um all of these are on there and I don't know, maybe one or two that are not on, on the slide at all. What do you reckon? You're right. All of these are on, on screen. Um And we'll cover each of these. I would, by the way, just one thing, um I wouldn't um class neoplasia as a cellular adaptation. It's a result of cellular adaptation going too far or it's not able to adapt to. Um, well, and you know, longstanding metaplasia or hyperplasia and we'll get onto that. But yeah. Um ok, fine. So I'll, I'll volunteer. Um So one other thing is hypoplasia or aplasia and don't let you get that, let you do, don't get that confused with anything that specifically is only relevant during embryogenesis. So when you know, literally, um humans or, well, any organism is being formed. Aplasia, refers to total lack of cell production in a particular limb or digit or anywhere. And then hypoplasia is well fewer as the name suggests. Um So they might have like a smaller limb or a smaller digit or anything like that or incomplete formed uh part and we'll go through these definitions. So I'll let you define them. So, what is hyperplasia versus hypertrophy? What is the difference? And by the way, um I will try to keep an eye out on the chat as well. So if you have any questions, uh you can put it on the ment screen or you can drop it on the chat as well. Um And yeah, we'll get around to it for sure. This is your best opportunity to just ask questions as they come on. But yeah, so what is hyperplasia versus hypertrophy? Um We're off to a good start. So just yeah, keep it going. Um Describe it. So literally simple. You can put it into like a few, as few words as possible. Hypertrophy equals hyperplasia equals go for it. I'm sure you know it, but we're just f building up from the basics, I suppose. So as I said, you've got one cell um or a group of cells, you put a certain type of stress on it and it starts to adapt and one of the ways it adapts is hyperplasia or one of the ways it adapts is hypertrophy anyone just go for it or if you're not sure, just write. Not sure. Oh, can you put the mention code the C mention? Oh sorry. Ok. Um my apologies. So let me go back to the code one second. So yeah, so 4733 47331139 139. Hopefully that's available for you now. Cool. So yeah anyone else um whilst um Samantha logs on to anyone else, if not, we can go through it if you're not sure. Just right, not sure honestly just so that I can then move on. Um but yeah, so hypertrophy um as you might imagine, especially like muscular hypertrophy, the cell um increases in size. So all the organelles within it, everything increases in size, hyperplasia is multiplication of the cell. So you get more and more cells um of the same type. So with that in mind, which tissues can only um undergo hypertrophy, they cannot undergo hyperplasia. So you can't produce more of them. Do you know which tissues there are? They are. And by the way, that's the definition of hypertrophy and hyperplasia increase in size of the cell hyperplasia, increase in number of cells. So yeah, which tissues can only undergo hypertrophy? Anyone? Oh, I see. Um my apologies. Let me has it hopefully started now. Maybe that's why I wasn't receiving results. My apologies. Oh, perfect. Ok. I can see some responses. Amazing. Sorry guys. My bad. I just thought you guys are not interacting like last time. So, my apologies. Good. Um Yes, absolutely correct. So, yes, cardiac tissue, um neural tissue, very good. Um Very good and then one other type. So very good. These are all examples of what permanent tissues aren't they? They, they are permanent, they lack stem cells, they cannot multiply in numbers. So, yeah. So cardiac muscle, that's the clue right there. That's the clue right there. If anyone picked her up cardiac muscle and then uh nervous tissue. So yeah, absolutely. Brain and uh neurons, et cetera. And then one other thing. OK. No worries. That's fine. We'll uh tell you it. Yeah. Skeletal mus. Exactly. Exactly. Fantastic. Good. Great. So yeah, and these are all examples, as I said of uh permanent tissues. Um Very good. So which organ, for example, this is a kind of a nice little like uh it's almost like a general knowledge quiz but again, comes in handy for sure. Um during part A or part B, which organ could easily be a part B question. Uh Which organ is the only physiological example of both hypertrophy and hyperplasia like that undergoes hypertrophy and hyperplasia at the same time. Does anyone know an I change the slide on here? So it is completely normal physiological. Um And this organ or tissue undergoes both hypertrophy and hyperplasia. Not quite hepatocytes, not quite hepatic sites. Endometrium. Yes. Very good. Very good. Yes, it's the, well, it's the uterus basically. Yes. Uh during pregnancy. Um So um undergoes both hypertrophy and hyperplasia. So increase in size. Um Good. Fantastic guys. Good. Next one. So eventually uh pathological hyper, so that was physiological by the way. So eventually pathological hyperplasia can lead to what? And it was one of the adaptations that we already mentioned earlier. Um But at the same time, can you also think of a pathological hyperplasia that won't lead to cancer? That's not necessarily, by the way, cancer is not the answer I'm looking for. It's similar but it's not quite. So what will pathological hyperplasia lead to um or can lead to? Oh, so on the chat. Uh Yeah, Sandy, I think you said Barretts esophagus. Yeah, I mean, in that particular area, if you get it. Absolutely. And Barrett's esophagus is an example of what then Sandy, what would you say it is? What kind of adaptation is it? How would you describe it? But yeah, you're not wrong. Uh Prostatic enlargement. Someone is uh answering the second question. Very good. So yeah, benign prostatic um you know, uh hyperplasia BPH is uh is one of the only examples of um pathological hyperplasia that won't lead to cancer. Good. It confers no risk or increased risk of prostate cancer. So fantastic and yes, metaplasia, exa. Exactly. So for example, pathological hyperplasia can lead to metaplasia, which is what uh Sandy was describing uh which is about it's esophagus very good and then that metaplasia could then eventually lead to neoplasia, which uh, is precancerous technically. Uh And um, yeah, and then eventually cancer and it doesn't have to be in that order, by the way. So you can skip metaplasia and go directly to neoplasia. But yeah, very good. So with that in mind, uh what is atrophy then guys? What ha what, so we talked about hypertrophy, we talked about hyperplasia. Um kind of briefly touched on menapia. Not yet though. What is atrophy? Mhm. Lack of cell growth? OK. Is it just a lack of cell growth or a actively anyone else wanna offer another explanation? Oh, you're not wrong. Like it's, it's just a bit more extreme than that. Yes, exa exactly. So yes. So someone wrote um you're shrinking size of cells or reducing number of cells and actually it refers to both and that's the, that's what a lot of people also tend to forget. So the organ, for example, gets smaller in size and it's usually due to a lack of stress um compared to what it has normally, you know, you can think about it like muscles, right? You know, when you know, unless you are training them and giving that stress by weight training, they're gonna atrophy and similarly um the same with any organ. And actually, yes, as whoever that person said is reversed to both fewer and smaller number of cells too. Very good. Fantastic. We're really knowing the definitions. Now, then what is metaplasia then? Um Well, we've already given an example. So Sandy has already given an example of Barrett's esophagus, which is fantastic. And then we already talked about persistent metaplasia that leads to um potentially neoplasia as well. So then I just want the definition of metaplasia then. So again, omenti what is metaplasia? How would you describe it again, this is really key for part A takers for understanding the concepts so that you can, you know, pick your choices rightly in the exam. But for part B takers though, you need to know your definitions because you need to, they will literally ask you to define it and you do need to be able to, you know, verb him like just say on the spot change in cell type. Yeah, that's as you know, like uh I was gonna say as basic as it gets but not in a bad way like that's exactly it. So yeah. Um from one cell type to another and that's due to a change in the nature of um stress. So yeah, very good. So um yeah, change in nature of stress equals change in cell type and is done via reprogramming of cells. An example is Barrett's esophagus uh which can lead to dysplasia. Um Very good. Can anyone think of any other examples of metaplasia? Does anyone know uh physiological example would be cervico epithelio? Yeah. Um cervical. OK. What else? Um mhm Yeah. Yeah. No, you're spot on there. Um But what, what would be examples of uh another pathological metaplasia? Anyone? It's a bit more tricky to be fair. But again, it could, uh, one that could potentially come up. So, uh, something called, uh X Malacia, if you guys know. So, you know, lack of Vitamin A and eyes, you know, we talk about night vision and, uh, you know, um, night blindness, like, right. So, um due to a lack of Vitamin A and that's because the um corneal epithelium changes from one cell type to the other. Can't quite remember off the top of my head. But um that's what it is. It's an example of pathological uh metaplasia. Good. And then finally, then what is dysplasia if you guys can? This is a popular one to know the definition of very much. So, I'd say, yeah, it's very important to know the definition of this one. And that will be that will be the key concept. One, cellular adaptations and we already covered aplasia and hypoplasia too. So, yeah, anyone wanna type up something quick for dysplasia? I'm sure you guys know it and I promise you I'll link everything together at the end of like key concept one and two. So you'll see what I mean. Anyone abnormal cell growth. Ok. Fine. Yeah. Uh I would describe it a bit more differently. It's crucial to say disordered cell growth. Um And actually just mention a proliferation of precancerous cell uh cells. And the key thing is that it's still reversible as long as the stress changes. So you're not wrong with abnormal cell growth, but it needs to be more specific. They like that specificity uh when it comes to um you know, defining these times a avior. Um but you're right, in terms of concept, I can see you definitely understand that. So disordered cell growth. Um and it's proliferation of precancerous cells and they are precancerous. It's not neoplasia and it's still reversible. Very good. Cool. Next up. So now, but that's the QR code just for the menting and up a periodic QR code just so that um if anyone's joined in late, they can join in. So we've talked about when cells can adapt to a new stress. But what happens when cells can't adapt and they therefore die well, they can happen one of two ways necrosis or apoptosis. So what is necrosis? Can you define it again? This will really help you understand pathology? Really? Actually because what is the difference between, I guess um apoptosis and necrosis? I don't mean you to answer like the third question because we will list the detailed differences. But yeah, so it's um so for necrosis, someone's pathological, that's a good keyword. It's always pathological, unprogrammed. They said fantastic. It's not meant to happen. It's because the stress exceeds the capacity of the cell um good and then death of a bo someone else but death of a body tissue which is not programmed. Yeah. Yeah. Exactly. Exactly. Good. There's one key element which I will um unless someone wants to have a go I will put so on program. That's key number one. like key word, number one. good someone else. But pathological death of cells lack of blood flow. Yeah. Lack of blood flow is a cause of necrosis. Um But it's not part of the definition I would say but like, yeah, so pathological is very good. So unprogrammed or pathological being the same thing, cell death and it's always followed by acute inflammation. That's the key concept. Number two of necrosis. OK. And again, we'll talk about what acute inflammation is and you know, all that kind of stuff, but only two things to bear in mind. So when you are, if you are preparing for part of the body, she needs to know two things on program and therefore pathological. And then two, it's always followed by acute inflammation. If we're talking key concept number three, then uh it's a bit more minor, but it's still important is it's energy independent and that's in contrast to apoptosis, which we'll come to. Ok. Good. Now, then, so here's so um bulky part. So there are potentially six different types of necrosis. Can anyone name the different types of necrosis? Um And it's, it's uh again, good to know, good to know it comes up sometimes and it's really important to know your concepts and nail, that nail these concepts. Does anyone know the different types of uh necrosis? Not the causes of the necrosis, which as someone else put earlier, lack of blood flow or hypoxia or hypoxemia, et cetera, et cetera. Someone's put liquefactive coagulative fat, caseous. Fantastic. That's four out of six. Bang on um someone's put oncosis swelling, uh pyrr pyroptosis, pyroptosis, heat. Um I think you're talking about signs of acute inflammation. I might be wrong. Feel free to explain on the chat what you meant if that's not what you meant. But um I think you're talking about that Dolo Rubor, all that kind of stuff, which are signs of acute inflammation. So you're right, swelling heat. They're all signs of acute inflammation. But yeah, someone else has put gangrenous necrosis. That's absolutely fantastic. Yeah, that's another type. So, yeah, very good. So, we've got five different types of necrosis so far. So, lique factor, coagulative um fat necrosis cases and then that's it. I think the sixth, I'm pretty sure I'll have the table in a minute. Gangrenous. I've just split into uh wet gangrene and um dry gangrene. I think. So. I'm just going through it in my own head before I do. I don't wanna cheat. So, liquefaction, coagulative, uh cases fat. Oh, there's one other type actually, but I'd be really impressed if someone else has got it. Um And there's a good way to remember it, which I'll show you hopefully. So the one other is fibrinoid necrosis. That's the only other one. So this is hopefully helpful diagram number one to break down some really important uh you know, concept of necrosis. So you guys almost smashed it, to be honest, like in fact, you did smash it. Now, the way I remember this um actually is uh three CS, two Fs and then 1 g. So there are three CS. So the alternative name for liquefaction, by the way, is colliquative. So three CS, two fs fat and fibrinoid and then gangrene, one gangrene, which is dry or wet and we'll talk about each of those. So just to, because I think it will get longer if I ask you a question about every single one of this, just talk to you a little bit more about coagulative necrosis. Well, this is necrotic tissue that remains firm after death. The cell structure is maintained but the nucleus is lost. It's kind of like a empty town. Basically everything's gone. And this is true for any solid organ except the brain. Uh because the brain undergoes liquefactive or colliquative necrosis because there's so much fat content and enzymes and enzymes digest all that and basically liquify it. Um And that comes up a lot um both in part A and part B. So not coagulative necrosis, liquefaction for the brain um which we'll go onto, but it's true for any other solid organ. Ok. So, heart, when there's myocardial ischemia, that's coagulative necrosis. Uh you know, he hepatic infarcts, that's coagulative necrosis. You gotta link these into your clinical conditions. Ok. Good. Then talking on about uh liqui factor or, or colic. This is uh liquefied due to enzymes, as I said. So anywhere you have rich enzymes. So brain from microglia, which I remember uh white cells of the brain abscesses because you have so much neutrophils. So, you know, you can all imagine what pus is like, right? It's liquidy and then pancreatitis that is very important to remember. There's uh you know, autolytic uh digestive enzymes, right? And then they so therefore, um digest the pancreas tissue on its own on their own. And therefore, that's colliquative necrosis as well. You mentioned caseous necrosis now and that's simply very easy. Conceptually, it's a combination of coagulative and liqu uh colliquative or liquefactive. Um It's necrotic tissue that's basically in between a solid and liquid uh state. And in fact, actually, I've gone through some pathology textbooks as grim as it is. They sometimes define it as in a cottage cheese like state, uh which is lovely. Not that I ever like cottage cheese. Anyway, um It's characteristic of granulomatous inflammation and we'll get onto that too. So classic thing TB or fungi, then we've got fat necrosis. Uh Can anyone put on ment on or on the chat uh quickly without reading it here. Does anyone know where we've come across fat necrosis? Typically we always sort of come across it in our sort of clinical medicine. Uh, the only place actually that I would argue that we've kind of come across fat necrosis. Exactly. Someone's a bit breast. I'm glad that some people are still listening to me yapping basically. But, um, exactly breast tissue. And that's because with fat necrosis, as the name suggests, wherever there's lots of adipose tissue that's been uh traumatized. Um, you basically get uh enzymes of fatty acids that link calcium with that fatty tissue. And that process is what's called saponification. And that's come up one or two times, I've seen that and to go on further, it's because um you get deposition of this calcium, right? And there are two types where you can get deposition of calcium, you can get dystrophic calcification or metastatic calcification. Now, don't get me wrong. Metastatic calcification is not in metastatic cancer. Although that confusingly does lead to high calcium levels too. Metastatic cancer is simply where there's a lot of uh calcium in the body and therefore it gets deposited in normal tissue. But dystrophic calcification which is this is um there's a normal amount of calcium but it gets deposited in the app abnormal tissue. Um And that's because it's been saponify in fat necrosis. So wherever there's lots of adipose tissue, that's the breast, for example, is the most common. But in pancreatitis two and it looks chalky white, that's the key thing to remember, you'll come to realize pathology is all about buzzwords and key words. Um So as long as you know, those kind of highlights, honestly, you have a fair chance and don't get me wrong. This is the tutorial that I wish I had when I was taking part A and part B I kind of, you know, did it on vibes, but this is the perfect, you know, it, it's not as detailed as the pathology textbook, but hopefully enough to get your head round some tricky concepts. So we've gone through three season one f fibrinoid very briefly. This has come up actually. And I don't know if I'm allowed to say it, but like, you know, on past papers, I'm sure that the uh official er team has released um fibrinoid necrosis that's due to malignant hypertension or vasculitis where you get damage to the vessel walls and fibrin leaks into the wall. Um On histology. Again, a highlight you need to know is it stains bright pink uh and lines of zahn are seen. Um And that's really important to remember and fibrinoid necrosis happens due to malignant hypertension or vasculitis. And then finally, gangrene. Well, actually, it's very simple. Dry gangrene is coagulative necrosis. Wet gangrene is dry plus an infection that leads to wet gangrene and that's liquefactive necrosis. Um Both are common in the gi tract and the lower limbs and that's literally it. So coagulative necrosis uh that resembles mummified tissue is dry gangrene which is a lovely thought. OK. So easy way to remember. Three CS two Fs 1 g. OK. Good. I know that was a long interlude, but hopefully that was worth it to get your head around it finally then. So we talked about what necrosis is. It's unprogrammed or unplanned pathological death of a cell always followed by acute inflammation. It's energy independent. These are already some three differences between um that and apoptosis. But what would you then define apoptosis as, what would you say are the differences than any others that you know, you can flip it obviously. So what is appetite? Can anyone just tell me? I know it's really dry guys. But yeah, you're doing really well and just hang in there with me and then we'll get through it. So Aventis is program solder and regulated. Very good. So it's planned. I would say, you know, that's really important. Um What's the flip of obviously it being uh necrosis being energy independent. Well, it takes energy, it requires ATP. Um And so yeah, very good. Anyone else maybe uh wanna give it a shout before I show you a table of some of the differences. Kind of move on just for timing. But apatite is internally programmed cell death plan. It's dependent on energy, it affects single cells by the way, as opposed to necrosis, which affects a group of cells. And that's true because as someone said earlier, there's a lack of blood flow, a lack of oxygen, you know, which leads to lack of like sort of hemoglobin or like, you know, energy dependent glucose getting delivered, et cetera. So it affects a group of cells in necrosis. It's not followed by inflammation that's key in hepatosis. And this could be physiological or pathological, but necrosis is always pathological. So a lot of it we've already sort of covered. OK. Very good. And this is that master slide that I'm kind of talking to you guys about uh from the beginning. So concept number one, concept number two, summarize. OK. So if we follow this journey, it is a single cell. OK. Happy on its own. We've exerted some stress on it. Now it can, the stress could be so bad that it just dies and that could be due to apoptosis. So it just gives up the ghost and programs its own death or there's a, there's a coding in its, you know DNA for when this much stress occurs, it's gonna program to be done like dead or it could be because of necrosis uh where it's pathological, lack of blood flow, all this kind of stuff. OK. And we've covered the six different types of necrosis that there are actually, however, it could also adapt. The stress is within its means and it adapts and all the ways that it adapts. We kind of went through hypertrophy increases in size, that same cell increases in number hyperplasia decreases in size or number. Remember is atrophy aplasia and hyperplasia or hernia androgenesis. Remember, but then the nature of uh stress changes. So the cell type changes. Now this circle becomes a square, a squamous episode in below becomes columnar. For example, that's metaplasia. Now this metaplasia. So this is long standing hyperplasia or metaplasia. Remember this could jump a step, then it eventually becomes a dysplasia. It the the stress is not so much that it dies but it just is too much for the sign. So it just starts growing, you know, randomly disordered cell growth is what dysplasia is. Remember, d equals d, dysplasia equals disordered cell growth. That's as simple as it gets. And then eventually that's uh you know, that's precancerous and then eventually that will then lead to neoplasia. And remember all of this until here until dysplasia is reversible as long as the stress is removed. Um So for example, in bars esophagus, if you take um gastric acid suppressing therapy, there's not enough, there's not much reflux, et cetera, it can then go down. But neoplasia is irreversible and neoplasia is a tumor. It's a tumor, it's a clump of, you know, cancer of cells and such. But what determines whether it's benign or malignant. And we'll talk about that in a minute when we talk about neoplasia, right on Q. So then what we've talked about all those guys, what is neoplasia? Then can anyone define it? Peace, by the way, I hope that slide made sense. Uh You obviously have the slides on the recording but that I think is if I may say so myself, uh uh I think of beauty to help me just really get the um order of what happens to a so basically, cos all these terms just start to merge together in my head. So having this visually here hopefully helps. So, yeah, what is neoplasia? Can anyone um give a little definition? Then again, if you're not sure, just stay safe and we'll go through the definition. That's all right. Anyone? Not sure. OK, cool. So, oh, abnormal cell growth. Not sure. OK. Thank you so much for actually saying, not sure guys. That's, that's really helpful. Um And no worries. So it's new unregulated tissue growth. So that's the key thing, isn't it? With the tumor? It's a clump of cells, it's unregulated. There are uh you know, no limits to this. It just starts growing and growing and growing more and more of them. And it's monoclonal and that's really important. That's what separates it from hyperplasia. And also normal repair of tissue where you got fibroblasts where you've got different cell types right here. It's just this, you know, say we've got dysplasia, which is disorder crosis. Some of these are growing a bit funny. And now in ne it's unregulated growth, it just keeps on growing and it's only that one specific cell type, it's monoclonal and that's key again, So that's very good. I hope that helps. Now, what determines and the earlier question I asked, what determines whether a neoplastic tumor is benign or malignant? Can anyone tell me the key concept? We always talk about it? I always used to think a neoplastic tumor means a malignant cancer ability to breach baseman. They are very good, very good because that ultimately determines what if it's invasive. Yeah, all of these things deter you're all right. What will that then lead to? So it's potential for what? Well, it's banana malignant is its reflects its potential for. So if it does start to breach the basement membrane and it invades past the basement membrane, it can then exactly metastasize. And that's literally it, whether we call a tumor benign or malignant is dependent on its ability to metastasize. So the classic example, I can then give you, for example, is a basal cell cancer versus a Melanoma. Basal cell cancer are known for its local invasion, but there's limited or no ability pretty much uh to, for it to metastasize whereas melanomas frequently do. And so therefore, there's a difference between benign and malignant. Now, here's some core, core pathology versus like hard core pathology. Now, how are tumors named? What is it based on? Well, that's a reabstract question and I think it's hard for me to expect you guys to know does, what does anyone know you, you might see as a clue from the different from the next, uh, few questions. Maybe the tumor nomenclature is based on anyone there. TNM is, uh, staging. That's, that's how they're staged. Um, TNM. But yes, origin cell type. Exactly. For example, sarcoma. Someone said absolutely. So they are literally, um, ok, that's, that's how they're diagnosed, histo histopathological investigation from biopsies. That's sort of how they're diagnosed. It's essentially exactly from glandular tissue or specialized tissue. It's, it's essentially talking about how they're named. Why do we call them what we call them? What is a sarcoma versus a carcinoma, adenocarcinoma versus a papillary carcinoma, all these kind of things. Well, it's because of the or like original cell type and not many people kind of think and stop for a second and think on why their name. So they are like, and that will again, really help you. So now I've got a good table because I think so if we talk about why, what do you call a benign or malignant of epithelial cell lineage, mesenchymal lineage, which is essentially connected to tissue. So for mesenchymal means connective tissue, right? For a long time, I didn't really know that. So that hopefully helps lymphocytes are white cells uh and the melanocytes of the skin um related cells. So what do we call a benign and a malignant tumor version of each of these? Well, let's look at this table and it will clarify everything. So if it's an epithelial cell, so it could be a squamous or a, a columnar cell, it doesn't matter where a benign tumor, ie one that doesn't have any potential to metastasize is called an adenoma or a papilloma, depending on what it is. And the malignant versions of these are adenocarcinoma and a pary carcinoma. Sorry that someone put on the chats uh uncontrolled, abnormal. So, sorry, that was my bad a little while ago, wasn't it? But yet you absolutely spot on. Um sorry, just moving back. Hopefully, this is helpful. So, yeah, yourself. So we can talk about it in the gi tract, for example, right? We see commonly what colon cancers they are adenocarcinomas typically. And so that's because and then uh whereas we know polyps are sometimes adenomas, we refer to them as that. And that's because polyp being benign, it's an adenoma whereas malignant is car adenocarcinoma same with papilloma. Uh for example, thyroid versus a papillary carcinoma. Again, a malignant thyroid cancer. Now, mesenchyme an example tissue, for example, is a lipoma um where it's benign, you know, tumor of the fat and lipomas we know are very common. Whereas malignant version is a liposarcoma and it's the same thing with um all sarcomas on their own, you know, like muscular tumors themselves, they um only are malignant actually. So this is not obviously like a ex exhaustive table, but it just helps to illustrate the differences, lymphocytes while there are no benign tumors of uh lymphocytes, uh tumors, you know, neoplasia shall we say it's not tumor, it's not solid um, tissue and therefore it's not true. Whereas malignant, obviously you have lymphoma or leukemia melanocytes. So, benign tumor, that's a mole, isn't it? It's a nevus. Uh, whereas a malignant cancer of me melanocytes, uh mal or malignant tumor is uh melanomas, as we said. So hopefully, that makes sense. Any questions, let me know on the chat or on ment. So, moving on, what are three different ways that uh these, you know, malignant neoplasias can metastasize what are the roots of metastasis? And that's really important too. And hopefully a lot of contests will start to link in slowly, probably running a little behind. So I just wanna, yeah, just give me, give me all you got hematogenous lymphatic and translam. Yeah. Lymph vascular. Yeah. Good blood. Someone said, yeah. Rsma. Yeah, absolutely. And then, well, yeah. Trans Kalem, you're absolutely spot on ie in other words, for other people, essentially, if you don't quite know what that is essentially seeding, direct contact, essentially. So, yeah, hematogenous um lymphatic and seeding direct sort of um you know, spread basically very good. So now we talked about some of the different types of cancers earlier, right? Like sarcomas, carcinomas, you know, all this kind of stuff. What type of cancers do you know that spread via lymphatic uh system? Do you know, can you tell me which type of cancers or you can give me examples by the work papillary thyroid. Yeah. Yeah. Breast cancer. Yeah. Yeah. Very good. Yeah, we do. Sentinel lymph node biopsies, don't we refer? Breast cancers are very good, but I'm looking for specific types and so it might be helpful if I show you what I mean, uh, which is carcinomas guys. So, you know, uh, epithelial um, cell tumors like adenocarcinomas, for example, very typically carcinomas that has that carcinoma. Typically not, it's not a rule typically spread via the lymphatic system. Whereas which type of cancer spread hematogenously? And do you have any examples? Next question on mental, which type of cancer spread hematogenously? And examples, leukemia? Well, you're not wrong. It exists within the blood. So, yeah, very smart, very true. Um Someone gave an example of uh a a type of thyroid cancer. Um What's the different type of thyroid cancer that again famously is hematogenous as opposed to um Yeah, sarcoma is very good medullary. Yeah. So good if we go through it. So renal cell cancer. Um so not medullary, sorry, by the way. So renal cell cancer via the renal vein, that's really important because um remember we get those uh you know, back up and a left sided varicocele and all of this, right? And that's by the venous system. Very good um hepatocellular carcinoma. So that's why the hepatic vein they spread. Um and then follicular cancers of the thyroid um as well. And then a choriocarcinoma. So sarcoma can do. Yes. Um But that's not so much the focus. It's, it's literally renal cell cancer. The famous example, hepatocellular carcinoma and follicular cancer of the thyroid. This is your classic. So remember pa papillary lymphatic and the follicular with um hematogenous and choriocarcinoma as well. Um For uh that too. Now, can you think of a cancer actually that seeds that I can think of? Maybe two I or you know, for example, trans as someone said earlier, there are 21 of which one example is why we never biopsied this cancer. And that's really important to know which, what are the two cancers that I'm uh talking about that can seed or, or trans kalic spread? What just give it a go testicular cancer? Very good. Yes. So that's the one that I'm talking about that you never biopsy. Remember you just do an ultrasound and then you go in pretty much um you don't biopsy because that can see it as you pull out the needle, it can start to spread the cancer further. Uh You guys had some good suggestions, but I'm gonna go with the ovarian one. That's the other one that is uh you know, because it's spread the metastasis is sort of. Um so the Mery and essentially all of that, uh I think someone said Wilms, I'm not too sure on that one. Maybe you're right. Maybe I'm not, I'm not, I'm not sure we might have to lift that arm up. I'm afraid um I'll be telling you fully the limits of my knowledge. So Ovarian is the other one that I've got. Um and that, that frequently has um metastasis of the Mery and uh the mental and basically, I think it's referred to as a mental caking, which is actually quite horrible. So, um now, then talking about again, more uh terminologies which are really important, like I said, all the pathologies, terminology definitions, keywords, buzzwords, what does the grade of the cancer refer to? And do you know any grading systems that might be relevant at our level? Uh at R CS level? How abnormal themselves are? Someone said? Very good. That's one good way of describing it. It's essentially, yeah, anyone else one more? Maybe you're right. It's essentially to the degree to which so we know these are abnormal but how abnormal are they? And the key is how differentiated or undifferentiated are they? So how well do they look like their native cells or how absolutely ugly and like nasty looking are they? And that's literally it. So sorry if I move to the definition here. Uh Oh, that's gives the answer to the next one. So we'll cover the next one together. And does anyone know any grading systems then that you might want to know potentially for MRC S both part A and part B actually not staging. So not TNM, I won't take any TNM suggestions, any grading systems. Does anyone know the grading system for breast cancer or prostate cancer. Those are the two big examples. I'll, I'll give you that clue. What's the grading system for prostate cancer, guys? I'm sure you must know it. Gleason. Very good. Exactly. Because remember what does Gleason score refer to? It's, it's, you know, out of five, essentially how differentiated or undifferentiated these cells are how nasty, how aggressive they are and you add the scores up, right. Um, the most frequently occurring and the second most frequently occurring, that's what it represents. So, Gleason is good and then anyone for breast cancer, uh don't worry, I'll tell you, Bloom Richardson. I think that's one of the thing that's worth knowing. It's on E MRC S. Um So it's worth knowing good. And then finally, in this key concept, what is uh staging? Um What does that refer to? Um And which is more important for prognosis of a cancer, the grade or the stage? And then do you know any examples of any staging systems? Now, this is obviously your classic stuff. So, feel free to answer whichever ones you want. So what does a stage of a cancer refer to? What is more important when determining prognosis? Is it the grade or the stage and then any examples? So I see this chat is going off dukes. Yes. As collars, I think I've heard of that. You're right. Can you remind me? Sorry, Brad, know which cancer that's relevant to? Definitely heard of it, but I'm not too sure where of uh that cancer is, but Dukes is one good uh staging criteria. Very good. Uh Not Gleason because we just talked about that grading uh had the cancer metastasized uh is one way to look at uh staging. Yes. Uh Essentially, it's talks about the size and the spread because it's really easy. If you think about it guys, if you look at your TNM, everyone knows the TNM, right? T refers to size. N refers to the lymph nodes and refers to the metastasis, just the metastasis. And that's literally it. So what are you measuring? You're measuring the size and the spread, aren't you? That's literally all staging. Is it reverses size of the cancer and the spread of the cancer? Um What's more prognostic? Do you think um someone said stage is key to prognosis more important than prognosis? Absolutely. So grade is good for prognosis. Like to determine prognosis because of how aggressive or, you know, more differentiated. It is more aggressive. It is the stage is far more important. If you've got a distal metasis, that's obviously a much poorer prognosis. And someone said TNM, we talked about uh you know, pre mentioned uh dukes are colorectal. OK. OK. As the collars. OK. Fine. Yeah. And then very good. And then some other ones especially for uh you know, lymphoma, leukemia. Well, lymphoma is an ar but that's really important. That's remember guys. And um what else? Did I put here uh Breslow thickness that's very important in um Melanoma. Good. Right. Moving swiftly on key concept number four. got it might run over 10 minutes guys if that's OK. But let's, you know, bang through it. Right next question. What is the difference between cytology and histology then, by the way? Uh just before, well, you guys, sorry, sorry, sorry, my bad eye. Uh Yeah. Yeah, I'll just refer back to the slide here. So we talked about key concepts so far and it all refers back to this original slide. Anyway, it's just a continuation of really stress capable of adapting to it. All these adaptations can't adapt anymore starts to have disordered cell growth. Uh With dysplasia, neoplasia is unregulated cell growth of only one type benign or malignant benign means uh does not invade the basement membrane or no potential for metastasis. Malignant means does and or can metastasize. Uh We talked about the original cell type is how they name the cancers. Uh And then we talked about how actually if the cell cannot adapt to the stress or it cannot adapt in the first place. Anyway, it dies if it's programmed and it's planned apoptosis. If it's not as necrosis or six different types of necrosis, we have covered a lot, haven't we so far? So we will uh try and get through the final bits. I hope all of this is sort of demystified pathology a little bit. So um cytology because a study of cells, histology is a study of tissue, fantastically phrased. I love that. So, looking at cells as cytology or tissues, as histology, very good. You could spell out the distinction between the two, a little bit better. Cytology. Looks at one cells. Histology looks a group of cells and there you go. That's my diagnosis. Sorry, diag, that's my definition. Anyway, guys, so fantastic. Amazing all it is coming in. Psychology looks at the cells individually. Histology looks at entire tissue in a block or a block of cells. Honest to God, I did not know this. So you guys are far ahead of the game. Um You used to confuse the hell out of me all, all the time. So what are the cytological features of malignancy then? And what are the histological features of malignancy? So um this comes up in part A and part B guys. Definitely, definitely that talking has definitely given me a dry throat, right? So what are the cytological features of malignancy? There are a lot. So you can list any one of them undifferentiated, increased mitosis. Someone said high nuclear to cytoplasm ratio. Fantastic answers. And then you guys are keeping me on what to, I need to check the chart as well. So Prodia says involvement slash invasion of the basement membrane are, well, this is why the definition is so important. So pregnant, we talked about what's the difference between cytology and histology? Didn't we cytology, you're examining an individual cell, you can only look at one cell. Now in cytology, then do you think we only looking at one cell? Do you think we can tell whether that cancer or whatever has invaded the basement membrane? Just looking at one cell? No. Right. You have to look at a block of tissue or a group of cells to look at its architecture and then to see if it's invaded past the basement membrane, right? And there is there is a difference between cytological features of malignancy and histological features of malignancy. So I'm really glad you brought that up. Um This is exactly what I mean by like learning, you know, on, on with the tutorial as much as you put in as, as you get out really. So cytology, you see metaplasia, dysplasia, neoplasia, histological breach of brain m and grading of neoplasia. Yeah. Yeah. Yeah. So I want to have like a proper list of them. So you're all right. Uh You know, I have a Pneumonic. So it's a bit silly. But anyway, like CNN, you know the channel CNN. So I just say damn CNN um like it literally is a, you know, pneumonic stands for dedifferentiation or undifferentiated your right uh abnormal architecture. So within a cell, you can still see abnormal architecture within the cell. That's KETO, it's within the cell. Um So cytoskeleton is disrupted, all that kind of stuff, abnormal mitoses or increased mitoses, you will actually spot on to whoever said that nuclear pleomorphism. So what does pleomorphism mean? Funny shapes, right? Different different shapes. So each cell looks different to the other nucleus looks different to the other co chromatin. Some things you just have to learn, right? Cause chromatin, thicken chromatin, nuclear atypia. Again, abnormal looking nuclei, abnormal nuclear to cytoplasmic ratio again. Exactly. So as someone said, so I remember it as damn CNN. OK. And you just have, that's one of those things. It's memorization. I love to explain concepts when I can. And I will also tell you honest upfront or you need to write memorize and this mnemonic helps me memorize. So we already kind of mentioned the histological features of malignancy. So as opposed to the psychological, so we'll talk about those as well. II remember this via thin. So tissue, it's, you have to kind of bear with me. I'm not gonna lie, but tissue architecture is abnormal. So that's thin, that's, that's the T tissue architecture. So as opposed to the cellular architecture, this is tissue architecture, there's hemorrhage potentially, that's one of the features invasion of the basal memory, which you guys love to mention. That's here, histological features. And then finally, the last end is, well, the two necrosis which we talked about many times uh or neovascularization. And that's really key. Remember Veg F uh that growth factor for neovascularization good. And we can sort of whiz through. So what are the advantages and disadvantages of psychology. You definitely need to know this for, um you know, part B if not part A at all. Uh definitely you would need to. So I'll, I'll kind of whiz through it. So it's psychology is quicker, cheaper and you're able to do fine ne aspiration because you're just collecting individual cells, right? And therefore it's less painful for the patient and therefore what the advantage of histology. Uh Well, it's opposite and disadvantages are also um similar. The key point, however, is the disadvantage of cytology. This is the key point in this part. So it's less accurate cytology because you're only looking at few individual cells. What if you miss on the cancer of cells? Well, you, you know, there's no guarantee, you can't tell anything about the whole tissue architecture. So, and this is really key because if you can't tell if it's invading the base membrane or not, then you can't tell between if it's an adenoma or an adenocarcinoma, that's the key. And that's exactly why with follicular cancer which is malignant, it spreads hematologist. Remember you cannot diagnose it on a fine, fine needle aspiration. Remember we M MS part A always, there's always a question on that. And so you cannot tell between an adenoma and adenocarcinoma because you can't talk about the base of membrane on cytology and therefore fine needle aspiration doesn't work. Does that make sense? Guys? I hope, I hope it does uh any questions. Let me know. And then disadvantages of cytology, histology. Well, vice versa. It's expensive. It's painful for the patient because you need to take a chunk of tissue out longer to report. And there's potential for seeding. There's more of a biopsy. It's, it's a proper biopsy. So, you know, you don't do an cancer cetera. Would psychology be better for grading than histology or is there a little difference? Oh, that's a good question. Actually, I never thought about it like that. Um, Amani. So, um I guess you're right. Uh Cytology would be better in my head anyway. Uh because you're looking at how undifferentiated uh that cell is how abnormal that cell is, right? But in reality, probably you can also probably tell um how, you know, aggressive, that sort a factor, isn't it in grading? How aggressive the cell is based on the histology because of how much invasion there is in the basement membrane, how much neovascularization there is. It all depends on the system that you use to grade I'd say is probably my sort of get out of jail uh answer. But I hope that helps um final concept and this is really important. I'll try and cover it in about 10 to 15 minutes. I hope you don't mind if you do or also need to go feel free. What is the purpose of inflammation guys? So now we've finally moved on to inflammation. That was all neoplasia, diagnosis, tissue, all that kind of stuff. What is the purpose of inflammation? What is, what does it do? Repair tissue damage? Yeah, good. Uh not necessarily repair also, I'll just be a bit quicker guys, obviously to just get through it. So uh just literally be rapid as much as you can. Uh but this has been fantastic so far. Loving the interaction. So repair absolutely is one. But to remember it, it's also involved in fighting infections, right. So actually the key purpose of inflammation actually is to allow these inflammatory cells. So yeah, exactly. For example, recruit other cell types but not just recruit but allow them to get to the target place. And that's the key. So remember in inflammation, you get uh basically more leaky endothelium and more leaky capillaries. Well, it's all because and you know, the neutrophils, you don't need to go in too detail in terms of, you know, like it margins, it rolls, you got cell adhesion CS and all this kind of stuff. Whole point of information is to allow these uh necessary cells to get to the place that they are needed uh to enter the tissue, go out of the bloodstream and enter the tissue. That's it. That's the most important. And then they will do whatever they need to do, whether that's repair as one of you guys said, or fight infection or anything like that. Ok. Good. Moving safely on this should be quick. What are the two different types of inflammation. I'm expecting a Bang Bang. Two different types of information that you know, acute and chronic? Fantastic. Let's go. At least I kept one of the questions quick. Um So what are the key features of acute inflammation? What would you say are the key features? Remember, buzzwords, what would you say are the key features of that? And one of the two primary causes of acute inflammation, I kind of mentioned the two causes earlier. So answer either question or both again, looking at the charts. Oh, thank you so much. So, Jen has kindly put um a feedback link on the chat. So if you do need to go, please obviously do. Uh but if you do feel like it's adding a little bit more and you can spare 10 more minutes happy to stay on. Um But I'd just love if you could um fill in the feedback form, guys, that would be very, very helpful infection injury. That's the causes of acute information. Absolutely good. And the key features, if we're talking about buzzwords here, it's characterized by edema and neutrophils and tissues. Um Yeah, yeah, you're right, you're right. That's the clinical symptoms of acute inflammation, which we mentioned earlier, which is swelling, which is kind of related to edema, redness, rubor and Latin heat. Uh you know, pain dull, all that kind of stuff. Very good. But yeah, the in the pathological definition, I guess is edema and the neutrophils in tissue, uh it occurs due to either infection or tissue, you know, necrosis or injury, basically. Good. Now, neutrophils come in first when there's uh acute inflammation. Yeah. What time point though? Do macrophages come in? Do you know in terms of I'm literally talking time as in like, are we talking days or weeks or hours? What, what, how long after the initial insult would you say macrophages come in? Um And then, well, I kind of answered the second question, which is what's the initial cell that's involved? Well, that's neutrophils. Anyone want to hazard a guess? At what time point, macrophages come into play. This is actually again relevant. I'm not just lecturing you on pathology for no reason. You know. Well, you know, one of the biggest, uh you know, like lies really is that people say, oh, you know, they talk about surgical pathology. Actually, it's just pathology. There's nothing like relevant specifically to surgery. They ask, you end up asking you questions to do with everything. Someone said hours. Uh You could say that I would probably not. Uh And that's because I would call it three days. Uh But the reason I said you could is you can say 48 to 72 hours. Very good. So after inflammation begins, that's when macrophages come into play. Uh cos remember they need to be a little bit more. They take the time to get into the tissues. Basically. Now these are again, further important concepts. What are the four different ways acute inflammation can end in? What's the resolution? And someone said days pregnant, said days, yeah. Spot on. What are? So you've got acute inflammation? Yeah, you've got an in insult or an infection you get in acute inflammation, what are the eventual outcomes of that? So everything goes well, everything doesn't go well, everything kind of stays in between as it is. What are the technical terms for all of this? Does anyone know? So you get a acute inflammation, you've dealt with the problem that's called, for example, I'll give you one of them resolution. For example, you then you try to deal with the problem but you can't and you just keep fighting an ongoing battle forever. Someone's for resolution, chronic inflammation, cell death spot on all of them. Very good. Um There's a couple more Prolia and again, I've got another nice mnemonic to remember it by. Um So let me get you through that. So Rosc people talk about obviously in, you know, cardiac arrests, right? Like Rosc, that's literally like the mnemonic that I use to return a sponsor circulation. Instead I talk about resolution. So you got an initial insult, you deal with it. Acute inflammation happens, you've repaired it or you've dealt with the infection, done res resolved or ongoing acute inflammation. So it's just persistent pus, for example. So it's not that it's become chronic, it's just ongoing acute inflammation. Um then you have s which is a separation or abscess formation, which is acute inflammation surrounded by fibrosis. OK. That's key, that's what defines an abscess essentially or separation. Uh And then finally, it results in chronic inflammation. So, you know, this body's been trying, body's been trying to deal with it uh for a long time now and it's become chronic and that's all it is. So we said the key features of acute inflammation are edema and neutrophils being in place. What are the key features of chronic inflammation? Does anyone know anyone just give me a shout or say, not sure. And we'll do it literally last five minutes. Bang out the last few uh questions and yeah, if you guys can fill out the feedback forms, all that great. Amazing, not sure. That's fine. Absolutely. So these are one of those again, like those are the definitions that you kind of need to know uh T cells. Yeah. Yeah. Very good. Well, lymphocytes. Yeah. So any white cell basically, but you're right. Uh T or B, you're right. Very good T or B specifically. Um good. So remember, not leucocytes as in any white cells, but lymphocytes specifically. Um and macrophages. Well, remember, macrophages are in acute um uh information, uh macrophages also in granulomatous as well. Of course, remember, so you're not wrong entirely either. So anyway, it's characterized by the presence of lymphocytes T ob and plasma cells. And that's I guess what refers to uh macrophages, they essentially what plasma cells producing, you know, b cells essentially or antibodies is delayed but specific response. Whereas acute inflammation is a generic response. Ok. And that's chronic inflammation good. Well, now moving on to that specifically, what is groin lymph inflammation and what are the characteristics of that? So now you can tell me it sort of macrophages or epithelioid cell fat necrosis. Someone said um not fat necrosis. Um we saw it in caseous necrosis, remember? But that's when we saw it, for example. Yeah. So what is granulomas inflammation? Well, again, sorry, just for the interest of time, I guess I'll define it. So, granulomas are a collection of epithelioid histiocytes which are essentially macrophages with a lot of cytoplasm. That's literally all epithelioid cells are, yeah, giant cells, for example, that's another like part of um granulomas is good. And the, well, these macrophages, the epithelioid histiocytes are surrounded by giant cells which are fused macrophages as one of you guys put and a rim of lymphocytes so very good. Um And then granuloma forming, for example, are tuberculosis and sarco, we'll get to that your spot on from you. Um How can you further subdivide granulomas then? And can you give me examples of each type last few minutes? Yeah, no worries. So, granulosis inflammation. Well, we can say it's either kind of what we talked about earlier or someone said it maybe on the chart. Uh oh, not sure. Yeah, that's fine. Um it's either caseating or non caseating. So, caseating, there's central necrosis which is remember cases, necrosis that we talked about and that's due to TB or fungi. Typically we see cases uh granulomas in TB, don't we? Whereas non caseating. So there's no necrosis in these granulomas. That's all the autoimmune stuff. It could be because of foreign material sarcoidosis. Crohn's all of these have uh you know, um giant cell arthritis has granulomas inflammation, all this kind of stuff. Ok. So that's cases non case. And that's how you can further subdivide. Finally, what is wound healing? Well, it's a arbitrary definition that I'll just list on the, on the slide here. It's when an injured tissue heals by structure um or function or with the return of its integrity and tensile strength. Um This will be amazing if you can sort of quote in your part. B uh for, for your part A, you don't really need to worry about it too much. But remember, these are all the different ways it can happen so it can heal by resolution, which is no scar formation. That's the key thing of what resolution means. It's not just that convict has been resolved, it actually specifically refers to no scar formation, that's resolution organization and repair, that will result in a scar. These two things, if it resolves by that will result in a scar or chronic inflammation. Uh which also is another way a wound can heal So what are the main principles that underlie wound healing? Uh which two process take place? Well, it's just simply repair and regeneration and what's the difference between them? Um I'm so sorry, I'm having to whiz through this just for the interest of time regeneration is replacement of damaged tissue with native tissue. So it's literally good as you. That's essentially what it is repairs. This is really key to remember if you guys wanna take that. Uh anything from these two terms. Take this one repair is replacement of damaged tissue with a fibrous scar. It's fibrous material basically. So for example, say you have a skeletal tissue, skeletal muscle that's been injured, you're now then replacing it with fibroblasts. That's just scar tissue, fibrous tissue, it's not the same and that's repair. Whereas regeneration would be, for example, hepatocytes that have been damaged but were replaced with hepatocytes. And that's exactly what we're gonna talk about next. So which tissues can undergo regeneration and which can't well, labile tissue that's constantly developing and renewing that be going change that skin bowel bone marrow that has constant turnover and that can undergo regeneration because it's good as new. It's got loads of stem cells produces more stable cells like liver cancer too. But typically don't, that's what we talked about earlier with the hepatocytes, a permanent tissue type like skeletal muscle, heart muscle, nervous tissue, which we mentioned cannot. And these are remember the only times that that sorry that these can only undergo hypertrophy, those three, which we mentioned right at the beginning, which is a throwback. And then finally, uh this will be good to define, this is really important. So I'll let you guys do it. Uh Can anyone define just primary uh well, wound healing by primary intention, secondary intention, tertiary intention, what are the definitions? Can anyone just drop down their definitions right out? And that's literally the penultimate question guys. Uh or nearly, I'm sure as you are leaving, uh please do fill out the feedback and also remember we are running the final set of uh lectures. We've got only three more in the series. Um This Thursday, next event and then next Tuesday and Thursday and then that's it. So you can watch all of them back, of course. But I hope this has been useful. Please do let your friends know if this has been useful to come along for the Thursday session as well. Um OK, I'll go through it. Yeah. So this is really key guys. This is the only thing that I would say like left to. Yeah, no worries. That's fine. This is really key. So obviously you have the slides, you can go through it again. The primary intention is when the wound edges are reapproximated on purpose and closed within 24 hours. So you made an incision as a surgeon. Finally, we're talking about actual clinical medicine. It's kind of a good refreshing throwback. Uh, you make an incision, you then suture it up, that's primary intention. You are reapproximating the wound just that's what it is. Secondary intention is. They're kind of put together, they're squashed together, but they're not really sutured together, they're not approximated properly or neatly. And actually it heals from the base up with granulation tissue. And that secondary intention is kind of left to heal on its own. Tertiary is when there's basically delayed closure, you kind of leave something open, you come back, you do procedures, you then uh leave it to sort of heal and then on its own again, because of infection or whatever, that's kind of tertiary intention. Good. What question? Um Where are we? OK. Yes. What uh what uh what is hypertrophic versus keloid scarring? Can anyone quickly tell me hypertrophic versus keloid scar? What's the difference again? A classic, another classic MRC S uh A ob what's the difference between a hypertrophy scar and a keloid scar? Keloid exceeds the limits of the scar? Exactly. So, remember this is a type of repair because it's repair. Uh It's, it's not the same tissue, it's fibrous or scar tissue, both of them because scaring the name and keloid grows out of its own site. Exactly like you guys said, whereas hypertrophic, it's an excess tissue but within the limits of its uh wound, which is fantastic. And then we could, you guys also would wanna learn things like curb phenomenon for example, where certain dermatological conditions then grow uh and are more likely to chemo and stuff like that good. And then the fi a very, very final question. This is really important as, as a concept. I wish I had a flow chart for you at the end. Unfortunately, I do not. But what are the stages of wound healing? Again? Another final, final, final pneumonic from me. This is the last lecture I'm doing so. Final pneumonic from me. Um think about as a hip. So three stages, hip H IP and then it could end in ROSC, which is what we talked about. Remember that's four different ways that acute inflammation can resolve in. Right? Well resolve is the wrong word but can end in which is resolution, ongoing acute inflammation, separation or abscess formation and then uh chronic inflammation. But what are the three initial stages then hip? So that's hemostasis. So when you have an acute injury, you wanna stop the bleeding, right? That's literally all it is. So hemostasis that's immediate. Then you have inflammation which by the way you can then break it down acute inflammation, you can break it out in many stages itself because then you have initial vasoconstriction to cause the uh hemostasis, then vasodilation to allow these inflammatory cells to get to the tissue, et cetera. So, hemostasis, then inflammation then proliferative phase. So this lasts from three days to three weeks where you basically have deposition of granulation tissue as the wound heals, for example. And then it ends in one of those four ways that I talked about. OK, Rosc, so hip then Rosc and breathe well done guys. That is that um that's my email. If you have any further questions, any tips on how to prepare, um go for it. Like I said, I know this is such a dry topic. It's something that's not really taught. Well, I hope that's kind of laid things out in a very orderly systematic format. I've told you which are just basic definitions that you just need to know. I've told you which ones you need to memorize versus you need to understand. So I hope it's been helpful. Um Thank you, Francesca. Thank you, everyone for interacting so well. Uh Please do fill in the feedback. Um And yeah, I look forward to thank you, Samantha King of Pneumonics. Yes. Like I said, you know, there's a, there's some things are useful to understand the concepts. Well, I try and understand the concepts all the time. Some things you just have to memorize unfortunately. So, yeah, I hope these pneumonics and these concepts have been helpful. Um And like I said, you know, we would love to have more of you here. Um So please do let your friends know um to attend and I'll hang around for a couple more minutes if you have any questions, but I appreciate you guys all being here over your scheduled time. Great. If everyone is done, if everyone's done, I will stop the broadcast.