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The cool. Let me send this again. Okay. Any way I can resend that first question again. See the first thing that s teams quiz anyway. Um evening everyone. I'm to rush. I am a final year student. Basically sat finals a couple of weeks ago. It was in your position last year. So I know exactly what path is about and exactly what histopathologic about. And I can tell you right now, it's not about much. All we really need to know for histopathologic is buzzwords. The most common cause of a wide range of things. And uh basically that's it. A lot of people get a bit bogged down with histopathologic. Uh's they think ours loads of slides of specimens in your exam. You literally will not get a single slide or specimen. They might give you a description. That's why it's important to know the buzz words, but you won't have to look at a neutrophil and like, oh that's a neutrophil. So everyone gets a bit nervous about histopathologic. Uh's, you've got to learn a little bit about everything compared to all the other path specialties. There definitely is the most content. However, in your exam you've only got 32 questions in total, which is the exact same number as all your other subspecialties, which means that you don't need to know in depth, you need to know a little bit about everything. And like I said before, be able to recognize the main conditions and the main buzz words, my top tip would be to learn the most common cause of something. For example, the most common uh risk factor in stroke is hypertension. That's literally all you need to know. You can learn some of the other ones. If you're struggling for time, learn the most common cause of something. The chances of that coming up are quite high. Most people don't find history path interesting. Um I certainly didn't last year, I thought it was a bit boring. But if you break it down, if you're interested in anatomy, if you're interested in how diseases happen, then history path becomes a little bit more interested be interesting because his the path basically aims to answer three key questions. The first one is how does disease happen? Secondly, how does that disease visualize in tissues? So what are you actually able to see? And thirdly how does these findings correlate clinically with what you see in the patient? So if you're able to answer all three of these questions, histopathology come becomes a little bit more interesting. And when we go through the conditions, if you think about these three questions for each condition. Um You'll start to understand histopathologic bit more. So, in this lecture, uh I'm gonna be covering Gynie breast, brain, bone and skin. I won't be covering heart lungs, g eye or renal and urology that will be covered by Johnny in the a later session. I think he's doing Thursday. The structure of this lecture is because I'm covering five topics will cover each one individually. We'll have 10 quizzes throughout the lecture with one SBA and one VSA in each. I'm going to try and use the Microsoft teams chat for it. If there's any problems uh care, just let me know what anyone put it in the chat or someone just shout out because I've never used the market of teens poor function before and the chances of it going wrong are quite high. So let's, let's start with Gynie. Um I'm gonna assume a bit of knowledge here because you guys are doing O N G this year and we're just gonna be focusing on the history, path relevant features. So basically, if we cover some of the anatomy first, um this is the female reproductive system. If you start distantly, you have the vulva extending approximately, you have the vagina, then you have the cervix and the cervical canal, the endometrium, the fallopian tubes and the ovary pathology can occur in any single part of this and we'll go through it step by step. But before that, I've got two questions for everyone and I'm going to try this feature again. Hopefully you guys got those questions here. Did you get these questions? Yeah, we can see them. So if you guys just want to go through and answer those questions, I'll give you about a minute and a half. The first ones that S P A second one's VSA and the second one will be as a word cloud. These responses will give her one about 30 40 more seconds, about 10 seconds and I'll close this now. Cool. Um So hopefully you guys can see the answers. Uh The answer to question one is d inhibiting tumor suppressor genes will cover this a little bit later. Uh But in principle, you have anchor genes, you have tumor suppressor genes, anca genes, our genes which cause proliferation and tumor suppressor genes are, well, it's exactly what it says in the name. They suppress the growth of the tumor. So if you were to look at this, if something is causing cancer, you're either going to have something which is activating the cell or something that's preventing the cell death. So just going through the options, um it's going to be A or D and then you need a little bit of extra knowledge, you know, specifically how HPV 16 and 18 cause cervical cancer that's through inhibition of protein Z six and the seven which will cover a little bit later, both of which are tumor suppressor genes. So the answer's D uh for question to a lot of you put ovarian cyst as the answer with a number of other options as well. Um I'll probably accept ovarian cyst is the answer. Maybe I didn't make it clear enough. The answer I was looking for was follicular cyst, which is a type of ovarian cyst. Um Once again, we'll cover cyst a little bit later. But the key features of this question are that the patient has non specific abdominal pain, be thinking a little bit more Gynie because once a month last for several days each time. So it's in mind with her periods. Um There's no red flags really and the hyper koink masses almost a buzzword for assist wherever you are in the body that's on the liver is on the ovaries anywhere it's likely to be assist was looking for follicular, that ovarian cyst I'll accept to start with. This is a very common pathology question that they like to ask a lot of people. They obviously revise all the different uh body parts like brain, bone skin. You, you will almost certainly get a question with a definition. So it's important to go through these at the start of lecture hyperplasia to increase the number of cells that's different too hypertrophy where you get an increase in size of the cells. So if you've got someone with Hachem, which is hypertrophic obstructive cardiomyopathy, you're cardiomyocyte increase in size, they don't increase in number metaplasia. As you get in Barrett's esophagus is a reversible change from one cell type to another dysplasia, which you get uh in sin, which we're gonna cover a little bit later too is when you get reduced differentiation of cells. Um, it's not cancer because the basement membrane is intact. And finally, neoplasia is when you get uncontrolled, abnormal growth of cells and tissues. Once again, uh this isn't necessarily cancer, but if it invades the basement membrane, it would be so, like I said, with the anatomy will start distilling work approximately, we'll start with the vulva and the vagina anatomically, the vulva consists of the vaginal opening, the labia majora, the labia minora and the clitoris. If you look at the normal epithelium of the vulva, um you've got this really nice, beautiful squamous epithelium on the outside. When you get Volvo intraepithelial neoplasia, as it says in the name within the epithelium and neoplasia, which is an abnormal proliferation of growth. You get the slide you see on the bottom, you get epithelial thickening and massive proliferation of cells. What epithelial neoplasia can be graded 1231 being the bottom third of the epithelium to being two thirds from the bottom and three being the entire width of the epithelium. There's two main types. Usual type and differentiated type. Usual type is caused by HPV, 16 and 18, smoking and immuno suppression, which are the same risk factors for sin and cervical cancer and differentiated type. Vin is often caused by like in sclerosis. And it's this particular type, which is more likely to lead to cancer of the vulva. So now I'm leaving on to cancer of the vulva when those cells invade the basement membrane. So initially, they were just within the epithelium. As soon as they invade the basement membrane, it is technically cancer. It's not vin anymore. There's two main types because you have squamous epithelium. That's going to be the predominant type in the Volvo and the vagina. Both squamous cell carcinoma and adenocarcinoma present in similar ways. You might get a visible painless lesion may be ulcerated. Um There'll be flaws and they'll often be itching. There may also be other skin lesions and a history of the risk factors. For example, of liken sclerosis or of HPV prime revolver carcinoma tends to occur in older women and clear cell carcinoma tends to occur in teenagers. It's very difficult to tell the difference when you look at this cancer macroscopically. Therefore, it's important to um take a really thorough history and try and ascertain some of the risk factors moving approximately from the vagina of the Volvo. You've got the cervix. Once again, it's important to understand the anatomy here. You've got the endocervix which is within the cervical canal. This is lined with Columbia, glandular epithelium on the outside. You have the ecto cervix which is continuous with the vagina. Here, you have squamous epithelium and the junction at which the endocervix and the ecto cervix meat, sort of just towards the lower end of the cervical canal is called the transformational zone. That's the area where Columbia and squamous epithelium meat. There's a high degree of cell replication there. So that area is extremely vulnerable to infection and to cancer, which is why when you see cervical intraepithelial neoplasia or cervical cancer, it often originates from the transformational zone just like in vin. Um you have cervical intraepithelial neoplasia. So just to orientate you, I don't think I did it in the last one. Um You've got the basement membranes going across the bottom and you have the epithelium um or expending all the way to the surface as with Vin. Um If you've got a proliferation of cells in the bottom third of the epithelium, that's in one, if those cells extend into the bottom two thirds, that's in too. And if they extend into the bottom to extend the entire width of the epithelium, that will be seen. Three sin and vin are both types of dysplasia. So, as we said in the definitions, that would be a proliferation of poorly differentiated cells. It's not cancer because it hasn't invaded the basement membrane. When those cells do invade the basement membrane, they become cervical cancer. Now, although I said that most of them occur at the transformational zone. Most cervical cancers are squamous cell epithelium because that's a little bit more on the outside. Some of them are identical cinema, which means that they're from Columbia glandular cells. The risk factors are the same for usual type Vin, unusual type bubble carcinoma. The main one being HPV infection with HPV 16 17. So as with the question before, how does HPV 16 and 18 cause cancer? So there's three main stages of HPV infection within the cervix if someone gets infected often, um the body clears it by itself in 80% of the cases. If not, the HPV doesn't actually cause any symptoms. It remains latent within the cells at times of immune suppression or stress. Uh The HPV may become activated and begin to use the cellular information within the squamous cells to produce more HPV and cause a degree of dysplasia within the cells. So you end up with cellular changes and you are able to visualize this on slides. Specifically how this happens is when HPV enters the squamous cell becomes activated, it encodes C six and C seven proteins which are two tumor suppressor genes. So they're not anca genes, they're tumor suppressor genes. E six specifically inactivates P 53 which is one of the most common TSG S involved in malignancy around the body where E seven inactivates the retinal blastoma gene which you also might see in Children in the eyes. The result of this is you get a massive uncoordinated proliferation of irregular epithelium, which is cancer. Just a little aside on the cycle cancer screening program, it's offered to all women, age 25 to 49 every three years and age 50 to 75 every five years. There's a couple of stages to it. And I got this slide from Shannon North Week Park for the first step. When someone gets a cycle, uh, screen is you check for HPV. If HPV is positive, you'll check for cytology and on cytology, you're looking for the degree of dysplasia. I, is there any sin or is there not if there is dysplasia? And if the normal cells are not present, then you'd refer this patient for colposcopy to better visualise a sin categorize it and potentially offer this patient a follow up treatment with core biopsy or let. So that's the cervix moving even more approximately two, the endometrium, you have a couple of layers, the first layer being the actual endometrium itself, which is almost the epithelium um of the womb. And then a lot, a little bit deeper to that you have the myometrium, which is the dense muscular layer uh within the uterine walls. The main conditions you need to think about for the endometrium are malignancy. Obviously, this would be endometrial cancer and people often get a little bit confused with fibroids as well because they are also technically proliferation of smooth muscle cells even though they're not cancer. Um It's important to consider these and they even have a cancer sounding name like leiomyoma, but like I said, they're not actually cancer and it's important to make that distinction. We'll start off with fibroids. Uh You have the endometrium deeper to that you have the myometrium. And if you have a proliferation of smooth muscle cells within the myometrium, that is basically a fibroid, it's extremely common in women. Uh over 40 and it's often caused by estrogen uh during uh menstrual cycles or during pregnancy. Macroscopically, you'll see these massive white wealth circumscribed bundles um of varying size within the endometrium. And if you were to examine those all under a microscope, you'd see these purple bundles of smooth muscle cells. So that's really the key word for fibroids. It's bundles or smooth muscle cells because if you remember, fibroids are basically proliferation of the myometrium myometrium muscle within the uterus. Uh just a quick touch on endometriosis. Um You guys probably know this already, but it's the presence of endometrial tissue outside the endometrium. It can be absolutely anywhere within the female reproductive tract within the abdomen. And I think there was a couple of reported cases of endometriosis within the thoracic cavity as well. It's caused by vascular or lymphatic dissemination of endometrial cells. So, the cells that are lining the endometrium, obviously, they have heavy vascular supply. And if you get retrograde dissemination uh of those cells through the the vascular or lymphatic tissue, it can literally spread anywhere locally or even distally. Two is often associated with infertility. And if you have endometrial tissue, remember, endometrium on the outside. If you have endometrial tissue within the myometrium itself, that's got a specific name called adenomyosis. Macroscopically, if you were looking at endometriosis, you'd see these red, blue, uh, or brown vehicles. It's almost as if, um, someone's got a cigarette and just put it out on the ovaries. Um, uh, obviously quite discolored and the buzz word for that is powder burns. These are called endometriomas. And if you see them on the ovaries, uh the buzz word is chocolate cysts. If you were to look at those cysts under a microscope, you see that darker purple tissue that's extremely dense endometrial tissue. So on the left, you've got the microscopic image and on the right, you've got the microscopic image moving onto endometry, ulcus to noma. There's two main types. You've got endometrioid and non endometrioid. Both of these are types of adenocarcinoma because proximal to the transformational zone. You have Colombia, Colangelo, a epithelium, which is therefore going to cause a Denna carcinoma. Endometrioid. Carcinomas are more common than non endometrioid carcinomas. They tend to affect perimenopausal women. And once again, it's associated with increased Eastern exposure throughout your lifetime. If you're struggling to remember which of the subtypes are an endometrioid and are a non endometrioid. Uh Someone in the air above told me a very simple pneumonic. Sarah eats meat. Paul can't stand it for the first three of the Endometrioid. The second three of non endometrioid secretary, endometrioid, mutinous. Sarah eats meat papillary, clear cell, serious, Paul can't stand it as you can see in the top. Right. That's basically a microscopic image of the endometrium. I didn't show you a normal one. Um, but I hope you're able to appreciate that a lot of the glands are proliferating quite irregularly. You can't see the cell type. But because this is completely irregular periphery, Asian within the endometrium, this is most likely to be endometrial carcinoma rather than something like fibroids where you'd see those dense collection of smooth muscle cells. Hell vic inflammatory disease. Sorry, we're rattling through some of these Gynie conditions. There are three key features of it. Number one, it's an ascending infection from the vagina and cervix upwards into the uterus and fallopian tubes. There is a heavy amount of inflammation which then in turn leads to the formation of adhesions. I thought that this image was really good. Um because you can actually see the adhesions that are being caused within the body. I see a lot of people talk about the wound being a little bit stickier, the fallopian tubes being a bit stickier. But when you actually see this, you can see all sorts of problems that happen with someone with pelvic inflammatory disease. This is why ectopics happen. Um the embryo just literally get stuck with in the fallopian tube. It can't go any further and you've got an ectopic which is really bad. There's a very rare condition called fits you Curtis syndrome. Uh We don't know exactly why it happens. But instead of getting these adhesions within the female reproductive tract, you somehow get these adhesions around the liver. It is associated with pelvic inflammatory disease and because of the appearance of the adhesions, uh someone described them as being like violin strings. Now, I don't know what sort of violin this guy's playing. Um But that's the buzzword and that's what we've got to know. Now, uh this is a little bit more micro, but it comes up all the time. You want to know the different causes of P I D. So it could be ascending uh from a foreign device like an IUD. It can be due to external contamination if someone's had an abortion or termination of pregnancy. Obviously, they're, it's likely to be a skin commendable bacteria like staph aureus and others around the world. Um In low middle income countries, there is a high amount of TB and schistosomiasis causing pelvic inflammatory disease. Now, onto ovarian cancer and ovarian cysts, people find this topic really difficult simply because there's so many different things and it's not very well taught. I'm going to give it a go. I'm going to try and simplify it in a way that I learned that last year, if you look at the anatomy of an ovary, there are three main types of cells. You've got epithelial cells, you've got germ cells and you've got stromal cells, obviously, epithelial cells around the outside germ cells are associated with follicles and stromal cells are associated with the tissue that binds all the ovary together. You can get cancer of each of these three different types of cell epithelial cell cancers are the most common. So if you're sure on time would recommend just looking at the epithelial cell tumor's along with the ovarian cysts going get scared by this table. Um This is a table that was used in the medal lecture in my year. I basically made a couple of modifications to it. I added loads of buzzwords. I reformatted it in a way which makes it a little bit easier to look at. So I'll just take you through it very, very quickly. You've got physiological cysts on the top. There are two main types of physiological cysts that you need to know. You've got follicular, which is the most common. You've got corpus luteal, which is common in pregnancy. Within the description. You've got a little bit of information about why this has happened. So in the question, uh you did a little bit earlier, you had a woman with non specific abdominal pain. Uh that was lasting a couple of days a month and it was only once a month. So follicular cysts, they're caused by a failure of rupture of a follicle and a failure of breakdown of a non dominant follicle. So if you think about the reproductive lectures, you might have had in year one year too. You have a follicle when it time for the following follicle to get released from the ovary, the majority of it becomes a secondary oocyte and gets released and whatever's left regresses to form a corpus luteal corpus luteum cyst, corpus luteum. Obviously, if the corpus luteum doesn't necessarily break down, you're gonna get corpus luteum cyst. Um If the non dominant follicle doesn't rupture, you're going to get a follicular cyst. So if you just work through this table line by line, um you've got a little bit of information about each particular one. I'm not going to go through it all now because it's way too much and you can have a whole lecture literally just on uh various lesions. You've got some buzzwords for histology and you've got some really key features to look out for in questions. But like I said, if you're really stuck for time and this table is all scaring, you just look at the benign epithelial tumors in the middle, the malignant epithelial tumor's and the physiological cyst. The other two, if you get a question on that fair play, but I really bet money that you're not. No, that was a whistle stop tour of Gynie. Uh So if you guys have got any questions, just whack them in the chat and I'll have a look at them. Now, if not, in the meantime, we will do a couple more guy, any questions just to finish off the section So fingers crossed. You guys get these questions now, just take a bit of time and give them a crack. I'll give you guys a minute and I have to do this as well. Give you about 20 more seconds. Last chance to get your answers in before I close. This can closing it now. Cool. So the majority for question one have gone with bundles of smooth muscle cells that's closely followed by powder burns. So it's not too far away. The correct answer is bundles of smooth muscle cells and it is deliberately meant to be a slightly difficult question where you're not 100% certain whether this might be fibroids or maybe endometriosis. I am assuming a bit of knowledge here. And if you didn't know it already heavy menstrual bleeding or menorrhagia is probably more likely to be associated with fibroids because your, if you got endometriosis, the endometrial tissue is often outside the um female reproductive tract is not actually going to cause bleeding. So, out of all the options, it's more likely to be fibroid. And as I said before, fibroids are proliferation of the myometrium which are smooth muscle cells within the uterine lining. That therefore the answer is b uh see powder burns is what you get in uh endometriosis, dense violin string adhesions is what you get in pelvic inflammatory disease. Rocket Danske protuberances. I think one person put that uh is associated with one of the ovarian cancers I can't even remember which one. If you go through that table, you'll be able to see, uh, next time Rocket Danske protuberances come up, you'll know exactly which ovarian cancer is. Uh, second one, most people went for dysplasia, which is the correct answer. Uh, displays is basically when you get proliferation of poorly differentiated cells, which is exactly what sin and vin are. So that is the correct answer. Cool. Uh That's the end of section one. We'll have a quick one minute break. I'll just look at the chat for some questions and then we'll move on to breast. Maybe I should have said if you guys have questions, just whack them in the chat and I'll look at them at the end of every speck. Shin good questions. Got a question. Let's have a look if you say Sinn pathological process. Is neoplasia. Is that correct? No, because neoplasia is a proliferation of new cells. Maybe I didn't make that distinction to clear was dysplasia is a reduction of um grade or poorly differentiated cells that already exist. So when you've got sinn, you've got no new extra cells, the cells which are actually they're themselves, they've changed, they've become more poorly differentiated. Therefore, it's dysplasia, not neoplasia. Okay. You guys think of any. Okay. Got another one in terms of cycle. Carcinomas are squamous cell carcinomas. Uh The most common. Yes, they are. Okay. It seems like it's stopped a little bit there. So we'll move on to breast. If you guys have more questions about Gynie, just whack them in and I'll answer them at the end of breast. Okay. So breast this once again has a little bit of overlap with Gynie. Um A couple of the conditions do tend to come up in the context of a um a pregnant lady or postpartum lady. I never really learned press that well, but when I came to revising it for finals, had a really good lecture on it which basically took me through from start to finish. And I couldn't believe that no one would really explain the actual anatomy of a breast to me. Once you understand the enough to me, it becomes really easy to understand the different types of breast cancer that exist as well as where some of the benign lesions may occur. So if you look at the anatomy here, you've got all these red dots in the middle in clusters. These are the lot Buell's. Um this is where breast milk milk is produced and stored, their breast milk then travels through the ducts, which are these blue lines all the way to the nipple um where it exits the body. So the milk flows from La Buell's through the ducks to the nipple. And you've got lymph drainage, which is extremely important in breast cancer which flows the exact opposite way. If you do, you understand the anatomy of the breast, it becomes really easy to understand some of the other conditions. So we'll move on to some more questions. Once again, you guys just want to answer the questions on the pole. I'll give you a minute and a half to two minutes to answer these. Give you about 30 more seconds, 10 seconds and then I'm closing, get last chance to get your answers in. Uh And of closed that. Okay. Oh, a real mix in the, in for question one, which is good. Uh The correct answer is D Doctor Carcinoma in situ. Most of you put fibrocystic disease uh and a lot of you put fiber adenoma as well. Um I'll explain why it's not both of them in a second. The reason why it is Doctor Carcinoma in situ is that this is a very common scenario or presentation that occurs in real life for patient's with a non invasive breast cancer. They turn up for their screening. Um They're completely asymptomatic and in one or maybe even both of the breasts, you can see these small microcalcifications. If someone has microcalcifications within the breast immediately, you should be thinking, could this patient have breast cancer? Micro calcifications is also a buzzword for D C I S. Um And even though this patient is completely asymptomatic, lots of patients with D C D C I S are asymptomatic. This is most likely to be the diagnosis in this patient. Fibrocystic disease. You also get uh micro calcifications. Fibrocystic disease is more likely to be multiple distinct areas of micro classifications, bilaterally across both breasts. It's also less likely to occur in a 62 year old woman as it tends to happen more. Um pre menopausally or perimenopausally, fibroadenoma is a good answer if you're not sure. Um If in doubt you can go with fiber adenoma. However, uh fibroadenomas are made of uh stromal and glandular tissue. You don't get calcifications in the breast question too. What is the single best prognostic indicator for breast cancer? You see the majority of you put lymph node, which is the correct answer. Uh There's a few, a lot of other people have put the receptor status. Uh The receptor status is more important when it comes to treatment. It's not necessarily a prognostic indicator. For example, if your breast cancer is estrogen receptor positive, it means that you can treat it with um entry estrogen medications like tamoxifen. If it's pr positive, you can treat it with Herceptin. So the receptor status is more to do with the treatment and doesn't actually confer um anything with the prognosis of the patient. Great. So if you break breast histopathology down into, into four main areas, you've got inflammatory breast disease, you've got benign breast lumps, you've got proliferative breast lumps which are pre malignant and then you have malignant breast lumps. So if you start to break down each topic into a couple of key areas, it helps you remember um the different types of pathology that might occur. Anybody that presents with a breast lump, undergoes triple assessment. This is really important for you guys to know near five. Also in finals, triple assessment consists of a thorough history and physical examination. Then relevant imaging. If a patient under 35 they're more likely to have an ultrasound. Um if they're over 35 because the density of the breast tissue, breast tissue changes, um ultrasound isn't as good. Therefore, we use mammograms. And finally, if there's a lump, um you would want to get a biopsy that could be the fine needle aspiration or a core biopsy to examine the content. So it's three stages to triple assessment. Once you've done all three, you're likely to have a really good idea of what the diagnosis is and be able to treat the operation appropriately. A lot of people get confused between fine needle aspiration and core biopsy. In very, very simple terms, find your aspiration is used if you're suspecting um the content of the lump to be liquid, for example, assist. Whereas core biopsy is used when it appears that the content of the lump is more solid or complex. So you can withdraw a piece of tissue, examine it under a slide. Both of these are used for grading. Um So it's not as if one's used for grading and the other isn't both, both are used for grading. The only difference is the type of material it extracts So we're going to tackle the first group of breast diseases, inflammatory breast disease, mastitis is basically inflammation of the breast. Patient's will present with a rhythm otis. Um tender painful breasts, there may also be some discharge from the nipple. There's two main types. It can be lactation, als or non lactation. All if it's lactation, all as it says in the name, it's occurring in women who are breastfeeding. If it's non lactation a little, um it occurs at any point after six weeks when um after after six weeks, postpartum, even if the patient is breastfeeding because it's mastitis, it's inflammation, you're going to get an abundance of neutrophils which are your the first cell which increase and migrate to an area where there's any inflammation macroscopically when you look at someone's breast, um it's very inflamed, it looks extremely painful. Um And the patient's offering often in quite a lot of discomfort. Uh I'm just quickly touch on the management because it can come up. This is one of the conditions that does come up in obscene guinea conservatively, you can use warm compresses, obviously use analgesia with the patient. The key thing is to continue breastfeeding bilaterally. Mastitis often occurs when there is a blockage of one of the ducts that leads to some inflammation and infection. So, if you encourage the patient to breastfeed bilaterally, um that is the optimal management because you're encouraging that milk to come out of the breast. If that doesn't work. You can give oral antibiotics because it's, it's caused by an extent infection. Staph aureus is most likely organism. You can give flu clocks. And if a patient presents with swinging fevers, extreme pain, uh fluctuance swelling, uh and they generally look systemically and well, consider that this patient might have an abscess and you might want to drain the abscess and then give IV antibiotics. The second inflammatory breast diseases, fat necrosis. uh This is an inflammatory reaction to damage adipose tissue. So, if a patient in a question has had trauma to the chest trauma to the breast, if they've been in a road traffic accident, previous radiotherapy, um and they have a small underlying mass that's changing a little bit acutely. Uh I think fat necrosis would be a very reasonable differential to have. If you were to look at fat necrosis under a microscope, you'd see damage fat lobules that are extremely big uh and are irregular within the breast tissue. Now, I'm moving on to benign breast uh lumps. A lot of you put fibroadenoma for the S B A fiber adenomas are benign neoplasms of either stromal or glandular epithelium. They're the most common lump in women aged 20 to 40. So if you're in doubt, statistically speaking, if you put fibroadenoma, you'll probably get the answer right. But you got to look for other clues in the question. Fiber, economies are driven by estrogen. Therefore, you get cyclical pain and they regress during menopause buzz, words to look for in a question are that it's extremely mobile. It's usually unilateral. There's usually only one. Uh and the patient may have noticed it if they were in a shower is often referred to as a breast mouse. Because if you ever feel it, it moves around quite a lot. So it's not tethered to the underlying skin in terms of management. It's not necessarily relevant for path but useful for finals. It's very, very simple. It's less than three centimeters, you do nothing. We usually go by itself. And if it's more than three centimeters or the patient is extremely symptomatic, you can take the fiber adenoma out by lord these tumor. Um Even though I put it under benign breast lumps, phyllodes tumor is a malignant tumor. It resembles a fibroadenoma. So when you get a proliferation of stromal or glandular epithelium that invades the basement membrane, this is what's called a phyllodes tumor. It's extremely rare, but it comes up disproportionately often in questions. So it's handy to have heard of it at least. And basically be aware that this is the malignant version of a fiber adenoma because it's very similar to a fibroadenoma. It's very difficult to tell the difference. Um You need a very expert specialist, um breast histopathologist to be able to tell the difference. And if you look at the slide on the bottom, right, it looks awfully similar to uh the previous slide where you've just got massive proliferation of uh fiber epithelium uh within the ducks. Buzzwords to look for are artichoke appearance. It's frowned like and it's branching. If you guys can see any of those things in the slide, you guys have got good eyes because I definitely can't moving back to benign disease. That was just a little aside on phyllodes tumor. You've got fibrocystic disease. These are basically fluid filled sacs in the breast. They tend to occur in premenopausal or perimenopausal women. Some key buzzwords look out for in questions uh that they're often multiple patient's describe lumpiness uh and cyclical pain along with their menstrual cycle, that's very similar to fibroadenomas. They're often well demarcated fluctuance, transluminal with clear or white nipple discharge when you send these patient's for triple assessment. Uh and you do find your aspiration and there's blood major, major red flag. Um You definitely want to refer that patient straightaway uh to the breast clinic for assessment if you do a core biopsy because you're not sure a fibrocystic contents can be quite solid if it comes. If you take a core biopsy is very cystic, it's very irregular. You're not exactly sure what the contents are. Refer that patient straight away. A lot of you put fibrocystic disease for uh the previous question, you can get calcifications within the cysts. However, it's going to be multiple, it's going to be across numerous breasts and it's more likely to occur in perimenopause or premenopausal women. Therefore, it wasn't necessarily the answer to that question on histology. Within the ducks. You can see some fluid filled cysts. Um And that is very characteristic of fibrocystic disease. It's not covering the um entire circumference of the cyst. Um It's just a little bit, but sometimes it can be the entire thing. So don't worry too much about the slides. Uh The main thing is the buzz words. Uh and finally, the last benign breast condition is duct ectasia. This is basically when a mammary duct gets blocked, usually buy milk stasis. Because of this, you get dilatation of the duct, you may get a lump and you may get a localized infection leading to green, yellow or brown discharge from the nipple because it's an infection, you get lots of deposition of protein, a cious material within the duct. And because it's an acute inflammatory uh sort of procedure, you often get infiltration of macrophages. Doctor Ectasia is more common in smokers. I mean, as I said, it may present with a mass with yellow green discharge. Obviously, we've been through each one individually. This is basically a summary table uh with comparing each four of the benign breast lumps very useful for revision just to go through the differences between them. Uh So I would recommend looking at this table along with the ovarian table in your revision. It's now on too proliferative lesion's uh just a couple of slides on these because they're really not that important. The only important one is intraductal papilloma. The reason uh for this being important is because it presents very similarly to malignancy within the name intraductal. It's within one of the mammary ducks and papilloma is just a growth of the tissue. It's not malignant because it doesn't invade the basement membrane. And uh it's defined as a nodule within a duct. It's common in perry and post menopausal women. And if it affects the smaller peripheral ducts, there may be a an Ariola mask. And if it affects one of the larger ducts, that's a little bit deeper within the breast, you may get some bloody or clear nipple discharge, which is why people often get confused with the breast cancer. You're not going to know the difference until you send this patient for triple assessment on histology. If you look at one of the ducts, you can see the growth of one of the tissues within the ducts. It's not covering the entire duct. Um but that is what is characteristic of an intraductal papilloma. Secondly, a radio scar, uh this is a benign sclerosing lesion scar, sclerosing caused by impaired healing, post injury. For example, if someone's had radiotherapy, more likely to have fibrosis of local tissue, more likely to have a radio scar, it can prevent present as a lump because it's a scar. Key, buzzwords to look for are fibrous and stellate because those words are associated with scar formation and if you look at the slides, you can see this very um it looks pretty nice. It looks quite artistic actually, um purple uh star shaped scar lesion in the middle, but I do definitely won't come up in your exam. So uh finally, on the proliferative breast conditions, uh there's a few pre malignant breast conditions to be aware of. These patient's are usually asymptomatic. They're picked up on breast screening or during an examination. You've got usual epithelial hyperplasia, flat epithelial atypia and in situ lobular neoplasia, there's a 33 malignant neoplasms, there's no easy way to remember these. So the way I remember it is the first one, it's the usual. So it's not that bad. Second one is atypia, which means it's a little bit different. So like a little bit bad and then if something has neoplasia, it's probably quite bad. Uh So if you just remember in that order, if it comes up in a question, you're more likely to remember it as being good, medium or really bad. And finally, with breast cancer, uh finally, with the breast diseases, we're talking about breast cancer. Uh this is the commonest cancer in the UK, affecting a lot of women. It's rare under 35 but it's becoming increasingly common and it's a very hot topic in exams. So I would recommend learning it properly. Risk factors for breast cancer are split into three main categories. You have genetics, lifetime estrogen exposure, uh and lifestyle itself within genetics. Uh you have the broccoli one and BRCA two gene mutation, which is autosomal dominant. So it's extremely important to ask about family history of breast cancer or ovarian cancer in these patient's lifetime. Eastern exposure is also really important when it comes to breast cancer as it was with endometrial cancer. Some components of lifetime eastern exposure include early menarche, late menopause nulla parity if you have a child really late on, and if you're taking the C O C P, if you have any of those, you have a lot more estrogen in your body during your lifetime and that increases your risk of breast cancer. Breast cancer can be split into two main types. You have non invasive breast cancer like it says in the name, it doesn't invade into surrounding tissues and then you have invasive breast cancer. If we look at non invasive breast cancer first, that can be within the ducts or within the lobules, ductal carcinoma in situ is more common. Um and it typically presents with microcalcifications in an asymptomatic woman. This image on the left is from a mammogram where you can visualize the microcalcifications within the breast. If you were to look at that or look at the lump under a microscope, you would see a typical epithelial cells uh that haven't invaded into uh the local structures. So that's the non invasive doctor carcinoma in situ is the most common and it's associated with microcalcifications on the other side, invasive breast cancer, this is usually uh really bad for the patient. They may need to have a mastectomy lymph node clearance. Um And these are the cancers that are more likely to metastasize to other parts of the body. Invasive ductal carcinoma is the most common breast cancer in women. So, if that question comes up, just remember, invasive ductal carcinoma, you also have invasive lobular carcinoma within the lobules and Paget's disease of the breast which is around the nipple. There's a few other types that are extremely rare. Uh but some of the buzzwords are below, but the main wants to remember would be ductal and invasive. Um And I think in our paper, they did ask just what's the most common type of breast cancer which would be invasive ductal carcinoma. Breast cancers are graded using the notting scoring system. You look at the cancer under a slide and an expert will assess it for nuclear pleomorphic is um's which is um what the nucleus looks like tubule formation within the cell and mitotic activity. They graded 12 and 33 being the poorly differentiated one associated with poor prognosis and outcome. All tumor's have their receptor status figured out they can be eastern receptor, progesterone receptor or her two receptor. This mainly guides treatment. It hasn't got any prognostic benefit. And as many of you said in the question, axillary lymph node status is the most important prognostic feature. Uh breast cancer because if it spread to the lymph nodes, uh the chances are it can spread around the body. So come to the end of the breast section and I'll just open the next poll. You guys have any questions, whack them in the chat and I'll have a look at them now, otherwise you've got a minute and a half uh to answer both of these questions, give you guys about 40 more seconds, 10 more seconds, less chance to get your answers in right. Closing the answers now. Okay. Let's have a look. Okay. A lot of you. Um Question one are split between C and E. Uh The correct answer is e the only difference between, see any is defined needle aspiration and core biopsy. The question is getting at a fibroadenoma. Uh This is a young woman uh with a very small spherical mobile, painless mass. These are all buzzwords, fiber adenoma. Therefore, because it's more likely to be a solid lesion, you're going to do a core biopsy rather than finding the aspiration. You almost only do fine needle aspiration if there's a cyst. And it's unlikely that that this patient has a cyst because Hamas is mobile. Um it's quite spherical, is very, you can feel it quite easily. Um So it's more unlikely to be a cyst. I can see why some of you might have thought that but in this case, fibroadenoma is just a little bit more likely question to uh Yeah, mostly you got most of you got this right duct ectasia. This question is buzzword, the law, sub Ariola mass, green nipple discharge, Berger's disease. If any of you guys know that it's associated with very heavy smoking, it's a vascular disease, um, and complex pro tenacious material which is deposited during the acute inflammatory response. A lot of these are all buzzwords for, uh checked Asia. Well, we'll have another minute break. I'll just have a look at some questions in the chat. If you guys have anything, just wipe them in there. Now, before we move on to brain, which is the last uh big topic and then the other two are quite small. What do you mean by friend? Like? Um, so if you've ever seen fronds, they just kind of go off in different directions. Uh I think that's just what it's getting at. What is the tick pole? I have no idea. Uh When would we prefer to use ultrasound first and mammogram vice versa. Yep, someone else in the chart has already answered too. That, that's correct. The, I mean, the guidelines say 35 because that's the age at which they've set it as you get older. The structure of the breast changes a little bit ultrasound is not as good. Therefore, use mammograms who used to say why it can't be 30 or 40. I don't know the guidelines say 35 any more questions before move on quickly. No, idea what this take, Paul is. Hopefully it doesn't happen again. We'll move on to breast, uh sorry, move on to neuro. Okay. So, uh the last big topic for this lecture is brain. We're still going to cover bone and skin, but they're both a little bit smaller. Once again, we'll start off with a bit of anatomy about the brain. You've got four main lobes, frontal, temporal, parietal and occipital. You have the cerebellum and you also have the brain stem. There's six key components of the brain, four lobes, cerebellum and brain stem a lesion in each one of those really regions will cause symptoms, which are specific for that region. For example, a legion within the parietal lobe will cause language and touch deficits because I think that's also where broccolis and vernick asses, occipital lobe will cause visual defects. Cerebella will cause balance ataxia, etcetera and brains them very lethal because it's where your cardio respiratory center is causes problems with breathing, uh heart rate and maintaining the autonomic function of your body. So the next quiz if anyone has problems with it, um just whack it in the chat. Hopefully it's not a tick box thing. Again, give you got 30 seconds quickly and seconds, get your answers in 32, put on closing the poll. Now, great. Got the responses in uh good. Over half of you uh put glioblastoma multiforme, which is the correct answer. Some of you put oligodendroglioma and some pilocytic astrocytoma as well. We're gonna cover brain cancer's in a little bit of detail later. But the key points of this question would be a two month of functional decline. So it's very, very rapid. The lesion has high mitotic activity, high cellularity and poor differentiation. I'm not sure why an MRI will show you that that would be a biopsy, which basically shows that this lesion um has a high grade, the cells are rapidly dividing and all in all this is a very aggressive tumor that this patient is experiencing out of all of these options. The most aggressive tumour is be a glioblastoma multiforme. It also tends to affect people over 50 which fits in with this patient, pilocytic astrocytoma um is usually grade one. So it's not that bad. Obviously, all brain cancers are bad, but uh patient's don't have this rapid functional decline and oligodendroglioma, it's unlikely to be um simply because of the rapid decline. This patient has, they may also be other symptoms associated associated with oligodendrocyte um which are quite specific and this patient doesn't have question too. Yep, most people have got this right. It's Polycystic astrocytoma. Uh The reason being is uh astro scitomas are the most common cancer in Children and in adults, some people uh have put neuroblastoma, uh glioblastoma multiforme. So, like I said before, glioblastoma multiforme is gonna affect older people. It's extremely bad. Um And you get massive functional decline. I'm surprised no one put medulloblastoma. I think that was the um other answer. I was hoping some people would put, but medulloblastoma as rm biological malignancies, they're the second most common brain cancer in Children. But astrocytoma is, are still the most common. So if it comes up in a question, astrocytoma, okay. Once again, we're gonna break brain down into four different parts. We've got stroke T I A tumor's chronic neurodegenerative disease and raise intracranial pressure will cover each one briefly. This should be uh some quick revision from year three. A stroke has the definition of a stroke has three key components to it. It's a focal neurological deficit of presumed vascular origin that lasts for more than 24 hours. The difference between that and A T I A is that T I A usually resolves within 24 hours and frankly, most people, it lasts less than 10 or 15 minutes. There are two main causes of a stroke. It can be ischemic or hemorrhagic. Most strokes are ischemic and the most common cause. Um or the most common path of physiology of an ischemic stroke is atherosclerosis with the second most common being thromboembolic. If a young patient, for example, a 41 year old gentleman comes in with a stroke and you can't find any obvious cause. It's really important to do a vasculitic screen on the patient because there may be hypercoagulable. Hemorrhagic strokes are not as common as a skeptic strokes. Most common risk factor for a hemorrhagic stroke is hypertension. And even though atherosclerosis was the most common cause of ischemic stroke, the most, the single most common modifiable risk factor for all strokes is hypertension. Even for a scheme. Ick, because hypertension and arthrosclerosis often go hand in hand. Um It's just identified uniquely here as hemorrhagic but it is for all strokes. If you've got a hemorrhagic stroke in a young patient, for example, the 41 year old gentleman, you do CT scan, they've got a massive bleed in the brain. You might want to consider if this patient has an A V malformation. And there are some rarer causes like cavernous angiomas as well. The main takeaway from this slide is the cause is um and once again, I'm going to reiterate the most common causes hypertension. But if it's in a young patient, consider vasculitis or navy malformation ischemia versus infarction, ischemia is basically just a lack of oxygen supply to the tissue is when, when the tissue is on its way to death, but hasn't actually died yet. Infarction is when the tissue is now dead because of the lack of oxygen supply. So you've got sort of two parts of the spectrum ischemia leads to infarction here. You've got a postmortem of uh someone, someone who's had a stroke here. I think in the left parietal lobe, you might, you can see a darker region. Uh that's basically the indicative of dead tissue and an infarct So it's likely this person has had probably an ischemic stroke, hemorrhagic strokes can either be non traumatic or traumatic. Like I said, hypertension is the single, most common modifiable risk factor in all strokes, particularly in hemorrhagic strokes. If you have an inter intra paran came or hemorrhage. So, within the parent chema of the brain, that's usually affecting the basal ganglia. And it's usually due to a spontaneous rupture of a vessel due to hypertension that's going to cause a hemorrhagic stroke. It's non traumatic because you haven't really had an injury. Second cause of a hemorrhagic stroke is a subarachnoid hemorrhage. Most of these occur from ruptured berry aneurysms around the posterior communicating artery. So if you remember your circle of Willis, um that's the artery right at the back or at the bifurcation of the internal carotid. Both of those places. Uh You often find berry aneurysms and the classic SBA association is if this patient has bilateral abdominal masses. Um and a family history of brain bleeds which points towards polycystic kidney disease. So that's a classic association. If you were to do a ct head of someone with subarachnoid hemorrhage, uh you can very clearly see the circle of Willis normally, you can't. So if you look at this one, you can see the white outline um which looked like vessels branching out from the center, that's what we call hyperten you ation around the circle of Willis. Usually can't see that if someone's had a subarachnoid. You can see that if you can't see that and you still think that this patient might have had a subarachnoid hemorrhage. You do a lumbar puncture, they has maximum uh sensitivity at around 12 hours and you can do it up to 72 hours, I think. And what you want to look for is basically blood in the lumber puncture, which indicates that the patient may have had a sub Barack. So that was the non traumatic causes of a hemorrhage. Now onto the traumatic causes of a hemorrhage. Obviously, with trauma, you've had some sort of injury, whether that's uh a road traffic accident, punch to the head or a fall at home that's caused a vessel in your head to burst. There are two main types. You've got extradural hemorrhage and a subdural hemorrhage. The extradural hemorrhage occurs when you get a fracture to vegetarian, which is around your temples. It's usually caused by road traffic accidents or if someone gets punched there. When you get a fracture of the bone, it often ruptures the middle meningeal artery that lives below it. And if you want to do a CT scan, you get a massive bleed into the brain that looks a bit like a lemon. So the buzz word for extradural hemorrhage is a lemon shaped CT scan, but contrast a subdural hemorrhage occurs due to rupture of some of the veins that are in your head. So it's not one of the arteries. It's one of the veins. It often occurs in patient's who drink a lot of alcohol because they lose the structural integrity of the veins inside their head. If someone's not on anti coagulation, if they have a bleed, it's more likely to continue the new bleeding. And as we get older, um we also lose the structural integrity of our veins. So, subdural hemorrhage is, are more likely to occur alcoholics if they're on anti coagulation and if they're elderly, it often presents with a banana shaped density on a CT head. So that's the buzz word for subdural hemorrhage, extradural hemorrhage, hemorrhage looks like a lemon and subdural hemorrhage. It looks like a banana. The only question I can think that they're going to ask about traumatic brain injury is if they just ask, what is the single um largest cause of death in under 45? Thanks, Steve gentleman um was very passionate about this topic. He spent a lot of slides talking to us about it. But the main takeaway from this slide is that if they ask you that question, the answer is traumatic brain injury clinically, I'm just trying to make it a bit more relevant. Some things to look out for uh fluid coming from the ears, fluid coming from the nose if that fluid is straw colored. So it's kind of pink, yellowy brownie. And if this patient has battle sign, which is a massive bruise around the mastoid process all of these point towards a traumatic brain injury. There are a couple of different types. You've got diffuse axonal injury. If you think about the anatomy of your brain, you've got the corpus callosum which binds the different hemispheres of the brain together. If you have a traumatic brain injury, those fibers may tear, uh causing a coma, that's really severe. Um Patient's very rarely recovered from it, but the more common one is a contusion, for example, in a road traffic accident, if someone has whiplash and they've smacked their head on the dashboard, your brand is obviously sat within the skull. The forces of your brain hit the front of your skull that's called coup and when it rebounds back and hits the back of your skull, that's counter coup. So if you're in a knee and you do an X ray of the head ct, you want to look at both where the impact of the injury was and the exact opposite side, but sometimes that can be almost as bad as the actual impact itself. Now, onto everyone's favorite topic. Um Brain cancers, everyone finds this a little bit trickier. Um But you don't need to know that much, like I said before. Astro sites are the most common cell in the brain. Therefore, astrocytoma are the most common cancer that in the brain. If you take anything away from next couple of slides, it should just be that statistically speaking, if you get it an exam you're more likely to be right. This slide has some anatomy of the brain. It might look complex at first, but I found it really useful in revision because it just highlights the different areas of the brain and the different tumors which pop up in those areas. The mainstream is, you need to know what astrocytoma as which we've covered and we're going to cover uh again, meningiomas, medulloblastoma as a pin demo, a a pin dioramas and to charity tumour. Those are the five main ones. Um And if we take, for example, how you can use this diagram. Uh If you look at the second red box from the top, it says astrocytoma and it says supratentorial inter axial. So you know that astrocytoma are super tentorial, they're above the tentorium and their intra axial, which means they're within the brain powering clima extra axial means they're not within the brain power and clima there to do with the soft tissue of the cranium or the tissue surrounding the brain. Brain tremors can be split into primary or secondary primary tumor originate within the brain and they can be intraaxial or extra axial. Astrocytoma are intra axial, which means they're within the brain parenchymatous or as an extra axial tumor's affect the cranium, the soft tissue or surrounding nerves, they're not actually within the brain. These are primary tumor's secondary tremors are the are more common in the brain. Um And they're often metastasis from other parts of the body. The three most common sources are lung, skin and breast. There's no real way you can remember that, but it does come up in exams because the brain is quite specific. And these three malignancies disproportionately metastasized to the brain. If you want to do an MRI, you see, well, demarcated solitary nodules and secondary tumor's with METS very, very poor prognosis. Brain cancers don't use TNM. But it's important to understand the difference between staging and grading staging is how far the chicken has spread. So, if the tumor has metastasized, somewhere grading is how differentiated the tumor cells are compared with the native cells similar to dysplasia. You're looking at the tumor cell, you're looking at the native cell and comparing the two to see how similar they are. If they're very, very dissimilar, it's going to have a high grade associated with poor prognosis. If they're kind of the same, it's going to have a lower grade with a better prognosis. So this is probably the most important slide for brain cancers. And it's really important to understand the different types of astrocytoma is that you get astrocytoma is ranged from pilocytic astrocytoma as all the way through to do your blastoma, multiforme, pilocytic astrocytoma as very indolent. They affect Children and their associated with quite a good prognosis. Diffuse gliomas are a little bit worse. The cell types are a little bit poorly differentiated and they affect people aged 20 to 40. So, in a slightly higher age group, and finally, you have the worst brain cancer, which is glioblastoma multiforme. Unfortunately, even though, because it's the worst, it's still the most common and associated with the worst prognosis in our exams. We got asked, um, what was the most common brain cancer in adults? And the add, the answer was vaccinated Multiform. As you get older, the grades of your astrocyte owners get worse. So that's another easy way to remember the progression. If you look at the histology below, you can see grade one doesn't look that bad, but grade two and grade three, you've got increased cellularity. Um And if you were to look at cell individually, you'll see increased mitotic figures and some microvascular vascular proliferation to compare grade four to grade one. And you can see a clear difference between the two. Grade four just looks way worse than grade one and that's associated with um with GM some other bread cancers. Um this to go through in your own time. Meningiomas can affect the meningea, the meninges or the arachnoid cells. Medulloblastoma is mainly affect Children, they affect the cerebellum. So Children get balance problems. A pen doma, I can't even say it affects the posterior fossa of the brain craniopharyngioma as and pituitary tumor's affect the pituitary seller. And um everyone knows maturity tumor's to cause bitemporal hemianopia, craniopharyngioma also caused that. But in the earlier stage, um you can tell the difference between the type of bitemporal hemianopia. They cause, for example, patootie tumor's go upwards so they cause an inferior uh wait perpetuity, tumor's grow upwards. So they compress the inferior fibers, therefore causing a superior bitemporal hemianopia. Whereas craniopharyngioma as start superior li they extend downwards, so they compress the superior fibers, therefore causing an inferior bitemporal hemianopia to start with hate neuro. But there we go. Uh now moving on to the final category which is a neurodegenerative diseases. Uh This mainly encompasses dementia and Parkinson's. If we cover dementia, first, dementia, by definition is a global impairment of cognitive function and personality without impairment of consciousness. Um That why it's really important to make that distinction between delirium and depression classic site questions. You've got the five A's that defined dementia, amnesia, apraxia, which is your inability to sort of do manual thing, things, a aphasia, your ability to understand or communicate um agnosia. Uh You um you can't recognize things again and I know Mia you forget the words of things. There's four main types of dementia. Alzheimer's is the most common then vascular, then Lewy body in front of temporal, important to learn that order as well because it does come up in exams quickly on an Alzheimer's Alzheimer's has two main theories. One you've got accumulation of beta amyloid plaques. And secondly, you've got hyper phosphorylation of TAU. No one really knows which theory is dominant, maybe it's a mixture of the two, maybe it's one of the other. We don't know if you were to look under a slide. Um You can see these beta amyloid plaques outside the cells. And on the right, you've got rough tangles of towel tau is associated in a number of other uh neurodegenerative diseases like frontotemporal dementia. And if you just keep this image of what a towel tangle looks like, I'll show you what it looks like in front of temporal dementia And you'll see that it looks pretty much exactly the same Alzheimer's affects the medial temporal lobes first because that's where the hippocampus is. That's what's important for your memory. If you were to do an MRI, you get global atrophy. When we get older, everyone gets a trophy, but atrophy, that's disproportionate to what's expected along with symptoms, points towards Alzheimer's dementia. Uh some buzzwords for vascular Lewy body in front of temporal dementia. Obviously, if someone has vascular, they're going to have uh cardiovascular risk factors and you get the classic stepwise deterioration, so they're fine and then the next day they're not and they're at that level for three months and then suddenly again, they've forgotten how to speak. So, in this really distinct steps, you get that. Did you get that deterioration with Lewy body? The buzz word is I can see little people running around. It also has a fluctuating course. So some days they're fine and some days they're not, which is different to the stepwise deterioration too. Don't get confused in questions in front of temporal dementia ache. A picks disease. Um It's also more dominant, it affects younger patient's. You get uh personality change, disinhibition, overeating because it affects that frontal lobe, which is responsible for your personality and the way you act, you get lots of pick bodies in front of temporal dementia. So if you look at the B slide here, um it looks very much like a towel tangle because pick bodies are basically just hyper force for related towel. So it can be very difficult to tell the difference. But um the pathophysiology of both is the same and somewhere along that line, they just end up with different presentations. I think the final thing on chronic neurodegenerative disease is Parkinson's disease. Parkinson's disease is a depletion of dopamine Europe dopaminergic neurons that project from the basal ganglia to the substantial Migra. It's caused by the accumulation of Louie bodies and Louie bodies are basically just bundles of alpha synuclein which have been disposed of by the cell. When you get lots and lots of Louie bodies within the nigrostriatal pathway, you get motor retardation and a reduction in firing of those neurons which leads to Parkinson's disease. People with Parkinson's often get an early loss of smell, which is when you get a loss or you get accumulation of Louie bodies within the olfactory nerve too. If you were to look under a slide, um you can see a Lewy body inside a neuron there and within the Nigris right or pathway, uh you get a lot of melanin deposits too that we're not 100% sure why. That is the case. Same Parkinson's plus in um syndromes. These are very, very buzz worthy. And if I were to look out for some, it would be that drug induced Parkinson's would get bilateral motor deficit. M S A multiple system atrophy. You get autonomic dysfunction. So they may have problems with their heart, with their bladder, with sweating and then PSP, you just get a vertical date, gays dysfunctions when they look up or when they look down, um they find it very difficult and they're not able to see all of them present like Parkinson's, but they had just have one additional feature to it and finishing off brain. We've got hydrocephalus, which is a, an increase in CSF within the ventricular system of the brain. The CSF is produced by the Corado plexus within the ventricles. So you've got your two lateral ventricles here. The CSF then flows through the interventricular foramen into the third ventricle and then flows through the cerebral aqueduct into the fourth ventricle and then out in the subarachnoid space is then reabsorbed into the superior sagittal sinus and makes that whole loop. Again, if you've got a blockage along any one of those ways, you get non communicating hydrocephalus. If you've got an increased production of CSF or decreased absorption of CSF, that's communicating because there's no blockage. And there's a really rare form of hydrocephalus called normal pressure where you get gait disturbance, urinary incontinence and confusion. So, a triad of those three things, if you were to do an MRI get massive ventricles, you're not going to miss it. If you see that. And the last slide quickly, if someone has raised intracranial pressure, for example, due to a tumor stroke, hemorrhage abscess, um there's an increased risk of uh herniation in different parts of the brain. You don't want to do a lumbar puncture in these patient's because of the increased pressure within the brain, they're more likely to get a tonsil herniation of the cerebellum and the brain stem through the foramen magnum, which can lead to cardio respiratory death. So that's the key um herniation to remember. Cool. We, we whizzed through neuro apologies if I went a little bit quick. Um But we haven't got long left. So I just opened the pole for the next one. I've seen a few questions as well. So just quickly answer those before you got the quiz, I'll answer the questions now as well. So we're not wasting too much time. I'll give you a minute, minute and a half to do that. What's the difference between a VM and cavernous angioma? Okay. So you've got arteries which then go into capillaries, which then go into veins at that junction. If so you got high pressure in the arteries and low pressure in the veins. Sometimes you can get leaking at that junction, which is an A V M, an arteriovenous malformation. That's what can cause a hemorrhage, particularly in a young person. A cavernous angioma. I can't remember off the top of my head. But, uh, from what I remember it's, you've got the cavernous sinuses within your brain which are the veins which drain blood from the brain. Um, if you have an obstruction there or if you have like a proliferation of the wall there, it increases the risk of a bleed. But cavernous angina don't, I'm not 100% sure on that one. Um So I would recommend just looking that up, you walk through the CSF pathway reabsorption again. Um Yeah, I'll get the image up. So it's easier. So, Andrea, you think you asked this question about the CSF absorption through the brain? I'll just go through it again. So CSF is produced by the Kuroi plexus, which is a group of cells within the ventricular system of the brain. So here in the middle of the brain, we've got the ventricles. Um there's two and they are on either side of the hemisphere. So they're two lateral ventricles, they produce CSF. CSF then drains through the interventricular foramen to the whole between both the ventricles into the third ventricle, which is the storage space. CSF then flows from the third ventricle to the fourth ventricle via the cerebral aqueduct and from the fourth ventricle, it goes out into the subarachnoid space which lines the entire brain from the subarachnoid space. It gets re absorbed into the sinuses which are often in the dural space. So that's the whole flow uh of CSF and the CSF thing gets reabsorbed back into the blood and it's never to be seen again. I can give you guys like 15 seconds more on the questions just quickly tourist just in the interest of time. Uh Just so you can get through the power point if everyone could like leave the question to the end. So we can finish the power point and then if you have any left burning at the end, then we can go through them. Just if, yeah, that's all right. Yeah, that's fine. The next two sections a little bit quicker. So perfect. Okay. I'm gonna close the poll now. Okay. Um So most people put lung for this one, which is the right answer. Remember lung, skin and breast, you've gotta wrote learn those three for brain cancer's. Um Yeah. The other ones can lead to mats. But if lung breast or skin are there, um then it's going to be one of those three. And alpha Synuclein is the correct answer for number to remember when alpha Synuclein MS folds. That's what a Lewy body is. Um And when that accumulates within neurons, at least Parkinson's disease. If you put Louie bodies, I'll also accept that answer. Cool. I'm just gonna skip the break, you can join this meme for like 10 seconds and then we'll move on. Um So we'll quickly uh whiz three bone as always important to understand the anatomy. Once you understand the anatomy, everything else becomes really easy. You've got the shaft of the bone, which is called the diagnosis. You've got the metaphase iss, which is basically the neck of the bone. So it's on both sides. The growth plate is located within the metaphase sis, it's called Fyssas. And then you have the epiphany sis, which is basically the end of the bone around the outside of the bone. You have cortical bone and on the inside, you have a medullary cavity which produces red blood cells with a deeper dive into what a joint looks like when two bones meet, each bone has cartilage because you don't want bones rubbing against each other between the cartilage. You have the synovial space which is basically fluid which lubricates the joints when it moves. The synovial fluid is produced by synovial sites which are specialized cells that produce the synovial fluid. Um We've got a couple more questions if you guys, uh I just want to have a look at these. You don't, I'll launch the poll, but if you do them really, really quickly and we'll move on, I'll give you 10 more seconds and then those people who're um haven't had enough time, but it's getting towards the end. Well, just close the pole and we'll talk about these. Um So the answer to one uh is a mccune Albright syndrome. Bit of a rare condition, but this kid basically has fibrous dysplasia. Um well done for a lot of you for getting it right mccuen. Alright syndrome is also triad to get cafe lay spots, precocious puberty and fibrous dysplasia. This patient has to all be it. It's quite descriptive. Third one, they have fibrous dysplasia, which will cover really quickly. And the last one, what is the most common bone cancer in adult osteosarcoma? Definitely, if you remember one bone cancer, osteosarcoma, I'm not going to go through the different types of bone fractures. Now, I'm just look over these when you've got the slides, when you get a fracture. Obviously, it's extremely painful. The healing of the fracture happens in four main stages. The first stage, you get the formation of a hematoma at the fracture site that delivers all the nutrients required for fracture healing. The second part you get deposition of new bone. This bone is immature but it provides the um the scaffolding for bone repair. The third part is you get mineralization of that new bone, which is why it's really important to have adequate vitamin D levels. And the fourth part is you get remodeling along weight bearing lines. So if you fracture your leg, once the initial fracture period is over, you want to start walking on it properly. So the bone starts to heal in the direction in which you walk that you is, um, is wolves, uh theory or wolfs, um, principle which you might come across in some of the earlier years. Uh, osteoarthritis, a very common bone disease. It is a degeneration of the articular cartilage. So, the cartilage that lines each bone if it starts to break down, that is osteoarthritis. As you can see on the histology, you've got a normal, very healthy looking cartilage and when that starts to break down, it becomes very irregular. Um it appears to be gaps within the cartilage as well. And that causes osteoarthritis, rheumatoid arthritis, not to be confused with osteoarthritis, you get chronic inflammation of the sino v. Um So if you remember the synovium is the joint space between the joints. It has the fluid which is produced by sina vo sites. If you get inflammation there, that is rheumatoid arthritis, it's caused by rheumatoid factor and anti CCP binding to receptors on the synovial sites, driving T cell and B cell autoimmune reactions and leading to general destruction of the joint. If you want to look at a joint under a microscope, because it's the synovial. Um you see sign of ITIS, you get proliferation of sino via sites which is reactive to the inflammation. You get uh inflammatory cell infiltrates particularly T cells. And because it's a chronic inflammatory response, you get fibrin deposition, um which leads to scarring around the joint with osteomyelitis. Everyone always focuses on the treatment. But what actually happens if you don't treat it well, the bone basically gets eaten away by the bacteria and you get lytic destruction of the bone and eventual detachment of the cortex within the bone. That's why it's extremely important to treat osteomyelitis because if you don't, it just completely destroys the bone from the inside gout and pseudogout, we talked quite a lot about these. Your investigation is to look at this under polarized light. Take a sample of fluid, look at it under polarized light with gout, which is the top left image, you get needle shaped crystals that are negatively beira fringe int if you were to do an X ray, you get rat bite erosions. It looks as if someone is bitten off part of the bone. If you compare that with pseudo gout, you get rhomboid a pap positively by refrigerant crystals. And if you were to do an X ray, you get white lines of calcinosis between the joint. So if you look at the X ray and the bottom in the joint space, you've got some calcium deposition um which is very, very characteristic of pseudo gout. Now, with the basics of bone cancer, they can be benign or malignant if you can't remember the names of any bone cancers. Um then it's important to just remember the differences between benign and malignant. If something is malignant, you are going to see a very distinct border between the cancer and the normal bone, it's going to be irregular, you're gonna get calcium deposition and it's going to be extremely painful compared with benign. It's probably going to be regular, isn't going to be not too dissimilar from the normal bone. Um, and uh there will be less pain or the patient will be less symptomatic. These are the main malignant bone tumors. You need to know. The main one is osteosarcoma. The most common brain cancer generally affects teenagers. And the most common site is the knee, the tibia or the femur with osteosarcoma, you get proliferation of the the the bone cells. So on the right, if you were to do an X ray, you get this classic cod mons triangle appearance where you've got the proliferation of the bone cells um leading to a sunburst appearance or an out bursting of the bone. If you see that very, very characteristic of an osteosarcoma, osteosarcoma, osteo comes from bone compared with chondrosarcoma, which is the second cancer here. Condo means cartilage. So yet proliferation of the cartilage doing sarcoma is highly malignant in younger people. So if someone has a rapid decline, just like glioblastoma, multiforme, you might want to consider ewing sarcoma fibrous dysplasia. We was the answer to one of the questions. Um It's when your bone is replaced by fibrous tissue. So it's not as dense. If you were to look at that under a microscope, you get this Chinese letter appearance, which is basically the fibrous tissue infiltrating within the bone parent chema. If you see the words Chinese letters or trabecular, within their question, it's gonna be fibrous dysplasia. Those are just the buzz words. And if you were to look at an X ray, you get soap bubble osteolysis. So if you look at the head of the femur, um you could potentially argue that um it looks like soap bubbles and you've got this very characteristic Shepherd script deformity um with Boeing of uh the metaphase iss is associated with mccuen Albright syndrome, which is a triad of fibrous dysplasia, cafe ole spots and precocious puberty. Well, that's the end of bone rapid 10 minutes on that. And then we've got even quicker section on skin. You guys should be pretty good at skin anyway, with all the dome teaching everyone gets, give you guys a minute to do these about 30 seconds. Okay. I'm gonna close it in 10 seconds to get your answers in quickly. OK. Closing it now, right? So question one, the answer is um most people got it right? Needle shaped crystals which are negatively buyer. Efren Geant. Uh The way to remember it is needle and negatively, they're both ends. And if you remember the image, they look like pins, they look like knives. So if you put them all together, you'll, you'll remember it that way. And the one person put rhomboid shaped crystals positively by reference Geant that is pseudogout. So gout is more common end end just works well together. So, per N N and gout together and the other one is pseudogout and question to sign of your sites is the right answer. Um This is rheumatoid arthritis. You get anti CCP and rheumatoid factor binding to the sino via sites leading to proliferation and inflammation of the synovium. It does this through um T cell and B cell activation, but you don't often get proliferation of T cells and B cells in uh rheumatoid arthritis. Cool. We will move on to down. So skin, like I said, you probably had loads of teaching on on down this year. Every dermatologist love going through the layers of the skin, quick recap. You've got the stratum corneum granulosa, um spin ocean and basil. The way I like to remember it is C G of the first to like Chicago grill on FPR spinous um is the spine. So it's like proper body. Well, in there, it's near the bottom and basil base right at the bottom. I got two questions quickly. Sorry if it feels a little bit rushed. Been a while. Sure, people to get a bit hungry as well. We'll give you 15 seconds and I'll close the pole. I'm going to close the pole in three seconds. Get your answers in closing coal now. Okay. Question one. Uh patient with malignant melanoma, which the following is associated with the worst prognosis. The answer is e depth. Although a two D are, are pretty bad. Um The depth of the malignant melanoma corresponds to Breslow thickness, which itself has been proven to be associated with the worst prognosis. Because the deeper the malignant melanoma goes, the more likely it is to metastasize, more likely it is to invade. It's local structures. Question too. And most people put bullous pemphigoid really tricky question. The answer is pemphigus, vulgaris, you often get a lot of people get really confused between the two. Um But hopefully, when I go through it in the next couple of slides, it will be a lot, a lot more clear. There's quite a few buzz words in this question too. And I'll try and give you a good way to remember it. So once again, we're done, you've got two different types of skin lesions. You've got inflammatory and you've got cancer. Well, just approach each one. So first is eczema. Uh There's two different theories about why eczema might be happening. You've got inside out theory and the outside, in theory, with the inside out theory, you've got the body's own reaction to internal I G which leads to dysfunction within the skin leading to eczema or you have the outside in theory, which is when the body reacts to two different allergens on the skin surface, which leads to I G E um sensitization and therefore an allergic response on the skin. Eczema is caused by mutations in the Filaggrin gene. Uh And it can be type one or type four hypersensitivity. If it's type one, that's your classic eczema. If it's type four, it's more likely to be contact eczema appears after a couple of days. For example, if someone wears a new watch and to get dermatitis around their wrist, that's type four, it usually occurs after a few days. It's more environmental. Um, it's more due to exposures at work as well. If you wanted to do a biopsy of the skin, you get thickening of the epidermis and spongy aosis, which is specific inflammation within the epidermis and fluid um collections which are pathological for inflammation. So thickening of the epidermis and spongy osis are your two key histopathological features of eczema psoriasis. Uh It's caused by T cell hyper reactivity within the epidermis that leads to proliferation of the carotid sites, which are the cells within the epidermis leading to epidermal thickening. Buzz word for psoriasis is para keratosis, which is release of lots of keratin proliferation of karate insights. You also get epidermal thickening recruitment of neutrophils. And if you rub a psoriatic plaque, you may get bleeding, which is called out spit sign. There are a few different types of psoriasis. Uh you can look at this in your own time. Now, the difference is between bullous pemphigoid and pemphigus vulgaris. The way I remember it is bullous, pemphigoid has bulla that are very, very difficult to break or to burst, which means that the buller must be really, really strong. And because the bullet are really, really strong, the word bulla is deserving in the name of the disease. Therefore, it's bullous pemphigoid. In comparison with pemphigus, vulgaris, the buller are very weak, you can break them, they can rip apart so they're not very strong. Therefore, the word bulla is not in the name. That's the way I remember it. Um If anyone has any better ideas, you can work them in the chat for everyone else, too. Bullous pemphigoid, you get an autoimmune reaction to adhesion molecules within the basement membrane of the epidermis. So the epidermis lifts up, there's a space between the epidermis and the dermis. Lots of fluid collects in there and that's the buller because it's protected by the epidermis. It's really difficult to burst. It's really difficult to rub it away with pemphigus, vulgaris. You get an autoimmune response to the adhesion molecules within the epidermis. So it's intra epidermal because it's a bit more superficial, you can easily rub it off. Therefore, they're very weak. Um the bowlers are there and then they're gone. So they don't have the word bulla in the name. Another one, pemphigus fallacious affects the elderly population. This is on the really superficial side of the epidermis. You get autoimmune reaction against the superficial keratinocytes which are then detached. This is just a quick summary slide of everything. Very, basically the antibodies, what they're targeting which layer of the skin and the result okay. I in the interest of time, I won't go through this. This is like the ovarian cyst um table and another one of the tables in the middle. This basically tells you the differences between basal cell carcinoma, squamous cell carcinoma and Melanoma. Basal cell carcinomas are the most common and Melanomas, the prognostic feature that's really important, Breslin's thickness. The most common Melanoma is superficial spreading. So that question came up in uh path exam last year. Melanoma's are more likely to metastasize. Therefore, they're prognosis is very bad. Whereas basal cell carcinomas, they're very slow growing, the indolent, they're unlikely to metastasize and they're not usually that bad. This is what all three looks like microscopically as well as microscopically. Uh If you look at the Melanoma one, you can see a proliferation of melanocytes um within or just above the basement membrane, a little bit darker purple and obviously basal cell carcinoma. Yeah. Proliferation of basal cells, squamous cell carcinoma. Yeah, proliferation of keratinous sites. So last bit of the lecture is just two more questions and then you're done. You don't have to listen to my voice again. I'll give you guys a minute, minute and a half uh for this and then we are done 30 more seconds, 10 more seconds, closing the poll in three seconds to born. OK. Polls closed. Good. Most of you got the right answer, which is C for number one, this patient, uh his boy probably has uh psoriasis. He's also got nail changes. Um So he's got a nickel isis and uh I can't remember what the white spots are, but basically the nail changes of psoriasis. When you got psoriasis, you've got t cell activation leading to proliferation of karate know sites and deposition of keratin within the epidermis ache. A hyper keratosis, filaggrin gene mutation associated with eczema. You wouldn't see on a biopsy, spongiosis associated with eczema can also happen psoriasis. Um but more associated with eczema, epidermal necrolysis is a dermatological emergency, raindrop lesion's associated with um got a psoriasis which this person doesn't have uh because it's been six months, they don't have a current infection. Question. Be superficial spreading is the most common type of malignant melanoma. Um Important to just remember the superficial spreading, nodular um lentigo malignant and all indigenous. So just remember a couple of them superficial spreading the most common, but it's nodular, it's probably gonna be worse because it's going to be have some depth to it too. So you can just think about it like that. Um You'll be really good for the skin. So that is the end of the lecture. Apologies. It's quite, quite long. Uh We covered the first three sections in a lot of detail, went through the last two sections a little bit quicker. But hopefully, you can see that histopathology is basically just understanding how diseases happen, what they look like and how they might present on a patient you don't have to know slides and specimens for the exam, but it helps you understand what is happening within the body. And I hope this exam goes really well for you guys. I know Johnny's giving a lecture on the other half of histopathologic, which I might say is probably more likely to come up because it's your cardio rest gastro that stuff is always going to come up a little bit more. Um So make sure you turn that lecture or watch it online. Any other questions? Drop me a message. Thanks to you guys for staying so late as well. Really appreciate to, I know you guys probably have a lot of the things they don't choose. They're not anyway, such as Sebastian. Thanks, Teresa. Fantastic lecture. It was a pretty comprehensive it and I think you could uh decently well and the amount of time that you had as well, so much a lot to cover. But I think the question is uh facilitate learning are pretty good as well. So again, thank you for giving every time as well. I know you're on holiday as well. So I really appreciate it. If anyone has any burning questions, if you can work from the chat now for Therese doesn't mind answering, but if not you feel free to look at that now, then please fill out the feedback as well guys. Thank you. We really appreciate it. It doesn't seem to be any questions I can't see any, it doesn't seem to be so I'll stop the recording then.