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I've been looking at the timetables recently. You guys have progress tests and mo so close to each other. I do not envy that. I hope preparation for it is going well, I'll just wait a few minutes. I'm just gonna send out a, um, a poll now because we have, um, uh, we have, um, this is supposed to be our last session before the Mock Iski. Um, but, uh, just sort of, I feel like that everything sort of ramps up in the next couple of weeks before the ISK and then we'll start again after the mock. Uh, I'm just wondering if you think it would be useful to have a, um, uh, a session where we just, uh, I just set out some example stations. So it would have the history itself. So I'd ask, what kind of questions would you want to ask? Then we'd go through what differentials we think we've got, um, investigations and how we describe that in the exam management. Um, I appreciate that. It's not one on one practice. I think a lot of other societies already practiced that. But since it's pretty much just me, it's just a little bit more difficult to do that. Um, uh, I am considering doing it later on before the is at the end, um, where it will just be some, one on one practice for like one or two stations that will just be on Zoom just to, so you can have a bit of a practice. Um, seems like the answer seems like. Yeah, so far we'll keep it up and see what people think. Um, You can say. No, I don't mind. I just, uh I hadn't really considered it before and I was like, you know what that would have been useful to me. Um, just cos it's a low stakes environment. Um No one can see what you're saying, cos it will be on men Yahoo or something. Um But you still get to practice it. We could then do a bit of a summary as well. Cos I know that a few people have been asking for more actual teaching on the conditions which I was just gonna push back and back until sort of near the is, but I can see only eight people who have responded to it. I'm assuming new people can see it as they join. Um But I've just got that poll and chat. If you can't see it, that would be great. Um Also can somebody just react to that to just tell me that you can hear me cos I'm assuming that there's a lot of people on the other end of this going. Yes, that sounds like a great idea or no, but I just need to, I just need to know if it's actually going through. Brilliant. Thank you. Um OK. Um All right. So I've put on the screen here, um put on the screen here. Um The mental code for today. Um This session is a, a lot more interactive. I've tried to keep the questions a bit more open because I would like to have a bit more of a chat sort of back and forwards about what you guys actually think. But I appreciate if you've not got, if it has your name associated with it, it's just embarrassing. Um So, oh, sorry, I just raised the chat wasn't available. So, um, yeah. Uh I can, it's kind of embarrassing sometimes you don't want to put your, your name out there with an answer just in case it's wrong, which you shouldn't be worried about being wrong. It's OK to be wrong. It's you were here to learn. Um, but you know, the vibe of some people is not that, you know, it's just sometimes a little bit uncomfy, but I want to have more interactions. That's why I've gone with the, the ment style. But if you want to put stuff in the chat, that's 100% fine. I can see that at the same time, I can't see the chat on ment for some reason, cos they appear and disappear. So the chat on here is better. But if you have something to say and I've not asked it, just put it on the slide, I will see it. Um, so I will put the, um, the ment code in the chart as well so that we all have it, but I am going to start 89406 going to start so that we can get on with everybody's evening. Um, so the first question that I put on the men, which for some reason I've not put the ment code actually on this slide, er was just what are people's concerns about data interpretation. Um It's something that you probably start been doing for several years now, but there's just something a little bit more nerve wracking when you're presenting it and putting your sort of stakes behind it in an in an is today we're focusing specifically on blood test results. Um And we've got, we're gonna do some on imaging ahead of the ey. Uh The reason that we've done blood test results is just that blood test results are more common come up. Um So let's have a look at what people are saying again, put it in the chat, put it on the mentor if you want, either way is fine. Um So I'm gonna pop this over here so we can see it. We go um So biggest concern about data interpreting, not having a clue what I'm looking at or where to start interpreting. Yeah, 100%. Um, everyone's biggest fear. I think that's worse with imaging as well if you were presented with imaging and you're like it looks normal but you're expecting it to be abnormal. That's always kind of worrying. Um, imaging sometimes just can't see anything. Yep, 100% double do imaging, ah, seems like that imaging one's gonna be really useful then. Um, looking at, I have no idea what's going on. Yeah, doing it under time pressure, not knowing what results may in turn the diagnosis. Yeah, just feel like I'm just saying what it says. Yeah, and that's actually something that we're gonna talk about is I think it's actually really useful. Um, even when you're looking at imaging, if you don't know how to interpret imaging, um just talking about what you can see shows that you're not just completely blank behind the eyes, right? If you're looking at an image and you have no idea what's going on, telling me what you can see. Um, or even what you can't see is really useful. Um I think I told you, I know this session is about imaging but I think I told you, er, a few times now in my ey patient history sounded like CO PD sounded like infective exacerbation of CO PD presented me with a chest X ray and I looked at it and I was like, this looks normal. I go through, I'm like, OK, I uh there's no evidence of pleural fusion, cardiac shadow looks fine, but it's an ap view all of that. And then they said, how would you manage an infective exacerbation of CO PD? And I looked back at this chest X ray with the context of knowing I was right when I said, I thought it might be CO PD the first time round and I look at it, I'm like, oh this is a hyper expanded chest and, but the only difference between me knowing that and not knowing that was the examiner saying, yeah, your diagnosis was right. And then I was like, oh, but now I can see it, I did point it out and I said, oh, that, that explains the hyperexpansion on the chest X ray despite the fact that I wasn't going to get any marks for it or the flattened diaphragm, despite the fact that I may or may not have actually got marks for it. I've just pointed to like I am thinking about what's going on. Yeah, sounding silly. There's another one. So the main thing that it comes to in excuse is is sounding confident being safe. Um And I think a large part of coming across as confident is having a clear structure so that it's clear that you know what you're talking about and going through, you've clear that you've done this before. Um It's a really scary place to do it, but on the wards or in GP is a really good place to do it where if you just tell whoever you're shadowing just before the ward round or before the day starts or anything, like I need to practice doing blood test results. Preface it with, I'm not very good, so I'm not very good, but I need to practice it. Do you mind if I present a couple of findings to you today and then just whatever patient you come across, just have a go at it. Um That's really useful. Um Because that way you'll learn how individual doctors do it too. Um And learning each individual doctor's like specific way of doing something is how you, how you, you want little bits from everyone. Like I saw somebody recently who, when they stick the form onto a blood test form, that little yellow bit that you peel off, they stick it back to it. So you don't have to put it in the bin. And I was like, oh, that's amazing. But I never would have done that if I wasn't paying attention to the doctor at the time. Um ok, so let's try and make sure that we don't sound silly and then we know what's going on. Um This thing as normal. This is where we are at the moment, imaging one sort of towards the end and then we'll do that big one at the end. Um I can see somebody said that they might want to do that session, if you're happy to either email me about it or something, whatever it would be that would make you interested in that session. Do just let me know. Um, but yes, we'll consider doing one in two weeks just to go through some common stations. So probably in here somewhere. Ok. Again, CBD, stuff, like I said, in the email, everybody who has sent me a CBD should have had an email back with the response to your CBD. If you have not, please send it again, I'm not intentionally ignoring you and if anybody else wants to send them through, please do right. Um So today we're going through FBC S LFT S using ETF TS and then how to present this specifically in an S station and then we're going through the example stations, we're gonna go through them as we go. Um All right. So data interpretation in uh the step by step that I would recommend to go through is to first read out your patient details, the type of test and the date this is just at the top of all of the pieces of paper that you are given. This is a pos fail part of this station. It is a red flag if you do not do this right. Er I did it in my mock ski and they were like, oh, you'll never make that mistake again and I made it immediately after on the next station. Um So it just really makes sure that you've got it in your head that you just read it out every time, then read out individually in normal language, whether each test is high, low and what those values are. This is useful to show the examiner. I am looking at the blood test results. It is useful for you because it gives you time to interpret what you're looking at and it makes sure that you don't miss anything because you have to read out all of them, then summarize everything you've just talked about in the technical terms. And then one of two things link that to your primary differential diagnosis or your new differential diagnosis. If it's changed or say, I don't know and that you would seek help from a senior. Um Sorry, I'm just checking that there's no comments. Um So how does that actually look in practice? Well, these are the full blood count test results for patient name. I would double check their date of birth with them. The date on the form is this date that's important because if that date was two years ago, I'm probably going to say I would see if there is a more recent one and if it's very recent, I would say I would see if there is a previous one to compare it to. So if it's a long time ago, is there more recent and if it's now, is there one to compare it to? You can't ever really interpret results from a patient without previous results because it may just be normal for them. So that the hemoglobin is low at 89 and the mean cell volume is high at 100 and five with a low B12 at 140. Everything else is within normal range. So whatever it was, I might read them out and then say the white blood cell count and the C RP are within normal range. I've not said they're normal. I've said they're within normal range because they may be abnormal for the patient. Then I've described that in our technical terms, this represents a macrocytic anemia. And then you can say this supports my most likely diagnosis of B12 deficiency or as I'm still unsure of the main differential diagnosis, I'd like to consult my senior with these blood test results using an SBAR approach. Now, hopefully you can see that that answer is not the same as I don't know. Right. You've told me specifically like, yeah, I don't know. But the important thing is what would an F one doctor do? What is safe and what were you able to do? And so you need to then say, well, if I don't know w what am I gonna do? Just give up, not interpret the blood test results. No, you're gonna do something with them. So I'm unsure, I'm gonna consult my senior. How am I gonna do that? I'm gonna use sbar So hopefully that all makes sense. Um We don't see any contra so far. If you have any comments or other, please do just put them in the chat. Um or on the, on the slider, we'll see them. Um But that's the basically the presentation that we're gonna wanna focus with. Same thing goes for imaging. Um And again, it's fine to say you don't know with imaging, just tell me where you're going next. Even if you, if you think yes, this sounds like B12 deficiency, but you're not sure you say this. Th this supports a diagnosis of B12 deficiency, but I'm shit still unsure that this is the most likely diagnosis. Therefore, I would like to consult my senior. OK. So hopefully I've left that up long enough for people who want to take notes, have taken notes or taken a picture. So let's work through them step by step. Now, FBC S you are probably all very familiar with at this point. Um But what do we actually need to be able to do and interpret for er an is um we need to know what the most important parts are. Most important bits are gonna be the hemoglobin, the white blood cell count and the platelets overall, it includes more than that. You got hemoglobin, white blood cells, platelets, red blood cell count, hematocrit mean cell volume and mean cell that mean called var hemoglobin. Majority of them not super useful and remember spot diagnoses, right? We need to have them then be easy and quick for people to identify in an, in an, in a, right. So how, how easily can the majority of doctors interpret the MC H on the fly? Not really, they don't really point to um they're not really pointing to specific er, diagnoses or anything. So they're less likely to come up, do bear in mind though, you might also be asked to interpret a differential uh white cell count. So that's your neutrophils, lymphocytes, monocytes, eosinophils and basophils. Um And often you're given CRP and iron studies alongside to be clear, those last two aren't part of the FBC, but they are often given alongside it. If you were presented with blood test results that look like these, you'd be forgiven for saying these are the full blood test results of. But you could just say these are the blood test results for patient name. Okey dokey. So what we've got here then are some main causes for high and low stuff. I focus specifically on the really and common and important ones. And you can see for some of them, I'm still, I'm having to push because a poly, a high hemoglobin is fairly rare. And so would I be surprised if they gave you polycythemia? Yeah. And like povera as a diagnosis in it, I would be surprised by um but you know, I put it on there because if you did see it, that's what I'd be thinking of. So majority of people are fully familiar with. You've got your low hemoglobin. That's things like anemia, common things that will come up gonna be your iron deficiency. Important thing to come up is gonna be a hemorrhage. Don't forget about things like aplastic anemia as well. And leukemias white blood cell counts. Remember, I've put these, these fancy bits in as your technical terms so that you can say, oh there's a low white blood cell count. And then when it comes to the technical count, you say, oh, there's a leucocytopenia. That's why that's there aplastic anemia, leukemia. Now, leukocytosis being your infections, your autoimmune conditions, um platelets, I've put itp on them. I don't think you're gonna get itp again but it PDI C and then high you can get it in infection. You can get it in CO PD as well. OK? Again, this is more for your own notes rather than me teaching you this in this moment, but they're all on. So hemoglobin, I've put on here some common um some common combinations of hemoglobin miso and that sort of thing so that we can try and guess if we were just presented with this, what would our diagnosis be? So there's four on there. Hopefully, 1234 people have a go at interpreting what they think. 123 and four are, some of them are a little bit more rogue than others. Um But I'll just give you a few minutes to have a little look and see what you're able to come up with. Hopefully, the slide has progressed so people can do it. Not had anything come through so far. So I'm hoping that it's all working. OK. Is it clear what my question is or are people just walk through it? OK. I've got one through. So I ii hope that's clear. So my question is, is what is the likely uh diet pathology with a low hemoglobin and a low mean cell volume? OK. Some questions are coming off you. Oh We've also got the Q and A open, by the way on the mentee. So if you have any long term questions, feel free to put them in. Um just whilst like that people are doing that, I can see uh in the chart, er acute inflammatory markers are affected by systemic steroids and immunosuppression. My understanding of that is that it suppresses your C RP. Um Yeah, because it's reducing your inflammatory response. Um But with C RP, you don't really have like a, a lower range for it. So I from my understanding, the majority of studies that have looked into it have looked into patients with a specific infection who were then treated with prednisoLONE or something like that. And essentially the C RP didn't rise as much from memory. I'm pretty sure the white cell counts were higher in patients that had steroids. I'd have to look at them again, but the C RP tended to trend lower than the people who were treated without pre, um, but that is my understanding. I'm not sure you'd be asked that in a, in a Cardiff is. Um, so right. I've got a few. Um, hopefully that is some sort of answer for you in the chart. Um, ok, so we've got some answers through on here. So we've got, I'm gonna push this over here so we can see it. Um So we've got low hemoglobin, low mean cell volume. And so for number one, we've got microcytic anemia. For example, iron deficiency, iron deficiency anemia, uh iron deficiency micro cystic anemia, microcytic anemia, microcytic anemia, iron deficiency anemia. Yes, I agree. We've got a mean cell volume. We've got a low hemoglobin. So number one, this is an anemia and then we've got a low mean cell volume. This is a microcytic anemia. So remember just cystic meaning cell micro, meaning small, most common cause that you will come across of microcytic anemia. In an issue is going to be your iron deficiency anemia. Brilliant. Second one along here. Then number two, we have B12 deficiency or alcohol misuse megaloblastic anemia. Er macrocystic anemia, er macrocytic anemia, macrocytic anemia like B12 deficiency B12 or folate deficiency. Yeah. So this is the opposite. This is a low hemoglobin with a high mean cell volume, which means not very many cells, but they're big. This is a macrocytic anemia. I agree. Most common causes of this are gonna be either your B12 or folate deficiency and also um your alcohol. Um So chronic alcohol use. Um Brilliant. Next one, low hemoglobin, low white blood cell counts and low platelets. So, let's have a look what we've got here. Leukemia, aplastic anemia, pancytopenia, aplastic anemia, uh hemorrhage, myeloprotect dysplastic, something microcytic. Sorry. Yeah. Um Yeah, brilliant. So, yeah, what we have here again, like break your words down. All of them are low. It's pan what are low? The cells cyto and then penia is low. So yeah, this is a pancytopenia, aplastic anemia, leukemia. So all of these are examples of where we're not producing enough of those things. Brilliant. Um And lastly high hemoglobin, normal white blood cells and low platelets. Uh What have we got over here? Um So not sure yet. I think this is the hardest one on here. I just put it on there because I was feeling bad for um uh the high hemoglobin polycythemia thrombocytopenia. It is thrombocytopenia. Yeah, because of the low platelets, polycythemia vera dehydration. Yeah. Um So yeah, this one here, that's the most classic quote unquote presentation of polycythemia where you've got a high hemoglobin and you have your white cells are unaffected. This isn't an effective or inflammatory thing, but you have low platelets. Um This is a difficult, if this is not really one of those like easy to get spot diagnoses that you get in a history. This is one that would take prolonged sort of investigations to figure out. Um, but just in case they give you a polycythemia, it's as a version of itp, that's what you're looking for. It's high hemoglobin. There aren't very many causes of high hemoglobin. Um, yeah, the reason why it might not be dehydration is the reason that dehydration makes the hemoglobin look high is cos you've decreased the volume inside the blood. So comparatively, it seems super concentrated. So the platelets would also go up or be normal. Uh It would be unlikely for them to go low. Hopefully, that makes sense. Um uh I've put here as well. The red one being the dangerous important one, not that other kinds of anemia can't be dangerous, but this is a proper red flag and I'd be wanting to get a senior involved quickly. So let's have a look at the white blood cell. So I've moved the slow on again again if you want to put these in the chart on the thing here. Uh Oh Sorry. OK. Um So um same thing again, but white blood cells. So what sort of pathologies are we looking at when we see these combinations? This from my perspective is the worst part of the F BCI think generally the full blood count is fine, but when it comes to these more complicated ones. So just whilst people are doing that in the chat, are you asking, are you asking if I have a patient who's got a high E sr cos I have like polymyalgia or, or something like that, if I give steroids will, what will happen to it? Are you asking if I give steroids in general health? What would happen to the E sr um and yes, feedback form pop that through. Now, I also, it also should pop up whenever you leave the thing and the slides will be available afterwards. Just I don't know about you guys, but I would sit here and take a picture of all of these slides and never look at the pictures again. Um So they should go up afterwards. So what did these combinations cause? So yeah, if, if, if the question is what would happen to the E sr the E sr should drop as well? Bezoar, I've got a couple of answers through. I'll just wait a few more minutes even if you're not actually interacting on mental or anywhere. Um um Then just have a think about it for yourself. Like what if you were presented with that in an exam? What you were actually thinking? Um Yeah, if you um in the chat about the previous recording and slides, if you want to uh email me and let me know which one it is that you're missing, they should be on there if you've done in, done the feedback form. But I know sometimes it doesn't upload properly. So just let me know. Um, ok. All right. So we got a few answers through, let's have a little look. So, um high white blood cell count, high C RP. So, one infection, infection, infection or inflammation, active infection, infection or inflammation. Yeah, this is the one that I would want to get in an exam and it's the one that you are most likely to get to an exam because an infection of any kind is very easy. Um, to, to give you a history about right. They just say that they've had a cough for a couple of days or that they've got dysuria or they've got vomiting and diarrhea like it's, it's very easy to give a history for that. Um Yep. So that's very common. Then we've got low white blood cells, low hemoglobin, low platelets. Um I've put this on here. People have said this very similar thing. I've put this on here because again, it's still affecting those white blood cells, but this is the same as the previous, it's a pancytopenia. So it can be like an aplastic anemia or an acute acute leukemia. Let's look at the next one. My email is in chat, by the way. Um The next one then w high white blood cells, low lymphocytes and high neutrophils. So this has got that differential white cell count involved. What have we got bacterial infection, chronic myeloid leukemia, acute myeloid leukemia, uh bacterial infection, uh bacterial infection. Yeah. So these are the ones that II think are quite challenging. Um I think they're all quite challenging themselves. Um, but this is a chronic myeloid leukemia. So I'll talk a little bit about it in a second. But, um, can, does anyone in that, in that same chat there anyone tell me why that's myeloid rather than lymphocytic. Why is that a myeloid leukemia? Yeah. So someone's had a lot of messed up neutrophils which are myeloid cells. Yeah. So basically, it's just your ability to know which ones are your myeloid versus your lymphocytic lineage. Um And yeah, so essentially the ones that I specifically look at again, the quick and dirty tricks. I'm not necessarily sure the what I would go to a hematologist with, but your neutrophils are myeloid, your lymphocytes are lymphocytic. So those are the main two that I'm going to be looking at when I'm trying to figure out what type of leukemia it is. So, since we've got high neutrophils, then it has to be myeloid. I'm assuming them people are clocking onto what the next one is. Um uh where we've got high lymphocytes but low neutrophils. So that therefore has to be lymphocytic. This could also be lymphoma because path pathologically fairly similar. Um somebody asked, no, no, nobody asked when we're talking. Therefore, to compare this with the acute stuff. So we know why these are myeloid and lymphocytic. Does anybody know how we can tell the difference between acute and not acute. And again I put these on here because they are hard. I do not expect you to be given these in an ey, but I don't want you to go into it and I didn't talk about it. Why are those chronic? Not acute? I'll only wait a few steps because I know that it's a, sucks. Yeah, it's the, yeah, immature versus mature cells. Yeah. So that's exactly it. So, the reason that our, uh, these are gonna be our chronic ones, um, is that these are the chronic, allows the development of mature cells which starts to actually affect the white blood cell count in the acute phase. Some of them won't count as the specific type of white blood cells that you're looking at. Um, cos you're not looking at lymphocytes, for example, you're looking at lymphoblasts and you're not looking at neutrophils, you're looking at myeloblasts. I don't know if that's making much sense. Um, so the main way, so what you'd see in the acute ones are going to be the l like an like your acute leukemia. So it's gonna be those low, low white blood cells, low hemoglobin, low platelets. Whereas in your chronic ones, they've started to count as real white blood cells. So how would you functionally tell the difference in real life if you're looking at either one of these? And you're like, 00, something's going wrong here, you're gonna do a peripheral blood smear and you'd look at those cells and then you would look at them and really, obviously, it would either be these are immature cells or mature cells. But the majority of acute leukemia patients are gonna be presenting with low white blood cells rather than high white blood cells. Is that making sense? Yeah. Yeah. Ok. Seems like people on the question are, are on board. I'll wait here for a second to wait. Um All cool with that. Hopefully. Yeah. Where's your lymphomas? I'm gonna show you increased lymphocytes and then different kinds of lymphocytes depending on what type you're looking at. OK. I'm gonna assume that we are happy with that because nobody's putting anything in. If you're not happy with it, pop it in the Q and A but essentially acute leukemia is low. Everything and then chronic leukemia will have some things high because they start becoming older. They're older cells because it's chronic. Your myeloid is your neutrophils. Your lymphocytic is your lymphocytes? OK. What's next playlets? Only two for this one? There's two on there. Low platelets, normal hemoglobin, normal white blood cell counts, low platelets, low hemoglobin, normal white blood cell count. What are these put this over here so that we can see as they come through. Mhm Honestly, I've literally only put this side in because of my a ski. I would never have put this in if I had, if I was doing a ski teaching before, I'd done the exam. I know I would be, I would never have put in a side on plane. Um Yeah, so they are both have an example of thrombocytopenia. Yeah, this is an example of anemia with normal white blood cell count. So if you wanna describe it, remember we're gonna describe it in like normal human words. First, the top one, an isolated drop in platelets is itp, that's why I TPS. It's either immune or idiopathic thrombocytopenia like low thrombocytes. Just the other one got low platelets and also anemia just wanna know what that is. Cos that to me is it sort of seems like you're bleeding, right. Hemoglobin's gone down, gone down and your clotting factors have been used up. Your, your platelets are being used up. What is that? Sometimes there can be a raised white cell count in it. It's not a nice thing. It's a, it's a scary emergency one. Anyone there. So, yeah, I would expect with autoimmune hemolysis, the platelets I would do, it would have to be chronic before I expect them to go down D IC. Yeah. So basically the difference between the two, the two is with D IC. Well, there's other differences with D IC. It's uncontrolled use of clotting factors. Whereas there's nothing wrong with the platelets in auto autoimmune hemolysis. There's something wrong with the red blood cells or the um, the antibodies are attacking the red blood cells. So, yes, the platelets will be used up. Just not like us to a severe degree. So would I say that that's a reasonable differential. Yes, 100%. But the big scary one I'm looking at for this one is gonna be D ICI. Hope that makes sense. Uh But yes, that's the trauma flight. Um, so ITP is just been by themselves. So you can see in this, in the scenario of what we had last year was a pediatric case child comes in with um increased bleeding and bruising is worried about cancer if a child comes in and says that to me, I am also worried about cancer, right? That sounds like leukemia to me when I'm presented with the one with the the blood test results. The only thing that has changed is the platelets, the hemoglobin is fine, the white blood cells are fine. So that's pointing me away from both my chronic and my acute leukemias. It's pointing me away from lymphoma. The only thing that's gonna just change those platelets is gonna be itp. OK? So what I have then is three cases on full blood counts. So we've not got a history here. We just have the blood test results in your head. How would you present this in your I remember patient details, talk it through step by step. Summarize it with technical terms. What is your top differential? Right? Practice that to yourself and then pop on the mentee or pop in the chat or what do you think this diagnosis is. So somebody has asked in what I would describe as harsh fashion, why does D IC cause low hemoglobin? Um So what, what happens in D IC is you've got uncontrolled activation of coagulation. So you get loads and loads of small clots, these block your blood flow, you get ischemia. This is then using up all of your clotting factors and it uses up your platelets, but then you've got build up of blood behind obstructions, um and no clotting factors. So any small amount of uh injury or trauma, both internal and external is then going to cause bleeding with no clotting factors, no platelets. And so that's what's gonna cause your low hemoglobin is just your blood, your bleeding, you're bleeding everywhere. Um Yeah. Um you've also got um slightly separately just whilst we're waiting for more people to pop in their answers. You also get um hemodilution. Um You get a bunch of fluid shifts um because of the changes because all of your closing factors are being used up, um which overall decreases the concentration of your hemoglobin despite, well, the hemoglobin is going down cos you're bleeding. But despite there being a fairly slowly decreasing, it will seem lower than it actually is, but the patients will be really unwell as well. Like in front of you, a patient with ITP and a patient with D IC would look completely different. Um Right. Uh I hope that answers if it doesn't again, just pop in that Q and A um say O um Right. OK. Yeah. So let's have a look at this one. So how are we going to interpret these? We are going to start off with just reading out the patient information. Um So these are the full, this is the full blood count test results for Mr patient name and I'm gonna double check that date of birth with my patient. Um I gave all of them the same birthday of today. Um which means that I haven't put any of the dates, but I would double check the date that this was taken. Um We're then gonna read it through step by step. So there's a low hemoglobin at 100 and T 10, low mean cell volume at 76 with normal white cell count. Oh, or white cell counts and platelets within normal reference ranges as best you can try to avoid abbreviations. Um A lot of examiners don't really like it. Um And so then that's my question to you is what do we think it is? And we've got iron deficiency anemia, iron anemia, microcytic anemia, iron deficiency, microcytic anemia. And then a lovely list of all the causes of microcytic anemia. Somebody's been on past med. Um Congratulations. Um I always forget lead poisoning as well. Oh, well, um check date of birth blood results for. No. Yes, there we go. So brilliant. So we've talked through it all step by step. And then we're summarizing using our technical terms. This represents a microcytic dynia which points towards my primary differential diagnosis of. Hopefully, we know our primary differential diagnosis from our history. If we don't, this is the point to make that primary differential diagnosis. And you've all given me brilliant examples of examples of causes of microcytic anemia. Brilliant. OK. So I'm gonna put on to the next slide. This is another full blood count interpretation here. Have a go at that one. Let me move to the next slide. Have a go at this one again. Think to yourself. How would you present this in an IY if that is what they give you just whilst people are doing that, somebody's asked in the chat, could the last one on the white blood. So slide also have been myeloma. Um Can I go back to see what was on the other side? Well, I'm not sure what the last one was on the white blood cell count slide. However, for myeloma, I would be looking for anemia, thrombocytopenia and then like a normal or a high white blood cell count. So that, that sounds vaguely familiar to one of them. So yes, but then have a think to yourself. What, what are the typical presenting symptoms of myeloma that you'd be thinking of as well? Um Going into that you don't have to answer that to me and I hope what your answer to yourself is to do with crap. Yeah. So hypercalcemia, renal insufficiency, anemia and then bony pain. Um I think some people also change it to Kr Krabi and I think the eye is for infection. Um But yes, if that's what the white blood cell count that could be by me. Yeah. Um All right, let's look at this one then. So as I present this, I would say these are the blood test results of missed patient name, date of birth there. I would check that with my patient just gonna double check the dates that these were done and compare them to a previous one. Looking at the hemoglobin here. Um The um white cell count is raised at 13.2. The CRP is raised at 100 and 10. The hemoglobin, the platelets are with no within normal ranges. Looking at what people have said over here, what do we think this is high white cell counts and ra CRP is infection infection, acute infection infect presentation. I agree. Oop, this is leukocytosis with raised inflammatory markers indicating an ongoing infection which is consistent with my primary diagnosis of community acquired pneumonia. Hopefully, this is sort of making sense about just getting into that same structure. And if you're practicing the structure that I'm talking about here, hopefully you can see the time that it gives you as you go through. So you just, you say it in normal words first, which gives you the ability to go. Ok. Well, it's got high white cell counts. That's leukocytosis, got ray cop those are inflammatory markers just to help structure it just as you're going through because it shows that not only are you going through all of them, you're not missing anything. You can summarize what you've been told and then you can link it to something else. Don't forget that it is OK to not know, just be honest. And like I said, use that bit of script that I talked about earlier saying that you talk to a senior last one for full blood count. Then what have we got here? What? And you haven't got any ideas, I'll talk it through as people are typing. So these are the full blood test results for Mr patient name, double check the date of birth of my patient and check the date of these results present. There is a low hemoglobin at 100 and five high white cell count at 25.3 and high platelets at 520. We've got one response so far, infective exacerbation of COPD anemia, chronic disease. Anybody else got anything to add? That's OK. So remember even if we have no idea what this diagnosis is, we are going to describe it with our fancy terms. So this re represents an anemia alongside a very high leukocytosis and a thrombocytosis. This points towards my likelihood diagnosis of. So, oops, what are we thinking? Then? Where's that? We've got an anemia leukocytosis. Yeah, malignancy. So, this is a, this is more of a cancer picture, right? Um, I've not given you any of the stuff specifically about which cells are up, but we're concerned here because we've got both white blood cells up and we've got platelets up. So, in my mind we're thinking about something myeloid here. This to me looks like chronic myeloid leukemia. But again, I'm bringing these up because these ones are hard, right? Not bringing them up because I think they're gonna come up, but it's worth seeing. And hopefully a few of you all sitting there going ah I don't know what that is. So what would you say? You would say this represents anemia alongside a very high leukocytosis and thrombocytosis. I don't know what the most likely diagnosis is at this point. So I would take these blood test results and present them to my senior with an sbar approach for their advice, right? But yeah, CML is our most likely diagnosis for this one, right? Use the knees. We may have to split this into two. It's going a bit slower than I was expecting. We'll see. So the most important bits of our urine electrolytes are sodium, potassium, urea and creatinine, which is basically all of it. Um The other thing is you got is you've got eg fr and sometimes you have some other electrolytes in there. Broadly, we are just trying to identify, are there any life threatening electrolyte? Imbalances. And is there an AK I? Those are the two main things we're getting out of? There are other things. But the main things we're looking out for is electrolytes. Is there any care? So, for our sodium and our potassium, these are our main things that we've got on here. Just remember that our hyperkalaemia here is the most important life threatening. One is the most likely one you'll be asked about. Um um I don't think that the majority of these things would come up in terms of Con Syndrome. Cushing's syndrome might. Addison's might, but I just think it would be a little bit nasty but I find those really hard to learn. Um which is why I've put them on here because I like to think it's not just me. Um So they're on here. They have very nice combinations of things. So when you see them, you should learn the pattern. So you instantly go. That's what I'm looking at again. This one here is more for your notes than for anything else. I'm not gonna talk through all of them and then we've got our urea, a creatinine and a eeg fr um You don't really have low urea and low creatinine. You can, you know, you don't really have a high EGFR again, you can. But yeah, it's not, it's not really worth talking about. Remember the important one with a high with your urea is just think about your gi bleeding it's a product of a breakdown of protein. Uh So if you have somebody who eats a lot of red meat, they might have high urea levels in the blood. But also if they've had an upper gi bleed and they're digesting that protein within the blood. Um But here, creatinine will also go up in rhabdo. But your creatinine or creatine kinase is a better measure of uh rab. OK. So let's go on. So, here we go. These are all presentations of things. Um What do we think is a exclusive this one? So what do we think these are representing? Now we're focusing specific thing specific specifically on your creatinine. Why do I think that that's CML? I think that that's CML because so the hemoglobin in chronic myeloid leukemia can be variable can be normal, low or high. Um But commonly leukemia will present with an anemia. The white blood cell count is up, our platelet count is up and platelets and white blood cells means we've got. So, so myeloid, the myeloid lineage is platelets, red blood cells, uh mast cells, basophils, neutrophils, eosinophils, monocytes, macrophages, right? So, the fact that you've got raised platelets and raised white cells to me is saying this has to be myeloid. Whereas if you've got raised white cells but not raised platelets, then that doesn't, that means that it has to be lymphoid. I get no feedback cos I'm just talking to the void. But hopefully that makes sense. Um, and, yeah, so, as you get the overproduction of some cells, that's why the an, the anemia will sometimes come about despite being from the myeloid progenitors is that you're overproducing those lymphocytes, you're overproducing those thrombocytes. Not all patients with CML will present with all three up. But that's how I know it's gonna be a myeloid one and it's not acute because the white cells were up. I hope that makes sense. OK. I've got one response through. So I'm gonna go through. No. Um ah there we have two. So what we've got achy eye, achy eye. I agree. High urea, high creatinine. That's our really classic one for an ache eye. It could also be for C KD. Er next one. We've got a super high urea and a high creatinine. Um few different ones, few different answers here. So high stage AK I prerenal AK or upper gi bleed a gi bleed hypovolemia. Yeah. So super high urea compared to creatinine is your dehydration. Um So I agree with a few of these ones here. So prerenal dehydration or hypovolemia. Yeah. Next one, high urea, high creatinine, low calcium, high potassium. And then you can see that the one below it is the exact same and it's got low sodium in it. What is this already? Just this first two anyone high urea, high creatinine AK I Yes. Good job. So this here is just this top one, right? AK IC KD So our question is, well, what's the difference between these two? So one of them's gonna be AK I and one of them is gonna be KD. The question is really asking you, are you aware of the main low electrolyte and abnormalities that come across with those two causes? And essentially our CKD has low calcium and A is tend to cause low sodium. Um So a low calcium in a patient with kidney failure indicates how chronic the disease is. I think the C for calcium and C for chronic. Thank you for that. Thumbs up. Um OK, I will move to the next one. Again. These are for notes, hopefully our sodium and potassium then have another brush at this. This one that I would hate. High sodium, low potassium, low sodium, high potassium, high potassium, high, low sodium, low potassium, high urea high creatinine. The worst thing to come across. I think I already talked about the white blood cell slide with myeloma that just came through as another new question. But I think that might have been a a glitch. Somebody said, I don't know. Um Just for, yeah, somebody knows. Number three. Number three is Rh though. Yeah, high creatinine kind is with a high potassium as well because potassium's inside your cells, your cells are dying, our potassium gets released. Yeah. Um I read this like um what's that Australian Mermaid show? Clio? What is that? Anyway? It's not important. Cons Addison's rhabdo Addison's. Yeah, so we can see that there's something endocrinological going on here, right? Um And that's basically what going on is just being able to identify the patterns that are going on here. So if we've got high sodium and low potassium versus low sodium and high potassium, this it's H2O it is H2O. Thank you. Er sorry. Um So what I'm thinking about in this case is um aldosterone antagonists are potassium sparing diuretics, they block the effect of aldosterone. So if they block the effect of aldosterone, that is the equivalent of low aldosterone, you get that in Addison's. So if spir spironolactone gives you a high potassium because it's an aldosterone blocker. Addison's gonna give you a high potassium because there is low aldosterone there. On the other hand, cons hyper aldosterone. So if our aldosterone blockers cause high potassium and that's low aldosterone, we're gonna do the opposite. So it's gonna cause low potassium. I am blinking and hoping that someone's like that makes sense. Um And that for me is how I figure out is I figure out the potassium based on the fact I know spironolactone and then I just, the sodium has gone over it. I can explain it again. All right. So we've got spironolactone which I think a lot of people already know side effect is high potassium. It's an aldosterone blocker, which means aldosterone is not working. That means aldosterone is low basically. And if our spironolactone, our aldosterone blocker causes high potassium that are addisons which has low aldosterone will be the same cos an aldosterone blocker is physiologically or functionally the same as low aldosterone. Cos it's blocking the effect of aldosterone or having no aldosterone. So they will cause high potassium. It's Addison's and spironolactone, high potassium because spironolactone is an aldosterone blocker and it was high potassium. If you didn't block the potassium, the aldosterone would cause a low potassium. So our cuts and our cushing's which result in high aldosterone are gonna cause low potassium. Well, I know, I know right. Um Is that, is that clicking? Is that making sense? Yeah. OK. Brilliant. OK. Cool. So we'll move on. I hope that makes sense. Like I think it really sucks but like that's how it works for me. So um we already said everyone already know this one. Brilliant Rhabdo. This isn't the Addison's couldn't be an emergency. I just think it's M rhabdo is more likely. Rhabdo came up in my exam in the medic medication review. One was where Rhabdo came up and this last one though. What do people say for this last one? Not super sure. OK. Low sodium, low potassium, high urea and high creatinine. So this here is vomiting, high urea, high creatinine is you sort of get like a dehydration ak I kind of picture which is what's causing the low sodium and the potassium is because of the hydrogen ions being lost. It's a little bit physiological. But when you, when you're vomiting, you're getting rid of hydrogen ions and your blood becomes super alkalotic. So your, your body goes oh no, we need hydrogen ions. So it swaps potassium K plus in your blood for hydrogen H plus in your cells and they swap like whoop. So the ph in your blood will become more significant, become normalized and the potassium goes into your cells functionally that causes a low potassium in your blood. So if you're ever having anything that reduces the amount of acid, your potassium will also drop down because it will try and replace those lost hydrogen ions. OK? I hope that is all right. What's left? What's this? Oh cases again, just continue to put in your er questions and stuff if you need. So let's have a little look then. So you and your interpretation, what would you do if you were presented with this in um exam, what would you talk through? Just practice it in your head? How would you talk that through? What conclusion would you come to? And I'll put this over here. So we can all see as it comes through. OK? If you got questions just pop down. OK? You got one answer. People agree. People disagree. Maybe you're up there. Tr remember, rub it as well and cause acute tubular necrosis cos the myoglobin gets released. It's toxic to your kidneys. So it will also cause kidney failure. Spiral lax lax stone. Okey dokey. So we've got a few answers in. So how would we present this same thing again? Just read it out. What have we got? There is a high potassium at 5.5 there is a raised urea, at 9.3 there's a raised creatinine at 100 and 25. I've got a lot of artists coming in now. Just pop them on here for everyone's due credit. Um Yep. So what have we got? This represents an acute kidney injury with hyperkalemia which points to my primary differential diagnosis of whatever it is that's causing the AK I or just AK I in terms of dehydration, the urea is quite up, it's not super, super high compared to the creatinine, but it is, it is like I would probably work out a ratio and see how much there's no like hard cut off between like what's dehydration and what's not and people with kidney problems will feel terrible and will, won't drink that much either. Um But yeah, brilliant. I agree with all of these. Could definitely be rab though like I said, got an A A I raised potassium. Potassium might also go up will also sorry, will also go up in a I nice good job with um look at this one. Here we go. Next one again. Continue to put in your questions if you want. What are we thinking? I'll get it pop this over here poop by the way. Just because I've just seen that the email come through. Um, uh, I previously clicked a button or metal that meant like only people who had like a fully registered account could watch the videos. I didn't mean to do that. It's just the default. Um, so what I would recommend is if you miss any of the previous ones have a go and see if you can watch them now because it should be available to just anyone just looking it up. Um But if it's still not working, I'll, I'll send it through. Um So dehydration A I again, what we got? Yeah, anybody else? Thank you. OK. Let's have a look through again. Talk through your, your electrolytes, talk through this. This is what it is. This is the name of the patient date of birth. When did it come in? So there is a slightly raised sodium. 100 and 48 there is a raised urea at 10.2 and there is urea is creatinine 103 and the potassium is within normal ranges. So, can you see in this situation what I mean about the, the, the massive Rais in urea compared to the creatinine. So this is you rise in urea proportionately greater than the rising creatinine alongside a mild hypernatremia pointing towards dehydration. This is also an A I but it's AK I most likely due to dehydration, furamide could be a cause of dehydration. Yes. A salty AK I Yes. Um yeah. Does that all make since I hope so? And I think somebody asked for a picture of this side. So I'm just gonna stand here for one second. Here it is you and e case one. Ok, I'm assuming that was enough time and in terms of this one, you an EK too. But yes AK is, are the most likely things that we're gonna come across pausing here for one more moment for the photo. All right, excellent. Let's go last one for your knees. What we got. I do remember as well just whilst you're thinking and talking to this. Um I said that one of the main ways that I revised for my s my lonely little world um was just me and track GPT. Um and text generators are a really good way to make little practice stations for yourself. Um So you can just ask like create a, a data interpretation station that includes full blood test results and then it will just create one. Um The only thing is is that I wouldn't, I wouldn't trust it for things like management. Um because often a lot of the stuff that it pulls from it. Well, it pulls from random online sources, but we're practicing specifically in the UK. Um And we use no nice guidelines specifically. Let's just be aware of that, right? Any a any answer so far. Ooh, people going bold for Addisons. Uh People must be confident with this, with these use and use things. That's all. Look. So um right again, so sorry, e for this person, date of birth, the date from the thing, what have we got? Well, we've got a low sodium at 100 and 30 a high potassium at 5.6 and we've got a raised er urea 8.1 and a borderline, raised creatinine. So we've got a combination of hyponatremia and hyperkalemia that slightly raised urea um most likely due to um adrenal insufficiency. And you wanna know what we get the urea, you can get an AK I in Addison's disease. You don't wanna know why you would, this is not the sort of Viber you get asked in an esky, by the way, the sort of vibes you get after are set like questions, but I just out of interest, that's fair enough. Um renal hypoperfusion. So um it affects the, it affects the blood supply to the kidney. So not, it's not that anything specifically is being released that is damaging the kidney or anything like that. It's not to do with dehydration. Literally just the blood supply to the kidney goes down and that affects the urea before it affects the creatinine because it's functionally if you don't put enough volume into the kidney, it's basically like dehydration. Yes. So, yes, exactly. So, slightly more physiological than I often go through, but lack of aldosterone, low BP, hypoperfusion. Yeah, somebody else how do I know that this is uh AK I not C KD. So it could be chronic kidney disease. It's just what is more likely AK is, are very common. Chronic kidney disease is less common. Um And for an is what are you gonna be presented with? You're more likely to be presented with an A I? Now, I would for yourself to think for five seconds, how would you tell the difference between A and ACDC D in real life? If you just had the blood test results in front of you, you can't ask the patient, have you got gammy kidneys? I would like to think that you're thinking I would compare this to previous results, right? The only way that I know that kidney failure or uh insufficient kidney function is new is that I look at what it was before and it's different. Um So yeah, you wanna have you wanna compare it? Um How would you c do it specifically if you had a blood test result that had calcium in it? Low calcium is chronic, normal or high calcium would not be chronic kidney disease? I hope that answers your question. But yes, it's it entirely fair enough. They could be CK DSI just think it's less likely, right? I am not going. Oh LFT S. Jeez. OK. LFT S uh how are we feeling? How is, how's stamina right now? Let I also getting hit down in uh good or bad. Let's put it in as a pole and see how people are going on. Cos we can stop this here and I can do, we can split it up or I can keep going. I got LFT S and ABG S that's what's next. But if we wanna split it up, I'm happy to cos I know or we can just start flying through it. So 5050. Ok? Because someone else weigh in and make it right. I'm gonna, it seems like I'm gonna, I'm gonna keep pushing on a little bit and then we'll see and then I'll ask again in like 15 minutes. But we'll try and we'll try and to pick it, pick up the pace cos I know not everybody's engaging on the mentee. So I just wanna make sure that we're being a little bit snappy. OK. Right. LFT. Right. What was important on LFT S? But mostly look at the A LT and Ast now I know people are thinking uh but cholestasis like, yeah, that will also come up. But A LT ast are the most important things that we need to really understand on this. What does the LST LFT S include A LT AST LLP, Bilirubin, gamma G TT and albumin liver function tests are fairly rare to interpret in cardiff is issues, doesn't mean we don't even know it. But broadly, we're looking to see is there liver failure and is there bili obstruction, two things that we're already coming out of it with. So, Ast A LT. All right, let's bash it out. Right. What is this? High A LT and high ast and high A LT? But even higher ast? So proportionally the AST has risen more than the A LT. What is the difference between these two? Yeah. Here we go. So, yeah, something's wrong with the liver. If our liver enzymes are messed up and then something here, if you've got a higher ast than your A LT, this is specifically caused by any sort of liver disease caused by alcohol use. So high A LT and high ast I've written here in, in all my infinite wisdom, hepatocellular injury. Um What does that mean? Hepatitis cirrhosis toxin, induced liver injury, cancer. Those are all things that cause hepatocellular injury, right? Hepatitis cirrhosis, any toxins like paracetamol and cancer. Alcohol also causes high A LT and AST, but characteristically causes a bigger rise in the ast. All right. A LP and GGT. Then what are S for? Oh yeah, that's good. Somebody's just said S for Stella. So Ast for Stella Artois, he I don't drink. What are these? The bottom one's a bit of a rare one, top one, I think majority of people have come across middle one sort of start coming across in year four, honestly. And the third one I think is a little bit rude, rude, rare. So we've got some answers to. So far so far we've got Billy obstruction obstruction, bone, bone problem and alcoholic liver disease. It's through your bone thing. Yeah, it's, it's a bone problem. Yeah, exactly. Um, so, uh, what we've got so far, so I've written here, cholestasis, obstruction is functionally the same thing. But if you've got a different reason that stuff is getting stuck other than obstruction, like you've still got peristalsis happening inside the biliary tree. Right. If that's not functioning, it doesn't really function so good. That's still cholestasis. Um high LP, normal gamma G TT. Yeah, that's, that's bone problem most commonly Paget's disease. But yeah, so A LP is a marker of increased burn, bone turnover. A massively raised A LP in the absence of anything else, any other changes is Paget's disease. So that's you get these osteolytic and osteosclerotic lesions, lot of holes where like the bone like eats away at itself and leaves these really firm margins around the outside. You also get it in fractures. That's why answer of bone problem, bone thing. And then I like this new one that just says bone, it's pretty good. Um All right, fractures would cause it because it's just replacing more bone. Oops, sorry. And yeah, this bone one here, alcohol causes a raised GGT with a normal AP. So those three are the three main things that can come up when you're talking about AP and TT this is the most common one and therefore, I think the most important. This one here is a dangerous one because it could be this, it could just be a fracture as well, but dangerous one cos it could be emergency. This one here rare to come up. They're more likely to ask you about the ast thing. Um, but it doesn't necessarily have to be chronic alcohol use. So, binging will cause this. Ok. I love the bilirubin. Why did do so much on bilirubin if I said it wasn't important, that's a bilirubin there. So we talked about unconjugated and conjugated here. More complicated. Cos we've got more stuff going on. Got one response so far. Oh, there we go. So a little bit on. So somebody said hemolysis, hepatocellular problem, the of the biliary obstruction. Anyone else prehepatic jaundice m liver disease, biliary tree? Yeah. Yeah, I agree. Um So I did them in order, which is probably really smart. Um Yeah, so hepatic and post hepatic meaning number one was the one, the other one. Brilliant, good job. So, yeah, exactly. And I think some people have given specific examples for it. So just as a little overview, your unconjugated bilirubin is what happens when you break down a red blood cell and you munch that hemoglobin it makes unconjugated. He er unconjugated bilirubin um that is like darker and then it, that's what it goes into the, it goes into the gut changes into bilverdin which is like green and then will change into the, the stuff that makes feces brown, right? So, that doesn't dissolve in water. And if you do have a, if you do have a build up of your unconjugated bilirubin, it will get filtered by the kidneys and makes you urinary duck. Um And that happens if it can't get out, it becomes conjugated then in the liver. So if you, there's a fly, sorry, um become conjugated in the liver and that is water solu soluble and that gets excreted in your bile and then it's a small intestine. Um Yeah, and people have given uh causes of everything. Again, the stuff in hepatic to be clear is the same stuff as hepatocellular injury. It's your hepatitis, your cirrhosis, your toxins and your cancers and cholestasis obstruction, something as as somebody said, something wrong with the biliary tree. So case let's go, what have we got here? Any thoughts on this one? Got one response in so far again, feel free to use the chat on med all as well. If you want close it close, it is something wrong on the biliary tree. Yep. All right. So everyone seems to be in agreement. Let's have a little look. So again, talk through what it is is a liver function test results for Mr a patient name but just double check that with my patient. Um Yeah, it goes. So someone says mmm main abnormality is a raised AP and gamma G TT suggesting a biliary or cholestatic picture. So yeah, go through step by step. Your A LP is raised at 100 and 56 and the gamma G TT is raised at 76. The bilirubin is slightly raised to 21. The other liver enzymes with normal range. This is the only one, by the way with the LFT S that I wouldn't, that, I think it's fine to abbreviate as best you can. Don't abbreviate, like, don't say, oh, I'll send the patient for PCA PCI. Say everything out loud. Um Just because otherwise like you're expecting them to assume that you know that it's right. But yes A raised A L pray GGT is your cholestatic but consistent with your primary diagnosis of gallstones, pancreatic cancer. I don't know whatever it is. Maybe not pancreatic cancer. But yes, toes. What's the main, what's a really common drug cause of cholestasis comes up all the time in P SA stuff? So a little bit of extra P SA prep at the same time. Got value for money here. How much do you guys pay me? Yeah. The combined oral contraceptive pill. Good job. All right. Next one. C OCP called, sorry to say that as a sentence. C ACP causes drug induced cholestasis. So if you get very classically like stereotypically and psa questions, you get like a 25 year old lady who's come in with sudden itching and yellowness, which drug is most likely to account for their symptoms. So watch this pato cellular injury. That's alcoholic liver disease. Let's talk it through as we go again, blood test results for this patient. This one A LT is raised at 80. The ast is raised at 60 um at six, at 60. Uh the bilirubin is raised at 68 and the A LP, the G DT and the albumin are normal. So we've got HEPAT. So people have said hepatocellular injury, alcoholic liver disease, hepatitis and biliary. So most likely thing in this case with a markedly raised A LT with a raised ast with bilirubinemia, it's most likely to be consistent with hepatocellular injury, which is most likely consistent with our hepatitis cirrhosis malignancy history. Um Why is it less likely to be biliary where our A LP and our GGT is normal? Why is it less likely to be alcoholic liver disease specifically? Could be? But classically the AST would be raised more than the A LT was no A SST fella. Thank you. Um All right. I'm gonna move on to the next slide. If you need a picture. Now's the time. Yeah, exactly. Good job in the chat. Oh, whoops. OK. Last one. Fifties. Oh, did I move it on? I did not. OK. What's this? Then? These are the most frustrating ones to interpret. Just cos you have so many. What are people thinking? Bone problem? Yeah. Um Yeah. So again, read through all the stuff at the top. Do not forget that the A LP has raised at 100 and 83 but all of your other LFT S with non ranges isolated range in A LP without a rising G TT points towards a high bone turnover such as in Paget's disease. Good job. Ok. All right. I'm gonna do one pole here and the question is you all want ABG S y'all or no? What do we think? Do you wanna go through ABG S or not? I know this says T FT S. Ok. Ok. Alright. It seems like people actually want ABG S they want ABG S more than they had stamina. 00 May as well. Yeah that's what I was thinking. All right, I'm not gonna I'm not gonna assume that I think T FT S is important to have on here but I'm not gonna spend a huge amount of time on it. T FT S here. These are the three different things for T FT S that you need to know, right? And I don't think that this is a massive challenge, this is what you know for an things like subclinical hyperthyroidism and the care veins and that sort of stuff not super likely to come up in an it they come up in a part of in your, in your progress that definitely revise it for that that's not what's gonna come up in this. Um So um anyone wanna jump in what they see things are so we can bash out ABG S if the bottom one I think is slightly more interesting. The bottom one will be a medication review station. R the Yes, we had hyper, no, yes, hyperthyroidism an hour. Um in my ski. So for the f what is it? I don't actually know what it says. Does it say? Second, hyperparathyroidism? I would struggle to comment on it just because I can't say anything about P th Yeah, that's what I was thinking but like, yeah. Um So yeah, basically, what have we got them? TSH tells the thyroid to make thyroid hormone if the TSH is super high and the thyroid isn't being made. That means this is hypothyroidism. If the TSH is super low, that means the, the thyroid hormone shouldn't be made. But it's actually I that's hypothyroidism. People here are talking about primary, these are both primary and what that, what that means is where is the source of the problem and the source of the problem in both of the problem. The pathology is the thyroid gland. The TSH says, gun, please make stuff and it says no, the th the TSH says, please don't make anything in the Thor LTA. No, most important one to know this one here could be sub subclinical hypothyroidism. However, given that it's most likely to pop up in a medication review station, anyone know what that might be. So, subclinical would present like this, I just think it's unlikely. And Iy this one, any ideas. Yeah. So this, yeah, this is an issue with compliance. This is the example of your, your TSH is really high saying, well, why aren't you making any thyroid hormone? And then they go, oh, no, I forgot to take my thyroid hormone, but they're gonna take my blood test tomorrow. So they take the levothyroxine on the morning of taking a blood test and so the TSH takes a while to come down. It just sort of lags. So it tells us that this person hasn't been taking the levothyroxine for a while. Yeah, equally just recently, go back onto it. Um OK, I will leave that on for one moment again, subclinical as well, but more likely for anky non compliance. OK. Let's do our ABG S. Let's go s so make sure you know how to do the scale comes up super scary to do on people really easy to do on models. Um except for the fact that you're really sticky, don't use the alcohol wipes on the ones that are in the clinical skills. A lot of people struggle with ABG interpretation. So find an explanation and a method that works for you. I am gonna go through one. It may not work for you. Hopefully it's not as scary as it seems. Um So I'm gonna move this on to the next one. Uh Right. So if you wanna ask questions, put it on that slide that I've just popped up. OK? Or in the chat. So this is the order that I look at an ABG in it is slightly different to the one that's recommended by SS someone slightly different to one that's on pasmed. This to me is we, we will give you the answer. The earliest ph the CO2 the bicarb, the oxygen, what this needs you to understand is that carbon dioxide is acidic, bicarbonate is basic or alkaline. That's number one. Hopefully we're all good with that. So our ph the question is, is it acidosis or is it alkalosis? It is acidosis. If it is a low ph, it is alkalosis as if it is a high ph when I say low and high compared to the reference ridge, if it's neither lower than or higher than the range, it's between the range. This is either a normal ABG or it is fully compensated. Compensated means something has changed so much that the ph came back to normal. Despite the fact that everything else still looks, I was about to swear them, it still looks messed up. Um So acidosis, alkalosis if neither it's normal or fully compensated. So we know that then we look at our carbon dioxide, our carbon dioxide is like our easiest way of figuring out what the cause is carbon dioxide is acidic. So if we have loads of acidic carbon dioxide, the PH should be acidic. If we don't have acidic carbon dioxide, the PH should be basic because you took it away. If the ph is matching the carbon dioxide, it is respiratory. What I mean by that is if the carbon dioxide is high loads of acid and the PH is acid that is a respiratory acidosis. And if the CO2 is low and the PH is high, cos you've taken away the acid that is a respiratory alkalosis, the PH matches the carbon dioxide pause if it doesn't. So you have loads of carbon dioxide which means it should be acidic, but it's actually alkalotic. That means it's metabolic. Again. Questions on the chat, questions on the Q and A or on the board. Hopefully that's ok. So far by up then at this point, we should know whether this is a respiratory acidosis, a respiratory alkalosis, metabolic acidosis or a metabolic alkalosis. Just because of the first two bits. Our bicarbonate is mostly telling us two things. If it is a respiratory acidosis or alkalosis, we're looking to see has the bicarbonate changed at all. If it has changed, this is a chronic thing, it has not changed. This is an acute thing cos the metabolic compensation is slow. So the classic example is a uh respiratory acidosis. So high carbon dioxide with uh high bicarbonate which is seen in chronic C or CO PD that are carbon dioxide retainers. It is a long term issue. So that bicarbon has had time to try to compensate but has failed to adjust the PH. If it is metabolic, the bicarbonate should match the PH IE if it is low, the PH should be high. If it is high, the PH should be low. But we should already know that if at this point, this doesn't make sense. So we've said, oh, it's a metabolic acidosis and then I check this over here and the ph actually uh sorry, the, the bicarbonate is actually low. This is now mixed, mixed me uh like acidosis and alkalosis just means it doesn't make sense, right? I've not seen any questions, comments. So I'm assuming we're all like really on it on the same side. OK. Um At this point, you just take your oxygen four. Is it type one or type two respiratory failure? Type two being when your oxygen is affected as well? I'm pausing here for, for you. OK? All good. You are unlikely to get a mixed to come up in your is it's even unlikely to come out in a progress test. It's unlike to come up in an is, but your main one is just if you can get these first two down, you can answer a decent chunk of it. Just remember that it is partial compensation. If the ph is changed, it is full compensation if the ph is in normal range. OK. I'm not seeing any questions come in. So I'm assuming we are all good with that. So, so and so I just put them all on the screen at once like here you go. Um Right. Have a bash do it on paper if you're not on the ment, what is going on here? What are these? Can I go back a slide? Yes, Tana. No worries. Ok. Back to the slight of the worst thing everyone's ever seen. Um, I've just lost the ment to. All right. Take care. Right. So you do it on the chart, you can do it on paper. Just have a practice at this regardless of what you wanna do, right? It seems like we've got loads loads of people coming in. It's a brilliant, good job. Ace looked then. So I'm gonna start to talk them through it. I appreciate it's not been loads of time. Take a picture of it and do it in your own time, like practice with yourself. But hopefully we're looking at them flat out and remember the most important thing in an exam is that we can say something. Hopefully we're looking at this and we're saying low acidosis, acidosis, alkalosis alkalosis. So at the very least we can say that. And then we've got the carbon dioxide ticketed so low Ph and a high CO2. My question is, does the CO2 match up with the low Ph? So CO2 is acidic, there is lots of acidic, the PH is acidic. OK. This matches up what have people said? Have people agreed that this is a respiratory yes, people are saying yes, this is a respiratory acidosis. I agree that this is a respiratory acidosis. People is this acute or chronic? It is acute. Yes, it is acute because the bicarbonate has not had enough time to change yet. And as a lot of people have said, because we've got a high CO2 and a low oxygen. This is a respiratory acidosis. More specifically, this is a type two respiratory failure. Next one, low ph acidic and low carbon dioxide. So low carbon dioxide. So there's not a lot of acid. So I'm expecting it to be alkalotic. But when I look at it, it's not. This is metabolic. Are people agreeing with that metabolic? Yes, we are with the normal oxygen. Why is the carbon dioxide low? If it's metabolic? Why is the carbon dioxide low? Mm God, I spat might squash. Um Yes, it has compensated. This is a partially compensated metabolic acidosis. Why is it partial? The ph is low? Ok. Next one. High ph so acid. Uh no, sorry. Basic uh carbon dioxide is low. So not a lot of acid which means it should be al um alkaline and it is OK. So this is respiratory people agreeing with that. Uh Yeah. Yep. Nice. OK. With a normal bicarbonate and a normal oxygen have people added anything else? That's a respiratory alkalis with no compensation because the carbon uh the bicarbonate is normal oxygen. Uh This, do you know what the most common cause of um respiratory alkalosis is? Yeah. Yeah. Hyperventilation. That's how I'll rephrase that. Yes. So hyperventilation due to anxiety, asthma um also caused by like aspirin and salicylat overdose. But that's a little bit rogue. Uh Can I explain how to know if there's compensation? Yeah. So at this point, once we've reached this point here, we should know that this lines up with that, right? Let's say we do know that this lines up with that. So acid, lots of acid, this is respiratory. So I check the bicarbonate. Now, the bicarbonate shouldn't change because there is a problem with the respiration, right? That's what's causing the acidic. So when I check the metabolic bit, this bicarb, it's not changed. And because it's not done anything, it's not compensating. So that is no compensation because I wouldn't expect it to change that. It's not. So it's just doing its normal stuff. Whereas if I compare that to the next one, it's low. Ph No, which we compare it to. Yeah, compare it to this one low. Ph H I check the carbon dioxide and the carbon dioxide is low, which means there's not a lot of acid which when I look at that, I'm like, oh, that doesn't make sense. I'd expect that to be high. So I now know that this is metabolic and that's, that's confirmed by the fact that my ca bicarb is high. So when I'm looking at the carb diets, I'm like, well, why is my carbon dioxide low? And it's because my respiratory center is compensating by changing the carbon dioxide level. So by this point here it come note said we should know if it's respiratory or metabolic, if it's respiratory with no compensation, only the respiratory stuff has changed and if it's metabolic with no compensation, only the metabolic stuff has changed. But since this, it's metabolic, the bicarb is high, that's what's causing the low ph but the carbon dioxide dioxide has also changed. It's gone down. That's how we know that there's compensation. Is this making sense? I hope so. Yeah. Um So yeah, if it's metabolic, just look at your metabolic ones should be the only ones change if it's respiratory, only the sy ones. Uh and let's just check this last one then high Ph and low. So there's not a lot of mhm. Not a lot of acid have I, I've done this one wrong, haven't I? One of these is wrong one second, I'll come back to it. Er If it's high Ph and low CO2 that to me says yeah, this should be high, shouldn't it? This one should be high everyone um doesn't make sense. High CO2 here does not make sense with a high Ph. So it must be metabolic. I double check it. It is metabolic. So this one here has to be a metabolic alkalosis. Sorry. How do I tell whether it's full or partial compensation, full compensation. The ph will be normal, partial compensation. The ph will be changed. So, partial conversation is it tried to fix it and didn't work. And yes, what you're saying there about respiratory and bicarb is right. And metabolic. Yeah. Co2, not co three though. Somebody has also asked, how do I know that it's more likely to be on a progress test than an esky vice versa. I done a lot of progress tests. Um, so I've done a lot of progress tests. I've done a lot of the questions that the uni has given out. Er, I've done the Iski and I've also had access to the previous Iski from the past couple of years as well. So just in terms of trends and the content, does that make sense? It's, it's just that it's just, it's just the sort of questions that are asked in is that's, that's how we know. Ok. Oh, can we request paper and pen and excuse, you can request that as a reasonable adjustment. Um, but the only station they give it to you in is the Sbar station. Um Yeah, sorry. The question was, can we request pen and paper in the? Um, yeah. Ok. So here you go, a little summary slide when they come up. No worries. Um Yep, I've tried to just keep in those super important ones that are likely to come up really common ones that are gonna come up or you're gonna be your, your CO PD and your hyperventilation. Um I can see a psych history with an ABG might be a, not, not one that they've tested, but one that I think might be a, one to think about. Right. I've got three. I'm sorry, it's going on for too long. Um. Right. Let's bash these out the last light, sorry. Ok. That's the last li full of cases again. It's not all of them, just the most likely ones to come up. You got it. No worries. Ok. Diabetes cases. Right. What have we got? And I have changed the ages by the way for these patients as well. It is worth being aware of how your, how old your patient is. It does change things. He's got quite a young patient this time and married literally unheard of at med school, right? Anyone got any ideas? Just boo boo boo. Here we go. OK. So we'll go through step by step. Yeah, and we'll use the same thing. So our Ph is up alkalosis. So we're gonna check our carbon dioxide and see, does that make sense? Our CO2 is acidic but it is low. So if you've got not a lot of acidic, I would expect the PH to be basic and it is so because the carbon dioxide makes sense with what the ph has done. It's respiratory. Are we all on board with why that's respiratory? Our ph is up. So I check my carbon dioxide, my carbon dioxide is acidic but at the moment is low. So if I've not got a lot of acid, that means that it should be alkaline which matches the ph. So there is a respiratory problem here. I will update the, sorry, somebody else, I'll, I'll update the slide. The one that had the wrong thing on it for the acidosis stuff. I'll update it when I put it up the slides. Nobody's responded. But I'm assuming that means that we are all good with the respiratory bit. So respiratory alkalosis, then we know oxygen 12.3 unaffected bicarbonate is 24. The bicarbonate has not changed. It's not tried to fix anything. It's not gone up, it's not gone down slight. So this is an uncompensated. There is no compensation here. This is a respiratory alkalosis with no compensation. Oh Yes. What is the most likely cause of this? Like we talked about already. This is most likely to be due to hyperventilation? OK. I'm gonna scoot you onto the next one. Where's it? Where's the next one? There we go. There it is. I put on 2004. What is this one? Then? Let me put this up here. I'll check again. Does our ph make sense with our carbon dioxide? Why does my camera keep going blurry. Do my little dance because people are getting it. So let's go through. So what have we got here again? Do all of your interpretation stuff. Our ph is low. Our carbon dioxide. Remember that's acidic Isler. If I've not got a lot of acid, I would expect the PH to be high, but my PH is low. So because my carbon dioxide doesn't make sense with my ph, they don't match up. This is metabolic because I would expect to have a high carbon dioxide with a low PH. But I don't have that. So just to say again, so just to say again, ph is low, carbon dioxide is acidic but it is low. There's not a lot of acid. So if there's not a lot of acid, it's alkaline. But then while I'm looking at it, it's not alkaline. That means that it must be metabolic, it's not the carbon dioxide that's caused this something else. So I'm thinking at this point, this is a metabolic acidosis. So I check my bicarbonate. That's the next thing on my list. Bicarb. Did it make sense? My bicarbonate here is low. Bicarbonate is basic. If it is low, I expect the Ph to be acidic because there's not a lot of base there. So the Ph is acidic. That is exactly what we've got here. So that bicarbonate makes sense with the Ph. And because the bicarb makes sense with the PH, it's not mixed. This is just confirming metabolic acidosis to the person. He said mixed. If so at the point where I've gone, oh, it's not respiratory. It must be metabolic because the carbon dioxide's gone the other way. And if I come to the bicarb and the bicarb was high, that is now mixed because it doesn't make sense in the context. But this does make sense because the bicarb is low, Ph is low. Our oxygen is normal. They're normal ranges. So yes, this is a metabolic acidosis with partial respiratory compensation because the carbon dioxide is different. It has changed in a patient. This young maybe looking at DK A likely diagnosis for a metabolic acidosis just gonna check the thing. See nothing. Yeah. OK. All right. Last one. Why is it not working? Last one. OK. We got this guys. We are so close to the end. Always taste it. I was gonna reward myself with cookies but not really hungry for cookies. Me, did I change the slide? I did. What are we thinking? All this one gonna give a few more seconds so other people can have a go. Yeah. OK. So I'll just talk it through one more time. So our Ph here is low. Yeah. Good job. Our ph here is low. I look at my carbon dioxide. My carbon dioxide is acidic in this situation it's high. So that means there is lots of acid. So I expect my Ph H to be acidic. I expect my ph to be low and it is so this means it's respiratory because the ph makes sense based on the carb induction scoot on down to the biop look uh 28 it's gone up and because the bicarb has changed and it was a respiratory, this bicarb is trying to compensate. It's just not done much. So this is a partially compensated respiratory acidosis and the oxygen is also low. What is the most so good job everyone did that, which is good. What is the most likely cause of this? A partially compensated respiratory acidosis type two respiratory failure because of the low oxygen. Yeah. Yeah, good job in chat as well. Yeah, this is CO PD. Just remember not all patients with CO PD are CO2 retainers. And so with the majority of COPD patients with the majority of COP D patients, you just give oxygen as normal but you would do an ABG just to check. Remember there's that pass med thing that says hypoxia kills. So whether you know if they are or are not, you're gonna give oxygen in an unwell patient. Um because the oxygen is what will kill them before the lack of hypoxic drive. Um Yep type two respiratory failure with partial metabolic conversation indicating it's chronic. So, yeah, see, can I actually explain the difference to type one? Yeah. So type the basically the easiest way. Um Yeah. Um the easiest thing to tell the difference between the two type two respiratory failure is two things have gone wrong. The oxygen has gone low and the carbon dioxide has gone high in type one respiratory failure. The oxygen has gone low. The carbon dioxide is fine, type one, low O2, type two, low O2 and a high CO2. Hopefully that is ok. No worries. We've reached the end. I'm sorry this has gone on for so long. I appreciate the remaining 21 people. All of you about the entire two hours. I think I just overestimated uh uh how long this would take? I apologize for that. Um How do I know it's chronic? So the bicarbonate takes a long time um to compensate. So the fact that we've got bicarbonate change at all means it's been going on for a while. Whereas respiratory compensation happens quick. It is the difference between me breathing now and breathing slightly faster. Whereas Binet that's a whole like acid base shift that's going on. So it takes a while. So that's how we know that it's chronic because it's actually been able to have enough time for the bub to catch up. So if there is ever metabolic compensation, you know, it's chronic. No worries. I hope that it was useful. No worries. I'm glad that you guys find it useful. I am, I am glad I am glad that that helped. I think I always talk brilliantly but we'll see. No worries. I'm glad that you found it useful. Oh, so lovely. Thanks guys. Brilliant. If you do have any other questions, just uh send them through. Oh, there are some more. It's going to be, oh, it wasn't a question. It was just a compliment. What conditions are associated. Yeah. Ok. Um So yeah, so the things that cause type one, respiratory failure is where you've got essentially a uh what's the word? Um, the a difficulty oxygenating the blood. Um So you've got hypoxemia, you've not necessarily got hypoxia, but you've got hypoxemia. Main things. The two main things that come up are your pneumonias and your pulmonary edema. Your pulmonary embolism also cause us pneumonia is your most common cause of a type one respiratory failure. So, pneumonia edema, pulmonary embolism and acute respiratory distress caused type one. Um and type two then is is more as a problem of getting rid of carbon dioxide, which means you can't take in enough oxygen. So that's your co PD um and things like neuromuscular disorders um and also severe asthma, you know, when the carbon dioxide suddenly go becomes normal and creeps up. That's type two respiratory failure. Um And so essentially type two, respiratory failure is associated more with hypoventilation because you're not getting rid of enough carbon dioxide. Does that make sense? Yeah, I hope so. Mhm. Um I did do a thyroid clinical if I my ask you um we, you know when we all split up and you do like half a morning in the hospitals in like year one in like on placement in like year one and year two, I got thyroid teaching then and then again on placement during C D2, I think. Um but I feel like I had to teach myself the majority of the clinical exams that is one that I don't think you get taught brilliantly. Um, whoever you are, if you want, uh, if you wanna email me, I'll put my email and chat again. I would, I'd be happy to send through like my, my notes on it. Um, on the main things that you have to do. Um, but remember that like, the majority of exams are just your ability to identify what specific symptoms you're looking for. So, if you're looking for a thyroid problem, I'm probably gonna feel the neck to see if you've got a goiter. I'm gonna see if you have tremor. I'm gonna see if you feel warm and sweaty. I'm gonna look at your nails for acropachy and I'm gonna look at your shins for edema. Um I'm gonna have a look at your hair nails. Um So if push came to shove you could, you could probably make it up as you go. But like I said, if you just send me an email, I can send you through the notes that I have on it. Um gee me has quite a good one too. Um Yeah, it involves a piece of paper and a glass of water which is why, you know when you walk in, that's what it's gonna be. Does type two respiratory failure have respiratory acidosis and type one respiratory failure have respiratory alkalosis. So, not necessarily type two, respiratory failure will be a respiratory acidosis. It may or may not be compensated. Type one, respiratory alkalosis doesn't necessarily sorry. Type one respiratory failure doesn't necessarily have to be a respiratory alkalosis. Um I hyperventilation is a good example of it. Um but you can have normal uh carbon dioxide in type one respiratory failure. It's just that it's not high carbon dioxide. You can have normal and you can have low carbon dioxide. But type one respiratory failure is the main issue is you can't get in enough oxygen. Type two is the main reason is you can't get rid enough carbon dioxide. No worries. I'm glad I hope it helps. I'm just gonna hang around for a little bit longer just because I think it was a lot. Well, I appreciate your coming. I hope that it was useful. All good. Awesome. Seems like we are all good. So I am going to wrap it up here. Thanks again guys. Good luck with the rest of your prep.