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Final Year Series - Haematology!

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Summary

In this on-demand teaching session, participants will explore a wide range of topics related to hematology including giving a hematologic history, diagnosing hematological disorders, anemia, high yield topics, and review questions. Led by a qualified F1 doctor and professional from Mindthebleep, the instructor will provide a comprehensive overview of hematologic conditions, evaluate possible medications that can affect hematologic functions, and answer questions. The course is suitable for medical professionals and those seeking a deeper understanding of hematology.

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Description

The 5th session of a 4 month Mind the Bleep Final Year Series! Dr Rimsha Khan (FY1 currently on haemato-oncology) will talk you through a summary of Haematology for finals! A topic often feared, we hope to break this down & highlight the most important things to be aware of! Come along to refresh yourself on the following topics:

·      Haematology history & examination

·      Interpreting blood tests

·      Anaemia

·      Thrombophilia

·      Transfusions

·      Emergencies

·      Malignancies

·      SBAs

Event date is 06/11/2023 from 7-8pm and we look forward to seeing you all there!

Please also remember to fill in the feedback form. All feedback is very useful for us and you will get a certificate of attendance after completing it!

Learning objectives

Learning Objectives

  1. Understand the importance of taking a hematology history from a medical patient
  2. Recognize the symptoms of anemia and how to quantify them
  3. Know the potential drugs which may lead to pancytopenia
  4. Have an awareness of the family and social history factors which can influence hematological disorders
  5. Be able to identify and explain the potential signs of jaundice and polycythemia from clinical photos
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hi guys, thank you for joining. Um Just gonna give it a couple more minutes to see if anyone else comes and then we'll get started. Ok, so I think we'll just get started. Um And then people can join um as they come. So um can everyone hear me? Someone doesn't mind just popping a message into the chat? Um Just so I know it's all working. Yeah. All good. Ok, thank you. Um So hi guys. So I'm Rome. Um I'm an F one doctor. Um I'm currently working on he oncology at Barts Hospital in London. Um and we've also got a man um on the call who's just helping with any questions and um is sort of the lead of all of the final year stuff for mind the bleep. So, um so yeah, um thank you mon and we'll just get started. So I'm gonna give you guys a lecture on hematology today. Um It's quite a complicated topic in general and I remember at medical school finding it really confusing. So I'll try and make things as simple as possible, but obviously, um just feel free to shout out with any questions that you have. Um, so in terms of the structure of the talk, so we're just gonna go through a few different topics, um, as outlined over here and then at the end, I've got some SBA questions. Um, I think there's just about five or six and we'll go through those. Um, and it shouldn't be more than an hour, hopefully, but we'll see how things go. Um So in terms of what we're going to cover today, um I'm gonna go through how to take a hematology history and examination. It doesn't tend to come up in ay too much. Um, but I think it's just important um to know how to do it in general because hes are part of so many different specialties. Um And then we'll go through some blood tests how to identify um different sort of hematological disorders, including anemia. Um some of the malignancies, any coagulation disorders, etcetera. Um And then the majority of the talk will be anemia because that's the sort of biggest thing in him. Um And we'll go through some high yield things at the end followed by SBA S. So I hope that's ok. So, um if we just start with how to take a hematological history, um it's important to just be aware that you may need to ask these questions in several different scenarios. So we'll go through how to do the history first. So, in a heme history, it's always important to ask about any symptoms of anemia. Um So could be things like any shortness of breath, um, you know, generalized tiredness. Um If they're really anemic in severe cases, then patients may often feel quite dizzy as well. Um, palpitations are super common because you've essentially got less blood being pumped around the body. So your heart has to work a little bit harder. Um And then again, in very sort of severe anemia cases, patients can also get chest pain for very similar reasons in terms of your heart working extra hard. Um And then obviously, we've got loads of different hematological malignancies. You've got the lymphomas, myelomas, all the leukemias as well. Um And all of them tend to in one way or another present with your b symptoms as we call them. So that's things like night sweats, weight loss, um fevers more than 38 degrees. Um and also any new lumps or bumps anywhere. So, lymphadenopathy, so always really important to ask about those things as well. Um And with weight loss, just remember to quantify exactly how much. So how many kilograms have they lost in the last three months or um in a year or whatever it may be. But yeah, really important to quantify that. Um And then the other thing is symptoms of infection. So um in lots of different heme disorders, which we'll talk about, um patients can often get either a low white cell count or a very high white cell count. But regardless, those can be indicative of some sort of infection or bugs going around. So, ask if, you know, in the last year, how many times have they been ill with coughs and colds and things like that? And have they had any hospital admissions requiring antibiotics, um, or you know how they managed all of these infections? Basically, because it's a red flag if someone's had, um, it's, it's sort of an arbitrary number but in, in him, we don't like them to have any more than um an infection a month. So if you're having, you know, if you're ill, two or three times a month for every single month of a year, um then everyone tends to get quite worried about that. Um So that's that bruising and bleeding. So, um if your platelets are low, which again can happen in several disorders, then you might have a lot of bruising, you might have bleeds which can range anywhere from, you know, just epistaxis and any mucosal bleeds to something more severe like um bleeding into the joints or, you know, massive um hemorrhages basically. Um So those are the four main things to, to ask about and those are the four main things that we worry about the most. Um But obviously just some other things to be aware of, so important to ask about their diet. So, um that will be particularly important for any nutritional deficiencies. So, you know, like the classic sort of do you eat green leafy vegetables for anemia? Um Are you vegan? Because if, if you know, vegans can sometimes have a low b12. So, so, yeah, um, just sort of general things like that. Um, and then drug history. So this is an interesting one. and I see it all the time on heme oncology. Um, but there are a lot of drugs that we actually give to patients with heme problems that can inadvertently also cause bone marrow suppression and therefore lower all of your counts. So your red cell count, your platelets, your neutrophils as well. Can you guys think of maybe if you just put it in the chart, any drugs that you know, that might lower some of your counts and cause sort of pancytopenia? Um Don't worry if not, but just wondering if you know anything off the top of your heads. Thanks. I um Yep. Carbimazole. That's a good one. Uh I'm not really sure if statins lower your counts. Maybe I've, I've never heard of it personally. Methotrexate. Exactly. CloZAPine. Yeah, you won't really see cloZAPine very much in um he patients. Um But yeah, definitely in psychiatry patients. Um The other one that I'm thinking of is Cotrimoxazole. Um So yeah, so the main, the main three that I would I would say are me be, be careful with methotrexate, Carbimazole and Cotrimoxazole. Um and Cotrim is often um something that we use to prevent people from getting infections as prophylaxis. So, um, and yeah, it, that I would say that's probably the commonest drug in him. So, just be careful with those. But yeah, um, excellent ideas. I'm not, I'm not sure about statins but, but maybe, um, so yeah, so that's that. And then in terms of family history again, you don't have to spend very long on this, but just asking them if they, if they've got a family history of any hematological disorders, um they often won't know what that means. So maybe just wording it um in something like, you know, have you got any um blood disorders that run in the family or has anyone been told that they've got anemia? Um et cetera. So, so yeah. Um and the last thing is social history. So obviously you'll ask this in any history that you take. Um but just some things to be aware of. So alcohol um or chronic alcohol abuse in large amounts can cause macrocytosis and we'll talk about this more when I, when I speak about anemia. Um And then the other thing is smoking which can cause polycythemia, which is essentially just um a very high red cell count and hematocrit um level. So, yeah. Um Can I write it up, please? Do you mean the um different drugs? I can definitely send them around later? Um But if that's what you mean just to reiterate. So the main ones that I was thinking of was methotrexate, carbimazole and um Cotrimoxazole as well. Fine. Um a and maybe if you just want to spell them in the chart, I don't know. Um But yeah, I can definitely send them around later. No worries at all. Um Yeah, cool. So we'll go on to the next slide. Oh, and then travel, malaria can often cause anemia as well. So just asking if they've been abroad anywhere recently, especially if you've got a very well patient uh or you know, someone who was previously very well and has suddenly come back from holiday. Um very unwell. So yeah, so um that was the history now, just some things to sort of look out for in a um examination of a sort of hematological person, I guess. Um we'll go through some of these things. I don't know if you guys can see my cursor but if we just start with the image on the top left hand corner, the one of the eyes, um any ideas what the main sort of finding is here, if you just put in the chat again or feel free to shout out as well. Yeah, fantastic. So jaundice um fancy word for the eye one for when it's in the eyes is um scleral icterus. Um So someone said iron deficiency. So good idea. But if you look at the other picture of the eye, so the one that's second in the bottom row, um that's more a sign of iron deficiency anemia and that's um conjunctival pallor. Um So you can see that the conjunctiva in that second eye photo in the bottom line and the conjunctiva are very pale. Um You'd expect them to be more sort of vascularized and more red, basically if you look at your own ones in the mirror. Um So that would be anemia, conjunctival pallor. But yeah, the top left one was jaundice um often seen in um hemolytic anemias um obviously in, you know, gastro patients as well with, with liver issues. Um So yeah, so that's that. So if we now talk about the second photo from the top. So the one of the, again, I don't know if you can see my cursor but the one of the red cheeks um a male or rash. Yeah, it does look like that. Actually, I don't blame you for saying that. Um I don't know very much cardio but yeah, it, it does look like that but in the context of a heme patient, what might you be more worried about? Yeah, facial plethora. Um So in his facial plethora, um you've got basically this, you know, bilateral redness of, of the cheeks of this woman. Um Do we know what kind of conditions in him can cause plethora? One condition? Really? Yeah. Ruddy cheeks is the other way they tend to describe it. Excellent. Yeah. Polycythemia, rubra, vera. Um excellent. So yeah, so basically um we'll talk about polycythemia but in polycythemia, you have an increased red blood cell mass. Um And when you've got all of those extra sort of red blood cells and hematocrit that cause it, that causes your blood to become a little bit thicker. And so you get all of this sort of swelling and vasodilation of all of your blood vessels causing um that sort of complexion. And the other thing, patients will often complain of with polycythemia is that this is, it can sometimes be very itchy as well. Um And although I've showed a photo of the face here, you can pretty much get this kind of redness anywhere on the body. So it may be on their palms and the soles of their feet, um like rarely in their nails as well. So, so yeah. Excellent. Um Yeah. And then the photo right next to that. So the one on the lips, what are we seeing there? Got it. Yes, perfect. So, um angular stomatitis, angular colitis. Um I think the terms are interchangeable, but um yeah, either one of those. So you can see that on the sort of on the sides of the um lip. So where the top and bottom lip meet, you've got all of these. It's not a very good photo, but you've got cracks and fissuring of the skin and the mucosa on the inside of the mouth. So, um yeah, and it's a sign of usually it's iron deficiency anemia, but sometimes you can also see it in b12 deficiency as well and it's usually a sign of very severe uncontrolled anemia that hasn't been treated for, um, months and months on end. Um So, yeah, be very careful of that. And then the photo right next to it. Um, I used to always get really confused of the difference between pete purpura and eys. So I've just put a photo on there to show you. Um, and I know you can't really sort of measure it by eye. Um But just take my word for it. So the way to sort of identify the difference between the three is petite, I usually very small and usually own anywhere between 1 to 3 millimeters, but no more than that. Um If you've got multiple of those coalescing together, then you'll get purpura which still look very blotchy, but um still sort of look like loads of separate different spots. Um And, and that's, that's purpura, but then ecchymoses is where you basically get a massive bleed into the skin. Um And you can't really, you know, separate out all of the different lesions in there. It just looks like one big blob of red basically. Um And that's just a massive massive bruise. Um So, yeah, so that's the difference between those three. Um And then the photo that I've got on the bottom left. So again, the one of lots of little tiny red spots, that's just another example of Petechia. Um Or at least I think it's Petechia. We don't know how big big they are, but I think they look small enough to be tech. Um And I think that's around the knees. So those are most of the photos. If we just now look at the one of the tongue, what are we seeing there? Any ideas? Cool. So um someone said Leukoplakia, you, you're right. It could be Leukoplakia actually and I'm not too sure how you would differentiate that from, from Thrush. Um So, and, and both Leukoplakia and Candida, you tend to get in very immunocompromised patients. Um So it's a great thought. Um But actually in this photo, um well, when I googled it, I was googling photos of Candida um oral thrush basically. So, so that's what this particular image is. Um And yeah, again tends to happen in immunocompromised patients because we've got all of this flora living in our bodies, but it just over proliferates if you don't have any immune cells. Um Some people also said Glyphis smooth tongue. I do agree. It looks a little bit smooth. They may have an element of anemia as well. Um But yeah, and yeah, I think Mon just said Harry Lela is typically on the side of the tongue. Oh Amazing. That's how you tell the difference. Um So yeah, and then the last photo I think um is, is more, is probably one of the most obvious ones, but we've got a swollen lymph node there. Um Just underneath um in sort of the angle between the chin um and the neck and it's probably, I mean, it's probably the one of the superficial cervical lymph nodes. Um But yeah, that's also quite concerning because you wouldn't expect lymph nodes that big just after a normal infection. Um So good, excellent uh is glossitis, enlarged tongue or smooth tongue? Um It's smooth tongue, maybe both, but I think we usually refer to glossitis um meaning smooth tongue. And so if you've got iron deficiency, you'll have a very smooth tongue, but it won't be, you know, swollen or anything like that. But the opposite tends to happen in B12 deficiency. You usually get a very beefy red tongue, um which you could, which sometimes can look a little bit enlarged. Um So I guess it can mean both just depends which, which type of anemia you're speaking about. Um Yeah. And yeah, petite, I are due to bleeding disorders usually due to low platelets. So if you've not got enough platelets, then any small insult to your skin, you know, if you've accidentally bashed your arm against a door or something, then that will cause um sort of superficial bleeding because your capillaries just burst very easily. Good. Um And then I won't spend too long on this slide. Um But there's not much to a hematological examination, but there are a few things to always, um watch out for. So the main two things that I always think of is always examine the lymph nodes and always feel for the spleen as well. So if you've got splenomegaly, you can see in the top right picture your spleen is obviously sort of on the left hand side of your body. But when it enlarges and when you've got splenomegaly, it tends to extend down towards your right eye, lap fossa. Um So it's always important that if you're feeling for someone's spleen, just make sure you also feel down to the right eyelet fossa and just to assess the sort of extent of enlargement. Um And then sometimes you can get hepatomegaly as well, less common, but we do see it in patients. And um yeah, I mean, that would just be, you know, an enlargement under your sort of right ribs. Um And then the lymph nodes, main thing to say about the lymph nodes is um we're most concerned about three areas which is the lymph nodes in the neck. Um the lymph nodes in the um underarm. So, in the axilla and lymph nodes in the groin as well, so just have a cyst of of sort of feeling them all. Um And I guess with the, the most complicated ones are the neck ones really. And um the picture on the left is quite helpful, but just have a system when you're examining them. So start at the top and work your way down or vice versa. Um And never forget your supraclavicular lymph nodes as well. OK. OK. Fine. So um just some differentials of all of our different examination findings. So, with lymphadenopathy, obviously, the commonest things that cause lymphadenopathy are infections. Um so E HIV TBA, lot of vaccines. So the COVID vaccine, for example, can also cause lymphadenopathy. Um So it might be worth asking if they've had any recent immunizations. Um and then some more uncommon causes are things like are the more concerning things really. So, lymphomas, um any other solid tumors that have metastasized to your lymph nodes. Um So a bad, it's a bad sign really. Um But in particular, your breast cancer tends to spread to your um axillary lymph nodes. Um It's just something to watch out for and then probably the most rare one, but sometimes in inflammatory disorders like sle you can also get lymphadenopathy. Um But I've never really seen it or heard about it to be honest. Um So that's for lymphadenopathy and then for splenomegaly. Um I think pass me or somewhere else online, used to say the three MS are the commonest cause of splenomegaly. So those are um chronic myeloid leukemia. Um The myeloid being that m and then myelofibrosis and malaria as well. So just good to memorize those three in case it ever comes up in case you have a splenomegaly patient in acies, you can sort of rule out those differentials. Um And then just some, I've just listed some other causes on there. Um So again, you know, lymphomas, leukemias, if they infiltrate into the spleen can cause splenomegaly, obviously, um anything causing portal hypertension. Um And then, yeah, a few other things on there as well. Um And then hepatomegaly. So, um again, a lot more sort of systemic causes for that. So, right heart failure can cause hepatomegaly due to backlog. Um again, liver issues. So, um liver cancer or METS um from any other type of cancer. Um and then some, some of the rarer sort of genetic things like hemochromatosis, myeloproliferative disorders as well. Um So someone's just asked, how are the erythematous features are iatrogenically affected by treatments such as anti coagulants and antiplatelets? Um um Do you mean can anticoagulants and antiplatelets cause the erythematous features? Um I'm not too sure what you mean, but I mean, yeah, theoretically anticoagulants. So things like heparin can also lead to bleeding. Um But obviously, we don't usually expect that. Um and we'd be quite worried if it caused bleeding in someone. And also um I think we usually with things like anticoagulants, we're more worried about bigger bleeds and sort of systemic bleeding. So things like um cerebral bleeds and and bleeding it everywhere else. Whereas when you've got low platelets, you get much sort of smaller bleeds. So things like all of your mucosal stuff. So like, you know, nose bleeds, bleeding into the gums, all the superficial stuff that I showed you photos of like petechia Aur. Um, so that's one of the differences, I guess. Um, but I don't know if I interpreted your question correctly. So just let me know if, if you meant something else. Um, but yeah, so let, just to talk about the full blood count, um, as well, very briefly. So, um, when we look at a full blood count in him, there's three main things that we want to look at first is the, um hb so hemoglobin, um the neutrophil count as well and also the lymphocytes and I've just sort of split it into um things that we are differentials if it, if the, if the counts are low and are differentials, if the counts are high. So, um if we just start with hemoglobin, um obviously, if your hemoglobin is low, then we're worried about anemia. There's several different causes. I'll go through them. But if you notice a low hemoglobin, the key things to do. I also check the M CV um and request any um hematinics. So your hematinic hematinics are basically ferritin B12 and folate. Um because that will allow you to further differentiate what type of anemia you're dealing with. Um But on the flip side, if your hemoglobin is high, um then we worry about polycythemia. Um and polycythemia split into primary and secondary polycythemia. So primary is genetic polycythemia. Um and you guys may or may not have heard of some sort of funky mutations that cause polycythemia rub. So things like the, um, Jak two and Kala mutations, I think they are, um, they tend to cause polycythemia rubra vera. And I think J two mutation is present in more than 95% of patients or something like that. So that's your sort of primary genetic, not a patient's fault or anything like that. Basically, um, secondary place cymia is um not inherited and there's several different causes. So we've got things like CO PD and smoking. And in both of these, what happens is you've basically got chronic hypoxia to the lungs. And so in order for your body to deal with that, it just produces more um hematocrit and more hemoglobin. Um so that, you know, you've got enough being pumped right your body. So, so that's why you get polycythemia in those lung conditions. Um And then sometimes, so with renal patients who are on erythropoietin because they don't make enough in their bodies is if you accidentally take too much of that or you prescribe too much of it, then again, your, your um your hemoglobin will be raised. Um high altitude is sort of similar to CO PD and smoking. It's just, you know, for your body to adapt to low oxygen saturations at higher altitudes. Um You know, if you're going like mountain climbing or you live in the mountains or something, then again, your hemoglobin will be raised. Um So, yeah, so that's sort of polycythemia in a nutshell. Um I think I do have a slide on it later on as well. Um But if we talk about the neutrophils now, so, um if you're neutrophils, neutrophils, I find a little bit confusing because sometimes they can be low in infection, sometimes they're raised in infection. Um So it's all a bit confusing. But what I've been told is that if your neutrophils are low, then we tend to worry more about viral infections. Um or the sort of non viral infection that we tend to worry about is TB. Um But if your neutrophils are high, then we're more concerned of a, it's almost always a bacterial infection. Um being the cause of a, of a raised neutrophil count. So low is viral. High is bacterial is the sort of generalized rule. Um But they can also be high after surgery, inflammation, um et cetera. Um The other thing is, so, um some ethnic groups also um tend to just have low neutrophils or have a higher um sort of probability of having low neutrophils and it's fine, it's not worrying at all. Um But I think it's Afro Caribbean ethnicities in particular, just have hereditary um low neutrophils, but they're not concerning and we don't do anything about them. Um So, yeah, and then drugs. So we, we already talked about some drugs that can lower our neutrophil counts earlier on. Um But uh but most chemotherapy um regimens also lower your neutrophil counts. Um And that's why you get neutropenic sepsis, which I have a slide on later as well. So just to be aware, any patient on chemotherapy always check their neutrophil count. Um And then obviously some autoimmune conditions as well. Um But yeah, and then just to talk about any, any any high neutrophil counts that you come across. Obviously, we talked about reactive um neutrophilia. The other thing is malignancy. So, leukemias as well can sometimes cause very high neutrophil counts. Um steroids as well can sometimes cause a falsely raised neutrophils. And you'll get people being really worried about this patient has an infection because their neutrophils are super high, but actually, it's just a reaction to the steroids. Um And then obviously, in some myeloproliferative disorders like um myelo leukemias, you can also get high neutrophils. Um Yeah. So those are your neutrophils then just moving on to the lymphocytes. So, um again, sometimes after surgery or trauma, your lymphocytes can be a little bit low, not really sure why. But um but yeah, and then COVID-19, you guys may or may not remember. But again, um typically patients would have low lymphocytes. Um and that would be a way to um you know, differentiate COVID versus another viral disease or bacterial infection, for example. Um and obviously HIV you get low CD four lymphocytes um and autoimmune disease. And then for high lymphocytes um annoyingly again, viral, some viral infections can cause high lymphocytes like EBV, um chronic things as well, like TB and then any uh malignancies that involve your lymphocytes. So the um lymphocytic leukemias, for example. Ok. Mhm. That's that. And then, oh, yeah. So just some um other things about just some other things to be aware of with your hemoglobin. So sometimes if you get a low hemoglobin, it may be a false result. Um, because if the blood sort of coagulates, then you may get um, the sorry, this is not supposed to have hemoglobin, not supposed to have platelets in the left hand side. Um So ignore that, that's my fault. So it should. So we're talking about basically causes of low platelets and causes of high platelets. Um So if we just start with causes of low platelets, um sometimes it's just a false result. Um So if you get platelet clumping, then your platelets will appear low. And the way to basically differentiate that is you need to get a blood film. So if you get a blood film and it's worth just googling this if, if you've got a computer next to you, but um on a blood film, you can see loads of platelets stacked on top of each other basically. And that tells you that you've got a falsely low uh platelet count. Um And then other causes include um your marrow bone marrow, basically not producing enough platelets. So that can be in like aplastic anemia where everything will be low. Um Chemotherapies, leukemias as well. Um and then obviously, either our marrow is not producing enough platelets or um our platelets are being destroyed somewhere in the body. So, um, it can be due to immune causes like IP um infections as well. Um, you know, D IC drug reactions, drug induced thrombocytopenia, uh sorry, drug induced um thrombocytopenia from things like heparin. Um And yeah, and the other reason is splenomegaly. So sometimes, um, if you've got splenomegaly, all of your platelets might pool in the spleen and basically get destroyed. So that will cause a low platelet count as well. Um And then for a high platelet count. So again, it could be reactive to several different things. Um Sometimes if you've got a patient with iron deficiency anemia, you might see that their platelets are also raised and it's just a reaction. I'm not really sure why, but those two things sometimes go hand in hand. Um And then obviously to things like infection, surgeries, malignancies, et cetera. Um and a bit like polycythemia, we've also got essential thrombocythemia, which is raised platelets. It's a myeloproliferative disorder. Um And yeah, those are the sort of main causes and yeah, just to reiterate, it should say platelets in that first column, not hemoglobin. Um cool. And then, so I've just got a question on the chart. So how do you actually differentiate um bacterial versus viral infections? Is it just fever and bacterial? Any other signs such as sputum volume or culture? Um So, usually, um, so I'm working on he oncology and usually, to be honest, it's based on all of the investigations you do. So, obviously you'll send, if, if a patient has got a fever or they're spiking, you know, they're spiking a temperature, they're unwell. You would send off blood cultures which may grow some sort of bacterial bug. Um, and you'll be told if it's gram negative, gram positive, et cetera. And in that case, you'll know they've got a bacteria infection and usually as part of the septic screen. So you'll do your blood cultures, you'll also send off a respiratory viral swab. Um Or if they're coughing, then you might do a sputum sample and send that off for M CNS. And, and that would also tell you whether um you know, they've got any bugs growing in their sputum or, or if any of their viral swab results come back as positive, then yeah, you'll know if they've got a viral infection. Um Oh, I think generally I remember often at medical school. Yeah. So you're right about the sputum color. Um Yeah, the procalcitonin is a really good point. Um So if you've got a raise procalcitonin, that tends to be a sign of a bacterial infection as well. Um And so you were asking about symptoms and signs. So, yeah, I know, I know at like medical school or generally people think that if you've got green sputum or yellow sputum, then that's a sign of a bacterial infection in real life or like with patients. I've not really found that to be helpful. Everyone pretty much has yellow sputum. Um, so I, but, yeah, theoretically, yeah. Or, or you should, and you should definitely ask about the color of the sputum and if it's like green then you're more worried but light yellow or yellow sputum, I wouldn't be, I wouldn't rely on it necessarily. Um, and, yeah, I don't ii think, I don't think there's any more anything else really. Sometimes the severity, you know, viral infections can be a bit milder. Um like, you know, rhinovirus is just a mild sort of cough and cold, whereas bacterial infections can be a little bit more serious and cause sep sepsis and bacteremia. So, so, yeah, but yeah, I don't think there's much else I can think of there. Um But yeah, so I've just got a slide here on how to approach anemia. So, um I think it's important to just understand what's going on with our red blood cells in order to understand what then happens in anemia. So everyone's been long on this, but basically our red blood cells go through several stages, both and the bone marrow and the blood as well. So initially, all of your red blood cells are pluripotent, um hematopoietic stem cells, which means they can basically become absolutely anything that they want. Um you know, they can become platelets, red blood cells, white blood cells, et cetera. Um And then eventually after some time and some cool complicated things happen, um They basically become reticulocytes and your bone marrow will throw out a load of these reticulocytes, which are basically immature red blood cells. Um And they don't tend to spend any longer than a day in your blood. Um But if you ever get a blood film, you'll often be able to see a few of these reticular sites because every day, some of them will be thrown out of your bone marrow into your blood. Um And then once you've got your reticulocytes after that, after a day or so, they will then turn into erythrocytes, which are your mature red blood cells. And these have a lifespan of about 100 and 20 days in your blood. Um after which they're destroyed um in the spleen. And then I've just got a photo just to remind you guys of um or, or to remind myself as well, really, this is what a hemoglobin um molecule looks like. So you've got your two alpha chains, your two beta chains, um And then your he molecule in the middle as well with iron atoms. Ok? Um It's fine, cool. So what can actually go wrong to cause anemia? There's three main things really. So either you're losing blood from somewhere. Um Again, many things. So cancers causing gi bleeds or ulcers causing gi bleeds, um trauma, surgery, heavy periods, um or you're not producing um enough red blood cells. We'll talk about what causes that um or you are producing red blood cells, but they're just very frequently being destroyed and aren't actually lasting in your system for 100 and 20 days. Um Yeah, and then this is just a nice um schematic to show you causes of sort of decreased production and increased destruction of the red blood cells. So if we just start with the left hand side, so things that cause decreased um production. So you've got your nutritional deficiencies that can be iron b12 folate um as well. Um and then also reduced bone marrow. So if you get bone marrow infiltration with things like leukemia and lots of white blood cells, then that basically stops your bone marrow from being able to produce all the other cell lines. So you might get low platelets, low red blood cells, but obviously have a very high white blood cell count because of the leukemia. Um And then sometimes when you've got a lot of inflammation in your body um or in genetic disorders like thalassemia, um you, you do get red blood cells being formed but they're just not formed in the correct um way necessarily or with the correct amount of alpha chains and beta chains. Um So there's that as well. Um And then if we talk about increased destruction, um so which, which is also called hemolysis, we split that into intrinsic and extrinsic issues. So, intrinsic issues are usually um problems with the actual red blood cells themselves. So they're either not the right shape or they're not working properly. Um Or there's a problem with the hemoglobin, for example. Um and usually most of these tend to be inherited disorders. Um So again, I've split them up. So if you've got problems with the metabolism of red blood cells, um so that's things like G six PD deficiency. Then again, you might get um lower counts. Um And in G six PD deficiency, for example, you get an inability of your red blood cells to respond to hypoxia. Um And so they, they basically get destroyed um under oxidative oxidative stress. So there's that and then problems with the red blood cell membranes. So, all of these funky disorders like hereditary spherocytosis where the red blood cells are very spherical shaped um or elliptocytosis as well. Um And elliptocytosis is rarer than the other one. Um And then obviously, we've sort of touched on the hemoglobin disorders as well. So thalassemia or sickle cell where your red blood cells are just shaped incorrectly. And so, again, tend to clog up in your blood vessels or get destroyed very easily as well. Um So that's of problems with the actual red blood cells themselves if we've got um problems outside of the red blood cells. So that's usually um either problems with the marrow or um anything that we do to the patient like transfusions um then again, we can get low counts. So um in autoimmune hemolytic anemia, you often, that's what A IH A is. You can get antibodies against your red blood cells attacking them. So they get destroyed very easily. And again, if you get um you know, incompatible transfusion reactions, which are very serious. Um then again, your red blood cells will become very destroyed very quickly. Um and then also, um we've got TTP um and D IC, which can basically um cause sort of mechanical trauma to your red blood cells and cause your red blood cells to just share within your blood vessels and, and get destroyed. Um So, yeah, and then um so this is probably one of the most important slides of the, of the whole talk. So, um if you remember back to, I said, when you look at your hemoglobin, uh hemoglobin level, you want to check your M CV as well if you've got a low hemoglobin. So, um we get low normal and high MC vs. Um And so of course, causes of a low M CV. So usually this is iron deficiency anemia or thalassemia as well. Um and sometimes anemia of chronic disease, but anemia of chronic disease tends to usually cause a normocytic anemia. So, a normal M CV. Um and then I've also put some rarer causes on there which you don't really need to know about, but just good to be aware of for SBA S So things like lead poisoning, um sideroblastic anemia and hookworm as well. Um So those are causes of a low M CV. Um And then if you've got a normal M CV, then the, the commonest one usually is anemia of chronic disease. So that may be due to renal disease or inflammation anywhere else in the body, um myeloma as well, for example. Um So yeah, and then also acute blood loss from anywhere in the body, um increased plasma volume. So if you're pregnant or you've got a lot of fluid overload, then your red blood cells will just get diluted. Basically. Um that can cause a normocytic anemia. And then sometimes um if you've got a patient who's just deficient in all of their nutrients, and if they've got a low iron, which causes a low MCV, as well as a low B12, which tends to cause a high MCV, then those will sort of balance out and give you a normocytic um uh and normocytic anemia with a normal M CV. Um and then hemolysis as well. Um and then causes of a high M CV. So that's the other end of it. So that, that's your B12 folate deficiencies, um alcohol or any sort of liver disease. Um And hypothyroidism is, is the other sort of main one. So yeah, and unfortunately, it's something you just have to memorize at some point. Um It may come up in Aussies, you may get a full blood count given to you and you have to sort of talk through your differentials um, of what it could be really. Um And then the other thing that, um, I never really understood at medical school, but, um, that people tend to look at a lot is the reticulocyte count. So, if you remember, I said reticulocytes are your immature red blood cells, the ones that only last in the system in your blood for about a day. Um So if you've got low reticulocytes, it means that your bone marrow is not, not throwing out enough of these reticulocytes. And basically, it's not able to make enough new cells um to then send into your blood. So with low reticulocytes, always think that you, you have a bone marrow issue going on. Um But on the flip side, if you've got a high number of reticulocytes with an anemia, then it means that your bone marrow is working because it's sending out uh it's, you know, pumping out all of these immature red blood cells. Um but the problem is happening somewhere outside the bone marrow. So the red blood cells are being produced. Um but either they're being destroyed or you're losing them through bleeding. Um, et cetera, et cetera. See you and then just to go into the different types of um anemia. So, obviously, the commonest type of anemia is iron deficiency anemia. And it's important to not just um you know, label a patient with iron deficiency anemia, we need to actually figure out what the cause of it is because there are just so many different things. Um And often with, depending on the gender of the patient and depending on the age, the patient, you'll be more suspicious about sort of different things. So if it's a woman um always ask about um heavy periods. So menorrhagia basically, um or you know, they may have stuff like fibroids which can cause a lot of bleeding. Um and therefore cause iron deficiency anemia. Um But if you've got say an older patient or a patient who's come in with, with other red flag symptoms, like weight loss, night sweats, fevers, um then be more worried about possibly a malignancy or a gi ulcer that's been chronically bleeding um or just sort of general chronic blood loss from, from anywhere else. Ok. Um And obviously, in relation to all of that, make sure you ask about any blood in the stool and the color of their stools as well because black stools were thinking Melina um from an upper gi bleed. Um and then just some other causes. So I've I told you about pregnancy causing dilutional anemia, um malabsorption. So, celiac disease h pylori. Um and yeah, just a couple of other things on there. Um And in terms of your uh test results, again, people sometimes find this quite confusing. Um But ferritin is basically the stores of iron in your body Um So someone just said you have to leave. Yeah. So our, our whole, this whole lecture is gonna be recorded and then eventually put on either youtube or be available on medal. So don't worry, you'll, you'll be able to access them. Um But thank you for coming. Um So, yeah, so ferritin is a store of iron in your body. So obviously, if you've got low iron, you'll have low stores of iron, therefore causing a low f low ferritin. Um And then transferrin is what basically binds to iron in the body. So, um if you've not got enough iron because of the deficiency, you, there won't be any of it or very little of it basically bound to transferrin. So the amount of transferrin that's saturated with iron will be low if that makes sense. Um And then serum iron will be low because obviously, you don't have any of it. Um But T IC which is your total iron binding capacity that will be high because it's sort of the opposite of transferrin saturation. It, it sort of means that there is a lot of capacity for um for you for the transferrin to bind the iron um because not much of it is bound at the moment. So that's why that's high. Um But yeah, I hope, I hope I didn't confuse that too much. Um And then the treatment, so several different ways you can replace iron. The commonest in the community is oral iron. Um we usually give that as either ferrous fumarate or ferrous sulfate. These oral iron tablets tend to have a lot of side effects in particular gi side effects and that should say nausea, not nausea. Um But yeah, people tend to get either constipated or have diarrhea can often feel quite sick with it. And we tend, we used to give people um a tablet three times a day, but most trusts have now moved to saying that one tablet a day is sufficient um because that's just much better tolerated in terms of the the gi side effects. Um And then, and also people tend to tolerate fumarate better than sulfate, but fumarate is more expensive, which is why people sometimes won't be happy to give it. Um And then yeah, it's recommended to take it, take these tablets of the Vitamin C because that increases the absorption of iron. Um but avoid tea and coffee around the times that you take your iron tablets because they can decrease um the absorption. So that's just good advice to give patients. You could get an AUS station asking you to explain um to a patient how to take the iron tablets. So important to say those things. Um And then it's much rarer, but sometimes if someone's got really low iron and they're not able to absorb oral iron, so maybe they've got celiac disease or they've had bowel resection, for example, then we could give them IV iron. Um but it tends to not be very well tolerated. Um And you just have to be very careful around giving it. Lots of people also react to IV iron. Um So they have to be very closely monitored. Um And then obviously in very severe cases. Um So on my ward, for example, where we've got all of these hematological malignancies, um patients tend to be very pancytopenic. So get daily um blood transfusions um to replace, to replace the, you know, low hemoglobin. Basically um a couple of questions. So um transfer, could you explain the transferrin saturation again? Yeah, sorry. So basically tran transferrin um binds to iron in your body. So if you've not got much iron in your body, it's not really gonna be bound to the transferrin. So your transferrin is gonna be basically very free to bind to loads of iron. Um So that's why the amount of transferrin that's saturated with iron is going to be low cos you don't have iron if that makes sense. But just let me know if that's confusing. Um Yeah. And then the next question. So are both fumarate and sulfate available on the NHS. Do you ever need to give a? So, yeah, they're both available on the NHS. It's just sulfate is cheaper. So um most GPS and initially in hospital, we tend to try sulfate. Um And if that doesn't work, then we can, we can try fumarate instead and then do you ever tend to give a prophylactic prophylactic laxative? No, never, never really. Um, because, I mean, I don't know the exact numbers, but I think diarrhea is probably equally as common as constipation. So you, you don't know which way the patient's gonna go basically. So there's no point. Um, and as far as I've seen patients, I think one tablet a day is ok for most people and tends to reduce the side effects significantly. So they don't usually tend to need anything. Um Or sometimes people recommend uh the other common regime I've seen is one tablet every other day. Um See you. Um What and the other question was, what about iron deficiency with a normal hemoglobin? Have I talked is that it's not really in my talk. Um Good point. I should have probably included a slide on that. Um But if I just go back to the causes. Um Oh, sorry, never mind. I misunderstood your question. Iron deficiency with a normal hemoglobin. I've never really seen that, to be honest, maybe a and can help out with that. Um But I, yeah, I've never really seen an iron deficiency with a low normal hemoglobin. Um I mean, if it's very mild iron deficiency, then maybe you'd have a normal hemoglobin and we wouldn't really treat that. Um We tend to get more what, what sort of happens is that a patient comes in very tired or whatever and you do a full blood count initially, you notice that they've got anemia and only after that do you send off um hematinics? So, iron levels, uh folate B12, et cetera. So usually it's, you know, we were triggered by a low hemoglobin and then find out that the patient has iron deficiency. Um So, yeah, I've, I've never really come across it the other way around, but that's interesting. Um So the next thing to talk about is um megaloblastic anemia. Um So that's where you've got a high M CV. Um And uh OK, I'm sorry, I was just reading the chart, interesting stuff. Um So yeah, so megaloblastic anemia. Um and what we, what we mean by this term is you've basically got um a da delayed maturation of the nucleus of your red blood cells. And that's because you've not got enough DNA being made. And there's two main reasons for why um we've not got enough DNA being made for our red blood cells, either your B12 levels are very low or your folate levels are low. And I'll talk about that in a second. Um But basically what happens when you've got these, you know, um defective red blood cells basically is that they um get a very reduced survival time. They're just not able to be present in the system for as long a period of time and what you will see on a film. And I think I've got an example of this on the next slide is you'll get these very large red blood cells because the M CV is big. Um And you'll often see multilobed neutrophils, which are basically just immature neutrophils um within the circulation. So, splitting it up into B12 and folate deficiency. So, um b12 is absorbed in your terminal ilium, which is why sometimes patients with Crohn's disease as well will have low B12 levels. Um But the sort of classic cause that you may see in SBS is um pernicious anemia where you get antibodies against your parietal cells. So they don't produce enough intrinsic factor and we need intrinsic factor to bind to B12 in order for it to be absorbed in your terminal ilium. Um So that's the sort of main cause of B12 deficiency to remember alongside, obviously, um you know, nutritional intake and being vegan, for example, or not having enough um as is in the photo, not having enough sort of eggs, meat, dairy products, et cetera. Um And then if you've got very severe cases of B12 deficiency, very rarely, you can get neurological symptoms. Um So, you know, you'll often hear about subacute combined degeneration of the spinal cord um which is where you basically get um your dorsal columns uh have undergo demyelination and that can cause a range of neuro symptoms. So, things like unsteady gait loss of proprioception, et cetera. Um And then we've talked about malabsorption. So, Crohn's gastrectomies um et cetera and then uh folate. So, main source of folate is your green leafy vegetables. Um and folate is absorbed in your um in the, in the upper part of your um abdomen. So the duodenum and the um jejunum. So again, any issues with those, then you may have folate deficiencies. And then the key thing is if you've got a pa patient who's got both B12 and folate deficiency, um always give the B12 before folate, not the other way around because you can then um you may trigger the whole sort of subacute degeneration of the spinal cord. Um and that sometimes comes up in SBA S actually um and then causes so dietary malabsorption we've said and treatment for folic deficiency is folic acid five mg once a day. Um I should have put it on here, but for B12 deficiency, um usually depending on how severe it is, we either give oral B12 supplements or in more severe cases, especially if they've got neurological symptoms, then we will give um injections of B12 as well. And then this is just a blood film very briefly to show you what um megal megaloblasts look like. So these are the, these huge red blood cells that you can see they're very big. Um And you know, we'd expect them to be a lot smaller and then in the top right hand corner, you've got a um hyper segmented multilobed neutrophil. Um And that's what it tends to look like. Ok. Um And yeah, someone just asked, but we'll just, um, sorry, we're running quite behind. But, um, here's a, here's just a slide for feedback. If we could just pause for a couple of minutes, you guys could just fill out the feedback. We'd be really grateful, um, takes no longer than a couple of minutes and it's just really helpful for us to, um, plan our future sessions and sort of see what went well, what didn't go well, et cetera. So I'll just pause here for, for a bit. And there's just a question on the chart. Can chronic use of PPI lead to B12 deficiency? Um You're, I think it's not very well studied, but you're right. There are some cases of um PPI use or high dose PPI use leading to B12 deficiency. Um We actually had a patient recently who had a, a low B12 that just wasn't improving. And then we found out that this patient had been taking um lots of lansoprazole without us knowing basically from wherever they sourced it from. So, and in that case, yeah, we basically stopped the, the PPI but the B12 didn't really come up so questionable, but there's definitely a um a sort of link that people have written lots about. Ok. OK. So I'm just gonna power on in the interest of time. Um So let's just talk about hemolysis. So, um hemolysis basically means a destruction of red blood cells. Um Obviously, it's, it's not normal. We don't expect this to happen and we tend to split hemolysis up into intravascular. So red blood cells breaking down within your blood vessels and extravascular. So that's um red blood cells breaking down in your other organs. So your spleen um or your liver as well. Um The main symptoms to watch out for with hemolysis are um jaundice. Um reason being when your red blood cells break down, you get a release of lots of bilirubin as a breakdown product. Um And that then basically causes jaundice. Um splenomegaly happens because when your red blood cells um are being destroyed, they will basically sequester in the spleen in order to be then removed from the um from your system. Um And then, so in the, on the image on the right, um I've got an example of a child who um probably has thalassemia, but you can see they've got a, they've got a lot of frontal, they've got what we call frontal bussing. So the forehead's just sort of enlarged and protruding forward. Um And the reason for that is because they've got chronic hemolysis. Um and their red blood cells are breaking down very often. Their bone marrow is working extra hard to then produce more red blood cells and your bone marrow basically enlarges and that can cause all these skeletal abnormalities um as well. So, so, yeah, um and then it's hemolysis usually gives you a normocytic anemia um with raised reticulocytes because the problem is not with your bone marrow. Your bone marrow is working fantastically, which is why it's enlarging and giving you skeletal issues, raised bilirubin and raised LDH as well. Um The other blood to look out for is haptoglobin. So, haptoglobin is basically a molecule that binds to any free hemoglobin in your plasma. So if you're having a lot of hemolysis, you'll have a lot of free hemoglobin in your plasma because it's being released from your red blood cells. So all of that will bind to your hemoglobin. Sorry, it will bind to your haptoglobin and then your haptoglobin levels will decrease. Um because they're all being occupied with a hemoglobin basically. Um And the other key thing is the direct antiglobulin test. Um So we often do this when we're suspecting autoimmune hemolytic anemia. And the dap test basically detects antibodies on your red blood cells showing us that um you know, yes, they've been marked for destruction. Um And we've got an autoimmune process going on. Um Yeah. So, so someone just said, can you show us the slide of the megalosticta anemia? So here it is. Um and, but the main points were really just you get these really enlarged red blood cells. Um again, ii should have put a picture next to it to compare to normal red blood cell sizes, but just take my word for it. These red blood cells are very, very big. Um and just very sort of perfectly circular, um, which, which isn't normal. And then you've also got a hypersegmented neutrophil. So, multilobe neutrophil in the top right hand corner. Um, which again is a sign of megaloblastic anemia? Oh, sorry, before that. Um, yeah. Did you want me to talk about anything in particular or did you just want to see the slide? Mm. I might just pop it back up at the end. Um, if we've got time, just, just cos I'm wary that it's eight o'clock and everyone probably wants to um have dinner or something. So just remind me, but I'll put the slide back up at the end in case you wanted to read over it or ask me any questions. Um So yeah, so um next slide, so I just wanted to speak about clotting very briefly. Um You just wanted to see the slide fine. Um So, so yeah, so clotting. So there's two main things to think about with clotting. Um So we have what we call sort of primary hemostasis and then you get secondary hemostasis as well. Um And if you just look at the picture on the right. So what happens essentially is when you get injury to a blood vessel, your blood vessel will vasoconstrict um to, you know, stop anything getting to it and then you'll get loads of platelets being attracted to the site as well. Um They all clump together to form a platelet plug and basically block off whatever defect was um made in the blood vessel. And this whole process of vasoconstriction and a platelet plug being formed is what we call um primary hemostasis. Basically. Um once that's happened, so once you've got your platelet plug formed, um you'll then get various sort of clotting factors being and you know, all part of the coagulation cascade also being attracted to the to the site of platelet plug formation. Um And this is what we call secondary hemostasis. So, secondary hemostasis is that whole sort of coagulation cascade that you may or may not remember from, from preclinical years. So, with our clotting disorders, it's just important to think about it in terms of, is this a problem with primary hemostasis clotting or is it a problem with secondary hemostasis? Um So, yeah, and just next slide again, I'm not going to spend very long on this because um it's a very preclinical thing, but just to remind you guys, um the coagulation cascade. So we have the extrinsic pathway which is measured by the prothrombin time. So pt and really, to be honest, we use the I NR um and the intrinsic pathway as well, which we measure using a PTT and eventually these two pathways basically converge um to um form the clot, which is, which is where you get fibrin formed right at the end from fibrinogen. Um So, yeah, but I won't go over the numbers, but just useful to, to recap. The main thing is remember, extrinsic pathway, prothrombin time, intrinsic pathway A PTT. Um So, um with abnormal clotting, um to think about what's sort of causing your abnormal clotting, we need to think about what the A PTT and the PT is. So, if you get a very long prolonged um A PTT, we're thinking about things like um heparin um hemophilia as well. Um Von Willebrand's disease because that um involves factor eight and then just a few other things on there as well like D IC liver disease, Vitamin K deficiency. And um if you sort of really look into all of these um different diseases or so with things like hemophilia, um A hemophilia B, et cetera, you'll, you'll realize that basically one of the factors in the intrinsic pathway will be going wrong and therefore causing a prolonged A PTT. Um And then it's just the opposite for prolonged PT. Um Warfarin can sometimes um cause both um as can Vitamin K deficiency um as can liver disease because they just sort of cause a generalized effect on the whole coagulation cascade. Um So, yeah, again, like I it, it's very difficult to sort of memorize these and learn these, but if it helps, just think back to what factors are actually involved in each of these diseases. Um And then when we're thinking about thrombosis, so abnormal clotting, basically causing things like DVTs P ES. Um Main thing to remember is Weal's triad, which is this sort of triangle on the right. Um Three main things that contribute to excessive clots in the body. So, stasis of blood flow, um any injury to the endothelium of blood vessels and also hypercoagulability. Um And obviously, um sometimes in an osk, for example, you may get a VTE risk assessment or um you may get a patient who's presented with a DVT or a PE. And it's always important to ask for any risk factors of thrombosis, um which are all of these things on, on the left hand side. So age, the older you are, the more likely you are to get a clot. Um immobility, which is why all of our hospital inpatients are on prophylaxis, um prophylactic rather low molecular heparin. Um And then all these other risk factors like obesity, pregnancy, malignancy, um flights as well to ask for. Ok. Um and then thrombophilia. So, um usually when you get um a patient who's had clots, so like DVTs or P ES um in nine times out of 10 people, it's not due to inherited thrombophilia. And it's usually just because of one of the risk factors listed on the previous page. Um But sometimes if you're in a bit of a um more nuanced situation, so you've got a younger patient us and, and the sort of arbitrary figure we use is someone less than 40 or someone's just getting loads of recurrent clots or they've got clots in a really sort of unusual site like the brain um or the spleen, for example, then you want to think about whether they've got something inherited. Um It's always good to check for the full blood count as well because um our myeloproliferative disorders. So things like polycythemia thrombocytosis, they cause our blood to become very sticky. Um and can also cause, you know, if your blood's sticky, that can cause clots as well. So just exclude those conditions. Um But after that, the commonest inherited disorder is Factor Five Leiden. Um And basically, if you've got this inherited condition, it causes protein C resistance. Um And again, you may or may not remember, but protein C and s are important in fibrinolysis. So, breaking down any clots in our bodies. So if we don't have these proteins, then our clots can't be broken down. And therefore, you know, you get clots basically. Um So, yeah, and then I've just, I'm not gonna go through them all, but I've just listed some other inherited sort of thrombophilias here. Um But main one to remember is Factor Five Leiden. Um Yeah. And then yeah. So the other big topic in hematology is um transfusions. Um So, and, and the main thing to remember with transfusions really is the types of reactions that patients have. So again, we've just got um five different ones on here. But if we just start with hemolytic transfusion reactions, so these are a never event, they're very, very serious. You hopefully will never see one because it, it just never happens or shouldn't happen. Um, but it's basically where we give the wrong blood to, um, the, you know, the patient or, or, you know, patients actually receive each other's blood, for example, but it's very bad. Um, and you'll see this reaction happen immediately. So within minutes, patients will present with things like um, vomiting, headaches, chest pain, shortness of breath. Um, and also they will, in most cases be hemodynamically very unstable. So their obs will be completely off. Um they'll be tachycardic, hypotensive, be spiking temperatures. So yeah, it's, it's a very acute situation and to manage it, obviously, the most important thing is immediately stop the transfusion. Um You need to inform the laboratory, um the transfusion lab um and the hematology lab of what's happened and check the id of the patient and just make sure that you, you or whoever hasn't actually given the wrong um blood. Um And then obviously get IV access fluids and bloods are very important. Um And then because they'll most probably they will be um their SATS will be low, you want to give them oxygen. Um and obviously escalate and get your seniors involved as soon as possible. Um The main thing to remember is stop the transfusion. Um And then you can also get what we call non hemolytic transfusion reactions. Um So these are basically where patients do get fevers um after starting a transfusion, but they won't really be hemodynamically unstable. So you won't get a low BP, um you know, tachycardia, um et cetera, or at least it won't be as severe. Um And they're usually caused by antibodies in the recipient's blood, um reacting to the blood that's being given to them. Um It's nowhere near as serious. We can manage it by just slowing the rate of the transfusion. So usually we give one unit of red blood cells over two hours. So I would just slow it down to one unit over four hours or five hours, for example. Um and obviously to manage their fevers, just give them some paracetamol. Um So yeah, and then the other common one, which is probably the commonest reaction we get to red blood cells is an allergic reaction, um which can be sort of very variable people. Patients might just get a bit of a rash or urticaria um or on the flip side, they may um get anaphylaxis to the red blood cells, which is again, very rare. Um It's more common to just have a bit of a rash um which if mild, you can treat with um steroids. So, hydrocortisone chlorphenamine as well. Um sometimes um our patients are just prescribed these things prophylactically anyway, in case they react um on the, on the P RN side of the drug chart. Um And obviously, yeah, again, slow down or stop the reaction, uh the transfusion for a period of time. And then anaphylaxis, I'm sure you will know how to manage adrenaline. Um And obviously, with anaphylaxis, you should stop the transfusion as well. Um And then we've got two very similar things. So we get taco and trolley. Um So taco um tends to basically happen in patients who've already got a problem with the heart. So, um they may have heart failure, for example, um or something else and it presents very similar similarly um to pulmonary edema. So you might get bibasal crackles, um peripheral edema, you know, in the hands and feet, um shortness of breath, et cetera, um and also hypertension. So, and I'll, I'll talk about Charlie in a second. But the main way to basically tell the difference between whether you've got Taco or Charley is that in Taco, you'll have a very hypertensive patient. Whereas in Charley, you should have either a normotensive or sometimes a hypotensive patient. Um But with Taco, um they're overloaded. So we want to slow the transfusion down. And with our heart failure patients, we give, we prescribe them the unit of blood much slower anyway, so about 4/4 hours um and obviously consider oxygen and furosemide is often given with the actual red blood cells. So it will run at the same time um as well as afterwards. Um if someone's having multiple transfusions, sometimes we just have a rule of furamide with every other unit of blood, for example. Um And then Charley So Charley presents a lot like acute um respiratory distress syndrome, um tends to come on a little bit slower than um taco. Um and again, does have very similar symptoms. So, respiratory distress, hypoxia pulmonary infiltrates. Um but um like I said, their BP will be either normal or low and they may have a fever as well and in terms of managing it. So, same as Taco stop the transfusion, um we don't slow it down, we tend to just stop it, give them oxygen as needed and escalate up. I would escalate with any of these things. There's an F one. But yeah, and then um just do a quick. So I'm not going to spend too long on neutropenic sepsis because it was covered um in the oncology talk that I gave a couple of weeks ago. Um But essentially um very important in hematology. It's the main um oncological emergency as well as hematological emergency. Um And usually we're just referring to a neutrophil count of the people have different cut offs, but sometimes it's less than naught 0.5 sometimes less than one. And alongside that, you'll also have either a raised temperature or um other signs of sepsis. Patients won't always have a raised temperature because if you're immunosuppressed, then you've not really got these sort of immune cells to actually produce a temperature. So, um it, we basically say neutropenia as well as either a fever or any clinical sort of indications of sepsis. Um, several different risk factors as I've listed there, um, with signs and symptoms. Main thing to note is that it can present very non specifically. Um So if you've got enough white blood cells, then usually your body is very good at, um, you know, pointing to the source of infection. So you'll cough if you've got a chest infection or you'll, you know, have an obvious sort of rash if you've got cellulitis or something. Um But with these patients, because they've not got any neutrophils, often, we, we'd never find the focus of infection, um which is difficult. Um And I think it's in about 50% of patients, we never know what, what the source was. Um So just be aware for someone who's generally very unwell, has got low neutrophils, be really worried about neutropenic sepsis. Um Obviously examine them very thoroughly and look for the source. So any coughing urinary symptoms, any pain or swelling around any of the sort of arterial or venous lines as well. Um And then with management, main thing to remember is um tazocin is the antibiotic that is pretty much trust guidelines everywhere. Um It's also called Pipracil and tazobactam. Um So, yeah, so that's, that's the sort of main thing. Sometimes people also add amikacin. Um But yeah, yeah, as long as you say tazocin, that's great culture, the patient do your sepsis six. And then in some patients, we would also give them G CSF, which you might see um named as Filgrastim, which is basically just a um stim dating factor that people get as injections. They're subcutaneous injections and it causes or it helps their um neutrophil counts recover um a little bit quicker than they would otherwise. And obviously call hematology if you've got a patient um with neutropenic sepsis. Um Quick note on myeloma, um main thing to say is you've got your um crab features um is the sort of pneumonic to remember. So, hypercalcemia, renal failure, anemia, and bone lesions. Um And in your SBA S, if you've got an elderly patient who's come in with hypercalcemia and worsening renal failure. So, you know, you, they'll tell you that their EGFR has decreased or their creatinine has exponentially increased. Um then be very worried about myeloma. Um And what is myeloma? Well, basically, um it's a, so your, your plasma cells basically clone. Um and you get a singular plasma cell clone which makes only one type of immunoglobulin. So that could be IgG um G so gamma or IgG G A um MD E et cetera, there's several different um immunoglobulins that you can make. Um but you basically just get one of them being produced. So we'll often say things like, oh, this patient's got an IgG G myeloma or IG um sorry, an IgG G A myeloma or IG GD myeloma or whatever. So it just means the main sort of immunoglobulin that's being overproduced. Um But anyway, you get too many of these immunoglobulins and they can then basically clog up your kidneys and therefore cause kidney failure. Um And they can also sort of build crowd out your bone marrow. And if that happens, then again, it reduces the capacity of your bone marrow to produce your um your hemoglobin. So you'll get anemia. Um And then all your other counts can be low as well as your white blood cells and your platelets. Um And then so in the image in the bottom left hand corner, um it's what I think. So some people call it a pepper pot skull. Um There's several different ways of describing it, but essentially, that's um bone infiltration of the myeloma plasma clones um across this patient's skull. Um And also sometimes as you can see on this red blood cell film, you can get stacks of these, of these, of these cells forming. Um which is also another sort of worrying sign of um of myeloma. Um And I there was a rouleau formation, I was trying to remember what the name of this is, but basically, we call so on that film that you can see um it's called a rouleaux formation where the red blood cells basically stack on top of each other. Um And then, yeah, I've talked about the, the, you know, the main features and then you can probably imagine what kind of symptoms patients would get. So, bone lesions will cause bone pain lead to pathological fractures and that's often how patients present. Um and anemia symptoms, bleeding infections, hypercalcemia. So that's your um there's, there's the other sort of pneumonics. So bones stones, grown's psychiatric undertones, et cetera. So just remember your hypercalcemic symptoms too. Um Cool. So just a quick note on um the hematological malignancies, they're very confusing. There's a lot of them. Um but I've just um sort of put the key points on here that you should remember for SBS, they won't really come up in Aussies. Um But obviously the way we split our leukemias is we've got the acute leukemias and we've got the um chronic leukemias. So, in acute myeloid leukemia, which is a l the main thing to remember is um sometimes in ba S you might hear the term A rods um which you, which there's a photo of and you can see that you just get this little inclusion separate to the nucleus of the um white blood cell. And basically, if you hear about our rods, you're thinking acute myeloid leukemia tends to happen in older patients. Whereas acute lymphoblastic leukemia is a disease of childhood. Um So in a ML or sorry, in an older person, be more worried about A ML than A LL. Um And then in A LL, like I said, it's childhood malignancy. It's got a very good prognosis in Children, but much poorer prognosis in adults. Um and the, the sort of symptoms you get across both are similar. So, with both acute uh acute myeloid and acute lymphoblastic leukemia, your hemoglobin will be low. So you get anemia, your white cell count will be um will it can be raised or low. But basically, regardless, you've got white cells that are very immature, not working very well. And therefore you tend to get a lot of infections. Um and then low platelets will of um will result in hemorrhages, um petite purpura, et cetera. Um And then, so you've got your chronic ones. So, chronic myeloid leukemia um is associated with the philadelphia chromosome, um which is basically um associated with this BCR able gene. Again, you may or may not remember from preclinical years. Um But it's good. Well, it's not good. But um the the thing is if you've got this sort of mutation, then we can treat it with a chemotherapy agent called imatinib um which is sort of targeted therapy to that chromosome and to that gene mutation. Um So sort of good and bad, I guess. Um with chronic myeloleukemia, you tend to get massive splenomegaly. Remember the, the three M causes um raised white cell count and then sometimes chronic myeloleukemia can also progress to um become a more acute leukemia and that often signifies very poor prognosis. Unfortunately. Um And then cll so chronic chronic lymphocytic leukemia, very high lymphocyte count. Key sort of buzzword to remember is smear or smudge cells, um, which I may have a photo of, I can't remember, but again, that often comes up in SBA S. So if you see that, think CLL um CLL is way commoner than CML. Um, and usually in elderly patients. Um, and it often actually it is just picked up as an asymptomatic high lymphocyte count. Um, and patients, some patients don't even need treatment um, until they start developing symptoms. So, um so yeah, it's very slow progressing. So that was all of the contents. I've just got some questions on here. Um A few SBA S I'll just make a pull for this one and then we'll be done soon. Don't worry. I think that should work. Let me know if not. So, so, um, so you've got a 56 year old man here. He's had fatigue, weight loss, hemoglobin is 105 low NCV. Um His stool has been darker than usual. What is the most likely cause of anemia that we're thinking of? Exactly. Ok. So, um, so most of you have gone for the correct answer, which is d which is iron deficiency anemia. So well done. Um So the main thing that I'm worried about here in this patient who's got red flag symptoms, so he's had weight loss, fatigue. Um and the fact that he's on a low M CV and dark stool. Um, the main thing I'm worried about here is a GI cause basically. So either a, um, gi malignancies. So that could be gastric cancer or colon cancer, um, or, um, something like a, you know, chronically bleeding peptic ulcer which is causing melena. Um, and therefore an upper gi bleed. And so in both of those cases, we'd be really worried about it being, um, I mean, in both of those cases, we'd, we'd be worried about it being iron deficiency, um, anemia secondary to a gi malignancy or a gastric ulcer. Um Some of the next most popular answer, the only other answer that people picked was anemia of chronic disease. Um It's possible but just remember that in anemia of chronic disease you'll get, usually, it's confusing but usually you'll have a normal M CV, not a low M CV. Um And it's very, very rare to get a low M CV. So for the purposes of exams, I would just, I would just learn anemia of chronic disease as a normocytic anemia. Not a um not, not a sort of low M CV. Ok. But well done. Um So the next question, I'll just make another poll. Yeah. So this is a um 26 year old man. He's had an episode of prolonged bleeding after he had a tooth extracted and he says his dad also had a bleeding disorder. You do his bloods. So, hemoglobin is normal. A PTT is prolonged. PT is normal. What's the most likely diagnosis? No. And I'll just give that a couple of minutes OK. So let's just talk through it. So, um this is a more difficult question and I think everyone was more um sort of torn about what the answer could be. So, um 42% of you went with E Von Willebrand's disease and then the majority of other people were thinking either hemophilia A or hemophilia B with a few of you picking C or D. So, um the answer in this case is e so Von Willebrand's disease. Um So in order to understand why it's Von Willebrand's disease, let's just talk about the other options. So, in hemophilia A, we basically have um insufficient production of Factor eight um which would cause a prolonged A PTT. You're right. Um However, with your hemophilias, both hemophilia A and hemophilia B, they tend to present with much bigger and much more serious bleeds. So people tend to get bleeding into the joints. Um and, you know, just very sort of large bleeds from a very young age. Um and it would be unlikely to present at the age of 26 years. You'd usually have a child coming in as a, you know, new diagnosis of hemophilia. Um the other thing is um both of these diseases. So, hemophilia A and hemophilia B and B, by the way, is a deficiency of Factor nine. But anyway, with both of these diseases, they are X linked chromosomal diseases um which would mean that he couldn't really inherit it from his dad because his dad wouldn't be the one passing on the X chromosome. His um his mum would be so, so, yeah. So that's why it can't really be hemophilia A or hemophilia B. Um, because remember you get your X chromosome from your mum and then the dad passes on A Y to make him to make him a, you know, male basically. So he wouldn't be able to inherit a hemophilia from his father. And the main other reason is you'd expect much more severe bleeds. Um Whereas with um Von Villa brand's disease, the key thing is that you get um mucosal bleeds. So that's much milder things. So things like uh nose bleeds, gum bleeds, um you know, pete purpura, things like that under the skin, but it's, you know, nowhere near as serious as massive hemorrhages into your joints. So, and yeah, and Von Willebrand's disease is in terms of its genetics, it's an autosomal dominant disease. So regardless of gender, it will be passed down and can be passed down from father to son. Um But yeah, I hope that makes sense. Um And then someone asked, so it can't be inherited from the father. That's the reason. That's one of the reasons. Yeah. Um But the other reason is also um it uh hemophilia A and hemophilia B wouldn't present with, with such mucosal bleeding and they would present with bigger bleeds into the joints. And the classic story would be oh, you've got a four year old child who presents with an inability to walk or mobilize or is, is just having, um, is, is not thriving basically and has poor growth. Um, and they, and they've got, and the reason why they can't mobilize is they've got massive bleeds into their joints. Um, typically the sort of knees, um, rather than mucosal bleeds, um, which are much milder and therefore caused by the milder Von Willebrand's disease. Ok. Um So you and then next question, oh, this is a bonus question. Um If the previous man with Von Willebrand disease developed more significant bleeding, what could you give him to stop the bleeding? Also, I appreciate we didn't spend long speaking about these inherited conditions just because we don't have time. Um But I will do my best to explain as much of them as we can and maybe we can have another talk going into those in more detail and here's a pole. OK. So again, sorry to rush you guys on just worried about time. So um let me just look at your responses, but I'll start going through it. So, uh 41% of you very mixed responses, but 41% of you picked, see um desmopressin, which is the correct answer. Um Reason being so desmopressin, um often used an endo but also used in heme for patients with Von Bilbray disease who are having bleeding that isn't stopping. So, you know, if they've got, um, nosebleeds that have now been going on for hours and nothing's helping. Um, the reason is that, um, I don't know how, but basically desmopressin um, stimulates the release of Von Willebrand factor from the stores of Von Willebrand factor in your body. Um, so that would basically cause more of it to be released and therefore help stop the bleeding. There is like a very severe funny type of Von Willebrand disease where um they don't produce Von Willebrand factor at all in the body. And so giving desmopressin wouldn't help because they don't have any stores. Um But for our purposes, we're just going to assume that this guy has the commonest type of Von Willebrand disease, which is just caused by um which yeah, in which he does have stores, they're just not released very well. Um And then factor some of you picked factor nine. So not really factor nine. Sometimes factor eight, concentrate can help, but we very rarely use it. Um It wouldn't be, we wouldn't give him platelets because there's not a problem with platelets in Von Willebrand's disease. And then Vitamin K is usually used for um warfarin reversal of bleeding. OK. And G CSF um like I mentioned earlier is to stimulate the production of neutrophils if you've got someone with neutropenia. Um next question. So um in this question, we've got a eight year old child brought in by her mum um because her mom has noticed this rash that you can see in the photo. Um There's no past medical history other than a chest infection one week ago, um you can see the full blood count there. Everything is normal other than her platelets are very low at seven. What's the most likely cause? Thanks. Ok. Um So quite an even split, the two most common answers that you guys have given so far are B and D so immune thrombocytopenia and reactive thrombocytopenia to infection. Um You're absolutely right to narrow it down to those two differentials. Um And I'll talk about why one's correct and the other isn't, but the correct answer here is immune thrombocytopenia. Um So let's go through the, so with acute lymphoblastic leukemia, um you would expect all of the other bits of the full blood count to be deranged as well. So, you know, you'd usually expect probably an anemia, so low hemoglobin and you'd expect the white cell count to be very raised. It might be in the thirties, forties, fifties, et cetera, whereas it's, it's normal here, it's, it's only nine. So that's why it's not. Um a and then, so I the correct answer is immune, um thrombocytopenia. Um Reason being this is just a condition that is um very common in Children and much more commoner in Children than adults and tends to have a very clear trigger um to, to causing it. So, in this case, this child had a chest infection just a week ago. Um And basically what happens is that um, antibodies are produced which attack the platelets and destroy the platelets, therefore causing this autoimmune reaction. Um And the main way to diagnose it is that when you have a full blood count, if you have an isolated low platelet count, meaning nothing else is deranged. It's just the platelets, then usually it is um immune thrombocytopenia. And that's why you've got the rash in the picture as well. So we've got this um sort of pinpoint um piperic rash over whatever part of the body um caused by low platelets, basically causing easy bleeding into the skin. Um Now I just want to talk about d while we're talking about um b so reactive thrombocytopenia to infection is very similar to immune thrombocytopenia. However, um it's not an autoimmune condition. So your platelets aren't really being destroyed. It's more of a case of it's, it's just a reaction to the infection really. And in reactive thrombocytopenia, you wouldn't expect such a low platelet count. Your platelet counts are more likely to be, you know, like 100 and 20 100 and 30. So, or even perhaps at the lower end of normal. So they may be 1 51 60 for example. Um but single digits, very unlikely, even double digits, very unlikely um to be reactive thrombocytopenia. So, the main way to tell the difference between them two is how low is the platelet count Um So yeah, and then um in D IC again, a bit like a LL, you'd expect more derangement of your, all of your full blood count and usually D IC will be triggered by a much more severe infection. So, something like um sepsis. And you'd have a, you know, very ill patient in front of you who's basically bleeding and clotting at the same time. Um And yeah, whereas obviously this patient's very unwell but, um, you know, isn't septic or anything. Ok. Question four. Um So here we've got a 75 year old man. He's got type two diabetes, hypertension, heart failure. He comes in fatigued. Um, hemoglobin is 56. So, uh he's sent to his local hospital. He gets two units of red blood cells, but halfway through the second unit, he um becomes very short of breath. You examine him, he's got crackles um to both of his lung bases and a raised GBP as well. What's the most likely diagnosis? This should be a bit more straightforward, hopefully almost at the end. Ok. So, um, so most of you have got the correct answer here, which is um, a taco and a few of you picked B so Charley and no one picked CD or E which is fantastic. And yeah, A or B are your two main differentials? Um The reason why it's a because we've got several risk factors here. So, remember I said that with T so transfusion associated circulatory overload. You've got an overload, overloaded patient, so, too much fluid in the body and he's got a past medical history of heart failure, which is obviously a significant risk factor for that. Um, he may have even come in partially sort of overloaded. You never know. Um So yeah, and then his raised JVP also tells us that he's fluid overloaded. Um So, so that's the main reason. And um, if he or with the, the symptoms, with the symptoms of the shortness of breath, the crackles, um it's less difficult to tell the difference between Taco and Charlie. But the main things here are the past medical history of heart failure and the raised JVP with Charlie. Um, you wouldn't really have a raised JVP. Um And I didn't give you a BP here, but just to reiterate BP would be normal or low in Charley and BP would be raised with T OK. Good question five. I think this is the last question. Um So 70 year old woman has a routine blood test feels well. Um You've got her full blood count there and blood film shows lots of big lymphocytes which are those purple blobs. Um, and smudge smudge cells which by the way, if you can see towards the bottom right hand corner, you've got a um lymphocyte there which looks a bit like a smudge of ink on a piece of paper. That's what, that's what we mean by the smudge cells. Um So yeah, and what's the most likely diagnosis? Ok. I'm not gonna spend any longer on this because most of you have got the correct answer, which is um b so the correct answer is CLL and this is literally just something to remember. So just looking at the full blood count, she's got a very raised um lymphocyte count. Um Hemoglobin is normal. White cell count is raised obviously because it takes into account your lymphocytes, um platelets and neutrophils are normal. So, and the other thing is the smudge cells. So if you remember, I said smudge cells or smear cells as they're often called, um is basically pathic of chronic lymphocytic leukemia. So that's just something you've got to learn. Um Yeah, so well done on that. I was wrong. This is the last question I promise I'm just gonna do last pull. So um here we've got a 67 year old man. He comes in with fatigue and night sweats for the last three months. Um He also complains that he's feeling very full and very bloated when he eats. Um, you examine him and he looks very pale. He's got splenomegaly right down to his umbilicus and also some mild um hepatomegaly as well. What's the most? Oh, I'm sorry. Uh You see a blood film which shows you tear drop cells, what's the most likely diagnosis? And again, I appreciate that we didn't really sort of cover these topics in detail. Um just cause there's so much to cover. But uh yeah, try your best. OK. Um So again, everyone's a little bit more torn in this one, but um about 70% of you have gone for D which is myelofibrosis. Um And then a few of you have picked um a couple of the other answers. Um So the majority of you are right, the answer is d myelofibrosis, reason being so myelofibrosis is what we call a myeloproliferative disorder. And if you remember, um these very commonly cause splenomegaly, um and he's got huge splenomegaly here and they tend to present with very um vague symptoms. So, you know, the fatigue and the night sweats that you've got here, um the sort of abdominal bloating, loss of appetite, et cetera. Um So, yeah, they tend to present very non specifically, but you could argue that those are also symptoms of some of the other things on here, like, you know, lymphoma leukemia, which are the other two common answers that you guys picked. However, um the key thing that gives the an gives away the fact that the answer is myelofibrosis is the blood film here. So, tear drop cells are basically, again, pathic of myelofibrosis. And it's worth just looking up a picture of these. I'm sorry, I didn't include it here. But um you get cells that basically look like tears. And the reason for that is when you've got a lot of fibrosis in your marrow, your marrow is not working very well. It's just full of rubbish, basically. And you know, fibrous tissue, um the cells that are then leaving the marrow have to be squeezed out of this very small space. And so they become squished and look like teardrop cells um and sort of, you know, become squashed on one end. So, so yeah, um again, main takeaway point, if you see teardrop cells mentioned anywhere, think myelofibrosis and pick that as your answer. Um So yeah, and that brings us to the end of the talk. We ran over a lot. I'm sorry, I promised an hour, but um thank you guys for listening. Um Let me know if you've got any questions and please do fill out the feedback form. Um You do get a certificate for attending um if you fill out the feedback form, which is nice for your C vs too. Um And yeah, like I said, just really useful for us to know as well what to improve on um in terms of future topics. And just to say that our next talk is this Thursday and is on endocrinology. Um So do come along to that as well if you're free. Um And it's, it's advertised on Med All and Facebook as well. But yeah, thank you. Yeah, it's, it's recorded, don't worry. Um We will be posting it on I think youtube All Med All. So it will be available. Ok? And Thank you Amon for attending and helping out. So. Ok, great. Thanks guys. I don't think anyone has any questions, so, um, I'll leave it at that. Um, enjoy your evenings. See you later.