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Week 11 - Part 2 - Bloods interpretation and "too much"

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Summary

In this illuminating session, Foundation Year One Doctor Josh introduces medical professionals to hematology, providing key insights into interpreting blood tests and decoding blood pathology. Beginning with the basics of understanding blood results, particularly for a full blood count, attendees are guided through an approach to investigate conditions like anemia and hemolysis, along with understanding the significance of haptoglobin, LDH, and reticulocytes. The session continues with details about the conditions of thrombocytopenia, thrombocytosis, and leukopenia. Key topics like polycythemia, myeloproliferative disorders, multiple myeloma, leukemia and lymphoma are scrutinized, enhancing attendee's abilities to diagnose and manage these conditions, further enriching their knowledge for exams. Join Doctor Josh for an engaging, comprehensive refresher course on hematology that's crucial for any medical professional.

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Description

Hi everyone! This is the video for the haematology part 2 lecture!

Learning objectives

  1. Understand and interpret the results of a full blood count, recognizing values for hemoglobin, white cell count, platelet count, and MCV.
  2. Understand the basis of anemia, including various types based on the MCV, along with appropriate investigations that should be carried out.
  3. Recognize the symptoms and investigations that may suggest there is a process of hemolysis occurring in the body.
  4. Identify thrombocytopenia, thrombocytosis, and their possible causes.
  5. Understand the categories of polycythemia, the causes of each, as well as general treatment strategies.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

You can still see it right. Uh Yes, it's like in the corner at the moment though for some reason, like, it's like half of the screen, like a quarter of the screen. I don't know why it was like that. Is it still like that now? It's not sharing at all? Oh, ok. Uh That's a weird, um, let me try sharing it again. Mhm. Oh powerpoint Life. Ok. Um, yeah, not bad. Is that better? Uh huh. Uh, yeah, this is full screen now. Oh, yeah. Go ahead and stop. Ok, great. Um, yeah, so, hi guys. My name is Josh. I'm one of the uh foundation year one doctors. Um, I'm here to talk to you about your uh second uh um set of hematology presentations. So, uh first of all, just start off by talking a little bit about interpreting blood tests and then we'll just talk about sort of too much in terms of blood pathology. So like leukemias, lymphomas, that sort of thing. Um, ii know hematology can be quite a uh a complex subject and, you know, it, it, you can go into a very thorough amount of detail. Uh But, you know, for like, but, you know, for finals level, I'll just give you the essentials that you need to know and, you know, uh we'll just get started. So we'll talk about bloods first because I think that will help you um understand like the following lecture as well. So we'll just go through um understanding uh blood results particularly for a full blood count. We're not gonna talk about like use and, and all and like everything else, but just full blood count and how it relates to hematology and, and a few other tests as well. So we'll just start off with uh what your full blood count consists of. It consists of things like your hemoglobin. And I'm given all the normal preference range values on the screen, uh your white cell count, your platelet count and your MCV. And you know, you can also um add on to that like a coagulation profile so that can check your prothrombin time and you activated um partial thromboplastin time or APTT, which basically just assess the different parts of the coagulation pathway. So we'll start off first by a very basic approach to anemia. So the first thing you'd want to do is check if the hemoglobin is low and that will confirm the anemia and then you look into um into uh into the MCV. And the MCV can give you a sort of indication as to what the cause of that anemia is. So, if the MCV is microcytic. It can be causes like iron deficiency anemia or thalassemia, which is like a genetic cause of anemia. Normocytic anemia are caused by anemia of chronic disease. Or when you, when you lose a lot of blood and you can and macrocytic anemia. So when those cells appear very large, that's because of b12 or folate deficiency, you will find it, you can find it a lot also in alcoholics and patients who have pre existing liver disease, you can also check uh uh go into more specific tests. So you can check the reticulocyte count, which we'll talk about in the next slide. Uh you can check ferritin. So if you're suspecting MYC anemia, you, you do ferritin and do like a full on hematinics to uh just to confirm an iron deficiency cause. And you can also check the B12 and folate levels and transferrin is also part of hematinics. We'll just talk about our approach to hemolysis. So, hemolysis is a destruction of red blood cells and that can lead to anemia or sometimes it could also be compensated. So you may not see an anemia. But here here are the key investigations that you should look for when investigating hemolysis. So the first is haptoglobin. Now, I like to think of haptoglobin as a sort of mop and basically when blood cells break up and they release these free hemoglobin proteins. Now, if too much of those proteins are just lying there in the bloodstream, it causes damage, it causes oxidative damage to the body. So you need haptoglobin, which is basically a protein that will just mop up all the free hemoglobin. Now, usually when you have uh in, in the setting of hemolysis, that heptoglobin will be very low because it's all being used up. Next, you want to look at LDH. So when cells break apart, they release lactate dehydrogenase. And so you would expect to see that go up in hemolysis. Um And then you can also look at reticulocytes as well. Now, reticulocytes are immature red blood cells. And usually when there is a loss of red blood cells, the amount of retic, the amount of reticulocytes would increase. And basically, it's a marker that shows that the bone marrow is working well and it's doing what it's supposed to. And in a way it's a way you can see how well the bone marrow is compensating for that red blood cell loss. Uh Next, we'll just look at platelets. So, uh you know, a platelet count of less than 150,000. You, you can characterize that as thrombocytopenia. And you know, there's a variety of causes to that. You can get immune thrombocytopenia, uh which is an autoimmune disease that destroys uh uh platelets. It can also indicate a bone marrow failure and a condition called D ID DD disseminated intravascular coagulation. And like, you'd find that in incredibly unwell patients, thrombocytosis is what you'd expect when the platelet counts are more than 450,000. And you know, there's a variety of causes to that. Um um as you may know, platelets are a uh are a um are acute phase reactant. So they tend to go up in the setting of infection or inflammation or they can even go up with essential thrombocythemia, which we will talk about in the next lecture, uh going over leucocytes. So when you have a increase in the number of leucocytes, um it's called leukocyte leukocytosis. A subset of these are neutrophilia. So that can happen in the setting of inflammation, infection or when patients are given steroids, lymphocytosis. So, you know, viral infections or with leukemias, eosinophils tend to go up with in the setting of allergies or parasitic infections. And you know, you can see leukopenia as well, which is a which is a decrease in the white cell count that happens because of bone marrow suppression, viral infections can also cause leukopenia as well as autoimmune conditions like lupus. So, so that was just a quick summary about interpreting blood results. Hopefully, it it should be just like a basic review for you guys. Uh What you have to do is you have to use a very systematic approach. Like I mentioned earlier. First, you have to look at hemoglobin and then uh consider the rest and you know, there's other tests as well like a peripheral blood smear ferritin and haptoglobin LDH that you use as you suspect according to what the rest of the clinical picture looks like and you won't have any questions about that. Ok. If there aren't any questions, I'll just, uh, move on to our next presentation. Um, I think we have around, ah, two hours for this. So II think we'd, we'd probably be done before that. Ah, but if anybody wants to have a break, ah, whenever, just, just let me know or I can stop halfway between our next presentation. Ok. So we'll start our next round then. So, hematology too much. And, you know, we'll just talk about um, basically the, uh, most essential exam, relevant, um pathology, clinical features, diagnosis and very basic management. Ok. And the topics we're going to talk about are polycythemia, myeloproliferative disorders, multiple myeloma, leukemia and lymphoma. And, you know, when I, and when, when you see these three stars on any of the text on the slides, that's usually that, that's a high yield point which you should know for your exams. So we'll start off first with polycythemia polycythemia. Very, basically is an increase in red blood cell mass. And you know, there can be, it's classified in different types, but you know, the first is absolute polycythemia, which is an increase in the blood cell mass itself or relative polycythemia in which the blood cell mass increases because the plasma volume is decreased. So, primary polycythemia is a, is a, is a myeloproliferative disorder called polycythemia rubra vera. And we'll talk about this later on in the presentation. Uh secondary polycythemia is when there is increased erythropoietin or epo. And you know, that's caused by usually chronic diseases. So you'll see it a lot in patients who have COPD, uh patients who have sleep apnea and you know, sometimes there are epo secreting tumors such as renal cell carcinoma that can also cause a polycythemia. There is also a relative poly and relative polycythemia. Like I mentioned, when the plasma volume goes down, that can happen as a result of things like dehydration. So, you know, the general features of polycythemia tend to vary with the cause. They, they can even be asymptomatic as well. Um But the the more like general symptoms you'd get are probably fatigue, headache, dizziness, blurred vision, and you know, to treat polycythemia, particularly with secondary polycythemia and relative polycythaemia is just managing the underlying condition. So you would ensure. So for example, if it happens in a COPD patient, you want to make sure that the COPD is well managed. If it's dehydrated, you want, you want to rehydrate them and figure out the cause of the dehydration and you also want to monitor for complications. So, thrombosis is a complication because you know, when the red cell mass becomes larger and there is more blood in, there is more blood cells in the blood. Things like thrombosis tend to happen. We'll talk next about myeloproliferative disorders So, myeloproliferative disorders is RN is like an umbrella term. Uh you know, there's, there's a few, uh there's like uh there's a few more other than these, but the ones that you need to know for your exam are uh polycythemia vera, essential thrombocythemia and myelofibrosis, particularly, we'll talk about polycythemia vera. So, like I mentioned before, Polycin is polycythemia that is driven by the JAK two mutation and that's really, really high yield to know uh to find. Now, you can diagnose this uh with patients who have a high hemoglobin and a low epo. And the reason that the EPO is low is because it's being suppressed because you're getting the JAK two mutation that's producing this large amount of red blood cells instead. So there is no need for the body to produce its own and that's why the EPO is decreased. And then you can also do jak two genetic testing. Now, uh posit it can also in, in, in I it can also result in increases in the platelets and the white cells too. The clinical features of polycythemia can be very nonspecific. So patients don't come in complaining of fatigue or it could even just be picked up on routine testing when they see a very high hematocrit on the patient's blood. One very key symptom to know is called aquagenic pruritus. Now, basically, in an exam question, you will see this as the patient is having a lot of itching. Um AAA after taking a warm shower and this is just caused by the release of cytokines. Patients also tend to have a have a ruddy complexion. You'll hear that in exam questions as well. Like the face becomes darker. A sort of interesting symptom is called erythromma. And basically, patients tend to have like burning, painful sensations in their tips or their fingers and in their toes. And this is caused by very, very small microvascular blood clots. Additionally, it can also result in hyperviscosity syndrome. And that's when patients can develop headaches, blurred vision because of the increase in red blood cell mass. Uh some complications like I mentioned before thrombosis and you'd see thrombosis in very weird locations. So for instance, you might get a Budd Chiari syndrome as a result of that, which is a thrombosis in the portal vein. Um uh polycythemia vera also places you at risk for hypertension uh gout because there's increased um uh blood cell turnover and splenomegaly. And there is also a risk of polycythemia progressing to acute myeloid leukemia or myelofibrosis, which we will talk about in, in the next slide and in, in a little bit later on in this presentation. So to manage polycythemia vera, uh it's managed with phlebotomy. So patients go and get their blood taken out and you know, they can get this donated as well. Uh It's mostly around monitoring for complications and preventing complications. So, patients are given aspirin as well. Now, if they are unable to manage it with phlebotomy. Then you know, you can give them cyto reductive therapy. So you can start them on jak two inhibitors. An example of this is a drug called Oxolinic and hydroxyurea. And this will help bring the counts down. And this is a slight area that just shows some of the key symptoms and signs you'd see in polycythemia. So next, we will talk about essential thrombocythemia. Now, this is a massive proliferation of platelets and it's also driven by the JAK two mutation. And you know, it's commonly asymptomatic, but you can get headaches, visual disturbances and you know, because there are so many platelets produced and a lot of these platelets aren't functioning well, there is a risk of bleeding and thrombosis. So you you can suspect this in patients who have a thrombocytosis that is not going away. And you know, you'd also want to investigate their LDH uric acid and you can do and you know, the the most definitive test is a bone marrow biopsy and that will show uh raised megakaryocytes and those are the precursors to platelets. Now, one thing that you have to rule out with essential thrombocythemia is you need to rule out a reactive thrombocytosis because like I mentioned earlier, platelets can go up for a number of reasons like infections or malignancy. So you have to rule that out first before considering this diagnosis and you know, this is treated with aspirin anticoagulation or cyto reductive therapies like we mentioned earlier. Now we'll just talk about myelofibrosis. So think about myelofibrosis as bone marrow burnout. And you know, this is because of primary or secondary causes. So for instance, it can be secondary to a disease like polycythemia which burns out the bone marrow because so much red blood cells are being produced and you and you know, the same applies to leukemia as well. And now essentially what happens is that there is a lot of fibroblast activity within the bone marrow and that causes fibrosis. So the bone marrow becomes non functional and this leads to symptoms such as fatigue, fever and weight loss. And you know, because the bone marrow isn't producing the blood cells, like it isn't producing functional blood cells that leads to problems like increased infections, bleeding and thrombosis. And you know, you would expect to see a splenomegaly and hepatomegaly because the blood, because the blood needs to be produced somewhere. And because the bone marrow isn't working, it's being produced in the liver and in the spleen. Now, a very characteristic sign that you'd see of myelofibrosis is something called dacrocytes. And those are basically these teardrop shaped rbcs that you see on a red blood, on a blood smear. You'd expect patients to have anemia as well. You can also do a jak two testing to see if there's any underlying cause. And you know, notably when you try to do a bone marrow aspiration, you'll get something called a dry tap. These patients are very, very difficult to get bone marrow samples from. And you know, you treat this with uh jak two inhibitors, uh hydroxyurea. And you know, in, in, in um in refractory cases, you can also offer patients a stem cell transplant. All right. Next, we'll move on to multiple myeloma. Now, this is a very high yield condition that you'll see a lot on your exams. And you know, we'll talk about the key features here. So, essentially multiple myeloma is when your bone marrow becomes infiltrated with malignant plasma cells. And you know, these plasma cells will produce a bunch of proteins, monoclonal proteins that are non functional. So it does. So you know, the production of these proteins leads to infection risk because these are because because the immunoglobulins don't work properly. They can deposit in the kidney, which is called myeloma kidney and it can lead to and it can deposit elsewhere in different tissues causing an amyloid doses. And you know, you assessed this with bloods doing a urine dipstick. So you are checking for protein in the urine. And you know, one of the more definitive investigations is serum and urine protein electrophoresis. And you'll hear the term M spike used a lot, which is when you will see a spike in the monoclonal proteins from myeloma. And then you would also use imaging to assess for bone lesions, which is very common in myeloma with either X ray or CT. And the definitive diagnostic test is with the bone marrow biopsy. You hear that being used a lot. Bone marrow biopsy is the definitive test for most of these cases. So what you really need to know for myeloma is the crab criteria. So it's an acronym. So to see is for calcium, you'll see, you'll see a raised calcium in these patients renal impairment because you know the myeloma proteins uh can deposit in the kidney and patients can develop renal failure as a result. You also uh you can also see an anemia which decrease the hemoglobin and you'll see bone involvement as well. And this can be li lesions which you can see right here, uh pathologic fractures and bone pain. And um you know, patients can also have these b symptoms. So things such as uh fever, night sweats, weight loss. A lot of times you'll commonly hear patients coming in with back pain too. I don't see a peripheral blood smear showing root. I had a picture here. It didn't, it didn't, I don't think it's saved. But uh it basically, it's like a stack of red blood cells. It's just a sort of a trivia finding. You'll find it's not really in every patient, but the key things to know is the crab criteria and it's a disease of older adults. Now, you uh myeloma is managed with chemotherapy. Uh the two drugs that are um quite common are om and L lenalidomide and you can also give steroids as well. Like dexamethasone. Uh patients can also be treated with a stem cell transplant. And bisphosphonates have been shown to um help for patients with bone involvement and you just want to treat any complications as well. A lot of these patients die from infection or from renal failure. So you definitely want to monitor for that. Ok. So now we'll just talk about our uh like one of the bigger topics in this is leukemia. Uh He here's where things can get a little bit complicated, but I'll try to uh keep things as simple as I can. So what, so what is leukemia? Leukemia is the malignant proliferation of white blood cells. And you know, leukemia involves a bone marrow blood or lymphoid tissue. So, in the lymph nodes and it generally causes an anemia. So, decreased hemoglobin infections and it can lead to hemorrhage because of low platelets. There's so much white blood cells being produced. So there's not enough room for other cells to be produced like uh like hemoglobin and the like red blood cells and platelets. Uh Leukemia can be classified into acute and chronic. So, acute leukemias are rapidly progressing and they affect immature cells and uh the immature cells are called blasts. Chronic leukemias are slowly progressing and they affect more mature cells. And you know, the and it can either be classified and it could further be and you know, acute and chronic, the effect is the lymphoid progenitors or the myeloid progenitors. Um you know, here's probably a throwback to uh to year one or year two when you're learning your basic sciences. But to put this simply, this is just the different cell lines that come from the stem cells. You can see these are the myeloid progenitor cells and these are the lymphoid progenitor cells. So, in your, so the leukemias that will affect the myeloid line are AML and CML. And in these conditions, you would see an increase in these different types of cells. Ok? And when you and the lymphoid line is affected by al or CLL and you will see an increase in these cells. Here, it's a very handy slide to have just whenever you get lost on different terminology of leukemia, you can always refer back to here to see what you would expect to see increased. Ok. So leukemias, so acute leukemias, um we'll start off first with acute lymphoblastic leukemia or al. Now, this is the most common malignancy in Children. And you know, very high yield point is that Children with Down Syndrome are, are at an increased risk. Now, uh i it's less common in adults and you know, when it does happen in, in, in, in adults, it's uh generally a very poor prognosis. So the mutations you'd expect uh that happen in A L are the 1221 translocation and that's the most common favorable prognosis. If you get the nine and 22 prognosis, that's not the, the the prognosis is poor. The leukemias can present in very similar way. So they, you'll have patients coming in and complaining of fevers, chills, fatigue, weight loss, having recurrent infections and having abnormal bleeding and bruising. There is a subtype of at cell A that can present as a mass as well and that can give compressive symptoms. So patients can have trouble swallowing, sometimes have trouble breathing as well. And you know, a is very, very responsive to therapy if it's treated early. So to diagnose al, you would do a bone marrow biopsy and when you have more than 25% lymphoblasts, that is diagnostic for a, you can also do a test called flow cytometry. Now, flow cytometry will assess the assesses the CD markers on the white cells and it identifies if they are a myeloid cell or a lymphoid cell. And this is really how you, how you differentiate between the two. It's treated with chemotherapy. Um one of the drugs is called vinCRIStine and you know, when you treat al, you also have to treat sanctuary sites. So you know, a can um can be present in the, in the cns, the brain and spinal cord or in the testes. So you have to give sort of focused chemotherapy to these regions. And you know, patients who are at very high risk can, can get a stem cell transplant. Next, we'll talk about AML. So, in acute myelogenous leukemia, now, I, in contrast to A LL, this is a disease of the elderly and you know, a L can arise from patients who have prior chemo or prior radiation for another malignancy or myelodysplasia. And you know, A L presents uh um similarly uh weakness, fatigue, anemia, thrombocytopenia, neutropenia. And you know, uh important thing to know is that A ML uh patients are at very high risk for D IC. And you know, there are different subtypes to AML, but the one that you should probably know is a translocation 1517. And that's for the APML subtype. So, acute promyelocytic leukemia. So, uh you know, you can diagnose AML with a bone marrow biopsy. And you know, I think the most, the most important thing to know is uh on a, on a, on a bone marrow biopsy, you will see something called in our rod. Now, this is just a fragment of cellular material in the cytoplasm. And you know, that's a hallmark sign of AML. Again, you can do flow cytometry to determine what type of lineage is affected. And you know, it's treated with chemotherapy. So you can give DAUNOrubicin and cytarabine and you know, patients can also get a uh patients at high risk, can also get a stem cell transplant. And the APML subtype is treated, not APML subtype that we mentioned earlier, is treated with something called all trans retinoic acid. And this is basically a Vitamin A derivative that will cause that will cause the immature cells to that will induce cellular maturation. Ok. We'll just move on to chronic leukemias. So, chronic leukemias will start with CLL CLL is chronic lymphocytic leukemia. And you mentioned earlier, these are, this is when it affects mature lymphocytes. Now, generally CLL is asymptomatic and it's usually a finding it's usually found on routine blood tests. A characteristic sign is patients can develop lymphadenopathy that comes and goes, it's painless. They can also be prone to repeated infections. You know, when you check the blood, you can see um some uh any of your patients can also have symptoms of anemia and thrombocytopenia. So, abnormal bleeding or bruising CLL has a risk of progressing to diffuse large b cell lymphoma and we'll talk about that later. But this is this is a phenomenon known as the Richter transformation. So to diagnose cll, you'd expect to see a lymphocytosis and sometimes you see cytopenias in the blood. A bone marrow biopsy isn't necessary for to diagnose cll. But what you'll see is generally see is a um is more than 30% lymphocytes. And you know, uh interesting finding here is on the blood smear, you'll see something called a smudge cell. And the reason why this happens is because when you put the uh blood film on the slide, these um these uh malfunctioning white cells are really, really fragile and they'll break and that's what causes the smudge. Uh again, you do flow cytometry and you know, patients who are asymptomatic, you can just monitor um their condition. Ok. Next, we'll talk about chronic myeloid leukemias. So CML, CML is a disease of maturing granulocytes. So, you know, when you, so like we talked about earlier, you'd see increase in neutrophils, basophils, metam myocytes and myocytes. And this is a disease of the elderly population. And you know, the the most and this is probably another really high yield point is that the hallmark of CML is something called the philadelphia chromosome. And this is caused by the translocation of chromosome nine and 22 and that forms the BCR able fusion gene. So just remember the Philadelphia chromosome is associated with CML. I've seen that question come up on exams and you know, it's very, very common. CML will present with fever, fatigue, weight loss, um and splenomegaly and night sweats. An important complication of CML is something called a blast crisis. So, it's when this chronic leukemia can develop into an acute leukemia into an acute myeloid leukemia. So to diagnose CML, um you know, you do your bloods, the bloods, you'd expect to see a severe leukocytosis. And you know, another hallmark of CML is an increase in basophil count. So if you see an increase in basophil count, particularly, let's look at just consider CML as a diagnosis, uh you can do a blood blood smear bone marrow biopsy and a flow cytometry. And one thing that you need to test for in CML is testing leucocyte alkaline phosphatase or lap. And you know this will differentiate CML from a leukemoid reaction. So what is a leukemoid reaction? A leuko reaction is the normal reaction to an infection which raises the white cells. So you need to determine how. So you need to differentiate CML from, from the normal response expected in an infection. So, in CML, the lap will be low. You would also do genetic testing for the Philadelphia chromosome. And, you know, CML is treated with, with tyrosine kinase inhibitors that is targeted therapy towards the Philadelphia chromosome. And when these drugs came out, they were quite revolutionary in how they changed, changed the management of this disease. Ok. So, now, ah, we'll just, ah, get on to, ah, lymphoma. Does anybody want, ah, does anybody have any questions so far or does anyone want to take a break? I'm happy to just power through this. Otherwise we're almost done. Ok. I'll, I'll guess I'll, uh, I'll just, uh, carry on then. So, lymphoma. So, lymphoma is a malignancy of the lymphoid tissues and it can be classed into Hodgkin's or non hodgkin's. So, Hodgkin lymphoma is characterized by reed Sternberg cells and that's very, very important. You'll see that on exams as well. And, you know, Hodgkin lymphoma is a type of B cell lymphoma. It has a has, uh, it occurs in both elderly people and in young adults. And you know, it's uh it it has an increased risk with immunosuppression, autoimmune disease and with Epstein barr virus infection. Now, there's different subtypes of this uh generally uh compared to non hodgkin's. Hodgkin's has a better prognosis. So the most common type of hodgkin's is nodular sclerosing. There is also lymphocyte rich and lymphocyte depleted. Hodgkin's and depleted has very poor prognosis. So, how does Hodgkin's present? It can present as a mass. Patients can also have a painless lymphadenopathy in different areas of the body. A a very strange symptom that you may see come up on an exam is pain with alcohol ingestion. So patients will feel uh pain in uh in those lymph nodes whenever they drink alcohol. It's a very weird symptom. It's possibly because of uh due to cytokine release, but just something that you should be aware of. Um patients can also have b symptoms of fever, night sweats and weight loss. Uh It's also, it's diagnosed with a lymph node biopsy and which shows we Sternberg cells. So this is a weed Sternberg cell right here. OK. And you might see it described on an exam question as owl eye nuclei. OK. Um And you might also the question, might also mention an inflammatory infiltrate around it. Uh Now, Hodgkin's is treated with uh chemotherapy and radiotherapy uh through ABVD regimen. You don't really need to know all of these key drugs just know that's treated with chemo. Um But if you did want, it's Adriamycin, bleomycin, vinBLAStine and uh carbazon. So now we'll just talk about non hodgkin's. Now non hodgkin's um has a lot of different subtypes. It's, it can be A B or at cell lymphoma and you know, it, the hodgkin's and non hodgkin's has an increased risk in patients who've had prior radiotherapy chemo patients who are immunosuppressed and it can also be caused by viruses as well. So HIV, EBV and HLT B virus, it can be divided into um into indole lymphomas or aggressive lymphomas. So indole lymphomas are um are for, for, for, for example, um follicular ly lymphoma, marginal zone or um CLL slash SLL. What's a little confusing is a CLL can also present as a lymphoma uh for follicular lymphoma, which is uh one of the more common of the ones. Um that translocation is 14 and 18. That's important to know aggressive non hodgkin's would be diffuse large B cell buckets T cell and male cell. The most you should know that diffuse large B cell is the most common of the non Hodgkin's lymphomas. And in Burkitt lymphoma, you might also see come up, it's caused by Epstein Barr virus. And you'll see, you'll see something called Starry Sky described in the question, which is basically the findings that you would see on a, on a bone marrow biopsy on a lymph node biopsy. So, uh you know, like I said we can go into quite a lot of detail with non hodgkin's. But uh I've just left this all here as a um as a um as a table, you can look at it in your own time. Uh But just generally, you see a note of points that I mentioned uh in the last slide. So non Hodgkin's is treated with an excisional biopsy. And, you know, once you do a biopsy, you, you find out what subtype it is exactly and treat it accordingly generally though there is a treatment regime called R chop. So you can give riTUXimab if it's A B cell, lymphoma, cyclophosphamide, hydroxydaunorubicin, Oncovin and prednisoLONE. OK. So uh does any, does anyone have any questions about, about what we've gone through so far? Because next, I'll just walk through some clinical cases if you guys want to get involved, feel free to just open up your mic and answer and answer the questions. Uh But it's just uh we'll just go through around four cases just going through what you'd classically see on exams in regards to each of these cases, in regards to each of the topics we've discussed. Josh. Yeah, I just thought before you start the cases just you can answer a couple of questions that have come up on the chat. Oh, sorry. I didn't see the chart. No, you're OK. Don't worry. OK. Yeah. Yeah. So what is flow cytometry? Right? So, flow cytometry is a test. Um, it's, it's sort of a, um, it's one of the, um, uh, it, it's, it's, it's one of the newer tests, um, newer diagnostic tests. So, basically, um, you would assess the, the markers that are present on white cells and, you know, these are called CD markers and depending on what CD markers you find, you can determine if it's a B cell or T cell related. And then, and then, you know, from there, those markers can also determine if it's a, if it's a, if it's a myeloid or a, or a lymphoid lineage that's being affected, would we need to know the chemotherapy regimes? No, not really. You know, you could see, you know, I would say probably r chop is a good thing to know just for non hodgkin's, that's probably the most common thing. It's highly unlikely. They will ask you like the particular types of drugs that are involved, that sort of, you might see that on higher level exams. But I think the finals, you should be fine in general. My finals didn't involve too much hematology. It was just more about those cases like myeloma, which is very, very key and polycythemia difference between leukemias versus lymphomas. Is it just the location of where the white cells are? Yeah. So generally, uh there's a lot of overlap in, in, you know, leukemias and lymphomas. And, you know, like I mentioned earlier, like a CLL can also present as a mass. So, yeah, you are. Right. It's just sort of, uh, you know, where the disease is located but there is a lot of overlap in there. Uh We did progress, we did progress this. Oh, ok. Um, I think that was, I think the last question was just in relation to another one. But does anyone have any more? It's just sort of brief whistlestop tour on, on hematology and, you know, II just tried to go through the points I felt would be relevant, would, would be relevant for like exams. So if we're happy with that, I can move on to our cases and you know, feel free to answer in the chat as well. So our first case is with a 55 year old male who's presenting with headaches, dizziness and itching after having a shower, you're also having some fatigue. Um Their exam findings are, are they have a facial plethora, ruddy complexion and palpable splenomegaly. Those are the blood results there if you want to have a minute to look at them. Um ok. So even without looking at the blood cells, does anyone have a suspicion of what might be going on? Yeah. So see in chat is uh polycythemia vera. Yeah. And yeah, it's a very classic case for APV. Um So how would you, does anyone know what you would do to confirm the diagnosis of PV? Ok. So to confirm the diagnosis of PV, um you just want to first of all, check the serum epo level. So, like I mentioned before, the EPO is gonna be suppressed in PV. And then you'd also check, you can also do a JAK two mutation testing. OK. Now, uh how would you manage? Uh how would you manage uh polycythemia vera? Yeah. So uh yeah, so fla flat is the, is the first way you'd manage it and with a JAK two inhibitor as well. Um And remember you'd also want to uh you, you, you'd also want to uh give them some aspirin to prevent thrombosis and you know, and you know, give them hydroxycarbamide or hydroxyurea. If the patient for sigh of reduction. OK, we'll move on to our second case. So this is a 68 year old female who is presenting with persistent back pain, fatigue, recent, recent history of recurrent chest infections. She's had some unintentional weight loss and she has some uh she has some tenderness over the spine. Those are her bloods right there. Uh Can anyone um So can anyone tell me what they um can what they think the diagnosis is? Yeah, getting a lot of responses. So this is this is very, very typical for multiple myeloma. You know, it's very clear, the crab criteria is here. You can see there's a, there's an anemia, uh waste calcium, the creatinine is high. So that's showing a degree of renal impairment and you know, the total proteins is high as well. And you know, she's having some bone pain too. So how would you confirm a multiple myeloma? Yeah. So, yeah. So you would do electrophoresis, serum and urine protein electrophoresis. That's like one of the, that's one of the steps to diagnosis. But if they ever ask you on a test for a confirmatory test, a diagnosis test, it will be with a bone marrow biopsy. Yeah. So um you know, you, you um you know, and then uh so yeah, you do serum protein, electrophoresis, urine protein electrophoresis. Uh you, you can also check for serum free light chains. But yeah, bone marrow biopsy is always gonna be the diagnostic test. And next steps to manage my myeloma. Any thoughts? Yeah. So you would give chemo, so that's the definity treatment. But you know, if you, but you'd want to manage some of the more symptomatic problems first. So you give them hydration to treat their renal impairment and the hypercalcemia you'd want to give with bisphosphonates because that's more of a because those are the two more acute issues in myeloma. Ok. So this is our third case. So you have a four year old who's pre who has Down syndrome presenting with fatigue, pallor and fever. He's been less active, he bruises easily and he has a petechial rash. Those are his uh bloods and blood film results. Anyone have any idea of what's going on? Yeah. So uh this is a very, very typical A LL case and how would you confirm the diagnosis for A LL? Yeah. So you would do a bone marrow biopsy and you know, another. And like I said, the next investigation would be flow cytometry and that's to identify the markers to confirm, to help confirm al. Ok. Uh Right. And w what would be the next steps in management for, um, for A LL? Yeah. So you do chemo and patients who are high risk could get, could also get a stem cell transplant. You remember you want to target the um the sanctuary sites as well. One thing to know is when treating all leukemias and lymphomas is that you want to treat you, you, you want to help prevent tumor lysis syndrome. So basically what happens is if you have a large amount of cells that are being destroyed with chemotherapy, they tend to release a lot of urea and uh and you know, that'll, that'll, that, that can put you into a very quickly. So, what you want to do is you want to make sure these patients are hydrated well, with IV fluids prior to giving chemotherapy and you can also give them allopurinol as well to prevent um to decrease the formation of uric acid. So that's a very, very important complication. You, you need to know uh for hematology, right? So this is our last case. So 62 year old male who presents with painless lymphadenopathy in the neck and you know, has become larger for the past three months. Also reports having night sweats, unexplained weight loss and occasional fatigue and, you know, these are, um, and you know, he's having um, non tender, painless lymphadenopathy. Uh, those are her bloods. Um, the, the, the, those are his blood. Sorry, anyone have any thoughts? Yeah. Yeah. So it would be, uh, so this would be like a lymphoma and, you know, to confirm the diagnosis. What, what would we do? Yep. So you would do a uh so you would do a biopsy. Now, in this case, it is a non hodgkin's lymphoma. And you know, like I mentioned earlier in, in elderly people when you're suspecting non hodgkin's, the most common form is the most common subtype is a diffuse large B cell. So you do a lymph node biopsy, you do flow cytometry. Uh You can also do a bone marrow biopsy to check if there is involvement of the bone marrow. And you know, you can also do a CT scan or pet CT to see if the lymphoma has affected anywhere else in the body. Um Next steps in management would be uh would be uh just doing chemotherapy, like I mentioned earlier, the r chop regime um and remember, always, always, always uh be on the lookout for tumor lysis syndrome as well. And another thing as well as neutropenic sepsis. Uh I don't know if you have a talk on like oncology emergencies to know but you know, um, um, tumor lysis syndrome and neutropenic sepsis are the most common complications. You, uh, you, you'll, you'll see on exams in your acies as well. So just be very, very mindful of that. Ok. So that's all I have for you guys. Anyone have any final questions about hematology? II, hope this has been helpful. Um, you know, I chose the most. I, if, if we wanted to go in detail, we could be here for hours. I don't think that's something you guys or e or either of us want. But, you know, hopefully this is, this is the most relevant material we'll see for exams if you have any questions, if you'd like the slides on this, uh, uh, you can just send me an email.