Transcription
So, first of the five cases, this is a 40-year-old man who presented to the emergency department because of worsening of fatigue and tiredness. He was referred by a GP to investigate because his white cell count was a bit high.
So, this is just Power 10 overview of the blood film. Maybe a few blasts. Yeah. So then I will go to Power 50 to magnify them on it. So, this is Power 50 and definitely a blast. Let me clear it. Yeah, sure. Was it a lymphoblast or my think it's a lymphoblast. So, definitely refer to a consultant without looking any further.
Yeah, what makes you think that this is a lymphoblast? Well, it's high nuclear cytoplasmic ratio. There's, there's no granulation as such. How old is he again? He is just 40 with no background history and he felt he started feeling tiredness, uh, a month ago and it was gradually worsening. So, GP thought that this is anemia. So, he did investigations for him, the routine blood test, and he noted that the white cell count is a bit high. Yeah. What was the platelet count? Platelet count was 90. Right. Okay. She looks dysplastic with blasts which are medium-sized and possibly these are very high granulated and cytoplasm. So, granular. The so that the margin is obscure. It looks like lymphoblast, but I think there's these are all stroyocytes. So, I will go to 100 power to maximize them. This is the picture of the cell. Let's find another cell for you. Yeah. Monocytes, lymphoblast. So, the granules are very few in it. We have another case as well where we will see the granules in it. Uh, uh, see a bit of a cleft there too. Now, these are two cells, uh, attached to one another. Chromatin is a bit loose and nucleoli is prominent. Yes. So, they are lost and they have very minimal cytoplasm. In the myeloid lineage, you will see some cytoplasm over there and they are very granulated. So, now I am looking for a diagnostic cell that should give you a morphological diagnosis on on the basis of which we pick this case. An AML? Thank you. This is one of the diagnostic cell. This film has few. Yeah, this is an L2 blast. Uh, L2 means because we do not use the FAB classification anymore. What is meant by L2? That means that that is cytoplasmic protrusion, that is a hand mirror appearance of the blast. Yeah, you got it. So, we saw many hand mirror blasts in it. Let's see if we have any other. And this one. Yeah, and this one is clear. Yeah. Right. So, you have, um, as a lab hematologist, you have seen the blood film and you have referred the blood film to the clinical hematologist now. Yeah, because this is an emergency. I need a, a report of this blood film from a clinical hematologist. How will you report this blood film? You are sitting in an Epath 2 exam. Any clinical hematologist who wants to report this blood film? All of the audience are the lab hematologists. They can't be. 13 people. RBC reduced in number, uh, mostly normocytic normochromic. Few schistocytes have been, uh, seen. WBC, uh, increased in number. Uh, majority of cells, uh, more than 90% of cells are small to medium-sized blasts, uh, with high NC ratio. Mhm. Dense chromatin pattern, inconspicuous nucleoli, like, uh, with few blasts having cytoplasmic protrusion, giving the picture of a lymphoblast. Platelets are scanty. So, my comment: pancytopenia with, uh, peripheral, um, increased blasts, suggestive of acute lymphoblastic leukemia. Okay. So, my advice: flow cytometry for confirmation of the diagnosis, molecular genetics and karyotype study, and also bone marrow study. So, always comment on the line, uh, first, which is abnormal. So, the blood film shows leukocytosis. There are multiple, uh, blasts in this, in this blood film with, uh, scanty cytoplasm and, uh, prominent nuclei. There is, uh, there is thrombocytopenia. No platelet inclusions. The red cell shows multiple schistocytes, uh, in this film. The impression is that of acute leukemia. We need to do urgent flow cytometry and further investigation like bone marrow biopsy in this patient to, uh, confirm our diagnosis. You should not say that this is acute lymphoblastic leukemia on a blood film, because, uh, we have seen multiple cases where we were thinking that this is acute lymphoblastic leukemia, they turned out to be biphenotypic, uh, acute leukemia, or they turned out to be, uh, acute myeloid leukemia. So, the safest term in the exam is to say this is acute leukemia. We need to do flow cytometry and invasive investigation like bone marrow biopsy to confirm our diagnosis. So, you, you send the blood urgently for the, uh, for the flow. And the flow shows that there is CD2 positive, cytoplasmic CD3 positive, CD19 negative, CD20 negative, CD5 positive, and TdT positive. So, what is the likely impression on the flow cytometry now? It is a case of, uh, T acute lymphoblastic leukemia. Yeah. T-ALL. And what is the usual presentation, clinical presentation of T-cell leukemia in, in, in real practice? In which patient you will usually? Mediastinal involvement is very common. Mediastinal. So, what are the, uh, poor risk features in T-ALL? CNS involvement, CNS leukemia, and, uh, early presentation, or if there is any marrow like one on C or HR? So, that can be a poor risk. Phenotypic. And, uh, what about cell count? Cell count, yes. More than one lakh if WBC count, it is a high risk. Poor risk. Yes. Genetic, like, like AML, cytogenetics, or molecular genetics, uh, like complex karyotype. Complex karyotype. Any hyperdiploidy? Yes. Uh, high WBC count. More than 100. And age factor as well. Higher the age, the poorer the prognosis. And in, in general, T-cell has poor prognosis. No one likes poor prognosis. No one likes T-cell, T-cell lymphomas, right? So, they can ask you in a short morphology question about the poor cytogenetics or poor risk factors in T-ALL. They can ask you what is the expected flow cytometry. Like that. What's the, sorry, what's the prognosis for the B-ALL? As compared to T-ALL, it is better. But, but again, we have to see what, there are factors like what the age of the patient, what is the white cell count at presentation, whether they have, uh, any complex karyotype or not, whether they have hypodiploidy or hypodiploidy, meaning deletion of the part of the chromosome, or they have associated translocations like 11;19, 4;11, 9;22. If these are present there, they have poor prognosis. But if they have, uh, translocation which is 12;21, 12 and 21, ETV6 or RUNX1, it is called like that, then it is considered as standard risk. Okay. So, uh, in general, T-ALL or T-cell lymphomas, they are considered bad risk than the B-ALL or B-cell lymphomas. But again, you have to see for multiple factors which will make the which will define their prognosis, whether they are bad prognosis for the patient or standard risk. So, why is it, um, good prognosis with a child? Why is it so poor for an adult? Now, because the research that we, that we have read up until now says that as the age increases, more than 40 or more than, uh, 65, the, uh, the response to the treatment decreases as well. And in adult people, you will expect more cytogenetic mutations than in children. If anyone can add to that, the comorbidities with the adults, including hypertension, diabetes, chronic kidney disease, all that adds on to the burden of, uh, morbidity and mortality during treatment. Whereas in children, most, most of them, almost 70-80% tolerate the expected dose and the duration of chemotherapy is maintained, the intensity is maintained. So, I think that is an important factor. Thank you. Thank you. Okay, Dr. Amir, could you please tell what treatment options do you offer in T-ALL? This is a very hard question for me. Sorry, because it usually comes in the pediatric cases and we do not deal with pediatrics. If anyone else can answer this question because I run away from T-ALL. Yeah, there is, there is an ongoing trial, isn't it? All together, which, uh, takes care of children and, I think, adolescents up to 23 or 24 years. That is the ongoing trial. And, T-ALLs are high risk, so most of them go through induction chemotherapy, four drugs, and there's consolidation, there's interim maintenance, and there's reinduction followed by maintenance. We have offered allogeneic transplant to all of our ALL patients, young patients, but not to any T-ALL up till now. Usually, we give them UK ALL 14, but add the nelarabine in it. Rest, I cannot comment because I have no interest in T-ALL and it's difficult. He will ask about it and then update you. Yeah.
So, this is another second case. 35-year-old female who presented to ED again with tiredness and fatigue. The full blood count shows hemoglobin of, uh, 101, white cell count of 12, and platelet count of 90. This is Power 10. Let's blast you again. Yeah, a blast is there. Any difference between this blast and the previous blast? Um, well, the NC ratio is not as great. See more cytoplasm. Yeah. Mhm. There's a bit hand mirror there. From Auer rods. Yeah. This patient has a lot of splenomegaly. A liver problem going on here then as well. Alcoholic. Alcohol. This is a case of AML because we are seeing blasts with cytoplasmic Auer rods. Where is that? This one you say that this is overall. So, let's magnify. I don't guys know rod. This is not, uh, the nuclear material is a bit separated from the rest of the body and it is elongated. So, on low power, it gives an impression that this is an Auer rod, but this is not. [Music] Anything? Maybe the nuclear morphology. Is it bilobed? Looks bilobed. There. This one is a bit because there's some separation here and this you can, this could be bilobed. I'm not sure. As there could be an APML. I'm not sure. I need to see a bit more cleft or bilobed. What about the nuclear morphology? Whether it is helping you or not? The nucleus has specific morphology here. Nucleoli suggestive of NPM1 mutated AML. Which shaped nuclear? Yes. Ring or C-shaped nuclear? Yes. I agree with that. A cup-shaped or fish mouth nucleoli. They are the feature of NPM1 mutated AML. Okay. So, the lab colleague have seen blasts in this blood film and he has carried it acute leukemia and referred the film urgently to the clinical hematologist. How would you report this blood film? So, someone need to report this blood film. Come on, say it. There is silence again today. Yeah, come on. The biomedical scientist or the lab hematologist is waiting for your report. One gentleman, Dr. Ata, is the first. Do you want to report the blood film, please? Then is Dr. MD Ashiq Zaman. Do you want to report the blood film, please? Uh, RBC normocytic normochromic, reduced in number. WBC, uh, increased in number. Start with the, with the abnormality first. Okay. Okay. WBC is increased in number with left shift maturation. Majority of the cells are medium to large size blasts with low NC ratio, loose chromatin pattern, prominent nucleoli with aurophilic granulation in the cytoplasm and few blasts showing cytoplasmic Auer rod formation. Nucleus, some of the blasts also shows nuclear cap-shaped, uh, abnormality. Platelets are scanty. So, my comment: this is a suspected case of acute leukemia, possibly acute myeloid leukemia. Should be confirmed by flow cytometry, imuno-phenotyping, molecular genetics study, and karyotype for risk stratification. And we should also do bone marrow biopsy. Okay. Right. So, the blood film shows leukocytosis. There are multiple blasts in the blood film with prominent nucleoli, open chromatin, and fishmouth appearance. There is thrombocytopenia. No platelet inclusions. And red cell shows multiple stomatocytosis-like pseudopods. The impression is that of acute leukemia. We needed to do urgent flow cytometry on blood and bone marrow aspirate and define to confirm our diagnosis. You have only 9 minutes in the FCB exam to, uh, attempt a question. And the question would include: write the report of the blood film, and what is the expected, uh, flow cytometry or what is the expected cytogenetics in this patient? What further investigation you would like to do? Or what are the differential diagnosis? Or what is the treatment option in this patient? Thank you. Okay. So, then, uh, according to the BSH guideline 2022, they have mentioned that we should do, uh, a minimum genetic tests on any new acute myeloid leukemia patient. So, what genetic tests would you like to do on any acute myeloid leukemia patient? We can do PCR for translocation 8;21 or, uh, ETV6-RUNX1 mutation, NPM1 mutation, PML-RARα, CBFα, FLT3, inversion 16, inversion 3. That should also be, uh, seen. And also, uh, we should do karyotype. Minimum. Yeah. So, there is a, so there is a table in the BSH 2022 guideline which says that what minimum genetic tests we should send for a new AML patient. They say that we should do FISH for inversion 16, 8;21, and KMT2A. This is one category. Second category is karyotype. Third category is molecular testing for FLT3-ITD, FLT3-TKD, and NPM1. And the fourth one is NGS panel. So, these four things, uh, that we should send in, in any patient with a new AML. So, if this patient has NPM1 mutation and also FLT3-ITD mutation, what would be the risk category according to WHO 2022? Favorable, intermediate, or adverse? Intermediate. Yes. It is intermediate. Mutated NPM1 and FLT3-ITD is an intermediate category. And you mentioned Auer rods. Which malignancies can have Auer rods? Then one M3. Certain. Sorry, I'm a very new hematologist. So, I don't know about T classification. Sorry. Okay. I'm old heart. Sorry. Yeah. So, APML is the one category which has Auer rods. What about others? Do you know any other which contain Auer rods? Think you can get them myeloid. I mean, in the form of leukemia. What other category of leukemia or what other mutations of leukemia or any other myeloid disease that is associated with Auer rods? NPM1 mutation, acute myeloid leukemia with maturation. Acute myeloid leukemia with maturation. Okay. NPM1. We have seen Auer rods in inversion 16 as well. And there is a category of MDS, MDS with excess blasts and Auer rods. So, Auer rods are not diagnostic of APML only. You can have them in multiple myeloid disorders. One subtype of MDS and three categories in AML they can have Auer rods. So, in the previous case, in the second case, before starting any treatment, what is the important step that you would like to take which would address your management as well, like affect your management as well? Any idea? We must do appropriate risk stratification first by molecular genetics study because now treatment is completely risk-stratified. So, which type of treatment I will take first? It depends on the risk category: favorable, intermediate, or high risk of AML. And then, if a patient is a, patient is transplant eligible, or patient has any comorbidity like cardiac or liver or renal function abnormality, we should assess this first because the therapy we are choosing will affect this. And do you remember the scenario, please? Can you, can you add, uh, again? I have just missed it. It was a 35-year-old female with fatigue presented to ED. And now she had this NPM1 blasts in the blood. Pregnancy? Yes. In every young female, you should do a pregnancy test because it will affect your treatment. If you do not mention pregnancy test in a young female in the, uh, hematology exams, you will suffer because the examiner will, you will tell all the treatment, everything, and in the end, when you stop, the examiner will say, "But the patient is pregnant." And then you will not have enough time to rethink on your treatment. Yes. She was young, she was fit for intensive therapy, and she had intermediate, uh, intermediate risk category, which needs transplant in remission. The category which is a favorable category according to WHO 2022, they do not need transplant. They do not need transplant in remission. But for intermediate category and worse category, you have to transplant them if they are transplant-eligible. Dr. Amir, to what age do we offer fertility preservation for a male and a female in the UK? For a female, it's like, uh, up to 50 is confirmed. Between 50 to 60, I would ask the patient. In case of a female, whether they have any plans for pregnancy in the future or not. But because 50 to 60 is an age in the UK where most people go into menopause. But for legal purpose and on the safe side, I should ask. And for a male, there is no age of, uh, like in females, menopause. But on, on the safe side and for legal purpose, I will ask them because a 60-year-old man and a 70-year-old man in the UK is considered as a young man. Mark, I am not lying. Yes, Mark, Mark is there, right?
So, this is a third case. This is again a young man, 35-year-old man, presented to ED with oral bleeding. He has noticed some gingival bleeding while brushing that is not normal for him. And when you did the blood test, the blood test shows hemoglobin of 110, white cell count of 19, and platelet count of 110. This is the blood film at low power, Power 10. So, any lab hematologist or from laboratory side who will see this blood film first, what will be their comment? Looks like now we have all clinical hematologists. Okay, let's resume. I am the lab hematologist. I have seen this blood film and I have seen a lot of granulated white cells in this smear. I am new to hematology and new to the, uh, new in the job as well, recently graduated. But I have heard that if there is any granular lymphoid, I should escalate that to the clinical hematologist. It can be acute leukemia or chronic leukemia. So, I have found you guys that there is a blood film which contains a lot of granular lymphocytes, granular white cells. I'm not sure whether this is acute leukemia or chronic leukemia. [Music] So, now the clinical hematologist should step in. Any clinical hematologist? I can. Okay. Severe leukocytosis of a patient was detected. Leukocytosis in which intermediate to large size granulated cells are typical. And beautiful Auer rods are present. But most, most of the cells are abnormal, like normal myeloid precursors. And these are granulated, granulated cells. I can see few schistocytes in the background. Mhm. And normocytic normochromic as well. And the platelet count is slightly decreased in the background. Mhm. So, peripheral smear is consistent with acute leukemia. Mhm. So, I would refer or I would order urgent FISH or flow cytometry or PML-RARα and bone marrow biopsy. Can you comment on these cells? Can we see some bilobed cells? Dividing cells? And these all cells, nucleophilic nucleus to cytoplasmic ratio is increased with lot of granules. Eosinophilic granules. Most likely this looks like APML. Okay. So, you picked that up that this is APML. Yeah. With the clinical history and this peripheral leukocytosis, abnormal blast cells, granular like granular cytoplasm. So, you have commented on the, you have given your impression. What advice would you give? We will suggest to start ATRA based on clinical suspicion, then send for further flow cytometry. Advise to do bone marrow biopsy, karyotype, NGS. So, to whom will you suggest to give ATRA? To the clinical hematologist who is taking care of this patient. Okay. This is your patient. Yes. So, I will start ATRA for my patient. The patient is female or this is a male patient? Fortunately, yeah. So, you will say, yes, the blood film contains leukocytosis. There are multiple blasts in the blood film with bilobed nuclei or kidney-shaped nuclei, like this one, kidney bean shape nuclei. There is thrombocytopenia. Red cell shows multiple schistocytes. The picture is consistent with the blood film is consistent with acute leukemia, most likely acute promyelocytic leukemia, which is a medical emergency. This patient needs to be admitted and started on ATRA as soon as possible with bone marrow biopsy. Next step of investigation. What other investigation would you like to do in this patient? We will send PML-RARα for the fusion. Then, patient is female, we'll do pregnancy test. It's a male patient. Male patient. So, population profile as you see is 19. The patient is at high risk. [Music] What are you interested in coagulation? What do you look for? DIC. Do you think this patient has DIC? Can be, because the patient presented with oral bleeding and the platelet count is low and fragmented red cells. He has schistocytes, which is common in the DIC. You will do, you will send the coagulation profile, fibrinogen in this patient as well, which, if it is low, less than one, then you have to give this patient fibrinogen concentrate or cryoprecipitate. Those tertiary centers in the UK who have HMDs, they send the PML-RARα stain and we get the result within 1 hour. Otherwise, PCR is the gold standard test, but it takes 48 hours. And FISH for, uh, PML-RARα takes 6 hours. So, if it is in hours, like between 9 to 6, then we can send PML-RARα and they will give us the result within an hour. So, this is, uh, high-risk APML or low-risk APML? High-risk APML. WBC was 19. And what is the definition of high-risk APML? Like, what is the cutoff of white blood count? I think, uh, 10,000. Yeah, more than 10, you consider them as high risk. So, what treatment you will give to this patient? We will start ATRA, arsenic, and chemotherapy. Either ATRA or arsenic, or ATRA and idarubicin. Which one will you start? ATRA and idarubicin. Okay. Right. And, uh, will you tell the patient about the side effects of ATRA? What are the side effects? Differentiation syndrome. Okay. And electrolyte disturbance. I think, uh, regarding the, I'm not sure, but I think potassium and magnesium are that is the requirement for arsenic. Whenever you give arsenic to the patient, you check potassium, magnesium, and QT interval. When you start the patient on ATRA, you regularly check their, uh, liver function test because liver function test can go off, and you then adjust the dose according to that. Hepatotoxicity, differentiation syndrome. And another, uh, significant side effect of ATRA. If the patient says I have a headache, and the patient is on ATRA, what would you suspect? Tumor lysis syndrome. Yes. Okay. So, would you give any prophylaxis for differentiation syndrome in this patient or not? Yes. You will give prophylactic steroids to these patients as a prophylaxis. What is differentiation syndrome? When all-trans retinoic acid is given to APML blasts, they differentiate into neutrophils. But these neutrophils are all abnormal at first, and they have many receptors, so very easily they accumulate on the endothelium and they pass through the endothelium, go outside the endothelium, then tissue space. They create like pleural diffusion, edema, and can pass the blood-brain barrier to cause CNS. CNS effects. Pericardial diffusion can occur. Yeah. Patient retains the fluid because of which their body weight increases and they develop, uh, fluid in the third space like effusions, ascites, edema, heat. And because of fluid, they become hypoxic. We have to stop ATRA once he becomes okay, then we can restart ATRA, uh, in them again. Okay.
All right. So, this is another 40-year-old patient who is feeling tired and weak. He went to the GP and the GP did blood test for him, and the blood test shows high white cell count. The white cell count is 35 in him. There is anemia, the hemoglobin is 105, and the platelet count is 130. So, this is the Power 10. This peripheral blood smear shows marked leukocytosis. Mhm. These monocytes appear here moderately enlarged. Yes. This is Power 10. So, I will go to Power 50 to make it clear for you, sir. Moderately enlarged, normal cells, cytoplasm, some cells are mature neutrophils. A lot of granulation in the cytoplasm. Mhm. This is mature. Some mature neutrophils. You can see some reactive cells. Few NRBCs are also present. And monocytes are also present. There's a bimodal peak. Most likely a myeloproliferative disorder. If the patient has splenomegaly? There is no splenomegaly. And this one, are these monocytes? Yeah, seems to be promonocytes. NRBCs are present. Hypochromia with WBC and monocytosis and marked dysplastic changes also present. Maybe something are these basophils? Which one? No. No, no. There is no basophil in this picture. Few blast cells are also present. Seems to be like CMML. Dr., can we say this is a dysplastic picture? Yes, if you are seeing dysplastic neutrophils, myeloid precursors, and NRBCs, this means you are seeing a dysplastic picture. So, now you guys have given multiple differentials. What is it? Oh, are you asking about the differential diagnosis or diagnosis? Report the blood film. And the prominent monocytes and, uh, dysplastic myeloid and the RBC is, uh, ARBC and NRBC are also, uh, somewhat reduced or poorly reduced. So, the peripheral picture is consistent with chronic myeloid leukemia or I can't say the exact word, but maybe motive disorder. Dysplastic, because it can be secondary to infection. You would say that there is leukocytosis in the blood film consisting of multiple promonocytes, monocytes, myeloid precursors, Auer rods, dysplastic neutrophils, NRBCs, and schistocytes, consistent with probable myeloproliferative disorder. You need to do a flow cytometry to confirm your diagnosis. There were multiple blasts as well, which we skipped. We didn't see any basophil to say that this is likely CMML. [Music] Okay. So, this is a CMML because you see promonocytes. Look at the dysplastic picture. And we have myeloid precursors as well. In RBC, this is a CMML. What category of CMML? Is it myelodysplastic CMML or myeloproliferative CMML? This is a myeloproliferative CMML. CMML-1 or 2? Not blast less than 2%. Perhaps the plot count. That maybe low. So, based on this, it is less than 2% or less than 5% that you call it as CMML-1. Yes. If it is less than 5%, then it is less than 5%. If it is less than 5% on peripheral blood film, then you call it as CMML-1. If it is more than 5% on peripheral blood film, then you call it as CMML-2. Right. How would you treat this patient? As the patient is young and, uh, as well as in myeloproliferative phase, so first of all, the cytoreduction to, uh, stabilize the patient based on discussion. Mhm. After that, if the patient, uh, is eligible for allogeneic stem cell transplant, criteria, then, uh, we can proceed for the transplant as well, but after discussion. Okay. So, cytoreduction. What set of reduction would you offer? Hypomethylating agent and chemotherapy. What is hypomethylating agent? I don't know. Can you tell me the name? Uh, I don't remember exactly. Azacitidine. Who wants to give azacitidine to this? Is it nice to recommend to give azacitidine to CMML-1? No, it's recommended for CMML-2. But Dr., I have a question. H, this patient, you said he's 40 years old. Usually CMML is a disease of old age. So, even the neutrophils, they show some toxic granulation. And how are you going to differentiate between some infective process or a clonal disease at this age? Even if the patient's age is 40, although the picture is suggestive that there could be a possibility of CMML, but still you have to rule out the common things first. First, I think at this stage, do you suggest we should directly jump to CMML in our reporting or we have to give a differential diagnosis? Could you please explain this? Let me find another. So, you never say that this is CMML on blood film. You confirm the things on flow cytometry. If this patient has an element of sepsis, then the blood cultures will tell you this patient has sepsis and the infection markers would. And the flow cytometry will come back as reactive. It will not tell you that this patient has CMML. So, you would differentiate it by blood, blood cells, by the, uh, blood test and by the leukocytosis. But the patient who has sepsis should not have promonocytes. They should have monocytes only, but not promonocytes. Usually in CMML, you get the atypical CML. They are not exactly of promonocyte morphology. But I want to know, okay, what should we write in the reporting in the exam? So, as we discussed, that the blood film can contain leukocytosis. There are multiple promonocytes and monocytes. There are, uh, hypergranulated neutrophils, myeloid precursors, NRBCs, and schistocytes. Because if it was a septic picture, I should not see promonocytes in there. And in how many, sorry, promonocytes are also equivalent to blasts? Yes, that's why we are thinking that maybe this patient has a myeloid disorder and we are sending the film. We are sending the blood for flow cytometry. In a very severe septic case, you will see NRBCs in the blood film. Otherwise, and how many septic or febrile patients have you seen NRBCs in the blood film or myeloid precursors? The blood. So, if you have seen promonocytes in the, in the blood film and there are myeloid precursors as well, and NRBCs as well, so I would be worried that this is some MPN. I should check the flow cytometry of this patient. If it is only sepsis, like this patient has, they have all sort of, like the one on the, on the front, in the, on the screen, this patient has a dysplastic neutrophil, band forms, myeloid precursors, and promonocytes, monocytes, everything is there because this patient was acutely unwell with the background of CMML-1. What would be my one-line opinion? You have described the picture, but what would be my most likely diagnosis? So, your most likely diagnosis is MPN. You need to confirm that on flow cytometry because you do not see promonocytes, NRBCs, dysplastic neutrophils in a normal septic patient or febrile patient. Very severely ill patient, they do have few NRBCs in the blood film. Otherwise, they do not appear. The NRBCs do not appear in the blood film or promonocytes do not appear. You will have hypergranulation in the monocytes, but not promonocytes in sepsis. And the film has a lot of monocytes and promonocytes. Normally, in a normal febrile patient or septic patient, the monocytes are not that much. And there were also blasts in the, in the film as well, which are suggesting that this can be some MPN as well, although less than 5%, but they are all blasts. So, you would not miss this patient by not sending the, uh, referred blood to the HMDs or flow cytometry. Hopefully, it makes sense. Yeah. Okay. One more thing. If there is a confusion between whether this is a CML or this is a leukemoid reaction, still you people send, uh, sample for flow cytometry to confirm. If I see basophils in it, then I would see, then I would send the, uh, blood for flow cytometry or BCR-ABL1. If there is no basophil, then leukemoid reactions usually do not contain basophils. Leukemoid reactions will have only high neutrophil count or band forms. That's okay. Thank you. But it is the basophilia that gives you an impression that this would be a CML. Yeah. But if you are sitting in your lab and you are doing this, you are seeing such smear, but if the situation would be different when you are sitting in an exam, in such high pressure, in such time limitation, if you can't find basophils and you are confused whether CML patient has very high basophilia, you will see basophils in the blood. It is not possible that they will give you any blood film which does not contain basophils and they would have labeled it as a CML. Okay. Thank you. And, and the CML has a myeloid peak. The leukemoid reaction usually doesn't have a myeloid peak. They contain only neutrophils and they are mature neutrophils. If they are under G-CSF effect or because of sepsis or because of any solid organ tumor the patient has high white cell count, you will not see any basophilia over there. Any myeloid peak over there. I should bring leukemoid reaction and CML in the next question.
The last case. This patient has returned from, uh, South America and now he is feeling feverish. What do you expect? What do you think? What are the differential diagnoses in your mind? Someone coming from South America after a trip and now feeling unwell. Malaria? But infectious mononucleosis. Uh-huh. What else? Trypanosoma cruzi. Trypanosoma cruzi. This thing. What is it? Have you seen this thing before? It is cruzi or bruzi? Cruzi. If you have identified that this is Trypanosoma, I think that is enough for us in the exam purpose. Because in real life, we do not deal with them. Whether this is cruzi or bruzi or something else, they are dealt by the infectious disease consultants. So, this is C-shaped. Goes for cruzi. C for cruzi, C for C-shaped. Mostly they are in C-shaped form. Trypanosoma cruzi. And what are the diseases associated with Trypanosoma cruzi? Or what are the diseases associated with Trypanosomiasis? Sleeping sickness. Chagas disease. Yes. So, these are the two cases. Because they can give you a scenario that the patient has come back from the, uh, from Mexico and now he has dysphagia, and he has given this blood film, and you will be looking for a blast-like picture that maybe this patient has esophageal carcinoma and invaded the bone marrow, and you may miss this thing. So, if you are more interested in the gems, you can read more about it. Like, one of them is Canis plus. I don't know which one of them. And what are the features of Trypanosoma brucei? What are the features of Trypanosoma brucei? How to differentiate them? But they are not required for the exam purpose. And to a maximum, they can ask you what treatment you will give to Trypanosomiasis. Do you know any treatment for Trypanosomiasis? What is the treatment of Trypanosomiasis? It's not stem cell transplant or Marata protocol or protocol. I'm sure about that. Pentamidine. Yeah. So, you need to know these things only for the exam purpose. If you are appearing in Part 2 exam, there will be one blood film which will be from a parasite. Either it will be malaria, or it will be Trypanosoma, or worm ova, usually, or it will be Leishmania. So, if you are working in the UK and you can go to your labs and your lab will have a lot of blood films from NHS related to the worms. The biomedical scientist and your lab will give you the collection and you should see them before the exam or start practicing on these blood films. If you are preparing for Part 2 exam, then you will not forget. Because in the exam, the blood films usually contain one or two gems in the lab. When you see them, the blood films are full of Trypanosoma, Leishmania, or worms. But when you sit in the exam, they have like divided the worms or gems in the blood film equally. You will see one or two of them. So, you should be vigilant in seeing them during the exam. You should see them a lot before the exam. Any question?