Transcription
You go [Music] oh spe fore speech fore hello everyone. Can you hear me? Can you hear me? Yes. Right, so let's start.
So this is the first case. A 30-year-old female patient with a background of sickle cell disease has presented with chest pain. This is the blood film. I would like you to enumerate the findings in the blood film.
So this is power 10. You will have one question in the exam which will say, "List the features or list the findings in the blood film." It will not say to report the blood film. It will say, "List the findings in the blood film."
Lot of nucleated RBCs there. Simiz? Yeah. So this is power 10. I will go to power 50 to make it clear. And then you have placed all the finding. Target off. Okay, anyone else? This could be like a variant, like an NC or something like that. He, a know, sickle cell disease patient and know has come with pain. Yeah, but the question is, what are the features in the blood? List the features in the blood. Yeah. You see sickle cell quite clear. Target cell, nucleated RBCs, thrombocytopenia. Maybe what's the platelet count? Platelet count was 234. Okay. On TOS as well. Are there some plasma cells? No, these are not plasma cells. NRBCs because the nucleus is a bit eccentric. Yeah, but this, but these are not plasma cells. The nucleus is very small and the cytoplasm is not bluish, just like the plasma cell. And the plasma cells' borders are not straight. The plasma cells' borders are wavy or flame-shaped, and the plasma cells are bigger than our RBC. So if there is a finding and you did not mention it in the exam, you will lose a mark. Everyone knows that this is sickle cell crisis, but what are the features in this blood film? Target cells are prominent. So they are target cells. This is one more. What else? Why you see the sickle cell there? Sickle cells. What else? Strange looking neutrophils. Uh-huh. And I say to assist different sizes. What is this one? Yeah, that's a microcyte. Now, this one or this one could be spherocytes. These are spherocytes. Patient, yeah, you have to mention all in the exam, otherwise you will fail the question. And you, you guys know that I have shown you the result of the people in which the people failed by 0.5 marks. The whole exam was failed just 4.5 more. So you have to pay 15,500 again. If they are asking you, "List the features in the blood cell," number one, sickle cell. Number two, target cell. Number three, NRBC. Four, microcytes. Uh, over there as well, granulated neutrophils over there. There were few Howell-Jolly bodies as well. Oh, yeah. You have to mention all the features, otherwise they will have a list of features with them. If you have not mentioned that in the, he will not get. What is the difference between this cell and elliptocyte? Well, there's more curve to the sickle cell. The shape pointed. Yeah, pointed tips. Cell, yeah. Um, cell is more, more straighter around the edge. Which one has the central pallor? Spherocyte or elliptocyte? Elliptocyte. Okay. A cell patient may be AR deficient as well, and AR deficiency can lead to ocytes. And this is a Howell-Jolly body. Okay. But why this patient has target cells? I'm saying most. So don't use the word SAR. It is an offensive word. Now, my God. Sorry. Okay. So, uh, if there are Howell-Jolly bodies or if there are target cells, it means the patient has hyposplenism. Here we have a lot. So, both shape cells and sickle cell. And at the bottom, there is a Howell-Jolly body. Right. Diagnosis is easy in the exam, but the full question carries 10 marks. You have to get a minimum mark to pass the question and to pass your exam as well. But it would come with practice. If you have your own slide bank and write on the paper, what is the report or features or what the next step treatment, acute treatment, uh, then you will be able to go through the exam. Dr., why can't it be thalassemia? Because in it, it also has target cells and NBS. Yes. So this patient is in crisis. If the patient is in crisis, he is hypoxemic a lot because the patient has spherocytes, reticulocytes, and bone marrow is under stress. That's why the NRBCs are coming to the, uh, blood. And the N, the target cells are there because a patient has hyposplenism. And there is another evidence of hyposplenism, which is the, uh, the Howell-Jolly bodies. If this patient has sickle beta-thalassemia, there would be some degree of microcytosis and hypochromia as well in this patient, which was not present in the blood film.
All right. The second case is a normal adult patient, 30 years old, and he has come to your AES unit for stem cell collection. And this is the blood film because the lab scientists have noticed that the WBC count is very high. This is power 10. So what does the lab scientist or lab hematologist think about neutrophilia? Okay. So why he has got? What, what are the differential diagnosis of NSF? Other, they are mostly left shifted. So I think it could probably be due to the G-CSF that he had for the stem cell collection. Yeah. Otherwise, it could be infection or steroids. What else is it? Differential diagnosis of neutrophilia? There is a CNL. Okay. Yes. Reactive neutrophilia. CNL. If you mention three or four, that is so you, that's abbreviation. Sorry. CNL. Chronic neutrophilic. So causes of neutrophilia are the leukemoid reaction, post-infection, steroids, use of the G-CSF. It could be secondary malignancy. CML as well. Or it could be chronic neutropenic leukemia, which is very rare. Yeah. So how would you differentiate G-CSF induced neutrophilia from other causes? From the leukemoid reaction, mostly the neutrophils will have toxic granulation and toxic vacuolation. If it's due to infection, um, and steroids, perhaps it would be the same. For the G-CSF, it will be mostly left shifted. Like they have hypersegmented features. And for the CML, they will have like, um, um, myeloid peak as well. So there would be like a lot of myelocytes. Two peaks, neutrophils and myelocytes. What else did we say? Um, and for the, there is no specific feature for chronic neutrophilic leukemia. There would just be lots of neutrophils which are of normal, um, morphology. Sorry, sorry. Oh, the platelet count looks a bit low. Yes. I, I think these are normal. Not look. He has enough platelets. Almost eight platelets in this field. Power 50. It looks more like a toxic picture. Cytoplasmic vacuolation, toxic granulation. Mhm. The reds look okay though. So the history is telling you he is a normal man and attending the AES unit for the stem cell collection. If he had fever or any features of infection, there would be a lot of toxic granulation in these neutrophils. But this patient has granulation, the orange granulation. He may have, we will see myelocytes as well. That shifting there. There will be a lot of band forms in this patient as well because the whole of the myeloid series cells, they will appear in the blood film. Even there may be one or two blasts as well. This one. But in CML, you will have basophilia. Eosinophilia must be there. So history and few of the features of the blood film will tell you this is G-CSF induced or this is infection induced or if this is CML. If this patient has a solid organ cancer and in the, in the history, no G-CSF history, then yes, leukemoid reactions are secondary to solid organ cancers as well. In case of CNL, chronic neutrophilic leukemia, all the cells are mature. All the neutrophil cells, they are mature. More than 80% neutrophils that you will see in the, in the blood film, they are mature neutrophils. There will be no band forms. There will be no blasts. And another important thing to differentiate CNL from rest of the neutrophilia causes is the mutation. CNL has a specific mutation. And that is what is the mutation of CML? CML PCR. CNL. Chronic myeloid leukemia. Right. Sorry. Clinical. This is a two-mark question. In the exam, it is CSF3R. Things which are not rare in real life, they are common things which are rare in real life. They are common in the exam. So be ready for the CNL cases or TPL cases or LGL cases in the exam. You will not see them in real life. I haven't seen any CNL case up now, but in the exam slides or in the exam, yes, they will appear. So this G-CSF induced blood film has a lot of orange granulation in the neutrophils. You will see myelocytes as well. A blast. G-CSF induced blast in the peripheral blood as well. Patient is usually normal. If he is an allogeneic stem cell donor, there will be no history of fever, no history of solid organ cancers in the patient. There will be no basophilia in the blood film, no eosinophilia in the blood. Okay. And if you, you have a transplant unit in your patient, you can see the blood film of a normal people with G-CSF. But if not, you may have lymphoma patient or myeloma patient, and your, um, in your units when they receive G-CSF, you can check the blood film to differentiate it from CML and sepsis induced leukemoid reaction. And in sepsis, in leukemoid reaction, you may see a lot of NRBCs as well because bone marrow is very much under stress. And the, why we don't give G-CSF in AML and MDS? Clinical, why you don't give G-CSF in AML and MDS? Can induce the cancer cells proliferation. What are the cancer cells? Myeloid series. That's why we don't do the G-CSF for that. It brings blasts to the peripheral blood film and the blast percentage increases falsely. So if your patient has G-CSF injections and you have sent blood for flow cytometry, they will say the patient has 22% blasts, and the MDS patient will be considered as AML. Now, it increases the blast percentage in the peripheral blood. That's why we avoid G-CSF in AML cases or in MDS. For those patients who are on palliative line and they are not responding to intensive therapies and not candidates for allogeneic stem cell transplant, then if the team decide the treating team decide to give G-CSF because of prolonged neutropenia, then we can give them G-CSF. Otherwise, in routine, we don't give them. So after the hydroxyurea, can we give the G-CSF? If the patient suffers from neutropenia. Sorry. After the hydroxyurea, can we give the patient G-CSF if the patient suffers from neutropenia? After the hydroxyurea. What is the cause of neutropenia in this patient? In this patient, are I'm asking about the hydroxycarbamide. If we give any patient, yes, what is the cause of the neutropenia in hydroxycarbamide patient? Myelosuppressive effect of the. And who causes myelosuppression? Hydroxyurea causes myelosuppression. Okay. So it is hydroxyurea induced myelosuppression. Stop the hydroxyurea, counts will come up. Okay. So there's no need to give the G-CSF for that. No, no. When we have a secondary cause for neutropenia, this is this is the hydroxyurea induced. We have an algorithm in a BSH guideline for hydroxyurea when when should we withhold or stop HX. So what, what are the basically indications for the G-CSF? So G-CSF, one is this one, mobilization of stem cells. And another one is chemotherapy induced neutropenia in lymphoma and myeloma cases. We give routinely because they are a part of the regimen. These are two main indications of the G-CSF: mobilization of stem cells and increasing the neutrophil count in lymphoma. Okay. In lymphoma and myeloma. Okay. Yes, because the autografting in lymphoma. Dr. Amir, can we give a neutropenic patient in hypocellular marrow like aplastic anemia? If there is an increased risk of infection and there is very low neutrophil count. So is there an? They don't have any functional marrow. The aplastic anemia patient have all, like fat cells in their marrow. You don't have anything. If there is any marrow left, then yes, we can give them. But in routine, we have nothing in the, in the marrow of aplastic anemia patient to mobilize them from marrow to peripheral blood. Then what is the standard of care? Means if there is a patient is not responding to the antibiotics and patient is going in sepsis, so what will be the standard care? So the routine care is that if the patient is septic, we treat the sepsis. And after sepsis, we know that this patient will have low cell counts. If the neutrophil count is less than 0.5, these patients are on long-term antibiotics prophylaxis. Antibiotic prophylaxis. 500 milligrams once a day. Can we get the granulocytes infusion? So granulocyte infusion is always a discussion of MDP. It has its own specific indication. When you think that this patient's neutrophil count will recover, then you give the granulocyte infusion. When you don't have any marrow left, any aplastic anemia, so then there is no way to recover the, for the neutrophil to recover. So we don't get G-CSF infusion in aplastic anemia patient. If it is an adult patient, he will go for stem cell transplant. So his misery will be over soon. If it is an old patient, then we have to try ATG and cyclosporine. Hopefully, that will solve the problem. Thank you.
So this is a 23-year-old female patient who is having fever and lymphadenopathy. The full blood count shows that hemoglobin is 12.2, white cell count is 17, and platelet count is 210. The blood film has gone to the lab scientist or lab hematologist. Let's see if he thinks this is lymphoma or LPD. This is power 10. Lymphocytosis and neutrophilia. Okay. Do you think this patient has lymphocytosis and neutrophilia? Let's go to power 50 then.
E, look more reactive. Why do you think this is here? Um, well, it's the large cell morphology around the reds, slightly basophilic cytoplasm, not classical though. So if the cytoplasm is and is lymphoid region, be with the clear cytoplasm, could be of lymphoid region blast. It is lymphoid because the cytoplasm is mostly clear. There were few blasts which have like granules, not in this one, but initially I've seen one with some granules. It would be a granular lymphocyte or LGLs. LGL. Yeah, that could be for that. It was only one cell with large granular lymphocyte, large granules or granular. But the rest of the cells don't have granules and cytoplasm is not clear. Right. So the lab scientists think that this is lymphoma because the patient has lymphadenopathy. He has read the history on the request form and now he has referred the blood to you, clinical hematologist. Report this blood. This is a very common exam question. Is it? The normal, normochromic and the platelet count is quite normal. So who is speaking? I'm speaking Dr. CNU. Dr. Sindhu. You may have heard from me before. Comment on the abnormal cells. Okay. Can you repeat what was the CBC count in this patient? Hemoglobin was 12.2, white cell count was 17, and platelet count was 210. WBC 17,000. 17. Okay. Uh, so I, on the low power, maybe there is a lymphocytosis is most prominent. Lymphocytosis. Mhm. B and these cells are intermediate in size with, which cell? These cells are intermediate in size. These cells are intermediate. Okay. Yeah. These atypical lymphocytes are intermediate in size with basophilic, irregular cytoplasm and nucleus is quite condensed and it is also irregular in margin and there is inconspicuous nuclei. There's no any prominence of nuclei. And while RBC, these are normocytic, normochromic and platelets, they are adequate in the background. So the peripheral smear is consistent with maybe lymphoma or LPD, lymphoproliferative disorder. What was the history? On examination, is there any lymphadenopathy? Organomegaly? Yes, this patient has lymphadenopathy. He has fever. Is that the T-PLL? T-PLL? [Music] I, I mentioned to you before as well. Concentrate on the history first. History may give you some clues as well. There are not much counts. That's why not. She is 23 years old. She has fever and she had lymphadenopathy. These cells are all atypical. One of the colleagues informed me that these are reactive lymphocytes. Infectious infection cells. None of the like CL cells are not like this. And you will not expect T-PLL in a 23-year-old. Follicular lymphoma cells, they have their own morphology with a cleft in the center. And there wasn't so much clear scalloping of the red cell around that. That's why maybe you have seen many which has very clear scalloping. And these cells are basophilic and a lot of cytoplasm in there. And you haven't seen any blast in in this LPD. So how do we differentiate between the lymphoma and, uh, because I have seen few cells having scalloping, but few lymphocytes are not much as reactive as in infectious mononucleosis. The others you have seen of the granular type of lymphocytes. The granular lymphocytes are also secondary to infections as well. They can be clonal only if their TCR reagent is positive, receptor is positive. And for that purpose, the patient should be elderly, should have history of autoimmune disease like rheumatoid arthritis or SLE, etc. And the patient, which lymphoma you were thinking that this patient has? As you said that large granular lymphocytes, maybe I'm telling that maybe there is LPD, lymphoproliferative disorder, which one, large granular lymphocytes, because size are these are large in size and quite few are granular as well. But there is a scalloping. Okay. So if in the exam, you get an LGL lymphoma, they will give you a history of neutropenia and a history of autoimmune disease. Okay. Okay. Secondly, this patient has Howell-Jolly bodies as well. You missed that in your reporting. You will lose marks for that because the examiner's report has mentioned the RBC contain Howell-Jolly bodies. Okay. Yeah. Always concentrate on the history. A 20-year-old cannot have a CLN and PCL. PCL has its own morphology. Mantle cell has its own morphology. Waldenstrom cells or marginal zone has its own morphology as well. They are not like this large, large cells with basophilic cytoplasm. And there is prominent scalloping. See, this cell is scalloping to four RBCs. So this is a common scenario in the exam. I think it did not appear in the last exam. So this exam, it will appear for, uh, LGL cells with scalloping. And especially this one. This is scalloping to the V. This one is scalloping here. Very prominent. [Music]
So the next case is again a 30-year-old with abnormal full blood count. Sorry, sorry. The previous case was an LGL? No, it was infectious mononucleosis. Oh, right. In LGL, the scenario would be that a 56-year-old man with a previous history of rheumatoid arthritis or ankylosing spondylitis or Sjögren's syndrome was referred to you because of neutropenia, and there will be a lot of LGL cells in their blood film. Let me check if I have any LGL slides. Dr. Amir, the granules, you said in infectious mononucleosis, there could be the granules and the lymphocytes as well. But is that granules will be the same as in LGL or that would be different? Same as LGL.
[Music] I think the slide has become old and the stain has faded. I would like to bring LGL slides for you because this one is now old and some of the. This is one of the large granular lymphocytes. Really cannot appreciate the granules in that. Yeah, because this slide has become old and like they appear like more eosinophilic. [Music] That looks a bit granular. Any other? Okay, if I manage to find another LGL slide somewhere. And this one has no scalloping. This one has also granules. At the top portion is marked with us. I am indeed. Yes. Do you have any fresh LGL slide with? I have this one, but this one is old and the stain has. I can't say. I haven't seen many LGLs. I always see the blood film of autoimmune disease patients and I hope to find LGLs in them. What is that? Is that a lymphocytosis? It's expired now. So the white cells appear very strange. That's why I'm looking for some nice LGL which is prominent. Staining is a bit strange though. It's not an MCG stain, is it? But it is an old slide. It's more than one year old now. So the stain has faded. Yeah. Try to produce. Right. Let's go to our own case. This is a 30-year-old male referred by GP because of the abnormal full blood count. Hemoglobin is 140, white cell count is 13, eosinophil count is 5, and platelet count is 250. What do you suspect if this patient, if this is the full blood count of a patient? Seems to be a lot. You may be reactive. Okay. Yeah. Eczema or like helminthic infection. What infection? Worm infestation. Parasitic worm infestation. If you are sitting in an exam, what will you do to find a worm? Go to low power first. You will go to low power. If there is any eosinophilia case in the exam with which the or the or the full blood count shows that your eosinophil count is high, you should start from power 4. Because in the native blood film, they have a lot of worms in the native blood film. And it is difficult to miss them. But in the exam cases, they will have one worm per slide. You have to go through all the section of the slide quickly to find. They appear on power 4. And if you could not find eosinophilia, you could not find worm, then you will go for other causes of eosinophilia. Have you got travel history on this chap? The patient? Sorry. Have you got travel history? This was the point that you picked. You snatched from my mouth. I was about to say it that if the scenario says this patient has traveled to any anywhere African countries or South American countries, then certainly there is a worm. But you are missing it. Okay. So this patient does not have a travel history, but the eosinophil count is persistently high since two years. Sometime five, sometime six, sometime four. This is what's the MCP? Like the CRP is normal. Is there any history of asthma or any allergic condition? No asthma, no allergic. Steroids? No steroid. He is a young man and completely fine. No background medical history. Is it dysplastic? Then you have to tell me. Yeah, it's not correct. You expect more granules than the granulation. Be, be orange granules. What are the clonal causes of eosinophilia? Chronic myelomonocytic leukemia. And lymphoid with mutations like PDGFRA, PDFGB, PDGFR alpha, and acute myeloid leukemia, especially inversion 16. And, uh, acute lymphoblastic leukemia, but there is translocation 5;14. But there, the eosinophilia is secondary to the reactive cause, not due to the clonal. And mastocytosis and other causes like CMML. There is also a can be a mutation which leads to the eosinophilia. And other, not otherwise specified cause. After WH 2022, there is no not otherwise specified cause anymore. If you want to mention it, you have to write in bracket. It can be the, yes, I remembered. The chronic eosinophilic leukemia is one. Myeloid neoplasms with eosinophilia and gene fusions is the second one. And if both of them are not present, then it is called. What is the difference between idiopathic eosinophilia and idiopathic hypereosinophilic syndrome? So the one has the organ damage like idiopathic hypereosinophilic syndrome has organ damage caused by the interleukin released by the eosinophils. And the idiopathic eosinophilia in which there is no any organ damage. So this is called idiopathic eosinophilia. Okay. Idiopathic eosinophilia is just eosinophilia. But if it comes with symptoms, then it becomes syndrome. You have mentioned the different genetic mutations that are present, rearrangement that are present in eosinophilia. And you have mentioned some causes of eosinophilia. The myeloid eosinophilia. Right. If this patient has hypereosinophilic syndrome, what is the first line treatment? So the first line treatment needs steroids. If the patient is steroid refractory, then imatinib, low dose imatinib, 400 mg for 6 weeks at least. Right. Eosinophilia is a common W case. You should remember. If the, what is the treatment of hypereosinophilic syndrome? What is the treatment of clonal eosinophilia with PDGFRA mutation or PDGFRB mutation or FGFR1? So before warming up this case, anyone can report this blood film for the exam. Uh, so this blood film is showing prominent eosinophils that are bi-lobed and with eosinophilic precursors as well. And there's a red cells are normocytic, normochromic and platelets are normal morphology. And [Music] I cannot see is what there is there is the dimorphic picture or like some normal and some few hypochromia. There is a bit of hypochromia. And that's it. Your report is not complete. There is little. I'm seeing vacuolation in eosinophils as well because they are dysplastic. That's why you are seeing vacuolation. Complete, complete your report. Means, uh, basically I would like to see neutrophils as well in this patient. There was no blast. However, and no neutrophils are also evident. Right. There are no neutrophils here. All you. Okay. Complete your blood film report. So, how to complete it? I'm actually not getting it. You have commented on the blood cells. What is this? What is your impression and what is your suggestion? The GP has sent this blood to you. So the blood film is suggesting of increased eosinophilia. I will request to GP to have a detailed history and examination and with the stool for O and C, and CRP to look for the CRP and infections to rule out the secondary causes. You know about the. Give him hematological advice. Okay. Then I'll advise him to PDGFRA and PDGFRB, FGFR1 mutation. Careful blood. I will ask the GP to observe the patient for the symptoms for some duration. Patient has eosinophilia since two years. Phenotypically. So the blood film shows lymphocytosis, most of which are dysplastic. There is a bit of hypochromia in the red cells and a pitted count is low. So this patient has eosinophilia which can be primary and secondary for hematological reasons. We will do a serum tryptase level and immunophenotype. And after that, the next step will be a bone marrow biopsy and genetics. Dr. Amir, can you please mute your? Okay, sorry. You said that history, examination, then serum tryptase and the immunophenotyping for that patient. The history and examination will be done by the GP. He would have done that to exclude secondary causes. He referred to you because this patient has eosinophilia since two years. So I will ask for the serum tryptase and immunophenotype for clonal causes. You need a peripheral sample for FISH. Okay. In the bracket, you can write for PDGFRA, PDGFRB, FGFR1, and serum. If there is any clonal cause, you will get it on these tests on FGFR1 on the peripheral blood flow FISH and on the immunophenotyping and tryptase. Why we are doing FISH for this patient? [Music] Synergistic. [Music] Mastocytosis. Eosinophilia panel consists of FISH, immunophenotyping, and serum. Dr. Amir, can we advise the serum vitamin B12 because it is also a marker of clonality? As I read in the books. GP would have done that. Okay. We only say if it is a new case, we advise the GP to exclude secondary causes. If secondary causes are ruled out, please refer back to us. And GP knows what are the secondary causes. Hematologists are not required to exclude secondary causes. It is also written that in the treatment, we give, we have to give strongyloides cover. Whatever the reason or whatever the underlying cause. So is that true that we have to give in every case? I heard that for ATL patients, but not for the steroid resistance in eosinophilia. If steroid resistance is not because of eosinophilia, why should I give the treatment for that? Because you have many eosinophilia patients in our clinics, but they are not using any worm-related treatment. If it is ATL, then yes, that is associated with strongyloides. And for that purpose, you have to give strongyloides cover. Otherwise, it is written in the BSH guideline. I mean, no. If it is the cause, then you have to give strongyloides. Otherwise, in eosinophilia patient, the patient has eosinophilia. Why would I give? If you can screenshot that paragraph and send it to me, because this is not the practice that we do. Okay. And if it is related to strongyloides induced eosinophilia, and the patient would go to ED, ID, infectious disease, not to us.
This is the last case. So among the exam candidates, Harmeet, I know you are the examiner. This is a 7-year-old boy who has been referred to a hematologist because of recurrent epistaxis, spontaneous osteitis, and the blood film goes to the lab scientist. The lab scientist has noted thrombocytopenia. This is power 10. Are you there? Kine is silent. Another person that I know going for exam is Rehan. Yeah. This is a child with recurrent epistaxis and the lab scientist says that this patient has nucleated RBCs there. You are from the lab side. Okay. Yeah. We need your comments first before referring this to clinical hematology. Well, it's from the thrombocytopenia that the age of the child is concerned. I'm looking for blasts, but I can't see any. Okay. So you have referred the case to clinical hematology because of thrombocytopenia. Yeah. On the age of the, of the child. So, Dr. Sona, you are the clinical hematologist. You have called her and she has come to report the blood film. So the blood film is showing marked thrombocytopenia with platelet anisocytosis. There is a leukopenia. Neutrophils. Please go inside to see the neutrophils. There are very few neutrophils in this patient. So neutrophils are also evident. And the red cell morphology is also showing normocytic, microcytic, and microcytes. Normal normochromic cells. So the findings are suggestive of thrombocytopenia that could be immune-related or that can be need detailed history. Can be viral induced, can be drug induced. What is this? How? Oh, yeah. You need to mention every finding in the blood film, otherwise you will lose marks. I mentioned that this has recurrent spontaneous. That's looking larger. Sorry. Got ITP. Possibly ITP with few large platelets can be seen with the thrombocytopenia. So I would investigate for the inherited any inherited platelet disorder as well. What inherited platelet disorder? I don't know. If it could be May-Hegglin, something like that. Large, large with with a large size platelet. The main is the Bernard-Soulier and gray platelet syndrome. But that doesn't look gray on morphology. But there are the evidence of nucleated RBC somewhere. I have seen some teardrop cells as well. So it could be with the gray platelet. Maybe these are not gray. The gray platelet is out of question. So why there are the NRBCs? These are not NRBCs. These are large. These are giant platelets. So the main differential with that was with the Bernard-Soulier. What are the differential diagnosis of large MPV? So it's a May-Hegglin, but not solar. Gray platelet. Cat 2 to G mutation. These are all in the macrothrombocytopenia. What else? Cas 22 is not common. G is not common. Bernard-Soulier is okay. May-Hegglin is okay. What else? Type? Yeah, this is common. You need to check for [Music] that. Okay. So Rehan should completely report because you have to report this for the exam. Yeah. So the findings are suggestive of macrothrombocytopenia. It can be inherited, but not so. Or advised. Patient is advised for. Patient needs to be referred to the hematology clinic for second opinion, urgent management and diagnosis and advice. Genetic mutation. The blood film shows through macrothrombocytes. The platelets are granular. The red cell and the white cells are okay. The impression is that of inherited micros atyia because of the given history. This thrombocytopenia needs further investigation, dash, dash, dash, to rule out the inherited. What investigations you would like to do first? I will, there can be light transmission aggregometry, cytometry, and genetic studies. And res and nucleation. Right. For more type to be storage, we will do the ATP ADP ratio for that. So one more blood screen, peripheral blood for flow cytometry and light transmission aggregometry. What is your expectation on light transmission aggregometry? Aggregometry and pro. This is Bernard-Soulier syndrome. So in the light transmission aggregometry, there will be absent response to ristocetin 1.5 mg high dose ristocetin. However, others will be normal. And in the Bernard-Soulier, I will get a CD42b, 342b positive absent. Sorry. Careful for GP12B, GP95, 1B9. It is the glycoprotein is absent. Right. This was the last case. They were the general today and they will come. I'm not an examiner, but they will come. So be ready for that. Do you have any questions? Sir, any question? Thank you. If no question, then enjoy the rainy Sunday for those who are in UK and see you next week. Take care. Okay. Am. See you next week. Thank you. Thank you. Thank you.