Transcription
Is the screen visible to you guys? Yeah. Okay. So, let's please let the people in 'cause I cannot see waiting in the.
So, this is the case. This is a 56-year-old man who is admitted in the oncology ward for, uh, chemotherapy. He has a background of pancreatic cancer and he has done some bloods and the blood shows that the good blood count is 80, plated count is 60 and white cell count is 12. This is power 10. And this is power 50. Oh boy. So, >> the drying platelets there >> the blood goes to the left side. >> Yeah. You can see this dry plate thrombocytoenia maybe. Yes. Do you know thrombocytopia? >> A lot of maybe >> are quite a lot. >> So you have not chromosyia sides. This thing is here as well. >> Okay. RBC and there are some other changes in the red cells as well. To target size. Someone is typing in the Teams but I cannot see the 'cause I'm sharing the screen. We can shout out >> something like a a TTP MH some form. >> Let's see. You're suspecting Mah and >> could be a few more maybe nuclear RBCs, but there's a lot to sites about. So what would you do then? >> I think I do a retake on this job. >> Dat sites maybe. >> Yeah, I definitely refer it to consultant. I'm a bit concerned about the Yes, >> there's nuclear RBC there as well. >> So, you're thinking about Maha NTP and uh uh you would like to refer this to the consultant hematology or register. >> Yeah. Yeah. Big concern about this size. And now we need the consultant hematology or restor hematology to report this blood pin is first on the list. You cannot be silent because your lab colleague is saying that this is TTP. You need to report this blood emergency. Second one is Rubina S on the list. >> Very shy here. >> Yes. Um I'm surprised that this is not certain situation. Sir. >> Awesome. Yes. >> Yeah, I can report. No problems. Yeah.
Okay. So, uh, this uh is, um, u blood film u show, uh, an isoccytosis, um, with many shistoides and, uh, um, a few hypogchromic cells, target cells, and, um, spherosides, few very few spheroxes also, and nucleated arbes and, u, wpcs. These are, um, normal in number and, uh, morphology, and, uh, platelets are, uh, reduced and the blood film findings are suggestive of, uh, uh, maha, um/TP, most likely GTP, uh, as patient history, uh, secondary to malignancy, uh, or treatment. Um, for confirmation, um, urgent, uh, uh, um, we need to, uh, inform the, uh, clinician, uh, as soon as possible, immediately to confirm with consultant. >> Yeah. Yeah. >> You, you are the consultant or register. We will call the DTP consultant, uh, to, uh, confirm the diagnosis and further, uh, to start the treatment as soon as possible and arrange the, um, blue light, uh, transfer to TTP center in case of TTP, uh, for plasma exchange and send admts 13 before it. >> Okay. Anyone else who differs with Shabana? Yeah, I think, uh, in the milling MC, uh, we, uh, we'll treat the underlying cause. Okay. Robia, what do you say? Uh, sorry, but I joined a couple of minutes, uh, late, so, um, the scenario, I didn't, uh, hear it from the start. >> This is 56-year-old man. >> Admitted in the ward. >> Waiting for chemotherapy. >> Because he has a background history of pancreatic cancer. >> Right. >> Blood has been done and a blood shows hemoglobin of 80 and, uh, break count of 60, white cell count of 12. The blood was >> Yeah. The blood film was seen by the biomedical scientists concerned. >> Yeah. >> And he thinks that this HTTP and MA, that's why he referred it to you urgently. >> All right. Okay. So, um, I agree with my colleagues in terms of the findings of the of the red cells. There is ancytologist with, uh, many fragmented cells and, um, many target cells as well. Um, and neglated RBC. Um, there is also like, uh, a giant platelets, um, reduced platelets with giant one and anocytosis. Um, this is what I saw so far and, um, neutrfil looks normal. Um, my impression, it's, um, it's, uh, there are also a couple of teardrops as well. So, it is, um, there is maha, but, um, I think it's not, uh, but not BTTP, it's, um, could be, um, due to medication induced maybe. >> Mah because of, yeah, secondary pregnancy and medication induced. >> So you think that this is not TTP? >> Yeah. >> We will ask Sami S as well and then we will discuss it. What do you think, Sam? >> Yeah, I agree with my colleagues. Uh, so, uh, feature suggesting Maha. So we need to, uh, find the cause. So you, we usually send Adam 13 in this situation and that will give us an idea is it immune or not, not immune. If Adam 13 came back normal or more than 10%. Uh, so this is can rule out TTB. So usually this discussion will be with the TTP center in line and and then we can decide the second stage of treat. Came back and it is less than one person. >> So this is TTP then, so we need to urgently transfer the patient. We are not a TTP center. So to TTP center and start treatment as soon as possible. Right. So, so this is a 56-year-old man and he has pancreatic cancer starting chemotherapy. Okay. There are a lot of fragments in the in the red in the blood film. Do not forget to mention other red cell finding as well and this film shows target cells as well and we had seen four jolt bodies in this patient as well. You need to mention all the findings that are present in the blood cl 'cause it may be written on the key of the examiner. If you do not mention target cell, they may deduct a mark from it. There are macro sites, everything is there. This patient has, um, pancreatic cancer and there is a maha. If the renal functions are abnormal, Shabbana said that we will confirm this with TDP consultant. We do not confirm with TTP consultant. We agree on TTP on TTP diagnosis with the consultant. If you open the TTP algorithm, it says agree with the TTP consultant because you don't have AdamTS13 when you are calling the TTP consultant or TTP send. You agree on the diagnosis. Yes, this is TDP. The renal functions are abnormal. There is an new anemia, new this is TTP. But what type of TTP is primary or secondary with a background of pancreatic cancer? This is secondary TPP. And in secondary TTP, yes, we do send AdamTS3 level. But we do not wait for the result. But here because it is secondary TTP, we do not do plasma exchange. We focus on the secondary port. If it was a primary TDP then yes, I would have, uh, blue light this patient to, um, to the TDP center, but if there is a secondary cause present over there, then we do not do this is how they would trick you in the exam. Reading the scenario is very >> Yeah. Uh, sorry, I'm, um, I think my impression was as a secondary TTP, but like that before even the atom 13, we would also like check the clotting and the hemosis screening for example, and kind of we're not using it, but like the platinum score that could give like a clue, um, if it's like a, a primary or secondary. And in terms of when, when you mentioned the history about the second, like malignancy, epetic cancer, I thought like it's probably secondary, so no, not for plasma exchange. If this patient was postallogenic stem cell transplant and he is using techrolyus, the picture is like this, okay, it is also mahaba, you may be thinking of tp as well at 13 maybe less than 10%. But he is post transplant and he's using techus, it is drug induced, you will not cause my exchanges. >> Yes. Yeah. They can give you this picture with normal plated comb, but the picture is just like this, a lot of red cell cytoides and >> I'm not sure, but got patient similar to this story, postrplant, and his Adam 13 was 50. >> 50. >> So, yeah, so I'm not sure if, if the Adam 13 like below 10%. How, how, how we say like, yeah, plasma exchange is not indicated. >> Because it is, there is a secondary cause present over there. It is not immune. You do plasma exchange to remove the antibodies. >> Yes. So Adam 13 will be, how will Adam 13 will be replaced? I guess when we have Adam 13 below 10%, we need to check for Adam 13 antibodies first, right? >> Yeah. So, for example, if it is trollimus related, we stop trollimus. We change it to solimus. We change it to cytosperine. If it is pancreatic cancer related, then we then we start chemotherapy for the patient. Yes, the patient will have low adamts 13 levels for a few weeks before the chemotherapy kick in. Then the, uh, the Adam say Adam TS3 level will go up. But the plasma exchange will not change anything in pancreatic cancer in induced, uh, TTP or any other cause of secondary TTP. In in the primary, it is the antibodies and the purpose of the plasma exchange is to remove the antibodies that is, uh, nullifying the adams 13. >> Uh, sir, I have a question. Uh, in malignancy, Adam TS3 will be low? No, uh, it will not low, right? >> In most of the cases, it is not low, but in some cases, yes, it gets low as well. Pancreatic cancer is a mucinous cancer. It absorbed everything. Okay. >> And most of the, most of the secondary TTP, you will see in pancreatic cancer. >> So in that case, uh, we just treat the malignancy. We will not treat, >> we do not, we will not go for the plasma exchange. >> Plasma is only for primary TTP, not for second. >> Yes, that is mentioned in the garden 2020. >> Sorry. Um, air, this is Kali. Um, I am with Sami. Yes, I know that, uh, that case was sent from, uh, our center to referral center, that one like alograph patient, something something, but we know that there are poor response. But what is the, um, guideline suggestion about kaplasab use up front in case if we are trying to liberate or release the platelet in circulation to prevent any bleeding complication? We transfuse them like >> Okay. >> here in leaves, we have a big, uh, allergenic stem cell transplant center as well. We, we find this situation quite often. >> Right. >> If, if the patient, um, is not responding by changing any imunosuppressive therapy, then MDT usually decide for blood transfusions. If no, if no response, then sometime they decide about either or. >> Okay. >> So this is, then MD decision, but there is no guideline for, uh, separate guideline for secondary TTP. >> Correct. >> Because, um, we, we quite often face this phenomena, maha, post transplant, or TTP postrplant, and their adine levels are low as well. >> Yeah. So we can, we can immediate, cuz we do show some quick response, like in that case, shall we consider like methile PR or RTUs up front? Cuz if we show like TTP directed therapy, cuz we know that TTP platelet transfusion is relative contraindication, lots of ho around the community. So I was just wondering on this point, please. >> I was just wondering on this point. >> If a patient is bleeding, okay, then you have to give platelets. The patient is not bleeding, >> then >> you have to wait. >> And the childon. >> I think in post transplant patient consultants usually avoid, uh, steroids, especially in my center, they do not give, they try to avoid steroids post transplant because they are already imunosuppressed. >> Steroid doses of steroids or p steroids may make it more imunosuppressive. >> Yeah. But again, um, I have little bit of hesitation in that point because of, you know, when we do see the grab versus source disease, like guard GBHD, so on so forth, then we end up offering steroid. So a separate thing. >> Different, different. Yeah. >> If a patient develop GBHD, then it is, then their treatment is steroid. >> Okay. Is steroid. >> Okay. Okay. No, nice, nice information. Thank you.
All right. This is a second case then. All right. So this is, um, 15-year-old boy, um, referred by the GP due to anemia. So in the, in the hematology clinic, he has some, he, he did some bloods. Hemoglobin is 110, platelet count is 161, and white cell count is 9. This is the power 10. Let's go to power 50 to there. Definitely is a DCT and red count. >> DCT is negative. >> It's negative. Okay. Got the retake count done. >> Count is high. >> Okay. Reticular site count done though. >> Yes. IC done is done in the R5. >> Yes. Right. It looks more like an autoimmune problem. >> The HP was okay though, wasn't it? >> Yes. 110. >> Yeah. Lot and I said to this super killer sites. >> There are a lot of things in this one picture, interesting film, and he's 15 years old. >> Yeah. So what do you think? You think this is, uh, someis going on? There's not many. I can't, you can't see any nuclear ABCs, but there's so many spherosites going there. Say it's a form of autom or maybe, um, yeah, there's no any lymphosytes around. >> Uh, one cell count is Okay. And licide count is okay as well. >> There it could be a bleed as well going on. >> No, there is no. >> I definitely, I definitely refer this one anyway because I'm, I'm concerned about the number of sperites. >> Okay. Got a lot of sperites in this one and other as well. Do you think this patient is bleeding or something? >> Could be a form of hemolytic. I, I say there's not that many nuclear ABCs about, but the swell sites is concerning for me. I don't know whether it's a HS or not. Um, autom possibility. >> Okay. You think this is >> Clinical hematologist. What do you think? Start. Um, can be, uh, I have a differential for, uh, this peripheral film. It can be, uh, can it be membranopathies? >> You need to report it. >> Okay. So the RBC there is n isoplocytosis and, uh, there is well macroytes plus 2 + 3 and along with electtosytes, spherocytes, and few pencil cells. Platlets are adequate on varicus smear, but I haven't seen any WBC here. So conclusion is, uh, it can be membranopeties by keeping history, uh, it is hemoglobin is around eight, so it's not sever anemia. >> Yeah, this is, I think lymphocy. >> How jolly body is about, I think. >> Yeah, how jolly bodies there. >> Uh, it's more like to me. >> You fragmented RBC's dear drop. So conclusion is maybe it is a heredity pyroytosis or herittoytosis is a differential I have. So advice for the IMA, uh, osmotic fragility test and SDS page and, uh, family studies and genetics CBC along with other parameters like MCV, MCH, Ipp. >> This is HP heridicular. You can see wide range of red cell features here. If it was electrocy, there should be no here and no drop and notoid, but it has macroytes, spherosides, teardrops, some, uh, strange hyrotes as well. Um, n isoperculosytosis and all of the blood fil is like this. So this goes with the, uh, most likely memoranopathy, the hereditary pyropiculy, but you need to confirm that on the investigations that you have mentioned. This patient has whole jelly bodies as well. Do not forget to write it in the exam because this blood film can be given in the exam in a different way as well. Write six different features present in this blood film. They may not ask you to report it. They may ask you write six features, uh, from this blood film. This blood film has a lot of features. This is hereditary pyropulyis and you need to confirm that on genetic testing. That's why he was not that much anemia. He will get anemia only in stressful condition. Right. >> This is a Niko slide. Those working in the NHS, they should go to the lab and see the nickel slide for HPP. It appears in exam.
The next patient is a 21-year-old female. Um, he is feeling generally unwell. This is power 10. Her hemoglobin is 130, plated count is 180, and white cell bound is 16. This is power. Okay, now. Yes. What do you think? I think you, you are the only biomedical scientist here. Any biomedical scientists? Okay, for example, I am the first year biomedical scientist. I have seen this blood con and I have seen a lot of atypical white cell and I think that this is all. Okay. And I have referred this blood to you guys to methology resistance and consult. So please report this blood. My suspicion as a first year biomedical scientist is that this is ALS because of these white cells. Denosa, can I speak up please? Um, yeah, uh, red cells normocchromic normocetic and, uh, there are some, uh, a liodies, uh, white cells, lymphocytosis noted. Uh, there is, uh, reactive lymphocytes with, uh, abandoned cytoplasm, bluish abandoned cytoplasm. Uh, some showing, uh, flow flowing cytoplasm, flowing around the red cells, making red cell, uh, uh, uh, indentation from the cytoplasm, cytoplasm making red cell indentation. Um, um, platelets are, uh, I didn't see the neutrfils. Oh, sorry, uh, nucleus show, uh, some chromatin clamping. Um, and platelets are normal. Uh, so I think this is more like, uh, reactive lymphocytosis, most probably due to, uh, mononucleosis, infectious mononucleosis. I will do, uh, Paul banner, um, IML antibodies, and CMV IG IM IGG and IGM antibodies. And as there is evidence of hyposplanism, uh, to assess further investigations of the auto scan abdomen to see liver spleen, you do BC and the HIV as well along with the monosport. But I am a first year biomedical scientist. I was thinking this is am all al. So how will you tell me that this is not all blast? These react? Um, because the morphology, the, um, there is nuclear, um, uh, the the chromatin, there is chromatin clamping, um, and, uh, there is no evidence of like, uh, immature like, uh, immature nuclear material. Mhm. >> But they told me that this patient has cervical lymphodenopathy, which which can be a fe, which is a feature of infectious monoconosis. They can have lymphocytosis, uh, mild splenomegaly, mild hepattoomegaly. Okay. That's right. Yes, you are right. These questions quite often come in the part two exam and people make it, uh, alll because is common in teenage. So when they see a patient of 29, 21 year old, or 20, or 19, or 18 with with such blood features, they think that this is a but here's the atypical lymphocytes, they have mature lymph, mature nuclear material and cytoplasmic material is bluish in color. Sometimes they make, uh, make skeleton ing to the red cells. But remember, scalping is not a feature of infectious moniosis or rectitoy. You may find scalping anywhere where there is high white cell count. We have seen, um, a monoplastic AML, whose slide is present in the ontology quizzes on the channel. That patient has white cell count of 132 and there were quite a lot of, um, red cell scal. Okay. So it depends on the scenario. White cell and then yes, you can say there is a cell scalping, but it does not necessarily mean that this is a reactive lymphocyto. 132 count cannot be reacts. And if a patient has interpre hemorrhage as well, and and blood thin shows a lot of atypical lymphocytes and scalping, you cannot say this is it depends on the scenario that they have given you the patient that they have given you in the scenario. As these nephosy are quite, um, reactive looking, the cytoplasmic is blue material is this is in practice monucle. Every alternate alternate epipath exam has one slide about infectious monosis. The next line is a 40-year-old female who is admitted because of, um, bruising and progressive tightness. The hemoglobin is, uh, 94, count is 80, and white cell count is nine. What? This is power 50. And and these are a few words available. Any biomedical scientists that want to comment on the blood feature? No. No. So again, I am the first year biomedical scientist. I heard from the, if the cytoplasm is bluish, then sometime they are reactive lymphocytes. So these cells appear to be bluish as well. So I have labeled it as a reactive lymphocytosis as well. But then for a second opinion, I referred it to you guys to clinical hematologist and consultant to see what is this. What do you think? All right. So any clinical hematologist, um, the blood film is, uh, showing anemia. Um, um, there are, um, medium to large size, um, monuclear cells with, um, nuclear, uh, with blob nucleus, a granular cytoplasm, um, and, uh, there is thrombocytoenia, so I couldn't see any platelets here. Um, yeah, blob nucleus and a granular cytoplasm. Um, a nuclear, uh, chromatin, uh, looks, uh, open, open nuclear chromatine, uh, couldn't appreciate any nucleololis, um, and patient presented with, uh, thness, I think, isn't it? So I would think about APML here. Anyone else with a different opinion? Uh, sir, we will, um, uh, write that, uh, uh, the blood film showing, uh, shows, uh, atypical monuclear cells, blast cells, uh, that are, uh, medium to large in size with abundant cytoplasm, open chromatin, and, uh, open chromatin nuclei, and, uh, with prominent nuclei, bophilic cytoplasm. And, uh, uh, red blood cells is an isopiculoccytosis, uh, with, uh, normocetic, and, uh, platelets are reduced. So, um, we will say it's, uh, um, the, uh, findings, uh, blood film findings are suggestive of, uh, acute leukemia, most likely acute myoid leukemia, and for confirmation, we will go for the flowcytometry and, uh, bone marrow, uh, with the cytogenetic and fish analysis, and APM Amen. >> It's not the typical APML. This is this is all or how can you say this is? You mentioned this is normal. >> Same. What is the question? >> This is AML or ALL. >> Why likely AML? >> Why? Why this is AML? >> Right. So the size of the blast, it's, um, kind of tends to be large, medium to large in size, and, um, in terms of the nucleus, it also like, it's, um, it's very open like chromatin rather than compacted chromatin. Um, what we can see in the liful blast, there is nucleololis in few of them. Um, the cytoplasm is not, yeah, it's not granular. It, it's not like, um, it tends to be granular in the like in terms of myoid, but it's not here. It's a granular, but like, it still could be either monocytoid or, um, yeah, it could be monoblast, rather than still, I don't think it's, um, yeah, for blast, this is the main things I think. >> Yeah. But, uh, some features favor, uh, lymphoblast, like less number of nucleoli, more, uh, regular rounded shaped blasts, and, uh, bluish cytoplasm. This favor alll more. AML blasts are like quite large, abnormal shaped, and the nuclear shape is also more abnormal, and they have like multiple nucleoli. So that is against that features we don't find here. So it could be ll also. >> It looks like monopolast for me. I don't know, maybe AML, I'm not sure, or M4, I'm not sure. >> Have you got any, um, typing result? >> Sorry. >> Have we got any result? >> No. >> I think these are my blast, not lymphoblast. >> What? >> Nuclear chromatin is not suggested of lymphoblast. It is like a reticular neutral material. >> In lymphoplast is a high NC ratio, but here is abandoned cytolas and, uh, so it's more suggestive of AML. >> We can send the nl, it will come within 1 hour or. >> It could be mixed, mixed phenotype acute leukemia, mixed phenotype acute leukemia can be both. I think also the polymorphism, uh, is more in myoid lineage rather than lymphoid lineage. So in AL, usually is monomorphic plus. >> That's why on the blood film, you always says that this is most likely acute leukemia. You do not say that this is AML or all unless you are very sure. But you may have seen that your seniors or consultants, they always mention for a blood thin like this, this is acute leukemia. Yeah, we need origen flow cytometry on peripheral blood to find out the mean that this is all or then yes, rest are the things you will do. You will do bone marrow biopsy on this patient or if there is an lymphodenopathy, you may do lymph biopsy if patient is refusing bone marrow. But this patient has cytoenia, so bone marrow biopsy is the next step. But the first thing we do is we take blood sample, drop it in HMDS, ask them to give us a provisional flow result to see whether this is myoid or this. These cells have a lot of cytoplasm. The cytoplasm nuclear ratio is not that low in in lymphoid cells. They have very minimal cytoplasm, but here the cytoplasm is quite a lot. Some of the cells have granules. Not all of them have. And I was looking for a cell which has, uh, our roots. In this blood pin, there are few white cells which contain our roots. Um, but when you try to find them again, they are lost. So the end result of this slide, this patient is currently admitted with us is a, a flow cytometry matches AML, and this patient has many different mutations. So we label it as complex AML. All right? So never say that this is AML or on a blood. Just mentioned the most likely this is acute leukemia. Leads urgent flow on per to find out the lineage. The, uh, further investigations will be vulnerable biopsy for cytogenetics, amino accept. >> S, if you don't mind me asking, why the RBC's in the background dish are looking like this? Like, uh, two RBC's are stabbed in most of the films, most of the fields that we saw, two RBCs were stacking together. Is there a reason for? >> I'm on the thick side, that's why because I'm searching for the a blast which which contain our walls. >> Okay, okay. >> If I go to the thin side, then there will be one and one cells, not, uh, side cells. Sir, I have a question. >> Uh, okay. I was just thinking that the patient's history was oozing from many sides. She was 40 years old female. Uh, although the TLC count is not very high, it is around nine. But, uh, some of these cells do show those, uh, um, nuclear foldings, um, with abundant cytoplasm and occasional we have shown us are showing, uh, these or rots. >> Can we give the, uh, possibility of APML also in it? Can we write like in our report that urgent flowcytometry on peripheral blood? So if you have seen the cells of the npm1 related, uh, AML, >> they are cells also sometimes shows holdings that make you think that they are ATML. They actually not. >> The ATML cells, they have two, uh, blob nuclei that are very characteristics. Like this one, this cell, which is present on the on the screen, if you tilt it a bit, you will think that it is like a boop cells. Actually, this is not a bop. >> Yeah, it's not, it's kind of a nuclear indentation. >> Yeah. So, and then secondly, our road, our road can be present in other hematological as well. A type of MDX contains our roads as well. Sometimes the in they will contain our roads as well. So our road is not a classical features of APM. You can find them in other conditions as >> Yeah, but oozing from many sites, that was also part. So I, I actually, I was stuck on, um, >> oozing oozing. Maybe the patient has thermosy, that may be the cause. >> Right. Right. >> So, uh, sorry to interrupt again. I was wondering like nuclear indentation or the cupping, uh, of, um, the nuclear shape, which seems mimicking bob. So is it the dd for npm1 mutation as well here in this case, if it was detected or not? >> So you do not avoid npm1 as a ded. We only say acute mid leukemia or alllenotypic leukemia, and they ask you about differentials. NPM1 mutated is like you, you are going too deep, uh, in the subcategories of AML. When you are sure this is AML, then you will say the nuclear, the the nucleus has a cup shape or fish mouth shaped materials. This can be one mutated as well. But you do not give NPM1 mutated AML as your detention. You always wait for the cyber genetics to come back. >> Yeah. Now, out of curiosity, as you said, like, as it was a complex carotype AML at the end in your center, so what was the NPM1 status? That's out of curiosity. >> It was not mutated. >> Okay. Okay. Thank you. Thank you. Um, if we put >> KM22 KMT2A mutated and, um, there were two other mutations, but the the patient has four or five different mutations. Yes. Someone was asking, yes, if we put, uh, uh, as a differential, uh, if we put, uh, APML at a differential, will deduct, uh, our marks. >> No, no, they will not deduct your marks, but if you mention, uh, answer the rest of the questions as APML, and their key answers are different, then obviously they will deduct marks. So >> Now I should bring APML slide now for you. It's going to be a Not. So this is a gain patient with epistaxis. Is that hyperdrenal? And let's find the typical HPML size. This one they are by low and as do they look different than the previous >> Especially this one? These are two different. Oh. So this is one loop and this is another loop. Another typical. This is a bean shaped cell, not a classical bal. This one is a typical bop cell. Does it look different than a previous blood? >> Yes. Yes. Yeah. Oh, these look different. This one is figure of a. And these are two different loop. One is this one and the top one is separate. You can see the mark. The hypoganular variant. They are usually panytoenic. You will not see a lot of bot cells in them. Will be one or two only. Sorry, hypogranular variant is with high TLC. I think. >> The most of the hypogranular variant I have seen >> are with low TLC and they can come with high TLC, but the most, the one that we have seen, they have >> low TLC and we had missed them as well. as, uh, we found out only on investigations. It has been reported by SGS that this patient has APF. But as I agreed that most of the hypoganal variants presented with higher TLC as far as four lakhs. Mhm. >> Oh, yeah. >> So that's why. >> Yeah, and that is the difficult differential, uh, with the monocytic ml, because that is hypo granular variant, and as well as, uh, two to three, uh, blobed as well. Then no one can miss this while set. You see this one as well. You will think that this is AML. Sorry, 8 mm. Searching for another by loop cell and. For example, And is this look different, you guys? >> Yes, it's totally different. >> This is figure of eight, and these are two typical boop cell. This is a separate loop and this is a separate loop, and they are hypog. I hope you will not miss APML in the in the exam because if you miss APML in the exam, they will miss you as well. They would like to see you again in the exam. All right. So, this was the last case. If you have any question, >> Thank you very much. Thanks a lot. >> A lot of things in the Teams but, uh, I cannot see during the session. So thank you very much. Um,