Transcription
For so this is the first case. Uh, 56-year-old man, uh, was brought to the emergency department because of C shortness of breath and abdominal P. The emergency doctor on examination noticed that there is suspected uh CR diffusion, which, which he confirmed on the X-ray. And there was HTO and spali as well. The full blood count shows hemoglobin of 110, white cell, white cell count of 10,3, L count of 110. So this is the blood p. And uh, I would request any of the lab staff to comment on the blood P. How would they report the blood P for a clinical hematologist? Do we have any lab stop? You comment on the blood P. I'm asking from the lab staff because I was told that I should give equal opportunities to both lab staff and clinical hematologist. So if there is any lab stuff available, he can come up and comment on the blood F, please.
Right, so I think you mean to say lab hematologist. Yes, any biomedical scientist, medical technologist, anyone like, because the blood film is first seen by them, and then they escalate us to, uh, escalate the film to us. And in previous sessions, many of the lab stuff, uh, messaged me that we need equal opportunities. So, uh, I want lab St first to come in on the F and then obviously this will go to clinical hematologist and then we will ask from the clinical hematologist to come in. Right, so we should wait for them. Right, so, uh, if the lab stop is not available, then I will act as a lab Stu, uh, for this life. That the blood F shows leucocytosis. The lymphocytes are the white cells are small in size with some projections from the cytoplasm. The Red Cell shows few schistocytes and there is thyia but no pled Clum seen. Refer to clinical hematologist for further opinion for further opinion due to suspicion of acute leukemia. So these are the commands that is made by the lab stop. So now this film has come to you. You are the clinical hematology register and you are sitting in EP for two exam. The first question is, report this film. I will make it to 10 again. All right, so now I need a clinical hematologist to comment on this film and Report the film. Anyone? I can try. Yes. So this is power 10. I'm giving you a general overview of the film. [Music] Right, and now move to power 50. Oils lens. Yes, so let's see few slides and then you can start reporting the blood pin. Sure. E. Yes, so report the blood F. You are sitting in F exam. How would you report this one? The film shows prom shows mainly small in size having high NC ratio, condensed nuclear chromatin, and some of the these atypical cells, they have GBS cytoplasmic GBS in them, inconspicuous nuclei. The ARBC morphology is shows mild anemia and few fragmented and popoyes are seen, and there is Mark and there is thrombocytopenia and okay. The peripheral f findings are consistent with the lymphoproliferative, uh, disorder, most likely TPP. And I would like to confirm my diagnosis with FL cytometry on peripheral blood for lineage specificity. I don't know whether I have to comment on the basis of this morphology that these may be DPP cells. They look like TPL cells because they are small, mature, and have cytoplasmic bloods, which is the feature of tpln. You would not say definitely that this this is TPL. You would say most likely it is consistent with, uh, TPL. So I need, uh, Clos hometry to con, to confirm my suspicion or to confirm this diagnosis. So what is the expected flow here? Um, usually these cells are CD2 positive, three is weak, they are five and there are seven positive. Any other significant marker that is important for treatment purpose, uh, is CD 52, I guess to give lm2 Zoom AB. Yes, cd52 is positive and that determine the treatment as well, which is. Are you aware of any genetic mutation? Yeah, mostly they have inversion 14 and also the abnormalities of chromosome 8 and on CY and on molecular genetics, they have, I'm not sure there is something M mtcp1 or tcl1 AB mutation. Also, they are also associated associated with aexa Tasia and they have ATM Gene rearrangement abnormalities. Yes, ATM Gene, um, mutation is associated with multiple things like mental cell inoma and multiple Myoma as well. But here more than 90% of the patient shows mtcp1 rearrangement and the Floetry you have mentioned treatment, you have mentioned which is, uh, a limit. This is sorry, more than 9% have which rearrangement? Mtcp1. Mtcp. Okay. Yeah, so this is TPL mature T leukemia and it comes as a short case in the, uh, part two exam where they ask the what is the, uh, report the blood frame, which cares six marks and then expected flow two marks, expected Cog gentics two marks, sometimes one marks, and then they ask you what is the treatment of choice for these patients, which is a limited amount and Transplant and pission if they are symptomatic. If not symptomatic, then watch and wait is the policy. The TP are small and their characteristic features in morphology are these blbs. They carry a lot of blbs like that. Some people call them Mickey Mouse s, but I think this is, uh, not correct. Sometime they have many blbs, not two blbs. So anything that can help you in retaining the information for the exam purpose, use all right, sir. How do you, um, comment on the chromatin on of these cells? Says for me, it is difficult to pick. Is it a blast or a mature P? Blast is usually large in size, um, and open chromatin with nuclear visible in it. While these cells were very small and the chromatin material was very dark blue and nucle were not visible here. So this is a feature of mature, um, Leia. You see these features in CL as well, in POC lymphoma as well. They are very small, their nuclear material is very, uh, dark blue in color and nuc is not visible. You will compare it with now another malignancy who has a large blast with prominent nucleoli, open chrom 10 and some have multiple nuclear as well. So you will see it in the second case now. So, sir, how we differentiate it from the meal blast which also have the production? Again, Mega Blast, they are a bit bigger than, um, this, uh, TPP cells and, uh, they have specific appearance. I will bring that film next time. I have one film for acute Mega blastic leukemia as well. We call it as bloody AML. I will bring this film next time and I will also show the TPL to you as well to see the difference between the two. The Mega Car blast, they are not as deeply blue color like these cells and they are bigger than the, uh, TPP and they are not as much in number as these TPL cells were. TPL one of the features of TPL is that they are very high in number. Usually when they present, they cross the mark of 100 in the per BL while the megao blasts, they are not that much. They are big in size, not that deeply blue color or bopic color and they have quite a lot of, uh, BLS and irregular markings of the cell. We will see that in in the next assessment, the acute Mega blastic. Thank you. Thank you much.
All right, so this is a second case. This is again a 56-year-old man presented to ED with significant weight loss and night sweats, decrease appetite. He has anginal and auxiliary lymphadenopathy on examination and he looked very tired and fatigue. This is the blood film from the patient. His white cell count shows hemoglobin of 98, platelet count of, uh, 93 and white cell count of 60. So again, I would need a lab stop first to comment on this film. So the peripheral film of this, uh, patient. Are you the LA stuff, sir? I'm lab hematologist. Lab hematologist. Okay, right. So, so this SP film is showing leyos predominantly, uh, uh, lymphocytes are seen of small to medium size and, uh, there is thrombocytopenia on this power of lens. Okay, so this is the power 50 now and this is a Nia slide. So the quality is a little bit, um, low as compared to other. Right, uh, so these are not lymphocytes. Um, they appear to me as monoplast. Okay, these are large cells, uh, with low NC ratio, um, these are large cells with low ratio, open chromatin, uh, few having conspicous nuclei and the cytoplasm is a granular. There is moderate to copious amount of cytoplasm. You cells having indentation, nuclear indentation. So this a blast, most probably of my light series. You said that the this is a granular, uh, at that power I can, I said a [Music] granular? Yes, there are granules but very few. You can see these blast have multiple nuclei, some small nuclei, some large Nu, but the car is multile and they are quite large as well. Yes, most probably the monol blast. No, they are lymp blast because we cannot see any, um, any indentation. The monoblos have very few indentation, but the cytoplasm here is not blue. There is no Ule and monoblast do not have this this like this clear nucle like this cell have. This is a lymp BL. Right, sir. Sir, are these large granular lympocytes? No, no, they, they may have very few granules, but most of them are without granules. Yes, sir. Like this one. I will make it to 100 power again. You can see they have multiple nucle is usually lymphoblast. They don't have the neutr. Initially we are we used to classify them on the basis of Fab when they were L2, then the L2 cells they have nucle, but usually neutralize not a feature of lymphoblast. There is one lymphoma whose feature is having large blast in the blood fil with multiple nuclei. So they have R nucular here. This one, this one. So the patient has features of b symptoms, lymphadenopathy, large lymphocytes, lymphoblast in multiple nuclei. Um, I will try to find out you lympho blast which carries vules as well. Blastoid where you, how you are going to differentiate between the blastoid variant, variant of some NHL and the lymphoblast on morphology? So the blastoid variant of mental cell infoma have blast, but they are not that much big. They are medium size. These blocks are very large in size with multiple nucleolo and patient has full-blown symptoms of lymphoma. So a lab Stu would report it like this. The blood P shows lucco yosis. The, uh, there are multiple block which which has Buon cytoplasm with open chromatin and multiple multiple nuclei. There are few smart cells as well. Red cells, uh, shows anisocytosis as you can see their shapes and size are different as well, and there is chenia and no plines. So this is the report for the, uh, lab scientist or biomedical scientist, and then they would say refer to clinical hematologist. Now this film is with you as a clinical hematologist and you are sitting in aath exam. So you have seen this. What comes in your mind as a differential diagnosis? Large lymphoblast with multiple nucleoli, lymphadenopathy in the patient. Say something, sir. LGL? Sorry, large LGL. LGL patient does not have the, uh, b symptoms like this severe. This patient has. This patient has lymphadenopathy everywhere. LGL comes in context of SLE, rheumatoid arthritis, sug syndrome in presence of any other, uh, autoimmune disease. This patient has all the symptoms of Lymphoma. So D can come. DB? Yeah, this is the feature of feature of dlbcl. Their blasts are very large and they have multiple nucle in their, uh, in their chromatin which is visible. Mental cyphoma or blastard variant of mental cell. They carry blast as well, but they are medium size and they carries only one nuclear La in it. This this patient has large loss with multiple nucle. You say some cells has three or four nucle and this cells has a lot of multiple nuclei, smaller in size. This is the feature of dlbcl. So if you are working in NHS and you have lab access, go to your lab and see the film number 2302. So this fil must be present in your lab in NHS lab 2302 and you can see the full comment of the babra ban on this film. He has mentioned as well that these These are large blast with multiple nuclei, features of this is most likely a highr lymphoma. We need to send blood for Urgent flow citometry, uh, and other investigations to look for any, uh, n node which is amenable to biopsy. All right, so this is a highr li fora and you have sent blood for flowetry. What is the expected flow here? Immuno hemistry expected. These as if they are dlbcl, then they should be cd10 and cd20 positive and should be five negative and also we ask for the make Gene rearrangement. If it is positive, then you go for bcl6 and bcl2 to label whether it's a double hit or a triple hit for. Yes. Okay, and let's say this patient is, um, fit for treatment and you want to assess this patient for cm profile AIS. What will you do to assess whether he is fit for CNS profile exis or not? For CNS profile, you will do the CNS IPI. Okay, so who are the patient to whom you will offer CNS profile access? I don't remember exactly, but maybe those who have stage three or four with extra nodal disease involving the tesses, the breast, the utus. Okay, so those patient who CNS IPI is High 4 to6 or if they have three or more extra nodal sites involved or they have specific anatomical sites involvement like testicular s, adrenal gland, renal involvement, or even intravascular dlbcl as well. And especially in a case of female, if breast involvement and and uterus involvement is there, then you offer the patient CNS profilaxis. What do you offer in CNS propy axis? Inal metot? It's not always inal Mex mexate. Yes, it is high do me mexate. If the patient has any contraindication for high inra intravenous meit like diffusions or, uh, po Ral function, then you go for inal meod transit. Otherwise, you just give them high do met I. In any sort of aites or infusions, you also avoid, uh, high dose mexate because there is a chance that the patient will accumulate met the trit over there and can lead to toxicity in the future. So these are the big cells of dlbcl. If you are working in NHS, go to your lab and see the film number 2302 and, uh, uh, you should see this High GR.
Right, so this is the third case. This case is directly for the clinical hematologist. This is again a 56-year-old male who is complaining of low back pain. The full blood count shows, um, anemia and thrombocytopenia. Hemoglobin is 90 and pled count is 90 as well. On examination, he has some splen splen as well. So low back pain, anemia, thomasenia, and, uh, Spen. Because of the persistent thrombocytopenia and anemia, bone biopsy was done and this is the Trine. So anyone who is volunteer for this case? Anyone? Enas Al Basher on the list? N Omar Iman Usman? Hi, hi Amir. So I have told you the scenario, yeah, and this is power four. I will just go through the refine to see whether this is a good size or not and and whether the there are enough tracular spaces or not. This is power four to give you an overview. Okay, so Tan usually have, um, some features that you should remember for the exam and once you see them, the diagnosis should be very clear to you. Like fular Loma has specific features, CL refine has specific features, MH monocytosis has specific features, dlbcl, uh, is very easy to pick. H infa, if you are able to see the overo cells, it is good. So this is, you can see a gym sustain. This is one clue to you. Why I have brought a gy sustain? Okay, similarly Milo fibrosis Trine has very specific features as well. So now you have seen the length, you have seen the tular spaces and you have seen the the tracula as well. I will go to Power 10 now. Okay, so this is power 10 and again, you have to comment on all the lineages if you know the if you know the diagnosis, doesn't matter, but you have to rep report it as it should be for the exam purpose, including length, cellularity, tular spaces, trul lineages, any abnormal features, and then your impression and suggesting, uh, hometry or imuno chemistry. If you have seen such Define before, the diagnosis will be very, very clear to you. All right, do you want me to go to Power 50 or you have found the enough features here? Sorry, my internet was had a full network. I was disconnected and come back again. Yeah, so do you want me to go to Power 50 or you have found the enough features here? No, can we go to Power 50 please? Because if I go to Power 50, most of the people will get the diagnosis on the spot. Those who knows should get the diagnosis now, just from this view. No, not so. Now you can. Okay, all right. No, no problem. You can report the, um, ine. How would you report? Okay, um, so is that similar to the aspirate? Like to comment on the initially on the L power on the simularity? Um, oh, the same approach for the aspirate. First, comment on the length and adequate, whether the sample is adequate or not. So this is a good length sample, a good length and adequate sample. Sometime you will find a Define slide which is fully crushed or end of the Define is crushed like this. Define is crushed at this point. Yeah, so good. So this is a good lens sample with crushing at one end, but the rest of the trul are preserved. The trul, yeah, they are thickened. They are thicken because of a because of the underlying disease. Okay, yes. Mega kites are present. You have seen a lot of Megas here. There are, yeah, yes. We cannot commend here on the, uh, my Lord lineage, because the stain is gser for that. Uh, H and E stain is better, but you have seen there is per tracular fibrosis and there are a lot of spindle shaped cells in the paricular area, which gives a suspicion of, uh, systemic MUSC cytosis, but that need to be confirmed on the imunohistochemistry and, uh, blood level of, uh, tripas. So these are all the spindle shaped cells. These are all the, uh, most SS. So if, um, if your hospital is a ter Hospital, there must be hmds. Usually most of the ter Hospital have hmds as well. You can get the performer, uh, of the Bon biopsy reporting from the from them. You can see these are all spindle shaped cells. They are own mustto sites. All right, yes. And Moc sites are better seen on gem sustain. So if in the exam, if you see any gem sustain, it will be for the purpose of systemic Moc cytosis, but presence of gem sustain does not mean that you jump to, uh, systemic musoc cytosis. See other features as well. Patient usually have, um, bony pains, they can have neuro psychiatric problems as well. Heeles, speles, anemias, because in systemic musoc cytosis we have either ulent form or smoldering form or advanc systemic monocytosis. Advanced systemic monocytosis usually comes with symptoms. Okay, sorry. But just for the spindle shape like cell, um, for me the cells look like more, you know, like it's like elliptic side or something, you know, like it's elongated, but, um, is that like where where is like the characteristic is pin? The shape of Master is yes, most cells are spindle shaped cells, mostly and, um, I don't have aspirate for this one and asate, they are usually elongated as well. All right, yeah. You see M cells in Wen stro as well. The the nules of Wen stom lymphocytes and refine are surrounded by Mell. This is the feature of Wen stom. If I get, I need to find for that. I will, okay. Dr. Am, if they have given you the gyza stain for systemic cytosis, we don't comment on the granulocytic lineage and arthropyosis. We just comment on the length adequacy, the length, the cellularity and the tacul and the main abnormality. We don't comment on ropes or lupis. If you are good in gy sustaining, uh, then you can, but I am not good in, uh, gym sustain refine reporting. I always use hn for, uh, refine report. But if you are asking for the exose, yes, um, ideally we should comment on the My Lord lineage and the ER lineage as well. But if you are, uh, confident whatever you are writing is correct, uh, is okay. But if it, if this was, uh, H and E, I would have commented on my Lord lineage as well on the, um, lineage. Megas were visible here, sir. Is there any other differential that should come in mind except systemic monocytosis if Bono tpine is given with James suen for the exam purpose, it is only the systemic monocytosis. But in real life, I'm not sure whether is there any other diagnosis which we made from JY suain? And in the lab, we make both both for, uh, both slides H stains and J suain for every disease. But for the exam purpose, it is the gem suain that comes for systemic to cytosis. Like if you have any bone marrow for myofibrosis, for et, for AML, they both would have, uh, gy suain and and h& stain. But the reporting is more on the, uh, h& for exam purpose. The lab staff, they are histopathologist and Consultants. They know what to pick from J sustain in in those cases. But I'm just talking about D purpose. Right, what is the criteria of systemic mastocytosis diagnosis? Is a major and a minor criteria. The major criteria includes the presence of dense clusters composed of more than 15% massels and Aggregates in the marrow or in any extracutaneous tissue. The minor criteria include more than 25% mass cells which are either spindal shaped or having an abnormal morphology. The presence of Kit mutation and cd2 117 and CD 25 expression on M cells and serumas CD. Four things in minor criteria. More than 25% abnormal spindal shap masses. Second would be the kit mutation. Third would be the expression of cd2, cd25 or I think 117 on the M cell. Sorry, 30. Okay, 30 on the mass cells and the fourth would be the serum St TR, which would be more than I think 20 Nano gr per ml. Right, if this patient has, uh, kit D d816v mutation plus pdgfr a mutation as well, what is a drug of choice? Mutation and PDG f a mutation. This is a lot of eils here. So the patient has pdgf and the kit mutation both together. What drug usually do you give? I don't remember exactly the name. It's pretended recently.
Okay, so this is the fourth case. This is a 25-year-old male with recurrent fevers. He didn't respond to antibiotics prescribed by GP and despite 3 days of antibiotics, he is spiking high temperature. His full blood count shows hemoglobin of 98, white cell count of nine and pred count of 180. This is the blood Fin and I want any lab Stu to come in on the PL plus any biomedical scientist, medical lab technologist, if you have any in the audience. Sir, I can't comment on this power. So this is power 10. I will go through the film to to show you an overview of the film and then I will move to power 50 and if required, power 100 as well. Okay, so you have seen few slides on power 10. Now let's move to power 50. I put some oil on it. Right, sir. So the b m of a 25-year-old male with blue HP and normal pled and white cell count is showing, uh, noritic normochromic red cells and the ring, uh, sing single delicate, uh, or single or multiple. I can see the two ring forms also infiltrating the red cells. Yes, sir. Ring form of most probably plasmodium falciparum. Yeah, so mostly. And you need to confirm this on RDT and net. So you mentioned that you are the lab stuff, right? Yes, sir. I'm a training, uh, for FCPS in Pakistan. I completed my training. All right, so then, uh, I would request you to report this film as well for the exam purpose. Like you are sitting in part two exam or FCPS 2 exam. How would you report? Uh, so the ring forms of plas plasmodium falciparum are seen. So we write like that. These are the nooc chromic nastic cells, infiltrated by the forms, uh, of plasmodium that are delicated in shape with the. You don't know yet that these are F. You need to confirm that on, uh, rdt and net testing because ring forms can be present in many other things. Yes, sir. It can. This affect the diagnosis? Affect the treatment options? Yes, why not? We will discuss the treatment, uh, in a second. Now G sir. Okay, so yes, comment on the blood fil, please. Um, sir, I have commented already and I don't know how to comment. So the blood film shows multiple, uh, ring trophozite of malal parasite. The red blood cell size is normal. There are few red blood cells with multiple rings in it. In some of the red cells, the ring is near to the red cell membrane. So this is equal, which is a feature of the, uh, plasmon. There are few shyo sites in the, uh, blood film as well with, uh, low platelet count and the white cell count is normal. The features of malal parasite is most likely consistent with plasmo ferum. We need to confirm this on, uh, rdt and net testing. You're right, sir. Okay, okay. Why this is not WX, sir? The differentiating points, uh, for the vix are, importantly that they invade the early precursors of the red blood cells, that that are reticul sites and that are large in size. So we can, um, and also, so the ring is not delicate, it is, um, with with thickened, uh, cytoplasmic membrane. And in this case, the plasmodium falciparum invade, uh, almost all kind of the cells and all also the mature SS. Mature RBCs. This is the double dot appearance. So the red cell size in WX is large and the the ring trophozite form of the M parasite is thick as well. So you must comment in your report about the red cell size, the ring features if they are thick or thin, near to the red cell membrane, multiple or single, and usually gyes are not seen in the blood films. If you are lucky, you will be able to see that, um, but in this film, I I searched for GTO side but I could not see the Cent form or banana shape form of the mod. Right, what is RDT? Rapid diagnostic test. Right, and what is the principle of RDT? Rapid diagnostic test. To, pardon, repeat your question, please. What is the principle of RDT? Sir, uh, it is based on the, uh, we use as ICT kits and there are two type of po kits. Either the, um, the the coating film is coated by antibodies against the parasites or they are coated with the antigens, uh, so they detect the, um, presence of the parasite and, uh, in case of heyum, there is histadine rich protein that is detected and in case of VX and other parasites, there is LDH. Okay, so it is a lateral low immunochromatographic antigen detecting test. Like it is a based on later Pro method. It is immunochromatographic antigen detection test which use a d label antibody to bind to the parasite antigen. Okay, and this complex makes a line in the result window. Just say it is immune immunochromatographic antigen detection test which use a d labeled antibody against parasite antigen and this complex form a line in the result. Is there any condition which gives you a false positive RDT? Rtic Factor, if present in a patient, can give you upholds, uh, positive. So we have seen even in the treated cases, uh, when there is no parasitemia, we cannot found any parasite in the blood, uh, in the treated cases, even ICT gives a positive result. Yes, correct. Right, so what is the indication of exchange transfusion and malaria? It's heavy parasitemia. I don't remember, but more than 30%, I think. More than 30%. [Music] And cerebral malaria, or if the patient, or if the patient is very ill because of the parasite infestation and the MTT decide that this should be, uh, treated by exchange transfusion. Usually the patient is refer to infectious disease team or tropical medicine team. They deal with the malaria and, yes, par index for, sorry, can you repeat? And the par index is 10% for exchange transmission. 30%. 30%. Oh, thank you. And, uh, ially, we we do not deal with the treatment of of malaria in terms of drugs, but if they ask in the exam, then they are the arate based medication for, uh, plasmodium fif. So remember the name of the drug for cerebral malaria or L mania or fasis, they will be asked in the exam. In real life, you do not deal with them, but for the exam purpose, remember the name of the drugs for these few infection, fasis, tronos, lishia, and malaria.
Right, the last case of the day. E. Okay, so this is again a 56-year-old man presented to ED with severe shortness of breath, failor, extreme tiredness. He is fiil as well. The full blood count shows hemoglobin of 70, platelet count of 45 and white cell count of 12. This is the blood F and I want any biomedical scientist or left stuff to comment on the blood F first, then I will go to clinical hematologist. Sir, sorry, how much was the white sound count? 12. Okay, thanks. Ignore these things. These are not pardes. This is just the oil related stuff moving here and there. Okay, so there is no biomedical stuff or lab stuff to commend, sir. The paper frame of the male patient, uh, is showing anisocytosis in the red blood cells. Uh, there is polychromasia, macrocytes. MHM. Uh, there are occasional tear drop cells. Okay, uh, I want to see spyes, but there is Central p in. I can identify the central F in many of them. You look like micros. Some of them don't have. Okay, so as a biomedical scientist, um, I will report it as the blood FM shows, uh, an an isop kyos with multiple polychromatic macrocytes, spyes, how jelly bodies and high pled come, no pled come seen. The neutr fils are hyper granulated. Suspicion of hemolysis secondary to any infection. The film is referred to hematology register for, uh, expert opinion. Now I need a clinical hematologist to report it for the purpose of farath exam. Yes, anyone want to report it? Yeah, uh, I can try. Yes. So you are sitting in FC paath exam, but not now. Yeah, and, um, this is the blood film for you. Yeah, yeah, and they want you to report it for six months. Uh, okay. That is an po cytosis. Um, the two rather two two morphological population present. When is macrocy macrocytes and the other is spherocytes. Um, there are oval joles in some of the cells. Um, yeah, and the PO I could see in the previous, uh, fields, some teardrop cells as well. Um, the nutrifil were having toxic. So probably spheros spherocytosis in splenectomized patient. Okay, sir. If this is, as there are, uh, velocites and I could not see any polychromasia. If there is, these are all polya. Oh, yes, yes. Large recites. Yeah, so probably there is hemolysis also going on, um, and the fyes might be due to the holis or maybe transfusion, uh, in a splenic M patient. The toxic might point towards the infectious, uh, trigger as a cause of hemolysis. Hope, yeah. The red cells are agglutinated. These red cells are uated. Oh, yes, there is not, there is no marked tination. Yeah, this one here. Yeah, yeah. So this question, an eath exam can come in two ways. One is a standard way, which is the report the blood F, and second one is the enumerate six points in this Blood fil. So you would say, for reporting the blood film shows severe red cell anos sitosis, if you are saying anisocytosis or anisocytosis, mention Red Cell because there can be anisocytosis as well. Okay, thank you. Containing multiple polychromatic macrocytes, microcytes or spherocytes, p drop cells, uh, H Jolly bodies. The nutrifil is, uh, hyper grain related, multiple Red Cell utenation, uh, are noted. The pled CR looks increased, but there is no anos sitosis and platlets. The blood film is most likely consistent with hemolysis secondary to infection. We need, uh, hemolytic screen and infection screen on this patient to rule out whether this is autoimmune htic anemia seconded to any infection or not. You commented on the blood F features, you give your suspected impression that this is hemolytic anemia secondary to infection, and you suggested hemolytic screen and infection screen. This can be autoimmune or this can be non-immune as well, but looks like, looks like this is autoimmune secondary to infection. Okay, and the h jly bodies, hypo hyposplenism. Okay, the patient, the patient may, the patient may have, uh, hyposplenic or low splenic function because of many reason, because of ongoing hemolysis, maybe this is not the first time he's coming to the hospital with, uh, hemolysis, maybe he had hyposthenic function because of other reasons, but there is H Jolly bodies, there is in sped count as well in hyperic patient. You see how jelly bodies and increased sped count, and this sped count can be second, increased count can be secondary to infection as well. Okay, yeah, thank you very much. Thank you. What are the secondary causes of autoimmune htic anemia? Secondary to the connective tissue disorders, as or autom, other autoimmune conditions. Yeah, so, yes, go on. So categorize it in four groups. Secondary autoimmune causes of secondary causes of autoimmune htic anemia can be because of four reasons. Cancers, blah blah blah, CL lymphoma. Oh, yes, infection, CMV, EB, bacterial infection, neopal, then immune Sid arthritis, etcetera. And then post transplant. Okay, post transplant. Postotic stems are transplant. Autoimmune htic anemia is very common. Yes, yes. Thank you. And what would be the treatment of this patient? Treatment of the underlying infection, underlying cause, underlying cause. Yeah, treat the underlying cause. The hemolysis will set right. So Dr. In reporting of this case, you will set your periferal findings are consistent with the hemolytic process and here we have to mention what would be the most probable cause or just we can say it's fin is are consist with the hemolytic process and then we advise the hemolytic screen. So as I as I mentioned in reporting that this patient has, um, the blood Fram is most likely consisted with hemolysis secondary to infection because this patient has redell utenation and, uh, hypergranulation of a neutri and the patient was fi as well in the history. The uations they are not very marked. Yes, they are not very because the patient is very very anemic and there are only few utenation, but they are all and usually when we see a gluten on, we think of cold autoimmune hemolytic anemia. Yes, but agation can be because of the infections as well. Tination has a lot of causes. So the left St will warm this and then he can repeat the blood if there is a quite significant and the non-immune causes of ftic anemia also includes infections as well as the autoimmune and the non-immune bo. Yes, so first you will do, um, htic SC screen to find out whether that test is positive or not. If that is positive, it is immune. If that is not positive, it is non-immune. And then according to the guidelines, you will ask, you'll think about few things. Whether first thing, first question according to the guideline is there any hemolysis? Yes, this patient has hemolysis. Is this hemolysis immune? Confirmed by that? So if that is positive, now whether this patient has any blood transfusion in the last three months and any drug that he has recently taken that can induce autoimun htic anemia. Any other cause? In case of infant, we think about hdfn as well. And if it is a anemia, okay, what type? So that will tell you whether it is warm or whether it is a cold, whether it is a CH, it is a mixed. Okay, now thank you.
Okay, so this was the last case. And, um, sir, I have a question. After lomy, the patient periphals may have nucleated red blood cells. What is the reason for this? How can we explain this? Because normally, if the patient are not in the periphal, he has no in nuclear blood cell, but after splenectomy, I have seen patient, they have lot of nucle R blood cells. So sir, what? So nucleated red blood cells can be present in severe hemolysis, like in the last few sessions when we had autoimmune hemolytic anemia patient, there were a lot of, um, NR red blood cells. But this autoimun htic anemia does not have any nucle blood cells. If you have severe DIC and your bone marrow is under under stress, you will have nucleated red blood cells in the blood film as well. If you have Luc blastic blood film picture, MDS or, uh, blastoid CML or blastoid mental as well, the bone marrow is under stress. You will see multiple nrbc in the blood film as well. And spom splenectomized patient, which is usually in tmia and in cyle cell disease, the spleen is the area of, uh, extr medary hematosis. When you remove the spleen, the bone marrow become under stress and then the blood film is packed with nrbc. So nrbc is not only in the per blood frame of splenectomy, they can appear in the peripheral blood film after many reasons, because of many reasons. Severe h is severe infection, MDS, BL, CML in Blast phase, um, also the the leukemic phases of follicular lymphoma, they all have an RBC in the peripheral blood. And tmia patient because there is extr hematosis going on is very large. That's why you have nrbc in the Press blood. And in in babies, in two days, two days old baby, if you see the blood film of two days old baby, they will have a lot of nrbc in the, uh, refer blood, which is normal for them because their spleen is not yet mature and the bone marrow is producing everything and bone marrow is under stress. So any any reason which make the bone marrow andpress, you will get an RBC in the G. Sir, thank you. So these sessions are free, but if you want to donate, these are the account details. And if you want to give me a, um, a Cofe, you can use this link and U subscribe the channel. Thank you for that and see you next week. Have a good week. Thank you, sir. Love. Thank you so much.