Transcription
e e e e e e hello everyone can you hear me can to hear me now yeah morning I'm here morning everyone we woke up and still going right so this is the first case this is a 56 year old who was brought to emergency department because he was feeling unwell bodyx uh fever and no energy the blood test shows that he has hemoglobin of 98 quel count of six and thed count of 13 the black grows first to theologist or clinical scientist scientist orist understand this is just a artifact anyone from you want to come in on the question first this is power 10 and then I will go to Power 15 okay what okay okay um there spes about yes there are few SP will go to High see mine I need another this one is power 50 must above I say this sorry what kill site kill site yeah it's like helmet c as well white cell yeah just Sid arees and some sides so poly chromia poly chromia maybe some the patient is anemia his hemoglobin is 98 but uh platelet may be dropped from more than 130 it was more than 130 then dropped Maybe the the result that we have got it shows count of 13 yeah it's just the SES there I think fragments what's the culation like is the other F done yes the CL honen was 1.9 1.9 that's okay yeah the PT and PT were okay okay CU I was thinking it could be something like see could be autoimmune does not have this much of fragments one thing I think the spes this one this one has no no wise one two 3 4 5 6 that's why I said the this yeah yeah I TTP on the fragments like there as well yes of them b as well PD maybe G6 should have BL F yeah yeah that's right and because of this much fragments obviously the clinical scientist or love scientist will you up I have a patient with anemia thyia and many segments in the in the blood yeah it's got to be in Maha some form then TTP di I the f is okay there fragments there so it's hiling so now can't see any rbcs though no no putc so so the clinical scientist think that this is mAh and according to our trust policies such things are urgently relate to the hematology consultant now I need a hematology personology person to this BL for the purpose of exam you are sitting in for exam and they have given you this and ask you to report it do have we don't have anyal hematologist today Russia is on the top in the list how you report this okay okay take that but I'm laboratory from the laboratory side can I yes appearing in regarding white white the SE there there are unremarkable morphology on the abnormality first you have seen the red pathology here Comm start with oh okay there is um anisocytosis including um fragmented cells spheroides poly chromia um regarding platelets um mild thrombocytopenia M so I um I advise for hemolytic workup agulation profile if it is not already here what is your what is your impression yeah uh my impression is the uh M first first of all Maha count done count is high right I would go with it but Dr said that blet counts one 3 Z right 13 Z okay but there are there nothing in to Me Maybe dropped from more more than 13 maybe but the first differential is Maha for cical coloration maybe the patient has valve replacement or hypertensive so I have to go for hemolytic work and coagulation profile fibrogen level okay so these things are usually done when a patient comes to Ed here the when the Bloods are sent it include full blood C function test liver function test ulation profile for the patient as well this patient are nor sorry they is AI you should have asked me this patient has anemia a lot of fragments in the blood P few cyes are there deted count is reduced no um no fled flug up there most likely this is M and it can be a TTP as well which is hematological emergency yes so this patient investigation need to be discussed with the TTP consultant or TTP Center 13 test as well to be done yeah so we need some history of this spti and other investigation like liver function test and LDH and then we have to discuss with the TTP Center if the TTP consultant agreed that this is a immune TTP and this patient need to be blue lighted to TTP Center we cannot treat it in all the hospital if this is immune TTP and there is no secondary cause for that then you have to Blue Light this station if there is a secondary cause for that then plasma exchange is not necessary you will treat the patient in your hospital sometime the patient is on cic mitigation Tiger Tiger Gill sometime they are on cing or post transplant medication stuff sometime they have any solid organ cancer thentic cancer is a commonest one and they come with this picture Maha picture we do not do plasma exchange for them plasma exchange is done foric poses if there is no secondary cause of TTP and we yeah in atic anemia there will be poly chromia there will be spides but there are no this this much fragments it can be only one or two fragments in the auto htic most of the cells in auto are poesia or spides this THM has a lot of cyes it cannot be ignored it it should be elaborated by the clinical scientist urgently by phone to the unall hematologist and call hematologist to discuss urgently with the TP Center to agree on the diagnosis of immun TTP e so in this Blood F I would like the candidate to list the abnormalities that you have seen in this Blood this is power turn they're all there the different myoid series I think now I will go to Power 50 to list the normal findings and then your differential diagnosis fromia what else what about this Masters there Ras no so I asked you list the abnormalities in this platform the master sites okay parite four times these blood cells don't have M otherwise they would have tell you that I am nrbc I am myosite I am dysplastic neutr yeah blasted picture what is in the exam in the exam you will be ask list the abnormalities in the blood well you got start from Red Cell series what do you see in the Red Cell you mentioned there are when they when they ask you list the abnormalities then you have to write the abnormalities not not an isopos cytosis you have seen stomates write stomato side number one number two there isite perite is micrite list a micros if there is any fragment if there and there is nrbc here as well list it as NBC Under The Heading of red C once you are done with the um the Red Cell series then go to the white cell and white cells we are seeing here mil is there this plastic neutr is there yeah you will see more yeah waito hypog hyp field tomato cyos is as we mentioned in the red Under the Red Cell head in quite this looks like a what's the um fet level defet level is normal normal okay this this one appear as hypers segmented yeah you will have one question in the exam that will ask you list the abnormalities in the BL F here the red cell look a bit hypochromic hypochromia is also a feature Under the Red Cell heading this is a bit tearing this one and this one this one we can WR drop what's the lft like lft is upd range the Abiline is 93 alt is 540 and alkaline is 600 which is well problem then patient has bilary sepsis all right okay so what is the differential diagnosis based on from what I see it's probably an MDS what's what's the age of the patient age of the patient is 50 okay I still think MDS do not forget U cck it series to comment on fromia is definely referral to a consultant sorry any repeat yeah it's definitely a referral to a consultant yeah so what is your thought what are you suspecting here I'm suspecting MDS MDS okay okay this film has now gone to clinical hematologist what Does the clinical hematologist thing I just ask is um what's the monite monite count the monite counts there was 1.0 that's normal well slightly elevated so what Does the clinical hematologist thing we have only two clinical hology this time one is Russia and other one is Iman very nervous gentlemen Russia and Iman if you can comment on this Blood okay um regarding the Y you want me to comment on the blood they report this Blood film report clinical scientists have referred this Blood film to you for a suspected MDF and the patient has B sepsis in ICU and this is the blood F I have told you the values as well the liver function test okay there is Lu Lu cytosis with the left shift granulitic left shift up to myoides neutrophils are hypog granular with the some this plastic features in the form of sudar forms some hyp segmented nuclear forms what isse I think rare hypers segmented I noticed why why you scroll the photo rare hyper sign I saw it's a birth of displasia anyway regarding rbcs there are yeah I notic this also abnormal segmentation of the neutri let's go to RBC comment there is anisob cytosis also includes nortic normal Chic occasional mcro sites few microtic hypochromic cells some Stato size also am I right I saw occasional NE rbcs or it was by mistake my eyes not occasional there are a lot of nrbc we have seen so I'm right so I will add the lopasic picture at the last of the report but regarding platelets there is thy opinion so what to recommend or what to advise is what is the impression impression is it goes with the my IL plastic syndrome so I have to assess first level of vitamin B12 LDH to rule out henic deficiency also iron profile and ftin level but F level is deceiving at this patient because you you mentioned that he he had the sepsis so iron profile vitamin B12 LDH just that maybe we we when the patient is out of infection we we can proceed for bommer am I right what is MDS how do you define MD I got your point I'm telling this patient has B subes the L function that is very abnormal so I will follow from my side I will follow up this patient has litic picture yes it can be seconded to infection as well MDS is unexplained cytopenias or abnormality in single lineage which is more than 10% but that cytopenia should be persistent this patient has developed thrombocytopenia because of the infection and liver disease his liver is very abnormal it is not secreting any thop right he has a lot of nrbc because the bone marrow is under stress due to sepsis he has all the lineage of the myoid you see this much myoides or this much band form in the the mostic syndrome mostic syndrome is usually very low counts but they are persistent not here we have a history that patient has B subes affecting the liver that's why the patient has stomato sides some of the cells are macroides as well because of the liver effect n RBC are there because B stress phocytes granulated nutrifil and band forms up there because there is infection thr thr cytopenia is there because liver is affected and infection leads toyia as well Milo dysplastic syndrome should have some blust as well there is nrbc Milo side this plastic neutr in MDS but they are persistent and longstanding every septic patient that admits to ICU or hematology W with abnormal PL does not mean there is MDS nowadays there is a lot of influenza A virus respiratory sensial virus every second full blood count in the NHS has thopia or neutropenia it does not mean that they have MDS We Will We Will suspect MDS only if it is persistent and longstanding there is no other cause this patient this patient has subis AB normal Li that's why you seeing the abnormalities you expect some toxic granulation then yes but I can't see anything there what's the CRP like CRP is 387 pretty conclusive no Dr IM the explanation here is during the infection the neutr can use its granules to fight the infection so at some level we can see the neutrophils hypog granulated during the course of infection it can be no problem some of them have gr here and they the blue dot ha as well yes yes I mean I mean it is not a m that we have we we have to see toxic grula I mean I expect to see a lot more myoc sites too to be honest and sever infection this patient has quite a lot of myoc and if you can see this death Crystal the blue crystal that's not good pretty much end stage isn't it yes SE say very severe Subs usually give you this death crystals as well okay so this was SES some people made it a differential of cmn last time which was wrong as well CML should have copil Basils and okay maybe lost as well now this next s is again 56 year old and he has developed some skin rushes which is not responding to any cream or antihistamines so this is power 10 white C count is 21 hemoglobin anded count is normal what Does the clinical scientist orat it's about lucis try know I am on the on the cells and make the pi for clear clear there maybe I would like to make it f big for you to see if you have any thought about it yeah that's a blast info blast Maybe what about the nuclear nuclear material being like that St isn't it sry how old is the fish 56 what about this noral this prosy this is a lymy what sort of lymy I'm interested you know what sort of lymy is this it looks like cells of Cesar syndrome cated nucleus why you think this is C do you have any features I couldn't see any CS as such could see any like I would say this is the best picture of a yeah there's like certain CFT in the center isn't it there are a lot of lines like the yeah cereum form well concentrating on this C do not forget that there are two our jelly bodies as well you have to report that in the exam otherwise you will lose Mar problem as well they may give you some history about that he has any from a road accident in the during childhood leading this one has a lot of groups yeah in the nuclear material yes some it's not very common but it is exam favorite the nuclear material is a bit immature but there are a lot of grooves just like the brain cereal yeah that's a lot clearer searching for other yeah this is a brain but without so what are the clues of having ciss syndrome here in the scenario what doctor what what are the clues like the skin manifestation is a patient has rushes patient will have fitis or rushes that is not responding to any treatment in that case you will be worried whether this patient has any skin lymphoma that is the cause of ising in this patient the nuclear material is a bit mature and not like a typical Blast One all right so what FL atry do you expect in ciss syndrome any is it CD4 positive cd8 positive or negative what do you think the loss of cd5 and cd7 it is cd7 negative negative as well what else or the clonality which marker you will check pity PCR Gene Arrangement and T cells we check TCR Gene okay let is see the it is cd7 negative it is cd8 negative 25 negative and the positive one are the CD4 is positive 2 and three are positive in this patient you have to exclude the other Tas to get a diagnosis but mostly depends on clinical features of the patient which is the unresponsive thitis or rashes eczema secondly the specific morphology of the P of the t- cells in the blood which is the cerebr form shape or you can see a lot of grooves in the nuclear material not like the L cells of other and they are cd25 negative cd25 is positive and T cell and ATL CD cd7 negative cd7 is strongly positive in PPL they are 56 57 negative as well is a feure of LG here cd1 negative cd10 is a feature of a among the T sets so these features will help you in the diagnosis of Cy syndrome and for all T Cell the cality is based on TCR there is no specific translocations or mutation and C syndrome like other T PPL is in version 14 the LGL has stat mutations but this one does that happen so ciss syndrome comes in the exam very frequently it is rare in the Practical life but common in the exam because it has morphological features that's what now you have seen T cell lymphoma and let's see other lymphoma to differentiate the lymphoid cells this is power 10 and you can say that the word CC come is more than 500 because only this one field contain more than 100 cells let's go to Power this is perh blood of a young boy with high words and very profuse epistaxis and there are some bruising on the the rest of the body as what do you see numerous blasts there they are all thrombocytopenia as well I count for the Blues in looks more like an one so you can see the difference between these BLS and the BL in the previous T cells they were a bit mature there were prob nucle but they were a bit the nuclear material was a bit mature and has a lot of groups here there there is per as well some of the cells has two nucle but a nuclear material is a bit open and they don't have any groes like why would be the patient bleeding one is thos is there any other cause of bleeding with the high wi C we have discussed this multiple time clinical hematologist if your Jor ask you why this patient is bleeding I'm giving him fed transfusion but still he is bleeding fled count after transfusion is 70 what's his coagulation profile like a isong okay a is so is a quop as well then but what is just 1.1 that should affect both PT and AP but this patient has only AP is it muscle be prolonged 70 that's very long as you had any um um hemophilia I factor ass says done yes one screen was done which contain factor a one antigen and Rec activity okay what do you want to know in the among these three some hematologist was expecting you to ask me this question the colleague from the lab is asking clinical question which is very I want to know which is very impressive High counts everywhere High counts lead to acquired one disease if it is high red cell count if it is High ped count if it is high white cell count it will consume your one multim leading to acquire deficiency of one disease we have read that in thrombocytosis we have read that in poly and we we reading it again and again in Al as well even CML patient or cmml patient if their counts are very high they can lead to acquired one because the one mul they are absorbed by these cell membrane and there is deficiency of anen leading to bleeding that's why if you replace p in this patient patient will still bleed Because the actual thing isir one syndrome how would you manage this patient acutely just one B answer this patient is bleeding white count is 900 what to do to stop the ble hello yes lucaris we will do lucaris to reduce the white cell because if I give him one will concentrate the white cell count is still high and it will be increasing more and more until I start chemotherapy in this patient I have to reduce this white with the reduction of the one in the patient will increase by itself and the patient will stop these are the question that are asked in the exam and people fail their exam because they have not answered the supplementary question in the exam yes everyone knows that this is Al but reporting of the blood film will carry only five mons there are other five marks as well which will have such question like this why the patient is bleeding what is the Urgent management what are the standard risk phog gentics what are the adverse risk phog gentics in this patient and that's why people people will come out from the exam yes I picked that up this was Al but when the result come they will fail Inc PA exams unfortunately .5 marks matter people have fill their exam by5 marks as well should very this slide is for estop theologist and clinical hematologist this is a 56 year old patient um with ezema and Oran this is power four and this is the I want you to pick up the abnormalities and your suspected diagnosis can it be hypocellular marrow with rein or fibrosis pointing to myofibrosis one pos you thinking about myofibrosis in the history I mentioned this patient has recurrent eczema and hpally and as well to add more patient has bony pains make it Power 10 to show you where is the fibrosis so you can see the bres which is in front of you are visible in background is very red due to presence of a lot of these this it has again fi rosis if I make it to 50 and then ask you to rethink on your diagnosis this is power 50 and this is the F fi what do you think is it's all cellular area MH this is cellular and any commments about this sun these are long slenders M sh sh so what are these cells nucleus is push on can it be MTO sites or or plasma cells no plasma cells are not like that um they are all cylinder shape elongated or spindal shape s this is the feature of monocytosis Moyes are like this oh yeah Mite but they said like they are almost like plasma cells but with the nucleus pushed to one side plasma cells have nucleus pushed to one side and here the other feature is that you can see the trabac they are distorted and thick we go to call the toac are quite thick and there is a bit of distortion as well and the other feature of system monocytosis is that they have fibrosis around the traul this is called paricular fibrosis the body part is okay but you will see fibrosis in these SP like here this part is Faus is here and in this fatic area you will see the must cell as another um feature of identifying most is from the type of slight they give to you in the exam if they give you any G sustain like this is a GM sustain which they usually do not give in the exam all the all the slides will be if they gave you any tan and it is G sustained you should think about cytosis because Moc sites appear better on G sustaining if they are giving you a g sustained defin SL then your first definion in your mind is that maybe I'm looking at monocytosis syic monocytosis the tracula are thick and disorted there will be fibrosis and monocytosis as we read yesterday the systemic mastocytosis is a cause of secondary Mero fibrosis you are seeing fibrosis here near the tular which is called per tracular fibrosis this is pular area and this is the this the body is okay but the fosis is around the peric area Trine there are a few Trine that will appear in the exam and these trines have features that you should PR for the exam purpose like syic MOS is have paricular fibrosis they will give you fular L for which will have very tricular infiltration they will have infiltration in the paricular area but here the cells are elongated spindle shape there Ina the cells will not be elongated they will have infiltration like these small cells a lot of cells will be we will see other as most cells they appear better on the gy sustain if you go to your hmds or lab and ask them how do you see muss in the lab they will tell you we use G sustain for visualization of most these dotted celles are allop systemic monocytosis is a cause ofilia and these all elongated cells they are most site this these are all side inated what would you see in the peripheral blood film then in peripheral blood film muscles are very rare there will be only the Cilia I have one blood film of Mel leukemia only which is very very rare in Practical life and it will not come in the exam it has few monocytes round monocytes in the peripheral blood and in the esperate aspirate in systemic mosis if you have Bonar aspirate you will see either elongated mus CS or around very granular deeply if I manage to find the asate somewhere I will certainly share with you but it is the time that usually come in the exam part two with systemes so we have if there is any question you can ask otherwise we will meet again thanks again thank you very much welome if there is nothing else then we will meet next Sunday again and