DIP Episode 203 - Leukemia’s and Lymphoma’s for the USMLE Step 2CK and Step 3 Exams

Okay, welcome. I am divine. I am a resident. This is episode 203 of the Divine Intervention Podcasts. And in this podcast I'm going to be talking about a topic that I don't know for whatever bizarre reason people tend to get this wrong like a lot on NV Me exams especially for step 2 CK. So it's going to be like a somewhat limited coverage of leukemias and lymphomas specifically for the USMLE step 2 CK and step 3 exams. So I'll just talk about some things that are high out that people tend to you know kind of screw up on these tests. And so be perfectly honest with you I think I'm going to set this up in a fairly unique way and it will be how to specifically on NV Me exams get questions correct that tests leukemias and lymphomas right. So the first big question and so this should hopefully be kind of like a shop podcast. So the first big question we want to ask yourself on NV Me exams is okay divine. How do leukemias classically present and how do lymphomas classically present. Here's the deal. The way leukemia will likely present on your test is you will see a person that has a disproportionately elevated white blood cell count. It's not always true but that is usually the case right. But I will say even more project is like this thinwear every other blood element will be low. So they'll have like low hemoglobin indicating that you have an anemia and they'll have low like a low pleclet count indicating that you have a thrombocytopenia.

So if you see either a high white disproportionately high white blood cell count or you see a normal white blood cell count but you notice that every other thing is low. The pleclet's are low. The hemoglobin is low. If you see that you absolutely want to think about a lymph sorry leukemia on an NV Me exam okay. Now on the flip side lymphomas people that have lymphomas the primary physical exam finding is almost always those people having some sort of lymphadenopathy. In fact they are for sure going to have lymphadenopathy on the exam and usually people that have lymphomas tend to not have CBC abnormalities right. So their white count may be normal. The hemoglobin may be normal. The pleclet count may be normal. That's something you absolutely need to keep at the back of your mind for tests okay. Usually they do not have CBC abnormalities and the primary presentation tends to be lymphadenopathy and it's almost always in young people. Yes can old people get lymphomas that's absolutely true again right but it's almost always in a young person right and then in addition to being in a young person the user also tend to have like chronic B symptoms so they'll see like over the last like X number of weeks or X number of months as far as I've been having like fevers, some outweigh loss although they usually don't have weight loss but you know fevers, night sweats and the like.

So that's the way you tell a leukemia apart from a lymphoma in a Q step right because the NV Me they're usually pretty good at writing these questions well enough to wait it's kind of hard to differentiate them so pay attention to these hard signs that I'm describing to you right now and then in the leukemia world there's this algorithm I use so once you determine that okay I'm likely to know with leukemia right there's an algorithm I typically use to say okay this is how I know the specific kind of leukemia they are asking about right so I look at the two extremes of life I look at old people and young people you know let's start with like young people first you know with the young come first right so like young people right and then we then have old people right so young people remember eight comes before seeing the alphabet so the young people will have ELL okay and then the old people will have CLL right those people usually have the extremes of age so super young people like kids five years old six-year-olds they get ELL and then you know old people like in the late 60s 70s 80s they tend to have CLL right and then in the middle of life right we have the ML ML for middle life right so we have a ML and C ML right that's the first step right so now what are some unique things you want to know about each of those things that you know they'll usually give it as a memory hook in the question that will tell you okay you are dealing with this versus the other again like I said ELL is gonna be in a kid right so if you see an adult and adult is not gonna get ELL on an in-beaming cell that's pretty much a given right and then remember that ELL has an association with Down Syndrome okay ELL has an association with Down Syndrome right you've probably heard of this the money that they all fall down to help you remember that ELL is found in people with Down Syndrome and then if

you look at the other extreme of age CLL right then ELL is rapidly fatal if it's not treated usually those kids can be dead in like weeks or something like that if you don't treat them quickly and then CLL the classic presentation will be an old person with recurrent infections right and you'll have a super high white count so you may say oh divine this person has a super high white count how are they getting recurrent infections the thing is CLL in and of itself is an immunodeficiency disease because the thing is yes you may have all those ferocious B cells running all over the place but the thing is those B cells essentially do not work so they may not make like a decent number of antibodies or if they make antibodies those antibodies will effectively not work okay so that's how you know that okay you're likely that's why those people tend to get recurrent infections right so again CLL they really high white count right tons of infections and it's usually like pneumonia and all this stuff like strecumal right you'll have a crazy high white count you'll be an old person right and remember if you look at the person's blood smear you're gonna find smudge cells okay they're gonna find smudge cells if they want then I guess maybe I should maybe go ahead and throw out there is it's a B cell problem right so the bog pattern since I'm almost discussing it as an immunodeficiency disorder will be practically bacterial infections okay so that's the big thing and then AML obviously AML you need to know the genetic translocation it's 1517 right so 1517 translocation and you you treat it with all transretinoc acid right then obviously if you're looking at the cells on the histology you're gonna see our right and our are you need to be extremely careful when you're when you're kind of manipulating those things because those people can absolutely get DIC those are words are very po

werful triggers of secondary hemostasis so those people can run into DIC with that right and then CML the big and the thing is one thing your friends at the MIMI can do is instead of putting all transretinoc acid as an answer for the treatment of AML right one thing they can do is they can put vitamin A derivative as an answer right so that's something you need to be careful about right because the MBMI one of the a cart like one of the most common stocks in treat is to essentially take what you know and just give it different words okay so instead of putting all transretinoc acid they can put vitamin A derivative right so don't fall for that on a test so that you don't get gimped and then CML right I mean you I feel like anyone that is taking step one was really magical for any length of time knows a you know decent amount about CML right so CML classic thing would be the 1922 translocation right that's a big one to know and then remember you create a fusion protein known as BCR able right aka the Philadelphia chromosome so the Philadelphia chromosome gives rise so that BCR able fusion protein and you treat this with a magnet okay you treat it with a magnet a magnet is a tyrosine kinase inhibitor and pretty certain I've given this fully in maybe like a video broadcast I've granted where I said that if a person has if a if a drug ends in nib that tells you right off the bat that that drug has to be a tyrosine kinase inhibitor so that's a very high yield thing to know for purposes of exams okay that's a very high yield thing to know for purposes of exams so that's the way you tell those different leukemia as a part right so the lymphomas I mean the big thing with lymphomas is you want to think about the two big classes right so again hotkins versus non-hotkins right so what are the big things to keep in mind with hotkins right obviously for president has hotkins lympho

ma again they will have again primarily lymph nodes that will be affected they will usually will not have CBC abnormalities it's usually going to be in a young person again these things are not always true but they are true the vast majority of the time on NV Me's right and you have chronic B symptoms right and remember the high light cell for hotkins lymphoma at the read Sternberg cells right the read Sternberg cells at the classic cells for hotkins lymphoma and one thing that the NV Me loves to do especially on step three and the also the reason step one is to make your well hopefully hope that you remember that hotkins lymphoma is almost like a nicer presentation of the bio-statistical concept of bi-modality right so it tends to shop in young folk right so you know like late teenagers like late teenagers or like you know like they're early 20s and then it also tends to shop in old people or it's people that are you know almost 60 years old or a little over 60 years old right so it's a bi-modal distribution right and then don't forget again your wristarm break cells I forgot to mention with CLL CLL the classic cell you think about are your smart cells I think I've mentioned it but I don't know why my mind is saying I need to say so I'm just saying adjusting case right and then again wristarm break cells versus non-hotkins you know non-hotkins lymphoma there's many different types you do not see the read Sternberg cells and pretty much most of these leukemias and lymphomas just involve these cells for the most part right and remember your different kinds of hotkins lymphomas I will just tell you this because there's many many different types the one I will just I just feel like there is like two key principles you want to or let's say three key principles you want to keep in mind with hotkins lymphomas because again there are many types you don't need to memorize every

thing about every type but there is like one unique thing you want to make sure you know about pretty much all of them and about these hotkins lymphomas the first thing is you want to know that if you have more lymphocytes in a hotkins lymphoma the prognosis is better okay if you have I'll say that again if you have more lymphocytes in a hotkins lymphoma the prognosis is better okay now the corollary to that is if you have fewer lymphocytes then the prognosis is worse right so there are two there is this kind of hotkins lymphoma that's called like lymphocyte predominant sometimes people call it lymphocyte rich and then there's another one that you call lymphocyte depleted by virtue of this principle I just discussed lymphocyte rich hotkins lymphoma has a much better effect that I'm fairly certain it has the best prognosis of all the prognosis is the wrong word prognosis it has the best prognosis of all the hotkins lymphomas compared to the like the compared to all the others and certainly a lot better than the lymphocyte depleted and then if they give you like a stock question on an MD exam and they're asking you about the kind of hotkins lymphoma the person has go with the nodules sclerosin variant okay the most common kind of hotkins lymphoma very high yield the most common kind of hotkins lymphoma is the nodules sclerosin kind of hotkins lymphoma and then if you see a person with hotkins lymphoma having a lot of paritis and they tell you that oh this the you look at the person's CBC and you notice that oh the no syofil count is like really high it's like 6% or 10% or something like that then you absolutely want to think about the mixed cellularity variant okay so the the things that are released by those your xenophils can cause a paritis although all the kinds of hotkins lymphomas can be associated with paritis and don't forget that your hotkins lymphomas right cl

assically they are CD15 and CD30 positive just remember CD15 and then double that number you get CD30 you're good to go on your test right and then some of the non-hotkins lymphomas I think I should maybe talk about right don't forget your brachets lymphoma starry sky pattern right 814 translocation right basically you have like a CMIC amplification and CMIC promotes like just crazy proliferation of lymphocytes right so starry sky pattern jaw mass in an African abdominal mass in a in a person that is not African right if 14 translocation CMIC amplification that's a very high thing to keep at the back of your mind for exams and then multiple my loma right again it's something I've talked about at NOSME many podcasts again don't screw this up on a test these people have crop symptoms right you have hypercocemia they'll have renal problems they'll have anemia and you have bone pain you have lidic lesions this is one of those things that causes lidic lesions on imaging okay lidic lesions it's a radiological term okay so hotkins lymphoma again keep I mean sorry multiple my loma keep that at back of your mind it's very easy to identify it right you do like your SPEP and your UPEP to make the correct diagnosis right and then don't forget that on blood on a blood smear right you see like a stack of coins formation of red blood cells that was classically known as the RULO formation and then I know that I talked about CML CML is actually one of those things called a mylo mylo proliferative the solder CML is a mylo proliferative the solder please do not forget your other mylo proliferative the solders right they love to test those things on ambient exams right like CML is a classic one there one other one you want to keep at the back of your mind is a polycypemia vera right for the most part these mylo proliferative the solders they tend to be associated with like jack two mutat

ions right so polycypemia vera these people have like a crazy high white blood cell count I mean sorry not white blood cell a crazy high hematocrit so you see these people hemoglobin is of like 20 hematocrit of like 65% right you're like that doesn't seem very normal and usually these people have like they'll have this thing called like like aquagenic parrhoid us right so you know they take a hot shower and they each like crazy right if you see that think about think about a polycypemia vera and another thing is another thing you may see on an ambient exam is these people may actually have like facial plethora so the faces are like super super super red if you see that yeah definitely think about polycypemia vera and the thing is because they have so many red blood cells there's almost like a feedback inhibition of the production of Ipo so their levels of Ipo actually pretty low right so because people have such high red blood cell count you know you try to bleed them out right so phlebotomies like the primary treatment you can also give these people like hydroxyurea remember that's a ribonucleothide reductis inhibitor that can help there and then another one you may see another mylo proliferative disorder you may see is like essential phymbolcypemia right the big thing is these people have like a crazy high platelet count crazy high may got a number of like maybe chiro sites I've actually seen this in the railroad you know it's kind of rare but it's pretty striking when you see it right so these people you may think that oh because they have a crazy high number of bleak list they are just gonna have thrombosis no they also gonna have a pretty large bleeding risk okay they're gonna have a pretty large bleeding risk and again it's actually they would jack two mutations and again the key thing you absolutely want to keep in mind with these things is this people have aga

in a super high platelet count so they have a high risk of forming clot but they also have a high risk of bleeding because again many of those platelets do not work right and then another classic mylo proliferative new plasma you may see something called a primary mylo fibrosis right for the most parts there's just something with the happen happens with fibroblasts and they essentially just obliterate the bone marrow right so basically you have like those tear drop ship red blood cells if you do a bone marrow's biopsy or whatever you get like a dry tap that's like a classic thing they love to test on exams right so again all of that CML that has the 922 translocation Philadelphia chromosome BCR able the other mylo proliferative disorders right like essential thrombocytemia primary mylo fibrosis and polycythemia vera associated with mutations in jack two okay the associated with mutations in jack two again that's very high you know and then one thing I want to talk about is like Harry Cell leukemia is just something that tends to pop up on exams right remember the classic thing when I keep in mind is you'll see a presence lymphocytes and those lymphocytes seem to have like these fine white projections if you see that like 3d long projections from the lymphocytes don't confuse this with a smudge cell smudge cell is CLL okay but Harry Cell leukemia again lymphocytes with like you know like long like stringy projections coming from it look up a picture of this is actually a good histology image to be able to identify on an mb-m exam and don't forget that it's positive for something in a strap okay touch rate resistant acid phosphatase okay so it's trapped so trapped so tetrate resistant acid phosphatase right and then one of that bizarre thing that I want you to keep in mind with with these leukemia lymphomas please do not confuse mylo proliferative disorders with somethi

ng called a mylo dysplastic syndrome okay please do not confuse you with something called a mylo dysplastic syndrome okay the thing is mylo dysplastic syndrome you know if you've had like chemo before or you've got a good in radiation therapy or you've been exposed to benzene all these things are bad because they can become like AML but basically I'll tell you this there are two critical things you want to keep again you may see the value of going all basic science on me here I promise you I'm not willingly going all basic science on you this stuff I'm talking about is super high to know for exams like literally for step two and literally for step three you don't need to believe me but I know what I'm talking about I promise you right so the thing is one of the two things you need to know with mylo dysplastic syndrome mylo dysplastic syndrome the one key thing one the first thing you want to keep in mind is there's something called the pseudo pelga hue weight anomaly right so the hue it I don't know if it's hue or hue it or whatever but what most parties hate you eat it okay basically I think of it as a neutrophil wearing glasses right so you see like a neutrophil that almost looks like a rich term break cell right like a neutrophil that has like a bi-lobe nucleus if you see that think about think about the pseudo pelga hue and anomaly in fact these mylo dysplastic syndrome they are set to be associated with high post segmented neutrophils not hyper segmented hyper segmented neutrophils the thinking of like a B12 fully deficiency of megaloblastic anemia but if you see like neutrophils and the mb me tells you that they are hyposecmented you absolutely want to think about the mylo dysplastic syndrome and then one other thing you may see with the mylo dysplastic syndrome is something called a pseudo blastic anemia right sorry like a rich pseudo blast so a rich pseudo bla

st does not always mean oh I'm just didn't see the plastic anemia does not always mean oh I'm just dealing with lead poisoning no you can also find a rendered pseudo blast in a mylo dysplastic syndrome again I promise you I promise you these things I'm saying some of you are gonna get this on an exam I'm gonna remember that you heard it in this in this podcast so I think those are kind of like the big things I want to see with these are leukemias and lymphomas but you know I kind of wanted to review them really well just again quick highlight for step two ck step three and hopefully you'll find this to be hopefully you find this to be to be helpful so I'm gonna go ahead and I guess maybe you know let me kind of end this with these translocations right just to kind of wrap them up right so 814 right is brackets lymphoma I've talked about that 922 is CML I've talked about that 1517 is aml right that's a good promo in the leclochemia 1418 is another weird one known as like follicular lymphoma and then there's one bizarre one 1122 but it's not a hematologic malignancy it's more like ewing sarcoma right it's more like ewing sarcoma right so yeah so I think I'm gonna go ahead and stop here like I said this podcast will be short as I do at the end of every podcast I do offer one on one tutoring and also a lot of group tutoring for a ton of exams right so step one step two ck step two cs step three preclinical med school exams 30th shelf exams if you're college student are you need tutoring for the MCA Ts for general chemistry or guinea chemistry physics biochemistry histology physiology I tutor for all those things right and then if you're a medicine resident are you need tutoring for the ebi-m board exam or the internal medicine intruding exam I offer again one on one tutoring for that and then I offer these booster courses it's like ten hours for step two ck step three 20 h

ours for step one basically I review the most notes that you need for those different tests yeah I review those most I review those most notes for those exams and then it's something that if you're like you know close to the end of your dedicated period or you just want to kind of like put everything together relatively quickly that's something you can always welcome to reach out to me for and then yeah I feel like if you're also you know like a medicine applying to residency so like an ira sap or a medicine applying to like med school so like an AMCA application again I offer like one on one coaching right so like personal stipend in application I did in rec letters mock interviews again I've worked with pretty large number of people are planning to like a pretty large number of residency programs I kind of know what these residencies kind of look out for so again most of people have worked with the pretty much all much that their first choices so again if that's something you're interested in do feel free to reach out to me and I'll be more than happy to point you in the right direction and then the final thing I guess I'll see some offerings on a large group US Emily courses but I'll need like five to seven people so if your group are you need tutoring it will probably be like over two or three weeks span pretty much go over everything you need either for step one or step two CK or step three if you'll find a group and you find a location just let me know and then reach out to me that through the website or you send me an email to find intervention podcasts with an SAB end at gmail.com and then we can kind of take things from there you know it's a fairly complicated process but actually it's not complicated it's pretty straightforward you just let me know and then we can set things up so have a wonderful rest of your day I hope you find this podcast to be helpful i

s one of those podcasts that are short but powerful they're very high for you exam so please listen to the stuff before you take any of your US Emily exams or any of your complex exams okay so I'll see you next time in episode 204 I guess so have a wonderful rest of your day God bless you thank you for listening please subscribe to the You Tube channel just search for divine intervention US Emily you'll find the You Tube channel please feel free to subscribe and also I have all this on Apple podcasts Google Play Spotify and also my Word Press website so you know please subscribe to all these things any positive reviews or negative reviews you leave helps that's the way I improve and again like I said if there is any specific podcast you want me to make you can either you know shoot me a comment on Reddit or something I think people are pretty visible on Reddit or you know just send me an email and I'll be happy to again if it's a reasonable request and I have the time like really probably the biggest lot jam on my time is just biggest in probably one of the bigger impediments to me not making podcasts is just time if I have more time I'd make a lot more podcasts but unfortunately I also have many of the life commitments so for one of our rest of your day I'll see you next time time to stop blabbing good night God bless you

Lymphadenopathy (enlarged lymph nodes).

Either disproportionately high WBC count OR pancytopenia (low Hgb, low platelets).

CD15 and CD30 positive; Reed-Sternberg cells.

t(9;22), creating the BCR-ABL fusion protein (Philadelphia chromosome).

Pseudo-Pelgergren anomaly (neutrophil with bi-lobed nucleus) and pseudo-blast.

Polycythemia Vera (PV).

Reed-Sternberg cells; positive for CD15 and CD30.

Burkitt Lymphoma; t(8;14) leading to cMYC amplification.

Lymphocyte-rich Hodgkin Lymphoma; more lymphocytes correlate with a better prognosis.

CLL shows "smudge cells"; HL shows Reed-Sternberg cells (and often normal CBC).

Hypercalcemia, Renal impairment, Anemia, and Bone pain/lesions.

Tyrosine Kinase Inhibitors (TK Is); they target the BCR-ABL tyrosine kinase activity.

Reed-Sternberg cells; positive for CD15 and CD30.

Burkitt Lymphoma; t(8;14) leading to cMYC amplification.

Lymphocyte-rich Hodgkin Lymphoma; more lymphocytes correlate with a better prognosis.

CLL shows "smudge cells"; HL shows Reed-Sternberg cells (and often normal CBC).

Hypercalcemia, Renal impairment, Anemia, and Bone pain/lesions.

Tyrosine Kinase Inhibitors (TK Is); they target the BCR-ABL tyrosine kinase activity.