DIP Episode 82 - USMLE Step 1 Hematology Review Part 4 (Oncology)

Okay, welcome. My name is Divine. I am a PGY1, a transitional year resident, going into a diagnostic radiology. And this will be the 82nd episode of the Divine Prevention Podcasts. And in this podcast episode we're going to continue a review of Himalc, spare the USML Step 1 exam. And today is probably going to be the day where I'm going to round up discussing oncology. So I'm going to talk about the lymphomas and leukemias today. And that will be it. But before I jump into talking about the leukemias and lymphomas, I'll just go ahead and say that there's probably like some weird, high-yield anatomical details and histological details you want to know, relating to like the lymph node for example. So I think it probably makes sense to sort of start off talking about those and then we'll sort of progress to the leukemias and lymphomas. And I mean obviously right, you want to know about your, like sort of like the different parts of your lymph node, right? So you want to know that for example your B cells, they sort of hang around within the, like the germinal follicles, right? So like the follicular areas of the lymph node, that's where you'll find your B cells. And remember if you're sort of looking into the spleen, right? So like the, the white pop in the spleen is where you'll find a lot of your B cells, right? And then if you're looking at sort of like the T cell region in a lymph node, right? You're looking at like the paracortex, right?

But remember there's something called the pals in the spleen, like the periodarial lymphatic sheath. That's where you tend to find your T cells in the spleen, right? Then obviously you should know that your thymus, right? Also contains the T cells. I mean that's where T cells be sort of kind of begin their lives. Actually the sort of kind of begin the bone marrow, but that's, that's a different story. That's more for the future immunology or podcast. And then don't forget, right? So like your medallary sinuses in your lymph nodes contain, you know, like macrophages. And remember that, you know, I mean you find macrophages in many different organs, for example, in the liver. Your liver macrophages are called copfer cells in the, in the lung. Your macrophages are called like alveola macrophages. Some things people call them dust cells. In the skin, your macrophages, you can call them like lunger-hung cells, right? So yeah, you find macrophages in many different organs of the body. I mean osteoclasts, a sort of kind of derived from macrophages as well, if I'm not mistaken. Okay. Now the thing is, what are some other, I guess, high-yield things to know about lymph nodes, right? Remember that there are many, right, cancers, right? Love to spread to certain lymph nodes. And those things, these are more like you either know it or you don't know it's sort of detail. So highly, highly encourage you to know these big ones, right? So for example, if a person has breast cancer, right?

On step one, you want to know that it goes to the axillary lymph nodes for the most part, right? If a person has like a higher lymphatic anapathy, right? You're probably thinking about lung cancer. So a chordosis also tends to present with a higher lymphatic anapathy. If a person has like, you know, like a supra-clavicular lymph node, right? Like supra-clavicular lymphatic anapathy, especially if it's on the left side, you sort of want to think about like abdominal cancers that have sort of metastasized, right? So like, you want to think about things like, you know, like stomach cancer, like pancreatic cancer, in fact, in some situations they call these left supra-clavicular lymphadenopathy, like a varicose node, right? And then if it's on the right, you want to think more about like lung cancers and like a syphagel cancers, and also kind of like Hatchkins lymphoma, under those circumstances. And that is generally not called a varicose node. Left supra-clavicular lymphadenopathy is what is known as a varicose node. And then some other high-yield cancers you want to know, right? So if a person has like, you know, like a T-cell lymphoma, right? I'll talk about that later in this podcast, right? They can have like, medias spinal lymphadenopathy. If a person has like a, sort of like a germ cell cancer, so like a testicular cancer, for example, right? You want to think about like the parallel lymph nodes.

And then if a person has like, you know, like a over cancer or a squamous cell cancer of the penis, chances are you probably go to the inguinal lymph node. So this is where you want to be careful, right? So like ovarian cancers, testicular cancers, they love the parallel lymph nodes, okay? But don't say, oh no, testicles pariotic. So the penis should be pariotic. No, testicles pariotic. The, like, squamous cell cancers of the penis, they love to go more to the inguinal lymph nodes, okay? If you sort of think embryologically, you'll see why that is the case. But I really don't have the time to go into that right now. I need to make this podcast relatively quickly so I can take a shower and I head to work. So, so what are some, I guess, other high-youth things to sort of know about lymph nodes. As you see, they will actually become important when I begin to talk about the leukemias and lymphomas is if, for example, right? There's a type of non-hatchkinz lymphoma that's known as follicular lymphoma. But the thing is there is also a phenomenon known as follicular hyperpleasure. Remember I told you that the germinal follicles are where you find B cells, right? So if you have like a region bacterial infection, you will have like a proliferation of B cells. So that will cause a hyperplegia of the germinal follicles, right? So the thing is, in the cellin of follicular hyperplegia, for the most part, you'll have a lot of problems. Yes, you have all the B cells proliferating, right?

But the thing is, if you take a histological section and look at a lymph node that has like a big proliferation of B cells in response to like some bacterial infection, the thing you'll notice is that the germinal follicles will still be very well demarcated from the paracortex, right? So the thing is, you'll see like basically the lymph node architecture will be well preserved. That is very different from follicular lymphoma where the lymph node will be completely faced with the neoplastic lymphocytes. So that's kind of like a high-yield thing to know. And the thing is that follicular hyperplegia, right? You don't just see it with bacterial infections, right? You can also see it like in early HIV, okay? And also certain, I guess, rheumatologic diseases, right? So like rheumatoid arthritis, and also like lupus, you tend to find a follicular hyperplegia on that of circumstances. And then remember, I told you that the T cell zone, right, is the region that has, I mean, the paracortex is the T cell zone. That's where you have your T cell sort of proliferating, right? So obviously if you have like some kind of like viral infection, right? You have hyperplegia of the paracortex. Also, I mean if you have like, I guess, yeah, I will see for the most part viral infections, those are probably sort of like the big ones you want to know. And please don't forget, if a patient has a de-jorge syndrome, right?

The paracortex will not be well developed because remembering de-jorge syndrome, your third and fourth pharyngeal pouches fail to develop. So your parathirides and your thymus are by-by, right? So, basically, if you are not having T cells growing in the thymus, then there is no basically like a feedstock for the paracortex of your lymph nodes. Kind of high up to know that. And then, I guess one other weird thing I will just go ahead and mention, because it's something that not many people sort of keep at the back of their minds, is in general, right? If a person has a bacterial infection, the way you respond is with a proliferation of like neutrophilts. But if a person has a bacterial infection where you see like, crap ton of lymphocytes responding to that bacterial infection, you really want to think about what's the name of this disease? So, you really want to think about a Bordetella pertussis. One of those is a circumstance that you remember Bordetella pertussis. If you're not an anti-vaxer, probably won't get this. And remember, if a person has pertussis, you want to treat them on the close contacts with a macrubin like erythromycin, right? Okay, so personally, I think that's what I'm going to say about like lymph nodes and just like some weird high yield stuff. And I guess I'll sort of live it there. And I know like some people may say, oh, divine. It's neutrophils and what not that respond to bacterial infections.

Why did you say that you would have hyperplegia of the, of the germinal follicles? If a person has a bacterial infection. So the reason I say that is, right? I mean, if you have like an infection, right? You obviously first of all, the respond will be neutrophils, right? But ultimately, if you want to say, for example, like, let's say you get, you get an infection and then you create antibodies so that you stave of that infection in the future, right? And that's what I'm going to say about that stuff. That germinal center reaction kind of has to happen. And I will say more about that when we get to the, when we get to an immunology podcast, really, to be honest with you guys, I really want to make more podcasts at a mock celerithic clip. But in turn years, just just gets quite busy. And sometimes especially when you're like internal medicine, I see you just makes it really tough. If you notice the last few podcasts have been making them largely like super early in the morning before I like prepared a good work. Okay, so back to this. So I guess we can sort of jump into the cancers now. And I think maybe I should go ahead and start with like, like non-hotchkins lymphoma, right? So the thing is, first thing is you want to sort of get the difference between a lymphoma leukemia, right? The thing is lymphomas for the most part represent cancers of lymph nodes.

One thing you want to keep at the back of your mind is these lymphomas can spread to things that are not lymph nodes, right? But for the most part, think of them again, they're exceptions to these roles, but I'm telling you what you need to know for your USMLE step one exam. Lymphomas for the most part study lymph nodes, leukemias for the most part study in the bone marrow and peripheral blood. Okay, so leukemias, bone marrow, blood lymphomas lymph nodes. Okay, and under the lymphoma class, you can have hotkins lymphomas that are characterized by the presence of rich, tempered cells and non-hotchkins lymphomas that are characterized by the absence of rich, tempered cells, right? And then under the leukemias, you can have acute leukemias and you can have chronic leukemias. I already talked about one of the chronic leukemias under the myeloproliferative neuroplasms in the last podcast. That was a CML and I sort of give you like an each algorithm that could basically help you determine like which cancer you're dealing with. I'm actually pretty useful algorithm or encourage you to go back and listen to episode I believe 81 to sort of get to the, get to the nuts and bolts of that. But today I was playing most of my time talking about CLL, right? Because if you're thinking about leukemias, right? You can have myeloy leukemias and you can have lymphoid leukemias, right? So like leukemias from lymphocytes or leukemias from myeloy cells, right?

And you can have acute or chronic for each one. So I'll talk about those. CLL is like the lymphoid acute that usually happens in kids and then CLL usually happens in all people with like white cancer like 50, 60, 80,000 with a smudge cells and like recurrent infections. I'll talk about that in a bit as well. And then you have AML with the only one they're going to test on you exam is the one that has our acute pro myelocytic leukemia with the 1517 translocation. So let's get let's get right to it. Right. So the thing is for your non-hotchkins lymphomas, right? So again, like I said, they generally tend to do not have rich thermberg cells pretty much. And most non-hotchkins lymphomas, most of them are right from B cells, right? Yes, I did T cells T cell long Hotchkins lymphomas. Sure, why not? But I'll say that for the most part on exams, you want to think more about B cells being the origin of non-hotchkins lymphomas. And the thing with non-hotchkins lymphomas, right? When people are learning they're like, man, this is a nebulous topic. There is a crap ton of stuff I need to know. That's actually no real true. They are just a few big things you need to recognize. And for the most part, you should be able to navigate your way through these things on exams, right? So like I said, again, they are no rich thermberg cells for non-hotchkins lymphomas.

And the thing with non-hotchkins lymphomas is that they tend to involve older people versus Hotchkins that tend to involve younger people and older people. In fact, many times you see that Hotchkins lymphoma is said to have like a bimodal age distribution. And I guess since I just mentioned the word bimodal, it's very high yield to know for the USML is step one. There is another classic thing that is tested in the context of like a bimodal distribution. That's people that are slow and fast-asseted leaders of drunks. Classically on exams, it's isoniasid. That's another one you definitely want to know. Right? So if you see a bimodal distribution, so don't make it as a concept in your head. You think about fast-asseted leaders. And you also think about the H distributions for Hotchkins lymphomas. Hotchkins lymphomas can shop in people between the ages of 15 to 34 and then people over the age of 50. Very high yield to know that. So this is the way you can connect those concepts in your mind. So non-hotchkins lymphomas, right? And the thing is I will try to keep making different, try to keep making like correlations. Oh, this is typical for Hotchkins. This is typical for non-hotchkins. But right now I'm talking primarily about non-hotchkins. Right? So in non-hotchkins lymphomas, right? So obviously it's going to involve lymph nodes. But the high yield thing you want to know is that it usually involves lymph nodes that are not contiguous. So what do I mean?

That involves lymph nodes that are not contiguous. The thing is you can have lymphadenopathy in many different spots in the body. Let's just put it that way. That is in strong contrast to Hotchkins lymphoma that tends to involve contiguous lymph node groups. Right? So it's like you have like a strong almost think of it as like a straight orderly line of lymph nodes that are involved in Hotchkins versus like a disorganized array of lymph nodes that are involved in non-hotchkins lymphoma. Now most non-hotchkins lymphomas, I mean there is many like high yield like scenarios you want to be able to identify on exams. Right? So obviously the big nasty bug, EBV, EPC bar virus plays a big really many non-hotchkins lymphomas. I mean if you want to think about like a patient with AIDS and like a primary CNS lymphoma that is almost EBV is almost always implicated in those kinds of lymphomas. Remember EBV also causes a lot of other problems. You can cause like Burkets lymphoma, I'll talk about that shortly. It can also cause like a nasal pharyngeal carcinoma. Right? I'll talk about that in a bit as well. Actually I'm not going to talk about that in a bit. Just know that association. So also don't forget right there. Certain like T cell lymphomas right that are associated with like a close cause in some HIV. Right? I think they are called like HTLV one the HTLV one virus. I think it's like human T cell lymphotropic virus. That's another classic scenario that we shop on exams.

But think about that in the context of a T cell non-hotchkins lymphoma. Right? And then you also thinking about the one of the most common causes at least if I will say the most common infectious cause of peptic ulcer disease, H by Laurie. Remember that's a URI positive bug. That's associated with a kind of non-hotchkins lymphoma known as a maltoma. Okay? I'll talk about that later down the line. And also don't forget right people with certain autoimmune diseases right? So like Hashimoto's if they describe a person like a thyroid mass that is rapidly enlarging and they have like a pass history of like Hashimoto's thyroiditis. You also want to think about a kind of more tumor right? I write in the thyroid blood right thyroid lymphoma one of the biggest if not the biggest risk factor for thyroid lymphoma is a past history of Hashimoto's thyroiditis. And then also if you're sort of thinking like a mouth like a mouth like an oral mass right in a person that has a history of show grints. You also want to think about some kind of like salivary gland and lymphoma. These are all examples of maltomas and they are all examples of non-hotchkins lymphomas. Now, so I guess we can sort of jump into the non-hotchkins lymphomas right? So I said that most of them are right from B cells. The ones that are right from T cells just sort of think of in fact you know what? Think of HTLV1 as being a cause of like a T cell lymphoma. That's probably all I'm going to say about that.

That's it's not very commonly tested on exams. So I don't consider it to be super high yield. So I'm going to move on from that. But the B cell non-hotchkins lymphomas right? So let's sort of work through them one by one right? And again just few things you need to know about these ones. So the first one I guess will be a Burkett's lymphoma. Burkett's lymphoma big things you want to know right? So it involves the 814 translocation right? So if you have that 814 translocation you basically have B cells that begin to proliferate like crazy right? In fact I think about these B cells as lift fast diome right? So they proliferate like a crap ton right? So it's a highly like aggressive mass when it arises in lymph node. But the thing is those cells they lift fast they die young. So as they die guess what? Macrophages will come and clear those clear the nastiness. The macrophages will come in and clear that nastiness right? So classically if you take a histological section through a Burkett's lymphoma you will see the classic like starry sky pattern on on our histology. And again EBV is classic in fact if they ask you about like a bug and Burkett's lymphoma think about EBV. Okay and remember again you'll 814 translocation basically you overexpress something called like the C-MIC oncogene. When you express that C-MIC oncogene you have like this just crazy proliferation of B cells and the person has a kind of non-hotch kinz and lymphoma.

And really the key thing you want to be able to identify guess in terms of like patient population they're actually like two types of this a Burkett's lymphoma. So usually there's one that involves the GI trucks that's more like in Americans in Europeans versus the African type that tends to involve the job. That's probably like the big thing you want to know there. And then if we're sort of jumping to the next one right? So if you're thinking about like the maltomas remember I already talked about H-Py-Lory. Remember H-Py-Lory is the most common infectious cause of a peptic ulcer disease. And sometimes you may see them refer to this as like a marginal zone lymphoma if you may. But again remember those three classic scenarios tired lymphoma which a history of Hashimoto's. Salivary gland lymphoma with a history of show grants and H-Py-Lory and a peptic ulcer disease. I mean occasionally you may see like the association with like an 11 18 translocation but that's kind of loyal so I'm sort of going to move on from that. But it's just one of those two 70 style questions where like a 11 18 translocation what where is that from? Think about these maltomas with that basically with that translocation you basically begin to overexpress an anti-phototic gene. So the cells don't die and then you begin basically cells don't die already essentially become immortal right? And then the person gets into cancer into cancer territory.

Now the next non-hochins lymphoma I'll talk about is follicular lymphoma right? So this one I've sort of kind of said many things about it already right? So remember the differences between follicular hyperplegia and follicular lymphoma right? So I've talked about those are those are high effects but the key translocation you want to know here is the 14 18 translocation right? Where you basically have like overexpression of a BCL to BCL to is an anti-phototic gene right? So if you overexpress it again the cells do not die right? And again remember the lymph node will be completely fixed right in the setting of in the setting of a follicular lymphoma. And really if you do a sting for BCL to right? You see like very high BCL to sting in the setting of follicular lymphoma as against a follicular hyperplegia. Now the next one I'll talk about is I guess I can talk about like diffuse large BCL lymphoma. This is actually the most common kind of non-hochins lymphoma and I will say that for the most part many of these non-hochins lymphomas if they want to go from like back to worse the progress to a diffuse large BCL lymphoma. That is probably all you need to know about diffuse large BCL lymphoma. I mean it has like a pretty crappy prognosis and I mean it can overexpress like BCL to BCL 6 bloody bloody blood. Basically I think of diffuse large BCL lymphoma is a non-hochins lymphoma that then acquires additional mutations and then becomes really bad.

And it's actually the most common kind of non-hochins lymphoma. And yes it has a bad prognosis but trust me the prognosis not as bad as the next one I'll talk about. Mantocel lymphoma. Mantocel lymphoma is the worst kind of non-hochins lymphoma. The life expectancy is pretty bad right? I mean it's almost like 100% mortality at like 5 years. If I'm not mistaken it's a pretty bad it's a pretty bad non-hochins lymphoma. And the key thing you want to know here is that you have an 11-14 translocation. So you basically overexpress this protein on a cycling D1. And the thing is cycling D1 what's its job in life? Its job in life is to make you keep going from G1 to S. But normally you would not want to go from G1 to the S phase if you have mutations that are like bad. But if you have an overexpression of cycling D1 you don't hear those messages of like you have a lot of mutation. Maybe you sort of claw back and going to the S phase. You don't hear those warnings anymore and you just keep going from G1 to S phase and then the person gets into trouble. Now one weird thing you want to know about these mantocel lymphomas is that they are CD5 positive. And why am I why you think I'm emphasizing this? The reason I'm emphasizing this is in general CD5 is something you find wonder the purview of T cells not B cells. So because it's kind of like a unique marker in B cell territory you sort of want to keep it at the back of your mind for example.

So mantocel lymphomas they are positive for CD5. Also if you look at like CLL right so like chronic lymphocytic leukemia it's also CD5 positive. But one way you differentiate between CLL and mantocel lymphomas that CLL is a CD23 positive. What mantocel lymphoma is not positive for CD23. So that's sort of like a nice way to differentiate between those two. So I think that's all I'm going to say about the B cell lymphomas. Again the T cell lymphomas I mean you can have like HTLV1 causing some of those. I guess if you want to think about the skin in the context of T cell lymphomas there's something called like myosis for goides and then there's something called a like a cesare syndrome. Basically the big thing you want to know about myosis for goides versus cesare syndrome is that myosis for goides is kind of like the more okay let's just put it this way. Myosis for goides is not as bad as cesare syndrome both are bad but myosis for goides is less bad. And myosis for goides for the most part tends to involve the skin right. If I classically they will show it usually involves the buttocks on a US Meli exams. So it involves the skin if you take a biopsy of the skin you'll see like T cells and the boss phrase you want to recognize on test is that they have like a cerebriform nucleus. So they sort of look like like the cerebral cortex in a sense. So they sort of look like gyre forming a sense. And then you may also see like clusters of these Abernthi cells.

When you see like a cluster of like four or five or more of these Abernthi cells the pathological name for those things are portray micro abscesses. Those are the big things you want to know. And then sometimes myosis for goides can also just present as just generalized like redness of the skin. Usually people call that a rethrote derma but if you're like divine okay how about the relationship between myosis for goides and cesare syndrome. If you see a lot of involvement of the blood and lymph nodes so if you see like prominent lymphadenopathy a lot of blood involvement. You want to think more about a cesare syndrome okay you want to think more about a cesare syndrome. And I think that's all I'm going to say about say about these non-hotchins lymphomas. Go ahead and jump to the hotchins lymphomas right so the hotchins lymphomas right again these are characterized primarily by the presence of of rich thermberg cells. And again remember the bi-modal age distribution already talked about that. So it shows up in people between like ages of 15 to 34 and people that are over the age of 50 okay. And the thing is these rich thermberg cells right there are like a kind of a B cell if you may. The sort of like bi-lobed or an inculge to sort of look up a picture of those they can classically show you a histological image with the rich thermberg cell like death center. And they need to know it's hotchins lymphoma.

And the thing is these rich thermberg cells right there like CD 15 CD 30 positive. And the thing is there are many types I mean there are few types not as many as non-hotchins. There are a few types of hotchins lymphoma. The big thing you want to know is that the more lymphocytes you have in your hotchins lymphoma the better the prognosis okay. So there's like lymphocytes predominant hotchins lymphoma. There's like lymphocytes depleted hotchins lymphoma. Lymphocytes depleted as a terrible prognosis lymphocytes predominant has an awesome prognosis in fact. If I'm not mistaken it has one of the best prognosis of the hotchins lymphomas. And obviously right the most common kind of hotchins lymphoma is the modulus clearosing type. I'll say for the most part hotchins lymphomas are probably more common in guys than girls. But the modulus clearosing type the sex distribution is kind of the same. It's sort of kind of like equally common in men and women. So I think those are probably like the big things I will say about like the hotchins lymphomas. I've talked about how more lymphocytes means better prognosis. And I guess let me go ahead and address this one question I've gotten from many people. So many people keep asking divine. How do I do I need to memorize the specific treatments for these different cancers? My answer to that is no you don't.

I mean there are certain things like oh if a person has like childhood cancers like ewinks, go ahead and give them what's the name of this drug. Go ahead and give them like actinomycin, deolactinomycin, fine. All those like high-yield specifics I mentioned them in the pharmacology podcast for hemorrhagic. But yeah to sort of say oh what is the regimen for hotchins lymphoma, do I need to memorize it? No you wouldn't. The thing is you need to know your hemorrhagic drugs but you need to know them mostly for like mechanism of action side effect kind of business. Not like oh use this big regimen for hotkins. No no no no no that is not how you have to know. And just wasting your time trying to memorize those are for example those are mostly for like medicine boards and things of that nature. So that's all I'm going to say about the hotkins lymphomas and I'm going to sort of move on from that. So the I guess last things I will sort of talk about I guess I can talk about CLL CLL already talked about it pretty extensively. I mean the last podcast so I'll just say like a few quick things and sort of move on. Remember CLL again it's a disease of old people can CLL happen in a younger population in the real world absolutely. But on USMLE exams if a person is like in their 40s they don't have CLL okay CLL usually a USMLE exam shows up in people that are 60s 70s 80s.

And the classic way in fact I don't think I've ever seen it presenting in in a different way on MBM is that you'll be an old person that has recurrent infections like although say like this is like this third episode of pneumonia in a year. And then you check the white count the white comes like 70,000 usually like some crazy high value if you see that don't waste your time reading the rest of the question it's CLL simple as that. And CLL right classically on the astrology you'll see smudge cells right sort of like a blood spatter kind of cell. And CLL this is actually one of those cancers we're knowing a drug that can treat it is useful. There's this drug in first state and I also talk about it in the in the podcast relating to like in fact I think I talk about it like in the immunopharmacology podcast there's like a podcast I have that is basically the monoclonal alphabet. So basically all the monoclonal antibody drugs you need to know for tests. I catalog them in that one podcast I talk about LM2 zoom up. It's a monoclonal against I believe a CD 52 it's actually used for the treatment of CLL those are one of those like one and done pieces of information you want to know for your exams. And really that is all I would say you need to know about about a CLL right and again remember I already said other high your things I said that it's positive for CD5 just like mantus cell lymphoma but it's also positive for CD23.

Remember CD23 positivity is found in CLL positive 23 negativity is found in mantus cell lymphoma which is a kind of non-hotchins lymphoma. Now I mean I guess another lymphoma you can sort of think about is like harry cell, harry cell leukemia sorry I keep mixing up these words. I'm talking about leukemias right so CLL right it's like chronic lymphocytic leukemia it's a leukemia apologize for that it's a leukemia although there's like a lymphoma kind of CLL called like small lymphocytic lymphoma but yes hotchins non-hotchins are the lymphomas sorry now I'm talking about a leukemias. So CLL old person it's a kind of leukemia already said the high offense there for for harry cell leukemia this one is pretty easy to identify on exams if you see a lymphocyte with like harry projections that's that's a harry cell leukemia. And really harry cell leukemia has a classic exam presentation that parallels primary mylofibrosis remember primary mylofibrosis is one of those are mylof dysplastic syndromes that I talked about where you have like the tear drop shaped red blood cells.

The thing is if a person has CLL you also for some reason when you do a bone marrow aspiration you get a dry tap okay so that's a classic presentation for primary mylofibrosis and also for CLL so it's kind of high you to know know for exams and the thing is patients with harry cell leukemia they tend to get just massive massive massive massive a split a hepato splinomageli and the thing is they are usually positive for this end as I'm known as a trap is thing is like a saturated resistant acid phosphatides I know I've seen that tested quite commonly on exams and that's really all I think I'll say about a harry cell leukemia. The acute leukemias again I sort of talked about them LL you'll be like a young kid usually it's like kids that are like five years old or whatever and remember these acute leukemias right classically you check the bone marrow and you find more than 20% blasts right remember I said like oh for the chronic leukemias they can have like a blast crisis where you don't have as many blasts at the beginning and then boom you sort of go to the accelerated phase where you have like between like 10 to 20% blasts in the bone marrow.

And then once you get over that 20% marker the person has a blast crisis right and that's obviously not a not a good thing in general if you don't treat these acute leukemias the person will be dead within weeks they are very sensitive to chemotherapy and all that stuff but you actually need to treat them if you don't treat them the person is going to die in a few weeks.

So LL right it's young kids again it does not show up in old people on NB Ms can it happen in old people absolutely okay absolutely but B cell LL on NBM exams is in young kids that is the only demographic you need to know for exams if you see a 40 year old it's not LL on your NBM exams very I you to know that so your acute like lymphocelin from chemia right remember the essential Down syndrome remember I talked about that in one of the early podcast for a him and remember that these cancers were positive for TDT TDT is known as a terminal deoxy nucleotide transfer is it's something I'll highlight some more when I do the immunology podcast but TDT positivity is something that defines the lymphocelin leukemias versus mylo peroxylase positivity that tends to TP5 the myloida leukemias and remember LL again in kids but if you say like a teenage boy with like an anterior medias spinal mass you want to think about like T cell LL that's like the classic presentation there so usually in those questions they will give you like a chest x-ray and you'll see like the cell sign that you classically see with like the thymus and think about a T cell LL under those under those circumstances and LL may also stay in positive for a periodic acid shape like PES but that's very really tested on exams I'll say that the TDT positivity is something that defines LL and then if you want to think more about what is good and what is bad in terms of LL right so if you remember when I talked about CML I said that oh you have the Philadelphia chromosome with a 922 translocation the thing is this 922 translocation you can actually also find that in the setting of LL and the thing is when you have it in the setting of LL that's usually a bad prognosis right and again this will kind of make sense remember I said that oh CML right you can have the chronic disease chronic form and then you can have a blas

t crisis and I remember very vividly from my previous podcast when I was talking about CML I said that CML when the person has the blast crisis it can degenerate to ML or it can degenerate to ML right you can have those blast crises so the thing is if a person has CML and it's degenerated to like a blast crisis that's obviously a bath and right so sort of use that in your mind to link up with the idea that oh if a person has a 922 translocation so the Philadelphia chromosome in the setting of LL that's a bad prognostic leisure okay and that's usually in a dot right because remember CML is a disease of a dot right so you'll likely find that 922 translocation in a dot as against kids kids with LL there's this I guess think of it as a 1221 translocation that's associated with a much better prognosis and it's a translocation that you find more common link kids and easy way to remember that is if you take the number 12 and you flip the letters it becomes 21 okay so that's an easy way easy way to remember for with that right and again because most L Ls are raised from B cells right you'll have like the classic B cell markers like CD 19 CD 20 bloody bloody blah they may also they'll also actually it's not they make they will also have CD 10 and you've probably heard of like the color and teaching like C.A.L.

L L.A. So it's like the LL and teaching it's a CD 10 so contrast that with the T cell L right like the and term of your stand on mass I can remember but though my ring in my head from a backing the day like and T. I mean just 10 months in a teenager if you see that think about the T cell L don't have more T cell markers right so like CD 3 CD 5 CD 7. Okay and then ML literally the only thing you want to know about the ML is that ML our odds 15 17 translocation so you have like an aberrant rate no Cassid receptor and you want to know that you treat this with a A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A.T.A And last thing I would say I promised before I round off is so I say that B.C.L.L.L. right? Express is like CD19 CD20 and like CD10. So that A.L.L.L. I'm teaching the T.C.L.L.L. right? I said it expresses more T.C.L markers right? So like CD3 CD7 bloody bloody blah. Usually those not express CD10. Okay. So that's another key difference. You sort of want to keep at the back of your mind. So sorry. This was a little horrid. It's a rush off to work. I have a large list.

I need to take care of what I was seeing the next podcast. But I think I'll say I'm right now officially done with the cancers. So really the major topics that are remaining are like the anemias. I'll talk about those. That's another like kind of like hairy topic for many people. And then I'll talk about like these like weird disorders like a PNH like a Paroxyximal, nocturnal hemoglobin, and all that weird stuff. So I'll talk about those in a little podcast. But I wish you all a wonderful day. And remember like I always say offer tutoring for med school exams, shelf exams, and this is private one on one tutoring. And again, you don't need to use any of this. I have videos and everything on the website that you can watch for all these exams. But I do offer one on one tutoring for med school exams, shelf exams, step one, step 2ck, step 2cs, step 3, the medicine boards, and also like the medicine in training exam. Believe it or not, I've actually treated people for these things. And I also have admissions committee experience. So I prepare I'm cast an era's application. So if you're, if you're a college student going into a med school or a med student going into residency, I can prepare your application. I can help with our personal statements like editing personal statements, doing walking interviews, and just share sharing my general knowledge with the residency process.

So if you have questions on any of those things or your med student that's preparing for intern year, and you're kind of scared and you sort of want to be prepared for like common situations you see as an intern, common conditions you have to work up as an intern. I sort of think of it as like my intern school. Feel free to reach out. I tutor one on one for those kinds of things. Just either email me through the website or you can send an email to the Vine Intervention podcasts. So that's podcast with an S at gmail.com. So have a wonderful day. I wish you all the best and God bless. Thank you.

B cells reside primarily in the germinal follicles; T cells are found in the paracortex.

Squamous cell carcinoma (SCC) of the penis.

In hyperplasia, the normal nodal architecture remains well-preserved; in lymphoma, the node is completely effaced by neoplastic lymphocytes.

t(8;14), leading to overexpression of c-MYC oncogene.

CLL is positive for CD23, while MCL is typically negative for CD23.

Cerebriform nuclei and porphyromicroabscesses.

Kupffer cells (liver), Alveolar/Dust cells (lung), Langerhans cells (skin).

Hodgkin tends to involve contiguous nodal groups; Non-Hodgkin often involves non-contiguous, scattered nodes.

15–34 years and over 50 years.

Chronic Lymphocytic Leukemia (CLL).

T-cells express CD3, CD5, and CD7; B-cells express CD19, CD20, and CD10.

t(14;18), resulting in BCL2 overexpression.

Kupffer cells (liver), Alveolar/Dust cells (lung), Langerhans cells (skin).

Hodgkin tends to involve contiguous nodal groups; Non-Hodgkin often involves non-contiguous, scattered nodes.

15–34 years and over 50 years.

Chronic Lymphocytic Leukemia (CLL).

T-cells express CD3, CD5, and CD7; B-cells express CD19, CD20, and CD10.

t(14;18), resulting in BCL2 overexpression.