Transcription
Hey guys, it's Medicos! Is perfection Alice? What a beautiful day today! Let's talk about a disease which is not so beautiful. Anyways, CLL—chronic lymphocytic leukemia—let's get started. But first, let me remind you of this challenge: Help me reach 25,000 subscribers, and Medicos, we'll start a new series. You can vote which of these would you like to see next, and we'll make it happen once I reach this number. So please help share my videos. Thank you so much in advance!
Let's review the previous topic. Leukemia is classified into acute and chronic. Acute can be ALL or AML. Chronic could be CML or CLL. Note: L here stands for lymphoblastic because the cells are immature, while L in CLL stands for lymphocytic because here those lymphocytes are mature. So, in CLL, the problem will be myeloid or lymphoid? The answer is lymphoid. Immature blasts or mature lymphocytes? The answer is mature lymphocytes. It's a chronic leukemia. What is CLL? It's a lymphoproliferative disorder. There is accumulation of lymphocytes. These lymphocytes morphologically are mature; they are mature in shape; they appear as mature cells. However, functionally they are incompetent; they are useless. That's why it's cancer—lots of good-looking cells that are evil from the inside. If there is a solid lymph node mass, we call it SLL—small lymphocytic leukemia. Together, we can call them CLL/SLL. Start as a leukemia, then lymphoma. Lemonade is to leukemia as lemon is to lymphoma.
Most common leukemia in Western countries is CLL. Contrast that with the most common leukemia worldwide, which is ALL. For CLL, the patient will be an elderly, usually Caucasian, probably male. CLL is usually asymptomatic. You guess the type of leukemia by age. Yes, indeed. Newborn to 14 years old is ALL. For you, sixty: AML or CML. More than sixty: CLL. So CLL is the oldest patient. Now I know that ALL can have bimodal distribution, so the elderly can get ALL as well, but I'm trying to keep it simple. Clinically speaking, CLL is asymptomatic most of the time. You can have lymphocytosis with the famous smudge cells. Now, if you have used Photoshop before, you know exactly what I'm talking about. There is a tool in Photoshop called the smudge tool. If this is a circle, okay, and you select the smudge tool from the toolbox on Photoshop, then you drag this tool all over the cell, this cell will come like this—smudged. This is called a smudge cell, exactly as in Photoshop. Lymphadenopathy can occur. Hepatosplenomegaly, of course. Anemia and thrombocytopenia. If you get anemia and thrombocytopenia, this is a severe CLL with bad prognosis. Usually, I don't talk about classifications and prognosis a lot, but here in CLL it's crucial; it's very important. We have the Rai system. It's a crazy system because it sorts with a zero; it's kind of confusing. So don't forget: Stage 0 is the first step. Start with lymphocytosis. Last stage: Stage 4—thrombocytopenia. Don't ever forget that it starts with stage 0, because some students know this clinical progression, but they forget that the first stage is stage 0, so they answer thrombocytopenia—stage 5 and stage 4, and they screw everything over. Don't do that! Starts with stage 0—lymphocytosis with a smudge cell; risk level: low. Stage 1: Add adenopathy to the lymphocytosis. Stage 2: Add hepatosplenomegaly to the lymphocytosis. Both stage 1 and stage 2 are medium risk level. Stage 3 is anemia. Stage 4 is thrombocytopenia. They have high risk, which means the prognosis is bad.
So let's do the prognosis and the Rai system again with visual mnemonics. So stage 0—lymphocytosis—we draw a zero inside the smudge cell. Stage 1: We add lymphadenopathy to the lymphocytosis, so we draw a one on the lemon, which represents a lymph node. Stage 2: Lymphocytosis plus hepatosplenomegaly. Hepatosplenomegaly—liver and spleen—so we draw a two between them. Stage 3 is anemia—here's the three. Stage 4 is thrombocytopenia—here is a guy doing the sign of number 4, and he has BTK.
Additional notes that you need to know: 10% of CLL patients will transform into diffuse large cell lymphoma, which is very aggressive. When patients transform, they start showing fever, increase lymph node size, and increase LDH in the blood. Why do we have cytokine in CLL? Three reasons: Number one, infiltration of the bone marrow by the ugly leukemic cells; splenic sequestration; antibody-mediated destruction. What are the favorable prognostic factors and the unfavorable prognostic factors for CLL? So you can read them, but I will just note that 13q deletion has favorable prognosis in CLL. Contrast that with the 5q deletion that had a good prognosis in MDS—myelodysplastic syndrome.
So here is a vignette for you. Can you solve it? Of course you can! 67-year-old woman, totally asymptomatic. Cool. Physical exam is normal. Cool. But on routine complete blood count, you have hemoglobin, hematocrit, and platelets within normal limits. White blood cell: 51,000—this is a lot. Lymphocytes are 78 percent of the total white blood cell count—this is again a lot. So we have high white blood cell and high lymphocytes. Peripheral smear: You have smudge cells. The question: What's the most likely diagnosis? And the answer, of course, is CLL. We have the smudge cells; we have the lymphocytosis; we have an old lady, older than 60 years old. Which stage of CLL? Okay, physical exam is normal; routine; we have only the lymphocytosis with smudge cell. So this is what? This is stage 0. How to manage? Watch and wait, or aggressive chemo, or stem cell transplant? And the answer is watch and wait. She is in stage 0; she has a very good prognosis and very low risk. That's it! I'll see you in the next video. Until next time, be safe, stay happy, and study hard.