Transcription
We continue our discussion about hematology and oncology. In the previous video, we have started talking about acute lymphoblastic leukemia. Today we'll talk about acute myelogenous leukemia. These videos are to be watched in order. I have a playlist on hematology oncology; watch these videos in order, ok? I made it this way for a reason.
AML: it's acute, so the patient is younger. It's acute; the onset is abrupt, which means rapid onset. It's myelogenous, meaning it's in the myeloid cell lineage. It's a leukemia, which means cancer of that—not actually the blood, but the bone marrow. You have abnormal cells in the bone marrow and then going pouring into the blood. Here are your myeloid blasts. This is the myeloblast, and this is the monoblast. If this mature—which is not gonna happen in cases of AML—it will produce neutrophils, eosinophils, and basophils. If this is to mature, it will produce monocytes.
Here is the hematopoiesis: we start with multipotent stem cells, myeloid and lymphoid stem cells. Here are the myeloid blasts; they are divided into myeloblast and monoblasts. Myeloblast has what? The Auer rods, which are myeloperoxidase positive, which makes sense—sense they're siblings; the neutrophils produce myeloperoxidase. Cool. Now describe the myeloblast: it's large, immature; there is more cytoplasm than the lymphoblast; the nucleoli are more prominent; it's granular; it has more granules than the monoblast; and and of course lymphoblast; they have no granules whatsoever, and they have the Auer rods, which are azurophilic needle-shaped granules. Monoblasts, on the other hand, yes, they are granular, but they have less granules; sometimes the cytoplasm is vacuolated, and again we have the prominent nucleoli.
For the ninth time, leukemia has acute or chronic subtypes: acute ALL or AML; chronic CML or CLL. Pay attention: CML can cause AML, and in this case we will call it secondary AML versus de novo AML, which arises on its own. Which leukemia is the most common leukemia? The answer is ALL. Can you guess the type of leukemia by age? Yes, I can. Roughly speaking: newborn to 14 years old, ALL; 40-60, AML (which is today's topic) or CML; more than sixty years old, CLL.
Factors for AML: same stuff—chemotherapy, alkylating agent, ionizing radiation, benzene exposure, myelodysplastic syndrome, aplastic anemia, PH, Fanconi anemia, myeloproliferative disorder. This is paroxysmal nocturnal hemoglobinuria, by the way. I've talked about this in a previous video. If AML occurs after any of these conditions, we call it secondary AML, and now it has poor prognosis. Genetic abnormalities can lead to AML; they include Down syndrome, Turner syndrome, and Klinefelter syndrome. Let's review some genetics: this is trisomy 21; 47 XX or XY; Turner syndrome is 45 X 0 or X 0; Klinefelter is 47 XXY. Great.
AML is an acute leukemia, really? Okay, acute myelogenous leukemia, of course, is an acute leukemia, which means patients are younger—not as young as ALL, but in their forties, fifties—a little younger than 67 or 89 or stuff like that. Since it's acute, you'll have blasts greater than 20% of the marrow, but this time they will be myeloid blasts. These myeloid blasts will proliferate and replace most of the bone marrow. You'll end up with pancytopenia. They will enter the peripheral blood, leading to leukostasis, metastases through the body, and you will end up with hepatosplenomegaly, painful—sorry, sorry—painless generalized lymphadenopathy, testicular enlargement maybe, and cranial abnormalities such as headache, normal teasing the cranial nerves, retinal abnormalities, meningeal irritation, bone pain maybe, skin abnormalities, and in AML subtype M5, there is gum infiltration or gingival hyperplasia.
High-yield classification of AML: if you don't have time, don't memorize everything; focus on the colorful ones. M2 is the most common; it's called myeloblastic with maturation; there is the translocation 8;21, and it carries favorable prognosis. M3, also known as acute promyelocytic leukemia—very important for your test—there is translocation 15;17; again, favorable prognosis. There is the M5 called monocytic; there is gum infiltration or gingival hyperplasia. A way to remember it: this is M5, and mouth has five letters. The way to remember M3: it's associated with DIC—three letters—and you can treat M3 with vitamin—three letters—of course, vitamin A. Did you know that we can cure cancer by giving vitamins? Yes, indeed; this is acute promyelocytic leukemia, AML subtype M3—pretty astonishing stuff.
Aside: genetics of AML. Lay a scary one—good prognosis—normal karyotype or this one; they carry intermediate prognosis; and these ones carry bad prognosis. So I'd like you just to remember this is good prognosis and this is good prognosis. Since this one is the most common subtype. Are the unfavorable prognosticators of AML: age greater than 60; white blood cell count greater than 100,000; poor performance status; secondary AML, which means I had a previous disease before getting AML; secondary AML has much poorer prognosis than de novo AML, which arises on its own; also mutation of FLT3; the mutation in NPM1 gene has good prognosis. Important for your exam is the M3 subtype of AML, known as acute promyelocytic leukemia. I'll talk about this in the next video, but for now remember it has t(15;17) translocation associated with DIC; it carries very good prognosis; why? Because we can treat with vitamin A, called all-trans-retinoic acid or ATRA.
Diagnosed this acute myelogenous leukemia: again, same stuff; we need the lab and we need morphological analysis to look at that myeloid blast; cytogenetic study, karyotyping to see the t(15;17) translocation and other stuff; we need molecular markings; we need cell surface or CDs; and cytochemical analysis. Usually AML is TdT negative but is myeloperoxidase positive; okay, it has a green color. This is different from ALL, which was TdT positive and myeloperoxidase negative. The lab results in cases of AML: here is the peripheral blood, and here is your bone marrow biopsy. You will get normocytic anemia, maybe microcytic due to folate deficiency; thrombocytopenia; again, red blood cell count can range from less than 10,000 all the way up to greater than 100,000. You'll see myeloid blasts such as the myeloblast with the Auer rod or the monoblasts with the vacuolated cytoplasm. These have the Auer rods, which are myeloperoxidase positive, azurophilic, needle-shaped granules. Bone marrow biopsy: hypercellular, blasts greater than 20%, and these blasts are which one? The myeloid blasts.
Are you ready for this vignette about leukemia? Of course you are. 49-year-old female comes in with fatigue, mucosal bleeding, infection—what I call pancytopenia. Bone marrow biopsy is ordered and revealed hypercellular with 40 percent of the cells described by the pathologist as large, immature blasts that contain azurophilic needle-shaped crystals. What are these? Do you know? These are the Auer rods. On immunohistochemistry, they are positive for myeloperoxidase. Thank you. So here I know we have pancytopenia, and here I know we have lots of blasts—could be ALL or could be AML. The age bracket makes ALL less likely; also myeloperoxidase positive makes ALL less likely. The needle-shaped crystals—Auer rods—makes AML very likely. So what's the diagnosis? AML.
Which of the following has bad prognosis? All right, how about that t(15;17) translocation? This is acute promyelocytic leukemia; it has an excellent prognosis; no, this is not the answer. t(8;21)? This is the most common subtype, and it has a favorable prognosis; so it's not this answer. Okay, what else? De novo AML? Okay, this is like a little vague question; it's trying to tell you that de novo AML is different from secondary AML; between the two, AML has bad prognosis; so de novo carries a relatively better prognosis. Or D: white blood cell count of greater than 100,000? Of course, this is the correct answer.
You are watching hematology oncology lectures by Medicosis Perfection, Alice. I'll see you in the next video. Don't forget to subscribe and share my videos with your friends. Thank you so much in advance, until next time.