 Welcome to MetSmarter Lecture Series. Today we will talk about high-yield hematology measures that are heavily tested on the exams. Before we start, just take a minute and subscribe so you can get notified when we post a new video. So let's dig in. Next we have hyper-segmented neutrophils. Hyper-segmented neutrophils can be defined as the presence of neutrophils with six or more lobes or the presence of more than three percent of neutrophils with at least five lobes. The presence of hyper-segmented neutrophils is an important diagnostic feature of megaloblastic anemia. Next we have bone marrow that is hyposellular for age and we can see that lacunar spaces are replaced by fatty cells. Where do we see that? We see in aplastic anemia. So aplastic anemia commonly is the result of an autoimmune mediated process. We can see infectious agents such as hepatitis A, B, C viruses can cause it. We can see allopyrinol, carbamazemine, benzene, they can also lead to it. Or it can be a result of loss of function in germ-sandline mutations due to DNA repair defects such as fincones anemia. Relox formation. Stacking of cells facilitates the rate of red-cell sedimentation, a phenomenon that may be seen on peripheral smear. Appearance of relox may be artificially caused by a poor preparation of this smear or by viewing this slide in a thickened area. When relox formation is truly present it is caused by an increase in such proteins as immunoglobulins and fibrinogen. Where we are going to see our relox formation or clumps of Arbisces, they are, they look like stacked plates. It's going to be in multiple myeloma and macroglobonemias. Next, pseudopergerhute anomaly. This is in, we see in inherited blood condition in which nuclei of several types of white cells such as neutrophils and esophils. They are involved. It looks like bilobed, peanut or dumbbell shaped instead of normal trilobed shape. And they are coarse and lumpy. We are going to see that in myelodysplastic syndrome and also in drugs such as immunosuppressants. In multiple myeloma, the plasma cells of multiple myeloma are going to show us blue cytoplasm, eccentric nucleus, and perinuclear pale zone or hollow. So this is going to show us clock face pattern of nuclear chromatin in plasma cells. Clock face is seen in multiple myeloma. Russell bodies. Russell bodies are considered to be aggregated and release immunoglobulin components as a result of a blockage in the normal secretion pathway of immunoglobulins. They are stored within the ruffinoplasmic reticulum or plasma cells and may totally fill up the cytoplasm and compress the nuclei. So you can see that they can totally fill up the cytoplasm and can compress the nuclei. Plasma cells containing them are sometimes referred at Mott cells. Where are you going to see Russell bodies in multiple myeloma? Read Stenberg cells. These are large about 30 to 50 microns, multinucleated or biolubed nuclei. They have prominent isnophilic inclusion like nuclei. So they resemble the owl eye appearance. They are CD30 and CD15 positive and the presence of these cells is necessary in the diagnosis of Hodgkin's lymphoma. In Burkitt lymphoma, we see steric sky appearance pattern. The tumor cells of b lymphoblasts which are large rounded indented nuclei and three or four nuclei with thin layer of basophilic cytoplasm are closely opposed to each other forming dark blue background. So dark blue background is going to be your lymphoblast. The surrounding macrophages with abundant pale, so this is going to be your macrophages. Formy cytoplasm is scattered among the tumor cells, the stars. So that's going to be your tangible bodies. So these tangible bodies are scattered macrophages, phagocytosing the cell membrane in apoptotic cells. These are going to be present in our Burkitt lymphoma. That's our non-Hodgkin lymphoma neoplasm of mature B cells. Chronic lymphocytic leukemia. A lot of times students have hard time understanding these. So this is easy. Okay, what we have? These are lymphocytes with darkly staining nuclei and skin cytoplasm. Okay, these cells are, these are known as chronic lymphocytic leukemia cells. Now there is one cell over here, smudge cell. So what are those? This is because of fragile nature of the chronic lymphocytic leukemic cells. They frequently get smudged during spear smear preparation. Hence incubation with bovine serum albumin prior to smear preparation allows better preservation of your chronic lymphocytic leukemia cells. So what are smudge cells? These are ruptured chronic lymphocytic leukemic cells. They appear on the blood smear of sickle cell. Sorry, your chronic lymphocytic leukemic cells. Okay, so and they said that it's going to be an important biological correlation is there. So smudge cells, a lot of times they said that like you squeeze the donut and the jelly gets out of it. Next we have acute lymphoblastic leukemia. So we can see the blast are there also. So many immature lymphocytes over here, many immature lymphocytes. So the difference between acute lymphoblastic leukemia and your chronic lymphocytic leukemia is going to be smudge cells. Over here, we will see smudge cells. And if you don't see any smudge cells, that is going to be your acute lymphoblastic leukemia. So large and heterogeneous lymphoblast that is going to be consistent with pre B cell acute lymphoblastic leukemia. Next we have hairy cell leukemia. These are mature B cell tumor and they have filamentous hairy like projections. Okay, that's our hairy cell leukemia. Acute myelogenous leukemia. They have increased circulating myeloblast and the characteristic of this one is our roads. They are large crystalline cytoplasmic inclusion bodies and myeloperoxidase positive chronic myelogenous leukemia. This is characterized by unregulated growth of myeloid cells in the bone marrow, resulting in the presence of large number of mature and immature granulocytes in both the bone marrow and the blood. And it's the form of leukemia caused by chromosomal translocation known as Philadelphia chromosome. So Philadelphia chromosome is de facto and unusually short because of reciprocal translocation. So translocation is 922 and contains a fusion gene that's known as BCR ABL1. So the presence of this translocation is required for the diagnosis of chronic myelogenous leukemia. So now over here what can you see is to like a garden garden of mature and immature granulocytes. Okay, in essential thrombocytemia we are going to see platelet clumps. Okay, and they have a massive proliferation of megakaryocytes and platelets over here. So increased numbers of platelets which may be large or otherwise abnormally formed. Last, we have hemophagocytic lymphal histiocytosis. This is going to show us stromal macrophages that containing numerous red blood cells in their cytoplasm. So numerous red blood cells in their cytoplasms are going to be seen and hemophagocytosis is phagocytosis by histocytes of RBCs, leukocytes, platelets and their precursors in bone marrow in another tissue. This disorder is seen more often in children than in adults. It's a life-threatening disease of severe hyper inflammation that is going to be caused by uncontrolled proliferation of activated lymphocytes and macrophages characterized by proliferation of morphologically benign lymphocytes and macrophages. They are going to secrete high amounts of inflammatory cytokines. So in light microscopy we are going to see numerous RBCs in their cytoplasm. In whose cytoplasm? In our macrophages cytoplasm. Thank you everyone. I hope this video was a source of information for you. Thank you.