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HemOnc 05

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This is the progression in RBC maturation. As we go from the proerythroblast to the mature (anucleated) RBC, the cytoplasm goes from blue to pink (lots of mRNA with little protein to no mRNA and lots of hemoglobin), the nucleus becomes progressively smaller (until there is no nucleus in the reticulocyte stage), and the nuclear chromatin pattern becomes more condensed.

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This is an example of erythroid maturation. The big cell in the upper center (blue cytoplasm) is probably a proerythroblast. The cell to the right of it is probably a basophilic erythroblast. The cells to the upper left of the proerythroblast should be considered polychromatophilic erythroblasts. The small cells with dark nuclei below the proerythroblast are probably orthochromatic normoblasts.

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More erythroid maturation. The 4 cells in the center are probably basophilic normoblasts. The cell down and to the left of them are probably polychromatophilic. The cells to the upper right of center are probably orthochromatic. (Notice that I've been using the word "probably"- it's hard to be precise, and you're allowed to be one stage off.)

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This is a picture of early myeloid maturation. The arrow is pointing to a myeloblast, the earliest recognizable form in myeloid maturation.

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The cell in the center is a promyelocyte, usually the largest cell in myeloid maturation. The red granules are primary granules. By this point, the nucleolus in the nucleus should have disappeared.

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Mid myeloid maturation. The two cells in the center of the field are myelocytes. These contain secondary granules, and have a clear zone adjacent to the nucleus. This is the last dividing cell in the myeloid series.

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Late myeloid maturation. The black arrows point to metamyelocytes, and the red arrow to a band. You should already be able to recognize the poly.

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Megakaryocyte. This is the cell which produces platelets. It is the largest cell in the marrow, and it is huge (compare it to the surrounding cells, most of which are of the same size as the cells in the previous slides. In fact, this cell is so large and distinctive that it was rumored that the chairman of the Anatomy department where I went to medical school could actually find and recognize this cell on a slide!!)

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Normal bone marrow biopsy. The clear white spaces represents fat. As we get older, there are fewer cells, and more fat in the marrow. The big cell in the upper left hand corner is a megakaryocyte. The small cells with round dark nuclei are red cell precursors. You can probably also recognize the polys (when you click on the image to get the full size view). Notice that it is impossible to identify a specific cell, cell by cell, as you can on an aspirate smear. Looking at the biopsy is like looking at the forest, while looking at the aspirate is like looking at individual trees. They are complementary ways to evaluate a bone marrow specimen.

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Peripheral blood smear from iron deficiency anemia. Notice that the RBCs are smaller than the normal lymphocyte in the field (microcytic) and have an increased amount of central pallor (hypochromic). The cells also vary in size (anisocytosis) and shape (poikilocytosis).

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Bone marrow aspirate from a patient with iron deficiency anemia. Notice that the RBC precursors are a little less pink than they should be (not enough hemoglobin) and have a ragged cytoplasmic border.

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This is a peripheral blood smear from a case of anemia of chronic disease. Anemia of chronic disease may be either normochromic/ normocytic (as in this case) or hypochromic/ microcytic. Looking at this smear without clinical history or laboratory values, I would be unable to tell (1) that the patient was anemic, or (2) that something was wrong.

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Bone marrow aspirate smear from anemia of chronic disease. The smear is identical morphologically to that seen in iron deficiency anemia (slide 20).

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Iron stains from bone marrow aspirate smears. "Dr. Ben-Ezra, if slides 20 and 22 are morphologically identical, how do I make a diagnosis of iron deficiency anemia or anemia of chronic disease?" I am glad you asked the question. Remember that the problem with iron deficiency is that the patient does not have iron, whereas in anemia of chronic disease, the patient has plenty of iron, but just can't utilize it properly. Therefore, if you absolutely positively have to know whether the patient has iron stores in the bone marrow, you do an iron stain of the bone marrow aspirate. In this case, it is a prussian blue stain. The panel on the left has blue staining iron; the patient therefore has iron, and in this case, would have anemia of chronic disease. The panel on the right has no blue, therefore no iron stores. This patient therefore has iron deficiency anemia.

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Prussian blue stain of erythroblasts. If the blue had not washed out on these figures, you would see that the cells on the left had no iron, and therefore were indicative of iron deficiency, whereas the cell on the right had iron (sideroblast= RBC precursor with iron), and in this lab was indicative of anemia of chronic disease.

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This is a peripheral blood smear from a patient with megaloblastic anemia. Notice that the RBCs are large (macrocytic anemia) and oval shaped, and the the poly is hypersegmented.

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Bone marrow aspirate smear from a patient with megaloblastic anemia. Remember that the problem here is that folate/ Vitamin B12 are essential for DNA synthesis, but not for RNA/ protein synthesis. There is therefore maturation of the cytoplasm, but not of the nucleus. At any stage of erythroid maturation, the nucleus is less mature than it should be; this is termed nuclear/ cytoplasmic dyssyncrhony. The chromatin of the megaloblasts is clasically described as being "open" or "rope-like".

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More of the same (megaloblastic anemia). Notice how large the cells are (megaloblasts). This is because the cell grows and grows, but can't synthesize the DNA it needs for mitosis. Notice that several of the cells have fairly mature cytoplasm (the color is less blue and more pink) yet the nuclear chromatin is still open.

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Once again, BM aspirate from a patient with megaloblastic anemia. This time, look at the granulocytic series. Notice how big the metamyelocytes and bands are (I can here the 1930s music now).

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Methylene blue stain of peripheral blood. This is a retic stain. Reticulocytes are RBC precursors which have mRNA, and represent young RBCs. If the bone marrow is responding properly, it will detect a low RBC mass, and will act by stepping production of RBCs. This results in the release of more RBCs into theperipheral blood, reflected by an increase in the retic count.

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Peripheral smear from a case of Hereditary Spherocytosis. Notice that the RBCs are small, and have lost their central pallor. The loss of central pallor is due to the fact that these are spheres, and not biconcave discs. The MCV may either be low (due to the small size of the spherocytes) or normal (due to small spherocytes + larger reticulocytes).
Hereditary Spherocytosis has the clinical triad of anemia, jaundice, and splenomegaly. It is one of the most common genetic diseases in Caucasians (classically from Northern Europe). 80% of cases are autosomal dominant. The defect is in the RBC membrane proteins (spectrin, ankyrin, etc.) The diagnostic test you would want to order is the osmotic fragility test. Because they are spheres, the RBCs can't expand as much in hypotonic solutions as can normal RBCs (with the biconcave disc). Therefore, RBCs in hereditary spherocytosis have increased osmotic fragility.

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Peripheral smear from autoimmune hemolytic anemia (AIHA). The morphologic features here are very similar to HS. The predominant RBC is a small spherocyte. One (soft) clue to the correct diagnosis is that there is more of a dimorphic population of RBCs here as compared to the previous case- we are seeing both normal and abnormal cells here.
This disease is caused by antibody coating the RBCs. This causes either the cells to be taken out of circulation by the spleen/ RES system (extravascular hemolysis), or to the antibody binding complement and causing intravascular hemolysis (a catastrophic event). The diagnostic test you would want to order is the Coomb's test (also called the Direct Antibody Test). This is a test, performed by the blood bank, which detects antibodies (directly) on the RBCs.

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Sickle Cell Anemia. The pathognomonic finding in this peripheral blood smear is the sickle cell, an RBC with 2 pointed ends. Also notice the target cells (a nonspecific finding) and the polychromatophilic cells (the large purplish cells). These latter cells correspond to reticulocytes if we were to do a methylene blue stain (remember that this is a hemolytic disease, so we would expect to see an increased reticulocyte count).
The molecular basis for this disease is one base pair substitution in the 6th codon of the beta-globin chain gene. This causes one amino acid substitution, which changes the whole biochemistry profile of the protein. The cell irreversibly sickles upon deoxygenation, causing sludging, blockage of vessels, pain, etc.

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Another peripheral blood smear from a patient with sickle cell anemia. In addition to the sickled cell and the polychromasia, also notice the nucleated RBC, another sign that the patient is putting out young RBCs to keep up with the increased hemolysis.
If we did not see these signs of a reticulocytosis, we would get worried, because this may indicate that the patient is going into aplastic crisis. This condition, associated with Parvovirus B19 infection, results in total shutdown of RBC production, and a severe anemic state.

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In addition to the sickled and target cells, note the cell with the purple Howell Jolly body near the right edge of the picture. This inclusion is a remnant of DNA. Normally, the spleen would pick these cells out of the circulation. However, in sickle cell disease, the patients have autosplenectomized by age 6, so they do not have working spleens. Howell Jolly bodies are seen in anyone who does not have a spleen (e.g. spleen removed because of rupture from an automobile accident).
The diagnosis of sickle cell disease is made based on a solubility test (quick, dirty, and cheap- just tells us if Hemoglobin S is there, but does not differentiate between carrier [AS], sickle cell disease [SS], or some other syndrome such as SC disease) or a hemoglobin electrophoresis (tells us all hemoglobins the patient has, so can distinguish AS from SS from SC from CC etc.)

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Peripheral blood smear from a patient with Hemoglobin C disease. Hemoglobin C is another pathologic hemoglobin caused by a single base pair substitution in the 6th codon of the beta-globin chain (a different mutation that Hgb S). The patient has a genotype of CC (2 copies of the Hemoglobin C gene). These patients are not as symptomatic as those with sickle cell disease. Hemoglobin C cannot be picked up on a solubility test, but can be diagnosed by hemoglobin electrophoresis.

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This is from a case of SC disease. As the name implies, the patient has one gene from Hemoglobin S, and one for Hemoglobin C. These patients classically have "folded" or "rumpled" RBCs. Once again, these patients are not as symptomatic as those with sickle cell anemia (SS).

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Peripheral blood smear from a patient with thalassemia. Thalassemia is the imbalance of production between the various globin chains. Beta thalassemia is a reduction (or absence) of the beta chains, and alpha thalassemia is a reduction in the production of the alpha chains. It is usually a hypochromic/microcytic anemia. It has both a production failure component and a hemolytic component. Production failure occurs because the RBCs don't have sufficient globin chains to make hemoglobin. The hemolytic component occurs because the excess chain (alpha chains in the case of beta thal, beta chains in the case of alpha thal) precipitate in the RBC, and the spleen removes from circulation cells with precipitated proteins.

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Another case of thalassemia. (Whoever took this picture liked getting a picture of RBCs in the act of extruding their nuclei).

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Peripheral blood from a patient with DIC. Notice the schistocytes (RBC fragments) and the thrombocytopenia (low platelet count). This is an example of a microangiopathic hemolytic anemia (a big term for a hemolytic anemia caused by trauma to RBCs in small vessels). There is increased clot formation and fibrinolysis, resulting in bleeding (using up of coagulation factors) and/or thrombosis. It is seen in association with infections, neoplasia, or sometimes pregnancy.
An identical blood picture would be seen in TTP (thrombotic thrombocytopenia purpura). However, the coagulation studies in DIC would be abnormal, whereas they would be normal in TTP. To make the diagnosis of DIC, one would order fibrin split (degradation) products or a d-dimer, looking for evidence of cleavage of fibrin clots.

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Case of ITP. What is missing from this picture?? Platelets. In ITP, there is an antibody produced against platelets. The antibody binds to the platelets, and the antibody/platelet complex is removed by the spleen. One can sometimes order a Platelet IgG test to detect this antiplatelet antibody.
An identical blood picture would be seen in a patient who has no production of platelets from the bone marrow. Occasionally, we perform a bone marrow aspirate and biopsy to determine the cause of a thrombocytopenia. If we see lots of megakaryocytes, we assume that the marrow is producing enough platelets, but they are just being destroyed (or sequestered) in the periphery. If we don't see megakaryocytes, the problem is that the patient is not producing platelets. (Notice that the diagnostic scheme is very similar to anemias- there, based on the reticulocyte count, we divided the anemias into poor production vs. increased destruction. Once we know which branch of the anemia [or thrombocytopenia] pathology tree we are on, we can hone in the likely diagnosis.)
CD2 / CD3 are characteristic of what?
T cells
CD10, CD19, and CD20 are characteristic of what?
B cells
CD13 / CD33 are characteristic of what?
myeloid cells
which antigen is found in nearly all cases of acute leukemia?
CD34 ("stem cell antigen")

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Peripheral blood from a patient with acute lymphoblastic leukemia (ALL). These are blast cells. They have an open chromatin pattern and nucleoli. Looking at these cells, I probably could not tell whether they were ALL or AML cells, but I could tell that they were blast cells. Notice the lack of platelets.

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Bone marrow from a patient with ALL. Notice that the marrow is hypercellular, and is virtually replaced by blast cells. This crowds out the normal hematopoietic elements in the bone marrow, leading to the clinical triad of leukemia- anemia (no RBC precursors to produce RBCs), infection (although there are lots of white cells, they are all nonfunctional blasts) and bleeding (no megakaryocytes to produce platelets).

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TdT stain of ALL. There are several ways to distinguish ALL from AML. (1) Morphology (looking at the cells)- the least helpful. If you see an Auer rod ( see below ) it is AML, but otherwise you can't tell just by looking at the cells under the microscope. (You are usually more correct basing your diagnosis on the age of the patient rather than trying to guess based on morphology. If the patient is under 20, guess ALL; over 20, guess AML.)
(2) What enzymes the blast cells contain (cytochemistry)- Myeloid cells contain myeloperoxidase, so we can stain blast cells for myeloperoxidase and if they are positive it is an AML ( see below ). Lymphoblasts contain Terminal deoxytransferase in their nuclei, so if they nuclei are positive for TdT it is an ALL. (Just looking at this slide, I would not know that it is a stain for TdT, but being told that this is a stain for TdT, I would see the brown, know the stain is positive, and therefore make the [correct] diagnosis of ALL.)
(3) What antigens the blast cells express on their surface- Lymphoblasts express lymphoid, either B-cell (CD10, CD19) or T-cell (CD1, CD2, CD3, CD7) antigens on their surface, while myeloblast express myeloid antigens (CD13, CD33) on their surface. Therefore, one of best tests to order to determine whether an acute leukemia is ALL or AML is flow cytometry, where we determine which antigens are on the cell surface of the blast cells.

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L3 variant of ALL. One special subtype of ALL is the L3 subtype. The cytoplasm is blue, and is vacuolated. This is the leukemic (peripheral blood and bone marrow) counterpart to Burkitt's lymphoma (see Lab 8). The leukemia has a mature B-cell phenotype (expresses either kappa or lambda light chains) and usually is associated with EBV. It has a translocation of the c-myc gene on chromosome 8 to the immunoglobulin heavy chain gene on chromosome 14 [t (8;14)].

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Smear from a case of Acute Myelogenous Leukemia (AML). I am able to tell that this is a case of AML because of the Auer rod (the red rod shaped thing in the big cell towards 1 o'clock) in one of the blast cells. Auer rods are crystallized primary granules. When you see it, it is an AML; unfortunately, only a minority of cases of AML contain Auer rods.

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Myeloperoxidase stain of AML. There is no way looking at this figure that I could say that this is a myeloperoxidase stain, but being told that this is a stain for myeloperoxidase, I would see the brown positive staining, and I would make the correct diagnosis of AML. Notice that the stain brings out some of the Auer rods. This is because Auer rods are crystallized primary granulocytic granules, which contain myeloperoxidase.

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Acute Promyelocytic Leukemia (FAB M3). This is a special subtype of AML. It is comprised primarily of promyelocytes (not blast cells), and often will have cells which contain multiple Auer rods (faggot cells [faggot= bundle of sticks]). It is important to recognize this variant because (1) patients with APL are prone to develop DIC; (2) it is associated with the t(15;17) translocation, and (3) the patients are treated with trans-retinoic acid (ATRA) as opposed to standard AML chemotherapy. The translocation of chromosome 17 involves the retinoic acid receptor gene, and the defect here is one of differentiation. Giving the patients ATRA helps the neoplastic cells differentiate towards polys.

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Acute Erythroleukemia (FAB M6). Another variant of AML. If you recall back to the CFU-GEMM, it can differentiate to granulocytes, erythroid cells, monocytes, or megakaryocytes. We therefore can have AMLs derived from granulocytes, erythroid cells, monocytes, or megakaryocytes. Notice that these neoplastic cells resemble erythroid precursors.

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Low power photomicrograph of peripheral blood with CML. The only thing that I want you to be able to recognize in this picture is that the white cell count is elevated.

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Peripheral blood smear from a case of CML. As compared to the AML seen in the previous lab, notice that here very few of the cells (if any) are blast cells. Chronic leukemias are characterized by a proliferation of more mature cells; in the case of CML, most of the cells are myelocytes or more mature cells. Also notice the increase in basophils, a finding common in CML.

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Bone Marrow aspirate smear from CML. Notice that (1) the marrow is hypercellular; (2) almost all the cells are granulocytic- we are not seeing a normal amount of erythroid cells (~20%); and (3) that the myeloid cells present are basically myelocytes and beyond; the sheets of blast cells characteristic of the acute leukemias is not present. Although one may see some blast cells in CML, it is usually in the 1-5% range, not the 80-100% range of acute leukemia.

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Low power picture of bone marrow biopsy of CML. The only thing to observe here is that the marrow is hypercellular; the cellularity is approximately 100%. The normal component of fat seen in the normal biopsy (remember lab 1?) is not present.

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Higher power picture of bone marrow biopsy from CML. The thing to notice is what we are not seeing ("and then there was the curious matter of the dog barking in the night..."); we are not seeing sheets of blast cells. The cells present are almost all myeloid cells at the myelocyte stage or mature mature. We are also not seeing erythroid cells (the small dark blue cells from lab 1).

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Peripheral blood smear from a leukemoid reaction. Once again, the only thing to really notice here is the increased WBC count.

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Peripheral blood smear from leukemoid reaction. We are seeing immature and mature white blood cells

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Another high power picture of peripheral blood with a leukemoid reaction.
A leukemoid reaction is basically the bone marrow putting out a lot of white blood cells, many of them less than mature, in reaction to stress (most commonly infection). This is a reactive, not neoplastic, proliferation of cells. It is important to recognize a leukemoid reaction because it is a common differential diagnosis for CML. Both a leukemoid reaction and CML will have an increased WBC count, and in both the cells will be predominantly granulocytes from the myelocyte to poly stage. In both, there may occasional (but not a lot of) blast cells. Some tests to help us differentiate between the two are:
(1) t (9;22)- CML must have a translocation between the abl oncogene on chromosome 9 to the bcr gene on chromosome 22. This can be detected either by classic cytogenetics or by molecular techniques (PCR). A leukemoid reaction will not have this translocation.
(2) Leukocyte Alkaline Phosphatase (LAP)- Normal granulocytes contain an enzyme called LAP. Granulocytes from a leukemoid reaction have a lot of this enzyme. For some reason (which I don't know), the granulocytes from CML have very little of this enzyme. Therefore, one can ask the lab to do an LAP score; if it is low, think CML, whereas if it is normal to high, think leukemoid reaction. (This test is not that specific and it is tech intensive, so I try to steer people to the PCR test instead of the LAP, but there are situations where it is helpful.)
(3) Examine and talk to the patient (not something that I do often as a pathologist- notice the small font)- if the patient has an obvious source of infection, think leukemoid reaction. If the patient does not have an infection and has a large spleen (almost always present in CML) think CML.
Notice that I have not put flow cytometry on this list. Flow is excellent for distinguishing myeloid from lymphoid cells. In this case, we already know that the cells are myeloid, so flow is not going to help us.

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Bone marrow biopsy with myelofibrosis. Notice that the marrow is hypercellular and that there is a lot of space between cells. This is due to fibrosis within the marrow. In myelofibrosis, the fibrotic process crowds out normal hematopoietic elements, and the hematopoietic cells take up residence elsewhere (extramedullary hematopoiesis), most commonly in the spleen. Remember that the spleen was a hematopoietic site during fetal development, so its environment is hospitable to hematopoietic stem cells.

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Reticulin stain of bone marrow biopsy in myelofibrosis. This stain brings out the reticulin fibrosis. Myelofibrosis is usually a reaction to something, whether it be to chemicals or as part of a myeloproliferative syndrome such as CML.

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Peripheral blood smear from myelofibrosis. Notice the teardrop shaped RBCs. As the RBCs are released by the bone marrow, they have to squeeze between the reticulin fibers, causing them to become misshapen. You can do the same thing experimentally by squeezing blood through a 30 gauge needle (very small opening).

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Low power picture of peripheral blood smear involved by CLL. Once again, the only thing to notice here is that the WBC count is increased.

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High power of peripheral blood involved by CLL. Notice that the cells here are all mature appearing lymphocytes. CLL is a neoplastic proliferation of mature B cells. Morphologically, on a cell by cell basis, these are indistinguishable from the normal lymphocytes you would see in my blood. We know that this is CLL because (1) there are a lot of them, and (2) we can perform immunologic testing to show that they are monoclonal B cells

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Bone Marrow aspirate from CLL. Notice that almost all the cells here are small mature lymphoid cells. The neoplastic process has overrun the bone marrow, crowding out the normal hematopoietic elements, leading to.....anemia, infections, and bleeding.

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Bone marrow biopsy from CLL. Notice that there are sheets of lymphoid cells replacing the normal hematopoietic elements. CLL is the leukemic counterpart to Small Lymphocytic Lymphoma.

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Bone marrow aspirate from multiple myeloma. Multiple myeloma is a neoplastic proliferation of plasma cells. In addition to the usual "leukemic" effects of crowding out normal bone marrow elements, there are a few unique features to multiple myeloma with which you should be familiar.
(1) Plasma cells produce immunoglobulins. A neoplastic proliferation of plasma cells produces a lot of immunoglobulin. Since it is derived from a neoplastic clone, the immunoglobulin is monoclonal. This can be detected with serum protein electrophoresis (SPEP).
(2) The neoplastic proliferations of plasma cells in the bone marrow lead to lytic lesions in the bones. This in turn may lead to bone fractures. It also provides us with another diagnostic test for multiple myeloma- a skeletal survey looking for lytic bone lesions.
(3) Patients with multiple myeloma are prone to develop renal failure. This can be due to (a) deposition of amyloid para- protein in the kidney, and/ or (2) the presence of the abnormal protein (especially the light chains) in the renal tubules. These abnormal monoclonal light chains in the urine are called Bence Jones proteins.

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Bone marrow biopsy from multiple myeloma. Sheets of plasma cells are present.

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Peripheral blood smear from a patient with multiple myeloma. Notice how the RBCs are stacking up, one upon the other. This is called rouleaux formation. It is a nonspecific reaction to the increased protein in the plasma.
Hodgkin's Disease is characterized by the presence of which cells?
Reed-Sternberg cells
which is more common: NHL or Hodgkin's?
NHL (NHL:Hodg = 2:1)
what infectious agent can cause Burkitt's lymphoma?
EBV
what infectious agent can cause T-cell lymphoma/leukemia?
HTLV-1
what chemicals/drugs can potentially cause Non-Hodgkin's Lymphoma?
benzene, dioxins, phenytoin, chemotherapy
discuss the staging of NHL and Hodgkin's
Stage I: one nodal group above or below the diaphragm

Stage II: more than one nodal group above or below the diaphragm

Stage III: involvement above AND below the diaphragm

Stage IV: extensive disease (bone marrow involvement)
compare the spread of HD vs. NHL
Hodgkin's: orderly spread by contiguity

NHL: more random spread, probably via blood
is extranodal presentation common in HD or NHL?
NHL
Hodgkin's Disease treatment
Stage I -- radiation

Stage II-IV -- chemo+radiation

if early relapse -- high dose chemo with BMT
diagnosis of NHL
neoplastic clones of lymphocytes arrested at or arising from discrete stages of normal lymphoid differentiation (most from B cells)
clinical presentation of lymphoid malignancies
weight loss, fever, night sweats

lymphadenopathy, fatigue, anemia
lymphadenopathy: when to biopsy
Any new node of >1 cm diameter not associated with documented infection, which persists longer than 4-6 weeks.
lymphoid system consists of what?
circulating T and B lymphocytes and the lymphoid organs (lymph codes, thymus, spleen, tonsils, and adenoids)
where do T-lymphocytes undergo differentiation?
in the thymus
where do B-lymphocytes develop?
in the marrow
what is the most differentiated cell of the B-cell system?
the plasma cell
what is the major function of lymph nodes?
to detect and inactivate foreign antigens arriving via lymphatics
spleen -- consists of what two components?
consists of filtering component (red pulp) and lymphoid component (white pulp)
T/F Lymphomas are clonal
T
most NHLs of children are of what grade?
high grade (i.e. aggressive)
T/F All B-NHLs demonstrate clonal rearrangement of the immunoglobulin gene
T (detectable by Southern blot of PCR)
what is the cell of origin of follicular lymphoma?
B follicular center cell
90% of FLs express which translocation?
t(14;18)
FL / Bcl-2
all FLs over-express Bcl-2, which blocks apoptotic cell death
Burkitt Lymphoma translocation
translocation of the MYC gene on chromosome 8 to the Ig heavy chain on chromosome 14
Follicular Lymphoma (FL)
Follicular Lymphoma (FL) -- effacement of nodal architecture by a proliferation of neoplastic follicular nodules; CD20+, CD10+, and abundant monotypic surface immunoglobulin
B-Small Lymphocytic Lymphoma (B-SLL)
B-Small Lymphocytic Lymphoma (B-SLL) -- diffuse effacement by a proliferation of small lymphocytes with round nuclei and dense chromatin (low-grade); CD20, CD5, CD23, and weak surface immunoglobulin
Diffuse Large B-cell Lymphoma (DLBCL)
Diffuse Large B-cell Lymphoma (DLBCL) -- diffuse proliferation of large neoplastic B-lymphoid cells; CD20+ and surface immunoglobulin
Burkitt Lymphoma (BL)
Burkitt Lymphoma (BL) -- highly aggressive lymphoma which occurs in children as well as adults (endemic in African children); diffuse proliferation of small noncleaved cells with a very high mitotic rate, and a background of "starry sky" macs; EBV plays important role in pathogenesis; CD20+, CD10+, and surface immunoglobulin positive
MALT Lymphoma
MALT Lymphoma -- usually low-grade lymphomas of adults that arise in extranodal lymphoid tissue, especially in the GI tract and lung
T-Lymphoblastic Lymphoma (T-LL)
T-Lymphoblastic Lymphoma (T-LL) -- rapidly growing anterior mediastinal mass in young patients, most often male, who may have respiratory or cardiovascular compromise and pleural or pericardial effusions; disseminate; tumor cells have a blastic appearance with a high nuclear to cytoplasmic ratio, finely dispersed chromatin, and inconspicuous nucleoli; thymic tissue is effaced by a diffuse growth of these monomorphic tumor cells that have a high mitotic rate; and invade the capsule
Mycosis Fungoides (MF)
Mycosis Fungoides (MF) -- tumor of small, skin-based T cells, predominantly of the CD4+ subset that occurs in adults; band-like superficial dermal infiltrate adjacent to, and invading the epidermis (epidermotropism) with formation of small collections of lymphocytes in the epidermis (Pautrier's microabscess); lymphocytes have a characteristic folded, cerebriform nucleus
Peripheral T-cell Lymphoma (PTCL)
Peripheral T-cell Lymphoma (PTCL) -- T-phenotype with loss or aberrent expression of pan T-cell antigens
Reed-Sternberg (RS) cell
diagnostic of Hodgkin Lymphoma

large binucleate cell with dispersed chromatin, inclusion-like macronuclei, and abundant eosinophilic cytoplasm
what is the characteristic immunophenotype of RS cells?
LeuM1(CD15)+, Ki-1(CD30)+, and LCA(CD45)-
what are the four types of HL?
(1) Nodular Sclerosis (NS)

(2) Mixed Cellularity (MC)

(3) Lymphocyte Depletion (LD)

(4) Lympocyte Predominance (LP)
is Nodular Sclerosis more common in young / old, male / female?
young adult females
Nodular Sclerosis (NS)
Nodular Sclerosis (NS) -- cervical adenopathy and/or a mediastinal mass; capsular fibrosis, and dense bands of connective tissue that efface nodal architecture and give a nodular appearance; most RS cells have a lacunar appearance where the cytoplasm retracts against the nucleus, giving the appearance of a hole or lacuna
lymphoma definition
Malignant proliferation of lymphoid cells
outside of the bone marrow
are high grade lymphomas seen in children or adults?
Both
are low grade lymphomas seen in children or adults?
adults
compare high and low grade lymphomas with regards to mitotic rate
high grade --> high mitotic rate

low grade --> low mitotic rate
of low grade and high grade lymphomas, which can be cured with chemotherapy?
high grade
can high grade lymphomas be seen in blood?
no, but low grade can
time new roman
time new roman

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