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65 Cards in this Set

  • Front
  • Back
Marrow smear from a patient with hemolytic anemia. The marrow reveals greatly increased numbers of maturing erythroid progenitors (normoblasts).
Hereditary spherocytosis (peripheral smear). Note the anisocytosis and several dark-appearing spherocytes with no central pallor. Howell-Jolly bodies (small dark nuclear remnants) are also present in red cells of this asplenic patient
G6PD deficiency: effects of oxidant drug exposure (peripheral blood smear). Inset, Red cells with precipitates of denatured globin (Heinz bodies) revealed by supravital staining. As the splenic macrophages pluck out these inclusions, "bite cells" like the one in this smear are produced.
Sickle cell disease (peripheral blood smear). A, Low magnification shows sickle cells, anisocytosis, and poikilocytosis.
Sickle cell disease (peripheral blood smear). A, Low magnification shows sickle cells, anisocytosis, and poikilocytosis. B, Higher magnification shows an irreversibly sickled cell in the center.
A, Spleen in sickle cell disease (low power). Red pulp cords and sinusoids are markedly congested; between the congested areas, pale areas of fibrosis resulting from ischemic damage are evident.
A, Spleen in sickle cell disease (low power). B, Under high power, splenic sinusoids are dilated and filled with sickled red cells.
"Autoinfarcted" splenic remnant in sickle cell disease.
Microangiopathic hemolytic anemia. A peripheral blood smear from a person with hemolytic-uremic syndrome shows several fragmented red cells
Megaloblastic anemia. A peripheral blood smear shows a hypersegmented neutrophil with a six-lobed nucleus.
Megaloblastic anemia (bone marrow aspirate). A to C, Megaloblasts in various stages of differentiation. Note that the orthochromatic megaloblast (B) is hemoglobinized (as revealed by cytoplasmic color), but in contrast to normal orthochromatic normoblasts, the nucleus is not pyknotic. The early erythroid precursors (A,C) and the granulocytic precursors are also large and have abnormally immature chromatin.
Hypochromic microcytic anemia of iron deficiency (peripheral blood smear). Note the small red cells containing a narrow rim of peripheral hemoglobin. Scattered fully hemoglobinized cells, present due to recent blood transfusion, stand in contrast.
Aplastic anemia (bone marrow biopsy). Markedly hypocellular marrow contains mainly fat cells. A, Low power; B, high power.
Aplastic anemia (bone marrow biopsy). Markedly hypocellular marrow contains mainly fat cells. A, Low power; B, high power.
Reactive changes in neutrophils. Neutrophils containing coarse purple cytoplasmic granules (toxic granulations) and blue cytoplasmic patches of dilated endoplasmic reticulum (Döhle bodies, arrow) are observed in this peripheral blood smear prepared from a patient with bacterial sepsis.
Follicular hyperplasia. A, Low-power view showing a reactive follicle and surrounding mantle zone. The dark-staining mantle zone is more prominent adjacent to the germinal-center light zone in the left half of the follicle. The right half of the follicle consists of the dark zone.
Follicular hyperplasia.. B, High-power view of the dark zone shows several mitotic figures and numerous macrophages containing phagocytosed apoptotic cells (tingible bodies).
A, Acute lymphoblastic leukemia/lymphoma. Lymphoblasts with condensed nuclear chromatin, small nucleoli, and scant agranular cytoplasm.
A, Acute lymphoblastic leukemia/lymphoma. Lymphoblasts with condensed nuclear chromatin, small nucleoli, and scant agranular cytoplasm. B and C represent the phenotype of the ALL shown in A, analyzed by flow cytometry. B, Note that the lymphoblasts represented by the red dots express terminal deoxynucleotidyl-transferase (TdT) and the B-cell marker CD22. C, The same cells are positive for two other markers, CD10 and CD19, commonly expressed on pre-B lymphoblasts. Thus, this is a B-ALL.
Small lymphocytic lymphoma/chronic lymphocytic leukemia (lymph node). A, Low-power view shows diffuse efface-ment of nodal architecture.
Small lymphocytic lymphoma/chronic lymphocytic leukemia (lymph node). B, At high power the majority of the tumor cells are small round lymphocytes. A "prolymphocyte," a larger cell with a centrally placed nucleolus, is also present in this field (arrow).
Chronic lymphocytic leukemia. This peripheral blood smear is flooded with small lymphocytes with condensed chromatin and scant cytoplasm. A characteristic finding is the presence of disrupted tumor cells (smudge cells). A coexistent autoimmune hemolytic anemia (Chapter 14) explains the presence of spherocytes (hyperchromatic, round erythrocytes). A nucleated erythroid cell is present in the lower left-hand corner of the field. In this setting, circulating nucleated red cells could stem from premature release of progenitors in the face of severe anemia, marrow infiltration by tumor (leukoerythroblastosis), or both.
Small lymphocytic lymphoma/chronic lymphocytic leukemia involving the liver. Low-power view of a typical periportal lymphocytic infiltrate.
Follicular lymphoma (lymph node). A, Nodular aggregates of lymphoma cells are present throughout lymph node.
Follicular lymphoma (lymph node). B, At high magnification, small lymphoid cells with condensed chromatin and irregular or cleaved nuclear outlines (centrocytes) are mixed with a population of larger cells with nucleoli (centroblasts).
Follicular lymphoma (spleen). Prominent nodules represent white pulp follicles expanded by follicular lymphoma cells. Other indolent B-cell lymphomas (small lymphocytic lymphoma, mantle cell lymphoma, marginal zone lymphoma) can produce an identical pattern of involvement.
BCL2 expression in reactive and neoplastic follicles. BCL2 protein was detected by using an immunohistochemical technique that produces a brown stain. In reactive follicles (A), BCL2 is present in mantle zone cells but not follicular-center B cells, whereas follicular lymphoma cells (B) show strong BCL2 staining.
Diffuse large B-cell lymphoma. Tumor cells have large nuclei, open chromatin, and prominent nucleoli
Diffuse large B-cell lymphoma involving the spleen. The isolated large mass is typical. In contrast, indolent B-cell lymphomas usually produce multifocal expansion of white pulp (see Fig. 13-11).
Burkitt lymphoma. A, At low power, numerous pale tingible body macrophages are evident, producing a "starry sky" appearance.
Burkitt lymphoma. B, At high power, tumor cells have multiple small nucleoli and high mitotic index. The lack of significant variation in nuclear shape and size lends a monotonous appearance.
Multiple myeloma of the skull (radiograph, lateral view). The sharply punched-out bone lesions are most obvious in the calvarium.
Multiple myeloma (bone marrow aspirate). Normal marrow cells are largely replaced by plasma cells, including forms with multiple nuclei, prominent nucleoli, and cytoplasmic droplets containing Ig.
Lymphoplasmacytic lymphoma. Bone marrow biopsy shows a characteristic mixture of small lymphoid cells exhibiting various degrees of plasma cell differentiation. In addition, a mast cell with purplish red cytoplasmic granules is present at the left-hand side of the field.
Mantle cell lymphoma. A, At low power, neoplastic lymphoid cells surround a small, atrophic germinal center, producing a mantle zone pattern of growth.
Mantle cell lymphoma. B, High-power view shows a homogeneous population of small lymphoid cells with somewhat irregular nuclear outlines, condensed chromatin, and scant cytoplasm. Large cells resembling prolymphocytes (seen in chronic lymphocytic leukemia) and centroblasts (seen in follicular lymphoma) are absent.
Hairy cell leukemia (peripheral blood smear). A, Phase-contrast microscopy shows tumor cells with fine hairlike cytoplasmic projections.
Hairy cell leukemia (peripheral blood smear). B, In stained smears, these cells have round or folded nuclei and modest amounts of pale blue, agranular cytoplasm.
Peripheral T-cell lymphoma, unspecified (lymph node). A spectrum of small, intermediate, and large lymphoid cells, many with irregular nuclear contours, is visible.
Anaplastic large-cell lymphoma. A, Several "hallmark" cells with horseshoe-like or "embryoid" nuclei and abundant cytoplasm lie near the center of the field.
Anaplastic large-cell lymphoma. B, Immunohistochemical stain demonstrating the presence of ALK fusion protein.
Reed-Sternberg cells and variants. A, Diagnostic Reed-Sternberg cell, with two nuclear lobes, large inclusion-like nucleoli, and abundant cytoplasm, surrounded by lymphocytes, macrophages, and an eosinophil.
Reed-Sternberg cells and variants. B, Reed-Sternberg cell, mononuclear variant.
Reed-Sternberg cells and variants. . C, Reed-Sternberg cell, lacunar variant. This variant has a folded or multilobated nucleus and lies within a open space, which is an artifact created by disruption of the cytoplasm during tissue sectioning.
Reed-Sternberg cells and variants. D, Reed-Sternberg cell, lymphohistiocytic variant. Several such variants with multiply infolded nuclear membranes, small nucleoli, fine chromatin, and abundant pale cytoplasm are present.
Hodgkin lymphoma, nodular sclerosis type. A low-power view shows well-defined bands of pink, acellular collagen that subdivide the tumor into nodules.
Hodgkin lymphoma, mixed-cellularity type. A diagnostic, binucleate Reed-Sternberg cell is surrounded by reactive cells, including eosinophils (bright red cytoplasm), lymphocytes, and histiocytes.
Hodgkin lymphoma, lymphocyte predominance type. Numerous mature-looking lymphocytes surround scattered, large, pale-staining lymphohistiocytic variants ("popcorn" cells).
A, Acute myeloid leukemia without maturation (FAB M1 subtype). B, In the flow cytometric analysis shown, the myeloid blasts, represented by the red dots, express CD34, a marker of multipotent stem cells, but do not express CD64, a marker of mature myeloid cells. C, The same myeloid blasts express CD33, a marker of immature myeloid cells, and a subset express CD15, a marker of more mature myeloid cells. Thus, these blasts are myeloid cells showing limited maturation.
Acute myeloid leukemia subtypes. A, Acute promyelocytic leukemia with the t(15;17) (FAB M3 subtype). Bone marrow aspirate shows neoplastic promyelocytes with abnormally coarse and numerous azurophilic granules. Other characteristic findings include the presence of several cells with bilobed nuclei and a cell in the center of the field that contains multiple needle-like Auer rods.
Acute myeloid leukemia subtypes. A, Acute promyelocytic leukemia with the t(15;17) (FAB M3 subtype). Bone marrow aspirate shows neoplastic promyelocytes with abnormally coarse and numerous azurophilic granules. Other characteristic findings include the presence of several cells with bilobed nuclei and a cell in the center of the field that contains multiple needle-like Auer rods.
Acute myeloid leukemia subtypes. B, Acute myeloid leukemia with monocytic differentiation (FAB M5b subtype). Peripheral smear shows one monoblast and five promonocytes with folded nuclear membranes.
Myelodysplasia. Characteristic forms of dysplasia are shown. A, Nucleated red cell progenitors with multilobated or multiple nuclei. Marrow aspirates
Myelodysplasia. Characteristic forms of dysplasia are shown. B, Ringed sideroblasts, erythroid progenitors with iron-laden mitochondria seen as blue perinuclear granules (Prussian blue stain). Marrow aspirate
Myelodysplasia. Characteristic forms of dysplasia are shown. C, Pseudo-Pelger-Hüet cells, neutrophils with only two nuclear lobes instead of the normal three to four, are observed at the top and bottom of this field. peripheral blood smear.)
Myelodysplasia. Characteristic forms of dysplasia are shown. D, Megakaryocytes with multiple nuclei instead of the normal single multilobated nucleus. Marrow aspirate
Chronic myeloid leukemia. Peripheral blood smear shows many mature neutrophils, some metamyelocytes, and a myelocyte.
Chronic myeloid leukemia (spleen). Enlarged spleen (2630 gm; normal: 150-200 gm) with greatly expanded red pulp stemming from neoplastic hematopoiesis.
Polycythemia vera, spent phase. Massive splenomegaly (3020 gm; normal: 150-200 gm) largely due to extramedullary hematopoiesis occurring in the setting of advanced marrow myelofibrosis.
Essential thrombocytosis. Peripheral blood smear shows marked thrombocytosis, including giant platelets approximating the size of surrounding red cells.
Primary myelofibrosis (peripheral blood smear). Two nucleated erythroid precursors and several teardrop-shaped red cells (dacryocytes) are evident. Immature myeloid cells were present in other fields. An identical picture can be seen in other diseases producing marrow distortion and fibrosis.
Langerhans cell histiocytosis. A, Langerhans cells with folded or grooved nuclei and moderately abundant pale cytoplasm are mixed with a few eosinophils. B, An electron micrograph shows rodlike Birbeck granules with characteristic periodicity and dilated terminal end.
Splenic infarcts. Multiple well-circumscribed infarcts are present in this spleen, which is massively enlarged (2820 gm; normal: 150-200 gm) by extramedullary hematopoiesis secondary to a myeloproliferative disorder (myelofibrosis). Recent infarcts are hemorrhagic, whereas older, more fibrotic infarcts are a pale yellow-gray color.
Thymoma. A, Benign thymoma (medullary type). The neoplastic epithelial cells are arranged in a swirling pattern and have bland, oval to elongated nuclei with inconspicuous nucleoli. Only a few small, reactive lymphoid cells are interspersed.
Thymoma. B, Malignant thymoma, type I. The neoplastic epithelial cells are polygonal and have round to oval, bland nuclei with inconspicuous nucleoli. Numerous small, reactive lymphoid cells are interspersed. The morphologic appearance of this tumor is identical to that of benign thymomas of the cortical type. In this case, however, the tumor was locally aggressive, invading adjacent lung and pericardium.