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Figure 9-4. (A) Pernicious anemia due to vitamin B12 deficiency caused by atrophic gastritis with decreased intrinsic factor production. Some RBCs are deformed as they pass through the splenic sinuses and appear teardrop shaped (dacryocytes). In addition, large neutrophils with a hypersegmenred nucleus (five to six lobes) can be observed (inset). (Reprinted with permission from Stiene-Martin EA, Lotspeich-Steininger CA, Koepke JA: Clinical Hematology, 2nd ed. Philadelphia, Lippincott, 1998, p 95. Inset reprinted with permission from Carr JH, Rodak BF: Clinical Hematology Atlas. Philadelphia, Saunders, 1999, p 143.) (B) Lead poisoning is shown in which the RBCs are microcytic, are hypochromic, and show basophilic stippling, which probably represents breakdown of ribosomes. Lead denatures sulfhydryl (SI I) groups in ferrochelatase within mitochondria that bind iron to protoporphyrin to form heme, thus inhibiting hemoglobin synthesis. As a result, unbound iron accumulates in mitochondria and forms ringed sideroblasts. (Reprinted with permission from Stiene-Martin EA, Lotspeich-Steininger CA, Koepke JA: Clinical Hematology, 2nd ed. Philadelphia, Lippincott, 1998, p 98.) (C) Iron deficiency anemia is shown with RBCs that are microcytic and hypochromic with a thin rim of l ib at the periphery. Iron deficiency is probably the most common nutritional disorder in the world. Iron is stored in the body as ferritin within the cytoplasm of cells and as hemosiderin within lysosomes. Some ferritin normally circulates in the plasma and is a good indicator of iron stores (iron deficiency: < 12 fig/1; iron overload: 5000 |xg/l). Iron is transported in the body mainly by transferrin, which is synthesized by the liver. The main function of transferrin is to deliver iron to cells, particularly to RBC precursors, which need iron for Hb synthesis. (Courtesy of Jean Shafer; Department of Medicine; University of Rochester from web site [email protected], Carden Jennings Publishing Co. Ltd.) (D) Howell-Jolly bodies after splenectomy. Howell-Jolly bodies represent nuclear fragments that arc normally removed from RBCs as they pass through the splenic sinuses. After splenectomy, increased numbers of RBCs with these inclusions are observed. (Reprinted with permission from Stiene-Martin EA, Lotspeich-Steininger CA, Koepke JA: Clinical Hematology, 2nd ed. Philadelphia, Lippincott, 1998, p 97.)

C. Spur cells in alcoholic cirrhosis, burr cells in kidney failure, target cells (Figure 9-5)

Figure 9-5. (A and B) Hemolytic anemia associated with alcoholic cirrhosis shows RBCs with a periphery consisting of sharp points called spur cells. (C ) Anemia associated with kidney failure (or renal insufficiency) shows RBCs with a periphery consisting of humps called burr cells. (D) Target cells (or codocytes) have a central dark area of Hb that is surrounded by a colorless ring followed by a peripheral rim of Hb. Target cells can be found in a number of pathologic states, including rhalassemia, obstructive liver disease, and iron deficiency. (Reprinted with permission from Stiene-Martin EA, Lotspeich-Steininger CA, Koepkc J A: Clinical Hematology, 2nd ed. Philadelphia, Lippincott, 1998, pp 92-93).

D. Chronic myeloid leukemia (Figure 9-6)

Figure 9-6. Chronic myeloid leukemia (CML). (A) Low-power light micrograph showing an increased number of granulocytes in all stages of maturation and many mature neutrophils. (B) Higher-power light micrograph showing neutrophils (N), metamyelocytes (M), myelocytes (ML), and promyelocytes (P). A characteristic finding in CML is the absence of alkaline phosphatase in granulocytes. The absence of alkaline phosphatase activity is used to distinguish CML from a leukemoid reaction. In 90% of CML cases, the Philadelphia (Ph) chromosome, which is a reciprocal translocation of DNA involving band q34 on chromosome 9 and band ql 1 on chromosome 22 |t(9;22)(q34;ql 1)], is found. This translocation results in the bcr-c-abl fusion gene, which codes for a protein with tyrosine kinase activity. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas of Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 179.)

Figure 9-6. Chronic myeloid leukemia (CML). (A) Low-power light micrograph showing an increased number of granulocytes in all stages of maturation and many mature neutrophils. (B) Higher-power light micrograph showing neutrophils (N), metamyelocytes (M), myelocytes (ML), and promyelocytes (P). A characteristic finding in CML is the absence of alkaline phosphatase in granulocytes. The absence of alkaline phosphatase activity is used to distinguish CML from a leukemoid reaction. In 90% of CML cases, the Philadelphia (Ph) chromosome, which is a reciprocal translocation of DNA involving band q34 on chromosome 9 and band ql 1 on chromosome 22 |t(9;22)(q34;ql 1)], is found. This translocation results in the bcr-c-abl fusion gene, which codes for a protein with tyrosine kinase activity. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas of Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 179.)

E. Chronic lymphocytic leukemia (Figure 9-7)

Figure 9-7. Chronic lymphocytic leukemia (CLL). (A) Low-power light micrograph showing an increased number of small, mature-looking R lymphocytes. (B) Higher-power light micrograph showing B lymphocytes with condensed nuclear chromatin and a high nucleusrcytoplasm ratio. CLL, which is the most common leukemia, is a disorder of mature (virgin) B cells that are unable to differentiate into plasma cells, causing hypogammaglobulinemia. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer IT-E, et al: An Atlas of Malignant Haematnlogy. Philadelphia, Lippincott-Raven, 1996, p 225.)

Figure 9-7. Chronic lymphocytic leukemia (CLL). (A) Low-power light micrograph showing an increased number of small, mature-looking R lymphocytes. (B) Higher-power light micrograph showing B lymphocytes with condensed nuclear chromatin and a high nucleusrcytoplasm ratio. CLL, which is the most common leukemia, is a disorder of mature (virgin) B cells that are unable to differentiate into plasma cells, causing hypogammaglobulinemia. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer IT-E, et al: An Atlas of Malignant Haematnlogy. Philadelphia, Lippincott-Raven, 1996, p 225.)

F. Hairy cell leukemia, Reed-Sternberg cells, Chediak-Higashi syndrome (Figure 9-8)

Figure 9-8. (A and B) Hairy cell leukemia. (A) B lymphocytes are shown with prominent cytoplasmic projections. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas oj Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 244 ) (B) Nomarski interference illumination clearly showing B lymphocytes with prominent cytoplasmic projections. Hairy cell leukemia is a relatively rare but distinctive form of chronic B lymphocyte leukemia that receives its name because of the distinctive feature of the cytoplasmic projections of the B lymphocyte. Massive splenomegaly is the most common physical finding. A positive tartrate-resistant acid phosphatase stain is a key to confirming the diagnosis. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas of Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 242.) (C) A Reed-Sternberg cell is a distinctive giant cell that is considered an essential neoplastic element in Hodgkin disease. The Reed-Sternberg cell is often binucleate or bilobed with a prominent nucleolus. (Reprinted with permission from Gatter K, Brown D: An Illustrated Guide to Bone Marrow Diagnosis. Maiden, MA, Blackwell Science, 1997, p 134.) (D) Chediak-Higashi syndrome is a genetic disease characterized by neutropenia and impaired phagocytosis of bacteria due to a defect in microtubule polymerization. Large abnormal lysosomes can be observed in the cytoplasm of a neutrophil. (Reprinted with permission Irom Carr JH, Rodak BF: Clinical Hematology Atlas. Philadelphia, Saunders, 1999, p 143.)

Figure 9-8. (A and B) Hairy cell leukemia. (A) B lymphocytes are shown with prominent cytoplasmic projections. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas oj Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 244 ) (B) Nomarski interference illumination clearly showing B lymphocytes with prominent cytoplasmic projections. Hairy cell leukemia is a relatively rare but distinctive form of chronic B lymphocyte leukemia that receives its name because of the distinctive feature of the cytoplasmic projections of the B lymphocyte. Massive splenomegaly is the most common physical finding. A positive tartrate-resistant acid phosphatase stain is a key to confirming the diagnosis. (Reprinted with permission from Mufti GJ, Flandrin G, Schaefer H-E, et al: An Atlas of Malignant Haematology. Philadelphia, Lippincott-Raven, 1996, p 242.) (C) A Reed-Sternberg cell is a distinctive giant cell that is considered an essential neoplastic element in Hodgkin disease. The Reed-Sternberg cell is often binucleate or bilobed with a prominent nucleolus. (Reprinted with permission from Gatter K, Brown D: An Illustrated Guide to Bone Marrow Diagnosis. Maiden, MA, Blackwell Science, 1997, p 134.) (D) Chediak-Higashi syndrome is a genetic disease characterized by neutropenia and impaired phagocytosis of bacteria due to a defect in microtubule polymerization. Large abnormal lysosomes can be observed in the cytoplasm of a neutrophil. (Reprinted with permission Irom Carr JH, Rodak BF: Clinical Hematology Atlas. Philadelphia, Saunders, 1999, p 143.)

Figure 9-9. Electron micrograph of a neutrophil. Although neutrophilic granules show considerable heterogeneity, two types are described: primary (azurophilic) granules, which are lysosomes, and secondary granules. Note the multilobed nucleus. (Courtesy of J. Parkin, University of Minnesota, Minneapolis, Minnesota)

Figure 9-9. Electron micrograph of a neutrophil. Although neutrophilic granules show considerable heterogeneity, two types are described: primary (azurophilic) granules, which are lysosomes, and secondary granules. Note the multilobed nucleus. (Courtesy of J. Parkin, University of Minnesota, Minneapolis, Minnesota)

Figure 9-10. Electron micrograph of an eosinophil. Note the conspicuous crystals within the granules. Although not apparent in this electron micrograph, the nucleus is bi-lobed. (Reprinted with permission from Fawcett DW: A Textbook of Histology, 12th ed. New York, Chapman Hall, 1994, p 197. Courtesy of Don W. Fawcett, M.D.)

Figure 9-10. Electron micrograph of an eosinophil. Note the conspicuous crystals within the granules. Although not apparent in this electron micrograph, the nucleus is bi-lobed. (Reprinted with permission from Fawcett DW: A Textbook of Histology, 12th ed. New York, Chapman Hall, 1994, p 197. Courtesy of Don W. Fawcett, M.D.)

I. Lymphocyte, plasma cell (Figure 9-11 ; see V E)

Figure 9-11. (A) Electron micrograph of a lymphocyte. (Courtesy of J. Parkin, University of Minnesota, Minneapolis, Minnesota). (B) Electron micrograph of a plasma cell. Although plasma cells secrete immunoglobulins (proteins), secretory granules are not observed. These cells possess a prominent Golgi complex, known as the Hof area (not clearly shown), and extensive rough endoplasmic reticulum (rER). Lymphocytes and plasma cells are related because B lymphocytes differentiate into plasma cells. (Reprinted with permission from Erlandscn SL, Magney JE: Human Histology: A Microfiche Atlas. Minneapolis, University of Minnesota Press, 1985.)

Figure 9-11. (A) Electron micrograph of a lymphocyte. (Courtesy of J. Parkin, University of Minnesota, Minneapolis, Minnesota). (B) Electron micrograph of a plasma cell. Although plasma cells secrete immunoglobulins (proteins), secretory granules are not observed. These cells possess a prominent Golgi complex, known as the Hof area (not clearly shown), and extensive rough endoplasmic reticulum (rER). Lymphocytes and plasma cells are related because B lymphocytes differentiate into plasma cells. (Reprinted with permission from Erlandscn SL, Magney JE: Human Histology: A Microfiche Atlas. Minneapolis, University of Minnesota Press, 1985.)

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