Color Atlas of Hematology - Practical Microscopic and Clinical ...

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106Abnormalities of the White Cell SeriesMyelodysplasia (MDS)Clinical practice has long been familiar with the scenario in which, afteryears of bone marrow insufficiency with a more or less pronounced deficitin all three cell series (tricytopenia), patients pass into a phase of insidiouslyincreasing blast counts and from there into frank leukosis—although the evolution may come to a halt at any of these stages. Thetransitions between the forms of myelodysplastic syndromes are veryfluid, and they have the following features in common:➤ Anemia, bicytopenia, or tricytopenia without known cause.➤ Dyserythropoiesis with sometimes pronounced erythrocyte anisocytosis;in the bone marrow often megaloblastoid cells and/or ring sideroblasts.➤ Dysgranulopoiesis with pseudo-Pelger-Huët nuclear anomaly (hyposegmentation)and hypogranulation (often no peroxidase reactivity) ofsegmented and band granulocytes in blood and bone marrow.➤ Dysmegakaryopoiesis with micromegakaryocytes.The FAB classification is the best-known scheme so far for organizing thedifferent forms of myelodysplasia (Table 17).Table 17Forms of myelodysplasiaForm of myelodysplasia Blood analysis Bone marrowRA = refractory anemiaRAS = refractory anemiawith ring sideroblasts( aquiredidiopathic sideroblasticanemia, p. 137)RAEB = refractory anemiawith excess ofblastsAnemia (normochromicor hyperchromic);possiblypseudo-Pelger granulocytes;blasts 1%Hypochromic andhyperchromic erythrocytesside by side,sometimes discretethrombopenia andleukopenia; pseudo-Pelger cellsOften thrombocytopeniain addition toanemia; blasts 5%,monocytes 1000/µl,pseudo-Pelger syndromeDyserythropoiesis(marginal dysgranulopoiesisand dysmegakaryopoiesis 10%) 5% blastsMore than 15% of thered cell precursors arering sideroblasts;blasts 5%Erythropoietic hyperplasia(with or withoutring sideroblasts);5–20% blastsCont. p. 108
In unexplained anemia and/or leukocytopenia and/or thrombocytopenia,blood cell abnormalities may indicate myelodysplasiaabcdeFig. 36 Myelodysplasia and CMML. a–d Different degrees of abnormal maturation(pseudo-Pelger type); the nuclear density can reach that of erythroblasts(d). The cytoplasmic hypogranulation is also observed in normal segmented granulocytes.These abnormalities are seen in myelodysplasia or after chemotherapy,among other conditions. e Blood analysis in CMML: monocytes (1), promyelocyte(2), and pseudo-Pelger cell (3). Thrombocytopenia.107
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iiiColor Atlas of HematologyPractic
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vPrefaceOur Current EditionAlthough
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viiContentsPhysiology and Pathophys
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ContentsixAcute Lymphoblastic Leuke
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2Physiology and Pathophysiology of
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Normal Cells of the Blood andHemato
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Normally erythropoiesis takes place
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34Normal Cells of the Blood and Hem
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Advancing nuclear contraction and s
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Note the granulations, inclusions,
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Page 66 and 67: 56Normal Cells of the Blood and Hem
Page 68 and 69: 58Normal Cells of the Blood and Hem
Page 71 and 72: Abnormalities of the White Cell Ser
Page 73 and 74: Predominance of Mononuclear Round t
Page 77 and 78: During lymphatic reactive states, v
Page 79 and 80: Extreme transformation of lymphocyt
Page 85 and 86: Monotonous proliferation of small l
Page 87 and 88: Atypical lymphocytes are not part o
Page 89 and 90: Deep nuclear indentation suggests f
Page 91 and 92: Cytoplasmic processes the main feat
Page 93 and 94: Plasmacytoma cannot be diagnosed wi
Page 95 and 96: Atypias and differential diagnoses
Page 97 and 98: Bone marrow diagnosis is indicated
Page 99 and 100: Conspicuously large numbers of mono
Page 107 and 108: Fundamental characteristic of acute
Page 109 and 110: The diagnosis of acute leukemia is
Page 111 and 112: Acute leukemias may also derive fro
Page 113 and 114: New WHO classification: AML with dy
Page 115: The cells in acute lymphocytic leuk
Page 119 and 120: The classification of myelodysplasi
Page 121 and 122: Prevalence of Polynuclear (Segmente
Page 123 and 124: Predominance of the granulocytic li
Page 125 and 126: Prevalence of Polynuclear (Segmente
Page 127 and 128: Left shift as far as myeloblasts, p
Page 129 and 130: Bone marrow analysis is not obligat
Page 131 and 132: In the course of chronic myeloid le
Page 133 and 134: Enlarged spleen and presence of imm
Page 135 and 136: Eosinophilia and basophilia are usu
Page 137 and 138: Erythrocyte and ThrombocyteAbnormal
Page 139 and 140: Hypochromic Anemias129Insufficient
Page 141 and 142: Hypochromic Anemias131BSGIron Ferri
Page 143 and 144: Small, hemoglobin-poor erythrocytes
Page 145 and 146: Hypochromic erythrocytes of very va
Page 147 and 148: Hypochromic Anemias137Hypochromic S
Page 149 and 150: Hypochromic anemia without iron def
Page 151 and 152: Consistently elevated “young” e
Page 153 and 154: Distribution pattern and shape of e
Page 155 and 156: Conspicuous erythrocyte morphology
Page 157 and 158: Unexplained decrease in cell counts
Page 159 and 160: Hypochromic Anemias149Differential
Page 161 and 162: Thrombocytopenia with leukocytosis
Page 163 and 164: Conspicuous large erythrocytes sugg
Page 165 and 166: In older patients, myelodysplastic
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Small inclusions are usually a sign
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PlasmodiumfalciparumPlasmodiumvivax
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Conspicuous erythrocyte inclusions
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Bone marrow analysis contributes to
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Thrombocytes: increases, reductions
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Thrombocytes: increases, reductions
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Variant forms of thrombocyte and me
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Thrombocyte proliferation with larg
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Cytology of Organ Biopsiesand Exuda
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Lymph Node Cytology175Anamnesis- su
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Reactive lymph node hyperplasia and
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Lymph Node Cytology179Contact witha
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Epithelioid cells dominate the lymp
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In cases of non-Hodgkin lymphoma an
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Accessible cysts (e.g., branchial c
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Tumor cells can be identified in pl
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Viral, bacterial, and malignant men
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191IndexAActinomycosis 179Addison d
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Index193Disseminated intravascularc
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Index195blast crisis 120-121bone ma
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Index197in hemolytic anemia 140orth
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