DOCSLIB.ORG

Red Blood Disorders Anemia Med.Pdf 14.44MB

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Red Blood Disorders Anemia Med.Pdf 14.44MB Lviv National Medical University Department of pathological physiology PATHOLOGY OF RED BLOOD PhD. Sementsiv N.G. In norm The number of erythrocytes: in female - 3,9-4,7·1012/l in male - 4,5-5,0·1012/l Hemoglobin in female - 120-140g/l in male - 140-160g/l Color index(CI) - 0,85-1,15 Globular value = 3 x Hb / the first 3 figures of erythrocytes. Reticulocytes - 0.5-2%, 0,5-2%0 changes in total blood volume normovolemia hypovolemia hypervolemia simple (Ht - norm), polycitemia (Ht > 0,48), olygocytemia (Ht < 0,36). A) Norm B) acut anaemia б) acute hemorrhage г) hydremia Pathological forms of erythrocytes regenerative degenerative cell pathologic regeneration Regenerative forms reticulocytes залежно від зрілості розрізняють: (Зернисті) Stippling (Сітчасті) Mesh Norm in a blood reticulocytes - 0,2–2,0%. Regenerative forms Basophiles substantial erythrocytes - cytoplasm remains basophilic normo blast. Polychromatophil erythrocytes (polychromasia, polychromatophilia ) – erythrocytes with basophiles substantial ( blue cells) indicates increased RBC production by the marrow Qualitative (degenerative) changes of red blood cell - poikilocytosis - different shape of erythrocytes; - anisocytosis - different size of erythrocytes; - anisochromia - different saturation of red blood cells by hemoglobin Degenerative forms Anisocytosis present in a blood different forms erythrocytes » normocyte (7,01–8,0 мкм) » microcyte(6,9–5,7 мкм) » macrocyte(8,1–9,35 мкм) » megalocyte (10–15 мкм) Degenerative forms Poikilocytosis present in a blood pictures erythrocytes different forms : elongate form , oval, ellipsoid and os. ОVAlOCYTE( ELLIPTOCYTE) – 5% all blood. Pathological cells regenerate Megaloblast mehaloblastyc cell type hematopoiesis Megaloblast oval cells in the diameter of 1,5- 2,0 times larger than normal erythrocytes is the final stage mehaloblastyc hematopoiesis. - pathological inclusions in the erythrocytes : Cabot rings Jolly bodies Cabot rings Jolly bodies Erythrocytosis Primary family (hereditary) forms Secondary Absolute (increased erythropoiesis) relative Vaquez disease Erythremia (true polycythemia) - chronic leukemia with the defect of cells of precursor of mielopoesis with unlimited proliferation hematopoetic cells. Blood picture: Hemoglobin (over 180g/l) Erythrocyte (over 6x1012/l) Platelets (over 400x109/l) Leukocyte (over 10x109/l) Hematocrit ↑ Anaemia Anemia -is a syndrome or disease which is characterized by the decrease of erythrocytes and hemoglobin amount in the unite of blood volume and accompanied by qualitative changes of erythrocyte. Cases of anemia The cases of anemia are numerous but the most important grouped whit in three major mechanisms that produce anemia: Blood loss (excessive bleeding) Inadequate production of red blood cells Excessive destruction of red blood cells Classification of anemia I. According to etiology: Hereditary and acquired II. According to pathogenesis : Diserythropoietic Hemolytic Posthemorragic IІІ. According to type of hematopoesis: 1. with erythroblastic 2. with megaloblastic ІV. According to color index (globular value): 1. normochromic 2. hypochromic 3. hyperchromic Color index(CI) - 0,85-1,15 Globular value = 3 x Hb (g/l) / the first 3 figures of erythrocytes. ІV. According to color index (globular value): Hypohromatic (c.i. < 0,8) Normochromatic (c.i. = 0,8– 1,05) Hyperchromatic (c.i. > 1,05) V. According to ability of bone marrow to regeneration: regenerative hyperregenerative hyporegenerative aregenerative Classification of anemia Over a mean diameter of erythrocytes (MDE) normocytic (mde = 7,2–8,0 мкм) microcytic (mde < 7,2 мкм) macrocytic (mde = 8,1–9,5мкм) megalocytic anaemia (mde > 12 мкм) Classification of anemia By type hematopoiesis Megaloblastic Erythroblastic Classification of anemia By etiopathogenesis Posthemorrhagic Hemolityc Dyserythropoietyc Classification of Anemia According to Underlying Mechanism I Blood Loss Acute: trauma Chronic: lesions of gastrointestinal tract, gynecologic disturbances II Increased Destruction (Hemolytic Anemias): III Impaired Red Cell Production Classification of Anemia According to Underlying Mechanism II Increased Destruction (Hemolytic Anemias): A. Intrinsic (intracorpuscular) abnormalities 1. Hereditary 2. Acquired B. Extrinsic (extracorpuscular) abnormalities Classification of Anemia According to Underlying Mechanism B. Extrinsic (extracorpuscular) abnormalities 1. Antibody mediated 2. Mechanical trauma to red cells: Extrinsic (extracorpuscular) abnormalities 1. Antibody mediated a. Isohemagglutinins: transfusion reactions, erythroblastosis fetalis (Rh disease of the newborn) b. Autoantibodies: idiopathic (primary), drug-associated, systemic lupus erythematosus B. Extrinsic (extracorpuscular) abnormalities 2. Mechanical trauma to red cells: a. Microangiopathic hemolytic anemias: thrombotic thrombocytopenic purpura, disseminated intravascular coagulation b. Infections: malaria Toxic hemolytic anemia Poisoning by hemolytic poisons: Arsine Acetic lead Phosphorus Nitrobenzene Phenylhydrazine Biliary acids Mushroom poison Snake venom Immune hemolytic anemia 1. Autoimmune anemia 2. Post transfusion anemia а) transfusion of АВ0-uncompatible blood б) transfusion of Rh- uncompatible blood 3. Hemolytic anemia of new-born Acquired haemolytic anemia Ethiology Immune injury : – isoimmun; – autoimmun. Injury caused by biological factors: the endo-and Some strains of microbes. Mechanical injury Thermal injury . Intoxication hemolytic poisons . A. Intrinsic (intracorpuscular) abnormalities 1. Hereditary a. Membrane abnormlities Membrane skeleton proteins: spherocytosis, elliptocytosis: Membrane lipids: abetalipoproteinemia b. Enzyme deficiencies Glycolytic enzymes: pyruvate kinase, hexokinase Enzymes of hexose monophosphate shunt: glucose-6-phosphate dehydrogenase, glutathione synthetase Microspherocytosis or Minkowsky-Shauffard disease [hereditary spherocytosis]. Membranopathy Blood picture : 1. The number of hemoglobin decreases. 2. The number of erythrocytes is decreases. 3. CI is normal - normochromic anemia. 4. The reticulocytes number increases - hyperregenerative anemia. 5. Decrease of erythrocytes osmotic resistance takes place. 6. Increase mean concentration of hemoglobin in the red blood cell (МСНС) more than 36%. 6. The number of unconjugated [indirect] bilirubin increases. Enzymopathy-deficiency of the enzyme Gl-6-FDG Blood picture : 1. Erythrocyte number ↓ 2. Hemoglobin amount ↓ 3. Color index (globular value) – normochromic. 4. Reticulocyte number ↑ 5. Erythrocytes osmotic resistance ↓ 6. Indirect bilirubin ↑ A. Intrinsic (intracorpuscular) abnormalities 1. Hereditary c. Disorders of hemoglobin synthesis Deficient globin synthesis: thalassemia syndromes Structurally abnormal globin synthesis (hemoglobinopathies): sickle cell anemia, unstable hemoglobins: Hemoglobinopathys are the anemias related to the violation of hemoglobin synthesis. Types of hemoglobinopathys : The 1st – is the hemoglobin chains synthesis violations; The 2nd – is the hemoglobin chains structure violations. Hemoglobinopathy α-thalassemia Blood picture : 1. Erythrocyte number ↓ ↓ 2. Hemoglobin amount ↓ 3. Color index ↓. 4. Reticulocyte number ↑ 5. Erythrocytes osmotic resistance ↓ 6. Indirect bilirubin ↑ 7. Target erythrocytes (codocytes) Sickle-cell anemia Blood picture : Erythrocyte number ↓ Hemoglobin amount ↓ Color index (globular value) – normochromic Indirect bilirubin ↑ Smear - Sickle-cell III Impaired Red Cell Production A.Disturbance of proliferation and differentiation of stem cells: 2. Defective hemoglobin synthesis a. Deficient heme synthesis: iron deficiency b. Deficient globin synthesis: thalassemias: Anemia of renal failure III Impaired Red Cell Production B. Unknown or multiple mechanisms: myelodysplastic syndrome, anemia of chronic inflammation, anemias due to marrow infiltrations Pathology of Anemias CLINICAL MANIFESTATIONS Acute: shortness of breath, organ failure, shock Chronic: With hemolysis: skeletal abnormalities because of expansion of marrow; growth retardation; jaundice and gallstones With defective erythropoiesis: iron overload, heart and endocrine failure Signs and symptoms of anaemia Most commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. Posthemorrhagic anaemia 1. Acute 2. Chronic Periods of compensation of acute blood loss 1. Reflectory 2. Hidremic 3. Medullary Acute posthemorrhagic anemia Reasons: 1. Wounding of vessels 2. Gastro-intestinal bleeding 3. Dysmenorrhea 4. Bleeding stomach ulcer 5. Lung tuberculosis Chronical posthemorrhagic anemia Causes: 1. Stomach ulcer 2. Stomach tumor 3. Hemorrhoid 4. Uterine bleeding 5. Renal bleeding 6. Nose bleeding By colour index - hypochromic Iron-deficiency anemia Blood picture : Erythrocyte number ↓ Reticulocyte number ↓ Hemoglobin amount ↓ Color index (globular value) ↓ Smear: microcytes, anulocytes , aniso/poikilocytosis, Target and “pencil” cells serum ferritin ↓ serum iron ↓ Serum soluble transferine receptors increase State of the oral cavity in anemias • Dietary iron deficiency anemia or anemia of chronic disease should be suspected in every case of glossitis, glossodynia, angular cheilitis, erythematous mucositis, oral candidiasis, recurrent oral ulcers, and burning mouth when no other obvious causes are identified Glossodynia Iron Deficiency Anemia
Load more

Recommended publications
  • Oral Diagnosis: the Clinician's Guide
    Wright An imprint of Elsevier Science Limited Robert Stevenson House, 1-3 Baxter's Place, Leith Walk, Edinburgh EH I 3AF First published :WOO Reprinted 2002. 238 7X69. fax: (+ 1) 215 238 2239, e-mail: [email protected]. You may also complete your request on-line via the Elsevier Science homepage (http://www.elsevier.com). by selecting'Customer Support' and then 'Obtaining Permissions·. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress ISBN 0 7236 1040 I _ your source for books. journals and multimedia in the health sciences www.elsevierhealth.com Composition by Scribe Design, Gillingham, Kent Printed and bound in China Contents Preface vii Acknowledgements ix 1 The challenge of diagnosis 1 2 The history 4 3 Examination 11 4 Diagnostic tests 33 5 Pain of dental origin 71 6 Pain of non-dental origin 99 7 Trauma 124 8 Infection 140 9 Cysts 160 10 Ulcers 185 11 White patches 210 12 Bumps, lumps and swellings 226 13 Oral changes in systemic disease 263 14 Oral consequences of medication 290 Index 299 Preface The foundation of any form of successful treatment is accurate diagnosis. Though scientifically based, dentistry is also an art. This is evident in the provision of operative dental care and also in the diagnosis of oral and dental diseases. While diagnostic skills will be developed and enhanced by experience, it is essential that every prospective dentist is taught how to develop a structured and comprehensive approach to oral diagnosis.
    [Show full text]
  • Age-Related Features and Pathology of Blood in Children
    MINISTRY OF PUBLIC HEALTH OF UKRAINE HIGHER STATE EDUCATIONAL ESTABLISHMENT OF UKRAINE «UKRAINIAN MEDICAL STOMATOLOGICAL ACADEMY» V.I. POKHYLKO, S.M. TSVIRENKO, YU.V. LYSANETS AGE-RELATED FEATURES AND PATHOLOGY OF BLOOD IN CHILDREN MANUAL FOR STUDENTS OF HIGHER MEDICAL EDUCATIONAL INSTITUTIONS OF THE III-IV ACCREDITATION LEVELS Poltava 2017 МІНІСТЕРСТВО ОХОРОНИ ЗДОРОВ’Я УКРАЇНИ ВИЩИЙ ДЕРЖАВНИЙ НАВЧАЛЬНИЙ ЗАКЛАД УКРАЇНИ «УКРАЇНСЬКА МЕДИЧНА СТОМАТОЛОГІЧНА АКАДЕМІЯ» ПОХИЛЬКО В.І., ЦВІРЕНКО С.М., ЛИСАНЕЦЬ Ю.В. ВІКОВІ ОСОБЛИВОСТІ ТА ПАТОЛОГІЯ КРОВІ У ДІТЕЙ НАВЧАЛЬНИЙ ПОСІБНИК ДЛЯ СТУДЕНТІВ ВИЩИХ МЕДИЧНИХ НАВЧАЛЬНИХ ЗАКЛАДІВ III-IV РІВНІВ АКРЕДИТАЦІЇ Полтава 2017 2 UDC: 616+616.15]-053.2(075.8) ВВС: 57.33я73 The manual highlights the issues of embryogenesis, age-related features, semiotics of lesion, examination methods and diseases of hemic system in children. The manual is intended for students of higher educational institutions of III-IV accreditation levels, and can be used by medical interns and primary care doctors. Authors: Doctor of Medical Sciences, Professor of the Department of Pediatrics No.1 with Propedeutics and Neonatology V.I. Pokhylko Candidate of Medical Sciences, Acting Head of the Department of Pediatrics No.1 with Propedeutics and Neonatology S.M. Tsvirenko Candidate of Philological Sciences, Senior Lecturer of the Department of Foreign Languages with Latin and Medical Terminology Yu.V. Lysanets Reviewers: O.S. Yablon’ ― Doctor of Medical Sciences, Professor, Head of the Department of Pediatrics No.1, Vinnytsya National M.I. Pirogov Memorial Medical University of Ministry of Public Health of Ukraine. M.O. Honchar ― Doctor of Medical Sciences, Professor, Head of the Department of Pediatrics and Neonatology No.1, Kharkiv National Medical University.
    [Show full text]
  • Anormal Rbc in Peripheral Blood. [Repaired].Pdf
    1. Acanthocyte 2. Burr-cell 3. Microcyte 1. Basophilic Normoblast 2. Polychromatic Normoblast 3. Pycnotic Normoblast 4. Plasmocyte 5. Eosinophil 6. Promyelocyte 1. Macrocyte 2. Elliptocyte 1. Microcyte 2. Normocyte 1. Polychromatic Erythrocyte 2. Acanthocyte 3. Elliptocyte 1. Polychromatic Normoblast 2. Pycnotic Normoblast 3. Neutrophil Myelocyte 4. Neutrophil Metamyelocyte 1. Schistocyte 2. Microcyte BASOPHILIC ( EARLY ) NORMOBLASTS Basophilic Erythroblast Basophilic Stippling, Blood smear, May-Giemsa stain, (×1000) CABOT'S RINGS Drepanocyte Elliptocyte Erythroblast ERYTHROBLAST in the blood Howell-jolly body Hypo chromic LACRYMOCYTES Leptocyte Malaria, Blood smear, May-Giemsa stain, ×1000 MICROCYTES Orthochromatic erythroblast Pappen heimer Bodies & 1. Schistocyte 2. Elliptocyte 3. Acanthocyte POIKILOCYTOSIS Polychromatic Erythroblast Pro Erytroblast Proerythroblasts Reticulocyte Rouleaux SICKLE CELLS Sickle cell Spherocyte Spherocyte Spherocyte SPHEROCYTES STOMATOCYTES Target Cells Tear Drop Cell, Blood smear, May-Giemsa stain, x1000 Anulocyte 1. Burr-cell 2. Elliptocyte 1. Macrocyte 2. Microcyte 3. Elliptocyte 4. Schistocyte 1. Ovalocyte 2. Lacrymocyte 3. Target cell 1. Polychromatic Erythrocyte 2. Basophilic Stippling 1. Proerythroblast 2. Basophilic Erythroblast 3. Intermediate Erythroblast 4. Late Erythroblast 5. Monocyte 6. Lymphocyte 1. Target-cell 2. Elliptocyte 3. Acanthocyte 4. Stomatocyte 5. Schistocyte 6. Polychromatophilic erythrocyte. 1.Pro erythroblast 2.Basophilic normoblast 3.Polychromatic normoblast 4.Pycnotic normoblast
    [Show full text]
  • The Clinical Application of Della-Porta Et Al Score in a Mexican Patient with Myelodysplastic Syndrome
    CLINICAL CASE Rev Hematol Mex. 2020; 21 (3): 158-171. The clinical application of Della-Porta et al score in a Mexican patient with myelodysplastic syndrome. Aplicación clínica de la puntuación Della-Porta y colaboradores en un paciente mexicano con síndrome mielodisplásico Juan C Marín-Corte,1,4 Eduardo Olmedo-Gutiérrez,1,4 Jeny A Marín-Corte,5 Roberto N Miranda,3 Carlos E Bueso-Ramos,3 Omar Cano-Jiménez,1 Arturo R Fuentes-Reyes,1 Elizabeth Hernández-Salamanca,1,4 Miguel A López-Trujillo,1,4 Rafael A Marín-López,1,4 Guillermo J Ruiz-Delgado,1,2,4 Guillermo J Ruiz-Argüelles1,2,4 Abstract BACKGROUND: The myelodysplastic syndromes are one of the most studied diseases in hematology in recent years. By definition and according to the World Health Or- ganization Classification of Tumours of hematopoietic and Lymphoid Tissues 2017, myelodysplastic syndromes are a group of clonal hematopoietic stem cell diseases characterized by cytopenia, dysplasia in one or more of the major myeloid lineages, ineffective hematopoiesis, recurrent genetic abnormalities and increased risk of de- veloping acute myeloid leukemia (AML). To identify in a quick way this disease, we designed a worksheet based on the article of Matteo Della-Porta et al to developed a systematic approach to assess the morphological features in the bone marrow smears of three cell lineages in patients with myelodysplastic syndromes and provide the basis to validate flow cytometric and immunohistochemistry data. CLINICAL CASE: A 47-year-old male patient in whom we applied a worksheet that we designed based on Della-Porta score criteria to each cellularity lineage in the bone 1 Clinical Laboratories of Puebla; Puebla, marrow smears and we obtained significant results according to the bone marrow Puebla, México.
    [Show full text]
  • Tumour-Simulating Intrathoracic Marrow Heterotopia in Thalassaemia Major
    Thorax: first published as 10.1136/thx.19.2.121 on 1 March 1964. Downloaded from Thorax (1964), 19, 121 Tumour-simulating intrathoracic marrow heterotopia in thalassaemia major C. PAPAVASILIOU AND P. SFIKAKIS From the Department of Clinical Therapeutics, Alexandra Hospital, University of Athens Haemopoiesis under certain circumstances can be flat frontal bones, and a hard arched palate. The liver supplemented by extramedullary foci of hetero- was slightly enlarged. There was general enlargement topic bone marrow located in other tissues. In of the lymph nodes, particularly in the axillae. addition to the normal phenomenon of extra- Chronic ulcers were present in the region of the ankles. The haemoglobin was 8-7 g./ 100 ml., medullary haemopoiesis in newborn babies and haematocrit 27%, R.B.C. 3,520,000 with anisocytosis, infants, such a process has been observed, as a poikilocytosis, microcytosis, target cells, hypochromia, compensatory phenomenon, in conditions asso- and anisochromia. There were 7,150 white cells per ciated with abnormal function of haemopoietic c.mm. with 60% polymorphs, 36% lymphocytes, 3% tissue, such as pernicious anaemia, macrocytic eosinophils, and 1% monocytes. There were 9 anaemia of hepatic origin, osteosclerosis, exten- erythroblasts per 100 white cells in the peripheral sive neoplastic infiltration of the bones (leuk- blood. The serum bilirubin was 0-9 mg./100 ml. direct aemia, lymphoma, etc.), erythraemia, erythro- and 0-48 mg./ 100 ml. indirect. The bone marrow blastosis, acholuric jaundice, and thalassaemia. showed marked hyperplasia of the red cell series, the in white cell series, and of the megakaryocytes. There copyright. Heterotopic marrow has been described the was no anomaly in the maturation of the red cells.
    [Show full text]
  • TR-507: Vanadium Pentoxide (CASRN 1314-62-1) in F344/N Rats
    NTP TECHNICAL REPORT ON THE TOXICOLOGY AND CARCINOGENESIS STUDIES OF VANADIUM PENTOXIDE (CAS NO. 1314-62-1) IN F344/N RATS AND B6C3F1 MICE (INHALATION STUDIES) NATIONAL TOXICOLOGY PROGRAM P.O. Box 12233 Research Triangle Park, NC 27709 December 2002 NTP TR 507 NIH Publication No. 03-4441 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health FOREWORD The National Toxicology Program (NTP) is made up of four charter agencies of the U.S. Department of Health and Human Services (DHHS): the National Cancer Institute (NCI), National Institutes of Health; the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health; the National Center for Toxicological Research (NCTR), Food and Drug Administration; and the National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. In July 1981, the Carcinogenesis Bioassay Testing Program, NCI, was transferred to the NIEHS. The NTP coordinates the relevant programs, staff, and resources from these Public Health Service agencies relating to basic and applied research and to biological assay development and validation. The NTP develops, evaluates, and disseminates scientific information about potentially toxic and hazardous chemicals. This knowledge is used for protecting the health of the American people and for the primary prevention of disease. The studies described in this Technical Report were performed under the direction of the NIEHS and were conducted in compliance with NTP laboratory health and safety requirements and must meet or exceed all applicable federal, state, and local health and safety regulations. Animal care and use were in accordance with the Public Health Service Policy on Humane Care and Use of Animals.
    [Show full text]
  • Erythroleukemia with Complex Cytogenetic Abnormalities: a Case Report with Review of Literature
    RESEARCH PAPER Medical Science Volume : 3 | Issue : 7 | July 2013 | ISSN - 2249-555X Erythroleukemia with Complex Cytogenetic Abnormalities: A case report with review of literature KEYWORDS Acute Erythroleukemia, Flow cytometry, Cytogenetic abnormality Pooja K Suresh Purnima S Rao Urmila N Khadilkar Department of Pathology, Kasturba Department of Pathology, Kasturba Department of Pathology, Kasturba Medical College, Mangalore (Manipal Medical College, Mangalore (Manipal Medical College, Mangalore (Manipal University) University) University) ABSTRACT Acute Erythroleukemia (AEL) is a rare type of hematopoietic neoplasm, having a prevalence of 3-5% of all Acute Myeloid Leukemia (AML). We present a case report of acute erythroleukemia, a rare type of AML, with complex cytogenetic abnormalities. A 54-year old male presented with low grade fever and significant weight loss. Complete hemogram and a peripheral smear revealed pancytopenia with 18% blasts. It also showed features of hemolysis. Bone marrow (BM) study showed eryth- roid hyperplasia with erythroblasts constituting 85% of all nucleated cells and 21% myeloid blasts among non-erythroid cells. Flow cytometry revealed 23% blasts positive for CD33, CD34, CD117, CD36 and HLA-DR. Cytogenetic study revealed hypotetraploidy with numerous structural abnormalities indicating poor prognosis. Introduction cells. Of this, the proerythroblasts comprised 35%. Dyspoi- The term Acute Erythroleukemia (AEL) /AML-M6 is defined etic erythroid cells showing multinucleation, nuclear budding as proliferation of dysplastic erythroid elements mixed with and nuclear to cytoplasmic dysynchrony were noted. Myelo- blasts of myeloid origin. The recent World Health Organi- blasts comprised 21% of non erythroid cells. Megakaryocytes zation (WHO) classification has a category of acute myeloid were normal in number and morphology.
    [Show full text]
  • Cambridge University Press 978-0-521-51426-2 — Anemia with Online Resource Edited by Edward J
    Cambridge University Press 978-0-521-51426-2 — Anemia with Online Resource Edited by Edward J. Benz, Jr. , Nancy Berliner , Fred J. Schiffman Index More Information Index aAA. See acquired aplastic clinical significance of, 187 through RBC transfusion, anemia of inflammation, 169 anemia dementia, 187 175 anemia of prematurity, 34 abdomen, physical examination epidemiology of, 185–6 with rhEPO, 172, 174–7 anemias. See also clinical of, 32 inflammation and, 186–7 pathogenesis of, 172–3 approaches; specific ABO incompatibility, 36 hepcidin levels, 186 pathophysiology, 198 anemias HSCT and, 181 leptin protein, 186 therapy-related toxicity causes of, xi, 1 acanthocytes, 27 MIF, 186 grading, 172 through blood loss, 24 ACD. See anemia of chronic TNF-α, 186 transfusion, 175 classification of, 24 inflammation vitamin D deficiency, 186–7 anemia of chronic inflammation through MCV, 24 ACI. See anemia of chronic management strategies, 187–8 (ACI) clinical definitions of, xi, 23 inflammation prevalence of, 185 cancer and, 172 comorbidities with, xi acquired aplastic anemia (aAA), aHUS. See atypical hemolytic case study for, 153–4 defined, 172, 185 128–32. See also uremic syndrome clinical presentation, 152–3, diagnostic approach, 23–4 paroxysmal nocturnal AIHA. See autoimmune 194 through bone marrow hemoglobinuria hemolytic anemia critical illness with, 151 aspirate specimens, 24 bone marrow with, 128 alcohol use, non-megaloblastic cytokines, 196 through peripheral blood clinical presentation of, 129 macrocytic anemias diagnostic evaluation, 153, smears, 24–5, 29 clonal hematopoiesis and, 129 from, 63 194–5 future approaches to, 230–3 diagnostic evaluation of, alemtuzumab, 134 epidemiology, 150–1 hemoglobin deficiency in, xi 129–30 ALI.
    [Show full text]
  • 10 11 Cyto Slides 81-85
    NEW YORK STATE CYTOHEMATOLOGY PROFICIENCY TESTING PROGRAM Glass Slide Critique ~ November 2010 Slide 081 Diagnosis: MDS to AML 9 WBC 51.0 x 10 /L 12 Available data: RBC 3.39 x 10 /L 72 year-old female Hemoglobin 9.6 g/dL Hematocrit 29.1 % MCV 86.0 fL Platelet count 16 x 109 /L The significant finding in this case of Acute Myelogenous Leukemia (AML) was the presence of many blast forms. The participant median for blasts, all types was 88. The blast cells in this case (Image 081) are large, irregular in shape and contain large prominent nucleoli. It is difficult to identify a blast cell as a myeloblast without the presence of an Auer rod in the cytoplasm. Auer rods were reported by three participants. Two systems are used to classify AML into subtypes, the French- American-British (FAB) and the World Health Organization (WHO). Most are familiar with the FAB classification. The WHO classification system takes into consideration prognostic factors in classifying AML. These factors include cytogenetic test results, patient’s age, white blood cell count, pre-existing blood disorders and a history of treatment with chemotherapy and/or radiation therapy for a prior cancer. The platelet count in this case was 16,000. Reduced number of platelets was correctly reported by 346 (94%) of participants. Approximately eight percent of participants commented that the red blood cells in this case were difficult to evaluate due to the presence of a bluish hue around the red blood cells. Comments received included, “On slide 081 the morphology was difficult to evaluate since there was a large amount of protein surrounding RBC’s”, “Slide 081 unable to distinguish red cell morphology due to protein” and “Unable to adequately assess morphology on slide 081 due to poor stain”.
    [Show full text]
  • Acute Erythroid Leukemia: a Review
    110 Apr 2012 Vol 5 No.2 North American Journal of Medicine and Science Review Acute Erythroid Leukemia: A Review Daniela Mihova, MD, FCAP;1* Lanjing Zhang, MD, MS, FCAP2,3 1 Pathology Department and Clinical Laboratories, Flushing Hospital Medical Center, Flushing, NY 2 Department of Pathology, University Medical Center at Princeton, Princeton, NJ 3 Department of Pathology and Laboratory Medicine, Robert Wood Johnson Medical School-UMDNJ, New Brunswick, NJ Acute erythroid leukemia is a rare form of acute myeloid leukemia. It accounts for <5% of all acute myeloid leukemia cases. According to the World Health Organization 2008 classification, it falls under the category of acute myeloid leukemia, not otherwise specified and is further divided into two subtypes: erythroid leukemia (erythroid/myeloid) and pure erythroid leukemia. Currently, erythroleukemia (erythroid/myeloid) is defined as 50% or more erythroid precursors and ≥20% blasts of the non-erythroid cells. By definition, pure erythroid leukemia is composed of ≥80% erythroid precursors. Acute erythroid leukemia is a diagnosis of exclusion and difficulty. This review discusses its differential diagnoses, which present with erythroid proliferation, such as myelodysplastic syndrome with erythroid proliferation, acute myeloid leukemia with myelodysplasia related changes, therapy related acute myeloid leukemia, myeloproliferative neoplasms with erythroblast transformation, acute myeloid leukemia with recurrent genetic abnormalities and other types of hematologic neoplasms. Additionally, reactive conditions such as erythropoietin treatment, vitamin B12 and folate deficiency, toxin exposure and congenital dyserythropoiesis should be excluded. As a result, the frequency of acute erythroid leukemia diagnosis has been reduced. Important adverse prognostic factors will be summarized, including presence of complex cytogenetic karyotype as the most important one.
    [Show full text]
  • Щетинин Патофизиол Ч2 Англ 9-10-19.Indd
    The Federal State Budgetary Educational Institution of Higher Education «Stavropol State Medical University» The Ministry of Healthcare of the Russian Federation The Department of Pathological Physiology PATHOPHYSIOLOGY, CLINICAL PATHOPHYSIOLOGY (WITH THE BASICS OF THE ORGANIZATION OF STUDENTS’ INDEPENDENT WORK) Specialty 31.05.01 General Medicine Part II STUDY GUIDE FOR FOREIGN STUDENTS OF THE ENGLISH-SPEAKING MEDIUM OF MEDICAL UNIVERSITIES Stavropol, 2019 1 УДК 616-092 (072) ББК 52.52я73 Р30 Pathophysiology, clinical pathophysiology (with the basics of the organization of students’ independent work), Part II: Study Guide / E.V. Schetinin, M.Yu. Vafiadi, G.G. Petrosyan, N.G. Radzievskaya, L.D. Erkenova, L.A. Parazyan, Yu.Yu. Gatilo, A.A. Vafiadi – Stavropol: Publishing house: StSMU, 2019. – 336 p. Authors: Professor E.V. Schetinin, Assoc. Professor M.Yu. Vafiadi, Assoc. Professor G.G. Petrosyan, ass. N.G. Radzievskaya, ass. L.D. Erkenova, ass. L.A. Parazyan, ass. Yu.Yu. Gatilo, ass. A.A. Vafiadi. ISBN 978-5-89822-595-7 Ч. I – 336 с. ISBN 978-5-89822-632-9 The study guide was developed in accordance with the Federal State Educational Standard of Higher Education and modern programs in Pathophysiology, Clinical Pathophysiology in the specialty 31.05.01 General Medicine. The study guide is designed for foreign students of the English-speaking Medium of medical universities to carry out practical work during class hours and homework assignments for each studied topic in Pathophysiology, Clinical Pathophysiology with the basics of organizing
    [Show full text]
  • Clinical Hematology 1
    CLINICAL HEMATOLOGY 1 CLINICAL HEMATOLOGY Editor Gamal Abdul Hamid, MD,PhD Associate Professor Faculty of Medicine and Health Sciences University of Aden CLINICAL HEMATOLOGY 2 PREFACE Clinical Hematology, first edition is written specifically for medical students, the clinician and resident doctors in training and general practioner. It is a practical guide to the diagnosis and treatment of the most common disorders of red blood cells, white blood cells, hemostasis and blood transfusion medicine. Each disease state is discussed in terms of the pathophysiology, clinical and paraclinical features which support the diagnosis and differential diagnosis. We bring together facts, concepts, and protocols important for the practice of hematology. In addition this book is also supported with review questions and quizzes. G.A-H 2012 CLINICAL HEMATOLOGY 3 CONTENTS Preface 1. Hematopoiesis 7 2. Anemia 26 3. Iron Deficiency Anemia 32 4. Hemolytic Anemia 41 5. Sickle Cell Hemoglobinopathies 49 6. Thalassemia 57 7. Hereditary Hemolytic Anemia 63 8. Acquired Hemolytic Anemia 68 9. Macrocytic Anemia 75 10. Bone Marrow Failure, Panctopenia 87 11. Spleen 95 12. Acute Leukemia 99 13. Chronic Myeloproliferative Disorders 125 14. Chronic Lymphoproliferative Disorders 137 15. Malignant Lymphoma 147 16. Multiple Myeloma and Related Paraproteinemia 171 17. Hemorrhagic Diseases 179 18. Transfusion Medicine 201 19. Bone Marrow Transplantations 214 CLINICAL HEMATOLOGY 4 Appendices: I. Hematological Tests and Normal Values 221 II. CD Nomenclature for Leukocytes Antigen 226 III. Cytotoxic Drugs 228 IV. Drugs Used in Hematology 230 Glossary 232 Answers 246 Bibliography 247 CLINICAL HEMATOLOGY 5 CLINICAL HEMATOLOGY 6 HEMATOPOIESIS 1 All of the cells in the peripheral blood have finite life spans and thus must be renewed continuously.
    [Show full text]