Clinical Hematology 1

Total Page:16

File Type:pdf, Size:1020Kb

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. The mechanisms responsible for regulating steady-state hematopoiesis and the capacity to modulate blood cell production in response to stresses such as anemia or infection consist of a series of progenitor cells in the bone marrow and a complex array of regulatory factors. It is the process of blood cell production, differentiation, and development. The hematopoietic system consists of the bone marrow, liver, spleen, lymphnodes, and thymus. It starts as early as the 3rd week of gestation in the yolk sac. By the 2nd month, hematopoiesis is established in the liver and continuous through the 2nd trimester. During the 3rd trimester it shifts gradually to bone marrow cavities. During infancy: all marrow cavities are active in erythropoiesis "Red Marrow". During childhood: erythropoiesis becomes gradually restricted to flat bones as; skull, vertebrae, sternum, Ribs and pelvic bones, in addition to ends of long bones. The shafts of long bones become populated by fat "yellow marrow". Blood Cell Development The pluripotent stem cell is the first in a sequence of steps of hematopoietic cell generation and maturation. The progenitor of all blood cells is called the multipotential hematopoietic stem cell. These cells have the capacity for self-renewal as well as proliferation and differentiation into progenitor cells committed to one specific cell line. The multipotential stem cell is the progenitor for two major ancestral cell lines: Lymphocytic and non-lymphocytic cells. The lymphoid stem cell is the precursor of mature T cells or B cells/ plasma cells. The non-lymphocytic (myeloid) stem cell is progress to the progenitor CFU-GEMM (colony-forming unit granulocyte- erythrocyte-monocyte-megakaryocyte). The CFU-GEMM can lead to the formation of CFU-GM (CFU-granulocyte-macrophage / monocyte), CFU-Eo (CF-Eosinophil), CFU-Bs (CFU-basophil) And CFU-MEG (CFU-Megakaryocyte). In erythropoiesis, the CFU-GEMM differentiates, into the BFU-E (Burst-Forming unit Erythroid). Each of the CFUs in turn can produce a colony of one hematopoietic lineage under appropriate growth conditions. CFU-E is the target cells for erythropoietin. Hematopoietic Growth Factors The hematopoietic growth factors are glycoprotein hormones that regulate the proliferation and differentiation of hematopoietic progenitor cells and the function of mature blood cells. These growth factors were referred to as colony stimulating factors (CSFs) because they stimulated the formation of colonies of cells derived from individual bone marrow progenitors. Erythropoietin, granulocyte-macrophage colony stimulating factors (GM-CSF) granulocyte colony stimulating factor (G-CSF), macrophage colony stimulating factor (M-CSF) and interleukin-3 are representative factor that have been identified, cloned and produced through recombinant DNA technology. The hematopoietic growth factors interact with blood cells at different levels in the cascade of cell differentiation from the multipotential progenitor to the circulating mature cell. CLINICAL HEMATOLOGY 7 Table 1.1: Human hematopoietic growth factors Growth Factor Source Major Function GM-CSF T-Lymphocyte, endothelial Stimulates production of cells, Fibroblasts neutrophils, eosinophils, monocytes, red cells and platelets. G-CSF Monocytes, Fibroblasts Stimulates production of neutrophils. M-CSF Macrophages, endothelia Stimulates production of cells monocytes ERYTHROPOIE Peritubular cells, Liver, Stimulates production of red TIN Macrophages cells. IL-1 Macrophages, activated Cofactor for IL-3 and IL-6. lymphes, endothelial cells. Activated T cells IL-2 Activated T cells T cell growth factor. Stimulates IL-1 synthesis. Activated B cells and NK cells IL-3 T cells Stimulates production of all non-lymphoid cells. IL-4 Activated T cells Growth factor for activated B cells, resting T cells and mast cells. IL-5 T cells Induces differentiation of activated B cells and eosinophils. IL-6 T cells Stimulates CFU-GEMM Stimulates Ig synthesis IL-7 T cells, Fibroblasts, Growth factor for pre B cells Endothelial cells Development and Maturation Erythrocytes are rapidly maturing cells that undergo several mitotic divisions during the maturation process. The Pronormoblast" is the first identifiable cell of this line followed by the " Basophilic normoblast ", polychromatic normoblast ", orthochromatic normocyte " and reticulocyte stages in the bone marrow. Reticulocytes enter the circulating blood and fully mature into functioned erythrocytes. A defect in nuclear maturation can occur. This is referred to as megaloblastic maturation. In this condition, the nuclear maturation, which represents an impaired ability of the cell to synthesize DNA, lags behind the normally developing cytoplasm. Reticulocytes represent the first nonnucleated stage in erythrocytic development. Although the nucleus has been lost from the cell by this stage, as long as RNA is present, synthesis of both protein and heme continues. The ultimate catabolism of RNA, ribosome disintegration, and loss of mitochondria mark the transition from the reticulocyte stage to full maturation of the erythrocyte. If erythropoietin stimulation produces increased numbers of immature reticulocytes in the blood circulation, these Reticulocytes are referred to as stress or shift reticulocytes. Supravital stains such as new methylene blue are used to perform quantitative determination of blood reticulocytes. CLINICAL HEMATOLOGY 8 Figure 1.1: Developemntal characteristics of erythrocytes Pronormoblast Basophilic Normoblast Size 12- 19 m in Size 12- 17 m in diameter diameter N:C ratio 4: 1 N:C ratio 4:1 Nucleus: Nucleus Large, round Nuclear chromatin more clumped nucleus Nucleoli usually not apparent Chromatin has a fine Cytoplasm: Distinctive pattern 0-2 nucleoli’ basophilic colour Cytoplasm: distinctive basophilic colour without granules Polychromatic Normoblast Orthochromic Normoblast or Size 11-1 m in nucleated RBC diameterN:C ratio 1:1 Size: 85-12 m Nucleus: Nucleus: Increased clumping of Chromatin pattern is tightly the chromatin condensed. Cytoplasm: Colour: Cytoplasm: Variable, with Colour: reddish-pink pink staining (acidophilic) Mixed with Basophilia Erythrocyte Reticulocyte (Supravital Average diameter 6-8 m stain) Size 7-10 m Cell is anuclear Polychromatic Erythrocyte Diffuse reticulum (Wright stain) Cytoplasm: Overall blue appearance Pronormoblast (1) basophilic normoblast(2) polychromatic N (3- 4) Orthochromatic normoblast (5-6) (1. CLINICAL HEMATOLOGY 9 The myeloblast is the first identifiable cell in the granulocytic series. Myeloblast constitutes approximately 1% of the total nucleated bone marrow cells. This stage lasts about 15 hours. The next stage, the promyelocyte, constitutes approximately 3% of the nucleated bone marrow; this stage lasts about 24 hours. The myelocyte is the next maturational stage, with approximately 12% of the proliferative cells existing in this stage. The stage from myelocyte to metamyelocyte lasts an average 4.3 days.The time requerd for the division and maturation of a myeloblast to a mature granulocyte is 5-12 days. Two stages of granulocytes are observed in the circulating blood: the band form of neutrophils, eosinophils and basophils and in end stage of maturation. The normal number of neutrophilic granulocytes in the peripheral blood is about 2500-7500/l. Neutrophilic granulocytes have a dense nuleus split into two to five lobes and a pale cytoplasm. The cytoplasm contains numerous pink blue or gray blue granules. Two types of granules can be distinguished morphologically; primary or azurophilic granules which appear at the promyelocyte stage and secondary granules, which appear later. The primary granules contain myeloperoxidase, and acid hydrolase, whereas lyszymes,
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]
  • University of Illinois College of Medicine at Urbana-Champaign
    UNIVERSITY OF ILLINOIS COLLEGE OF MEDICINE AT URBANA-CHAMPAIGN PATHOLOGY - VOLUME I 2014 - 2015 PATHOLOGY TEACHING FACULTY LIST Jerome Anderson, MD Farah Gaudier, MD Richard Tapping, PhD Department of Pathology Dept. of Pathology Associate Professor. McDonough District Hosp. Carle Physician Group Dept. of Microbiology McComb, IL 61455 [email protected] [email protected] Phone: (309) 837-2368 [email protected] Teaching Assistant Nasser Gayed, MD Lindsey Burnett, PhD Brett Bartlett, MD Dept. of Med. Info. Sciences [email protected] Dept. of Pathology 190 Medical Sciences Bldg SBL Health Centre 506 South Mathews Avenue Mattoon, IL 61938 Urbana, IL 61801 Pathology Office [email protected] [email protected] Jackie Newman Phone: (217) 244-2265 Frank Bellafiore, MD Nicole Howell, MD [email protected] Dept. of Pathology Dept. of Pathology Carle Physician Group Carle Physician Group 602 West University Avenue [email protected] Urbana, IL 61801 [email protected] Zheng George Liu, MD Dept. of Pathology Allan Campbell, MD Carle Physician Group Dept. Of Pathology 602 West University Avenue UICOM Peoria IL Urbana, IL 61801 [email protected] [email protected] Gregory Freund, MD Steve Nandkumar, M.D. Head, Dept. of Pathology Pathology Course Director 190 Medical Sciences Building 249 Medical Sciences Building 506 South Mathews Avenue 506 South Mathews Avenue Urbana, IL 61801 Urbana, IL 61801 [email protected] [email protected] Page 2 Pathology M-2 Introduction INTRODUCTION Pathology – study of the essential nature of diseases and the structural and functional changes produced by them. ( Pathos= suffering; ologos = study) Pathology consists of two major subdivisions.
    [Show full text]
  • Modelling of Red Blood Cell Morphological and Deformability Changes During In-Vitro Storage
    applied sciences Article Modelling of Red Blood Cell Morphological and Deformability Changes during In-Vitro Storage Nadeeshani Geekiyanage 1 , Emilie Sauret 1,*, Suvash Saha 2 , Robert Flower 3 and YuanTong Gu 1 1 School of Mechanical, Medical and Process Engineering, Science and Engineering Faculty, Queensland University of Technology (QUT), Brisbane City, QLD 4000, Australia; [email protected] (N.G.); [email protected] (Y.G.) 2 School of Mechanical and Mechatronic Engineering, University of Technology Sydney (UTS), Ultimo, NSW 2007, Australia; [email protected] 3 Research and Development, Australian Red Cross Lifeblood, Kelvin Grove, QLD 4059, Australia; [email protected] * Correspondence: [email protected] Received: 28 February 2020; Accepted: 27 April 2020; Published: 4 May 2020 Featured Application: Red blood cell (RBC) storage lesion is a critical issue facing transfusion treatments, and significant changes in RBC morphology and deformability are observed due to the storage lesion. RBCs require high deformability to sustain in-vivo circulation, and impaired deformability leads to several post-transfusion adverse outcomes. Therefore, improved understanding of the interrelation between the morphological and deformability changes and the quality and viability of the stored RBCs is essential to prevent or reduce the transfusion related adverse outcomes. To support this requisite, the influence on RBC deformability due to several aspects of the storage lesion, namely, the changes in cell morphology, surface area and volume, RBC membrane biomechanics, and cytoskeletal structural integrity are explored numerically in this study. Abstract: Storage lesion is a critical issue facing transfusion treatments, and it adversely affects the quality and viability of stored red blood cells (RBCs).
    [Show full text]
  • Cytology of Myeloma Cells
    J Clin Pathol: first published as 10.1136/jcp.29.10.916 on 1 October 1976. Downloaded from J. clin. Path., 1976, 29, 916-922 Cytology of myeloma cells F. G. J. HAYHOE AND ZOFIA NEUMAN1 From the Department of Haematological Medicine, Cambridge University SYNOPSIS A cytological, cytochemical, and cytometric study of plasma cells from 195 cases of multiple myeloma showed that, contrary to earlier reports, flaming cells, thesaurocytes, and intra- nuclear inclusions are not confined to IgA-secreting cases but are common also in IgG and Bence Jones varieties of myeloma. IgA-secreting cells are not larger, nor do they have a lower nuclear- cytoplasmic ratio than other myeloma cells. On average, for a given mass of tumour, Bence-Jones, IgG, and IgA varieties of myeloma produce amounts of paraprotein in the ratio 1 to 1 6 to 2-7. In 1961 Paraskevas et al reported a correlation the results of a larger scale survey carried out some between the morphological features of plasma cells years ago but previously unpublished. in myeloma and the type of immunoglobulin secreted. The cases studied included 12 with y1A Material and methods (f2A, IgA) myeloma, 30 with y (IgG) myeloma, and six myelomas without M protein (probably Bence The study was performed on bone marrow smearscopyright. Jones myelomas). Flaming cells, thesaurocytes, and from 200 consecutive patients newly entered into a intranuclear, PAS-positive inclusion bodies were comparative trial of treatments in myeloma, under found only in cases of IgA myeloma, and flaming the auspices of the Medical Research Council. Five cells especially were present in most cases and in patients were subsequently excluded as not confirmed high percentage in several.
    [Show full text]
  • Evidence-Based Practice Center Systematic Review Protocol
    Evidence-based Practice Center Systematic Review Protocol Project Title: Serum-Free Light Chain Analysis for the Diagnosis, Management, and Prognosis of Plasma Cell Dyscrasias I. Background and Objectives for the Systematic Review Plasma cell dyscrasias (PCDs) are a spectrum of disorders characterized by the expansion of a population of monoclonal bone-marrow plasma cells that produce monoclonal immunoglobulins.1 At the benign end of the spectrum is monoclonal gammopathy of undetermined significance (MGUS), where the plasma-cell clone usually does not expand. Multiple myeloma (MM) is a plasma cell disorder at the malignant end of the spectrum and is characterized by the neoplastic proliferation of a clone of plasma cells in the bone marrow with resulting end-organ damage, including skeletal destruction (lytic bone lesions), hypercalcemia, anemia, and renal insufficiency. Whereas monoclonal plasma cells generally secrete intact immunoglobulin, in about 20 percent of patients with MM these cells only produce light-chain monoclonal proteins (i.e., light-chain multiple myeloma [LCMM], formerly known as Bence Jones myeloma) and in 3 percent of patients they secrete neither light- nor heavy-chain monoclonal proteins that are detectable by immunofixation (i.e., nonsecretory multiple myeloma [NSMM]).1 In two-thirds of patients with NSMM, a monoclonal protein can be identified by the serum-free light chain (SFLC) assay. Patients with LCMM develop complications related to tissue deposition of light chains, including amyloidosis. Amyloid light-chain (AL) amyloidosis is the most common form of systemic amyloidosis seen in the United States and is characterized by a relatively stable, slow-growing plasma-cell clone that secretes light-chain proteins that form Table 1: Diagnostic criteria and clinical course of selected plasma cell dyscrasias (PCDs)2 Disorder Disease Definition Clinical Course Monoclonal gammopathy of .
    [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]
  • Canine Multiple Myeloma
    Canine Multiple Myeloma Meredith Maczuzak, DVM; Kenneth S. Latimer, DVM, PhD; Paula M. Krimer, DVM, DVSc; and Perry J. Bain, DVM, PhD Class of 2003 (Maczuzak) and Department of Pathology (Latimer, Krimer, Bain), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388 Introduction Multiple myeloma or plasma cell myeloma, is a neoplasm of well- differentiated B cell lymphocytes typically originating from the bone marrow. Neoplastic cells can metastasize widely, having a predilection for bone and resulting in osteolysis. The malignant transformation of a single B cell can secrete a homogenous immunoglobulin product known as paraprotein, which will mimic the structure of normal immunoglobulins. Overabundant production of paraprotein, consisting of any of the immunoglobulin classes, will appear as a sharp, well-defined peak or monoclonal gammopathy on serum electrophoresis. The most frequently encountered multiple myelomas secrete IgG or IgA paraproteins, however IgM myelomas (macroglobulinemia) have also been diagnosed in companion animals. Light chain disease is caused by plasma cell overproduction of the light chain segment of the immunoglobulin complex, consisting of either the lambda or kappa light chain. These proteins are referred to as Bence-Jones proteins and are the most commonly observed immunoglobulin fragments in the monoclonal gammopathies.2 There are rare instances where a malignant plasma cell neoplasm will be nonsecretory. These tumors occur in approximately 1% of all cases of multiple myeloma and are referred
    [Show full text]
  • Chapter 7: Hematologic Disorders and Kidney Disease
    Chapter 7: Hematologic Disorders and Kidney Disease Ala Abudayyeh, MD,* and Kevin Finkel, MD, FACP, FASN, FCCM*† *Division of General Internal Medicine, Section of Nephrology, University of Texas MD Anderson Cancer Center, Houston, Texas; and †UTHealth Science Center at Houston Medical School, Department of Medicine, Division of Renal Diseases and Hypertension, Houston, Texas MULIPLE MYELOMA chains precipitate with Tamm-Horsfall protein (THP) secreted by the thick ascending limb of the Pathogenesis loop of Henle and produce casts in the distal tubule. Multiple myeloma (MM) is a hematologic malig- Decreased GFR may increase the concentration of nancy involving the pathologic proliferation of light chains in the distal tubule and enhance the terminally differentiated plasma cells. It is the formation of casts. Therefore, hypercalcemia, vol- second most common hematologic malignancy ume depletion, diuretics, and nonsteroidal anti- behind non-Hodgkin lymphoma, with an annual inflammatory drugs can exacerbate renal injury. incidence of 4–7 cases per 100,000 in the United In some cases of AKI associated with MM, cast States. Clinical symptoms are due to osteolysis of formation is rare on renal biopsy. Instead, renal the bone, suppression of normal hematopoiesis, injury is attributed to the direct toxic effects of and the overproduction of monoclonal immuno- urinary free light chains (FLCs) on proximal tubule globulins that deposit in organ tissues. Clinical cells (5,6). After reabsorption, lysosomal degrada- symptoms include bone pain and fractures, anemia, tion of FLCs can activate the NF-kB pathway lead- infections, hypercalcemia, edema, heart failure, and ing to oxidative stress with an inflammatory renal disease. response, apoptosis, and fibrosis.
    [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]
  • 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.
    [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]