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Konon Eagles
Konon Eagles

Morphology Of Blood Disorders PDF



Morphology of Blood Disorders, 2nd edition is an outstanding atlas with over 800 high-quality digital images, covering the whole spectrum of blood and bone marrow morphology, with particular emphasis on malignant haematology. Originally written in the Italian language by two world leaders in the field, the book has been expertly translated by the renowned haematologist and teacher, Barbara Bain.




Morphology of Blood Disorders PDF



This book explores the major topics of haematological pathology, blending classical teaching with up-to-date WHO classification and terminology. Each image in this book is derived from material obtained for diagnostic purposes from patients with serious haematological conditions. Morphological details are supplemented by detailed descriptions of the output and role of automated instruments in disorders of the blood.


Morphology of Blood Disorders, 2nd edition is an essential reference source for diagnosis in the haematology laboratory, designed to be the go-to guide for anyone with an interest in blood cell morphology.


Health conditions that affect the blood can be life threatening, but effective treatment is often available. In the United States, blood diseases accounted for 10,066 deaths in 2008, mostly different types of anemia.


Red blood cells have a slightly indented, flattened disk shape. They transport oxygen to and from the lungs. Hemoglobin is a protein that contains iron and carries oxygen to its destination. The life span of a red blood cell is 4 months, and the body replaces them regularly. The human body produces around 2 million blood cells every second.


Bone marrow produces red blood cells, white blood cells, and platelets, and from there they enter the bloodstream. Plasma is mostly water that is absorbed from ingested food and fluid by the intestines. The heart pumps them around the body as blood by way of the blood vessels.


The platelets in blood enable the clotting, or coagulation, of blood. When bleeding occurs, the platelets group together to create a clot. The clot forms a scab, which stops the bleeding and helps protect the wound from infection.


Blood groups are important during pregnancy. If a pregnant person has RhD-negative blood, for example, but the fetus inherits RhD-positive blood, treatment will be necessary to prevent a condition known as hemolytic disease of the newborn.


Blood is essential for maintaining the health and life of the human body. It has many functions, including delivering nutrients and oxygen. The four main components of blood are red blood cells, white blood cells, plasma, and platelets.


The classification of myeloid neoplasms and acute leukemias was last updated in 2016 within a collaboration between the World Health Organization (WHO), the Society for Hematopathology, and the European Association for Haematopathology. This collaboration was primarily based on input from a clinical advisory committees (CACs) composed of pathologists, hematologists, oncologists, geneticists, and bioinformaticians from around the world. The recent advances in our understanding of the biology of hematologic malignancies, the experience with the use of the 2016 WHO classification in clinical practice, and the results of clinical trials have indicated the need for further revising and updating the classification. As a continuation of this CAC-based process, the authors, a group with expertise in the clinical, pathologic, and genetic aspects of these disorders, developed the International Consensus Classification (ICC) of myeloid neoplasms and acute leukemias. Using a multiparameter approach, the main objective of the consensus process was the definition of real disease entities, including the introduction of new entities and refined criteria for existing diagnostic categories, based on accumulated data. The ICC is aimed at facilitating diagnosis and prognostication of these neoplasms, improving treatment of affected patients, and allowing the design of innovative clinical trials.


The major categories of myeloproliferative neoplasms (MPN)3 remain unchanged in the ICC; however, continuous integration of new molecular data and improved understanding of morphology have sharpened the proposed diagnostic criteria.10,11


In chronic myeloid leukemia (CML), progression to advanced phases12-14 (Table 2) is a consequence of continued BCR::ABL1 activity, induced proliferation of leukemic cells, and further genetic instability and DNA damage.15 This invariably leads to clonal evolution and acquisitions of mutations both inside and outside the BCR::ABL1 kinase domain and additional chromosomal abnormalities (ACAs). Therefore, the presence of major route ACAs at diagnosis or the acquisition of major route ACAs on treatment are considered as the hallmark of CML in accelerated phase (CML-AP),14,16 although most ACAs were defined prior to the use of tyrosine kinase inhibitor therapy. A bone marrow (BM) trephine biopsy is indicated for patients who meet any of the criteria for CML-AP or blast phase (CML-BP) and for patients who have a clinical history suggestive of disease progression (eg, progressive splenomegaly). Importantly, an increase in BM reticulin fibers at the time of diagnosis is correlated with a decreased major molecular response rate in the first year of tyrosine kinase inhibitor therapy.17 The ICC has maintained a blast percentage threshold of 10% to 19% and at least 20% in the blood or BM to establish the diagnosis of AP and BP, respectively. Increasing numbers of lymphoblasts (>5%) in peripheral blood (PB) or BM may indicate impending lymphoid BP and thus should prompt further laboratory and genetic studies.18 Of note, other classification and risk stratification systems that include the International Blood and Marrow Transplant Registry,19 M. D. Anderson Cancer Center,20 and the European LeukemiaNet21 have defined a higher blast threshold of more than 30% for BP and are frequently used as eligibility criteria in clinical trials.12,21


The classical BCR::ABL1-negative MPN subtypes include polycythemia vera (PV) (Table 3), essential thrombocythemia (ET) (Table 4), and primary myelofibrosis (PMF) (Table 5). The principal objective in the classification of these cases is to reduce diagnostic uncertainty especially in initial/early disease stages presenting with elevated platelet counts and to optimize clinical management of patients.10 The integration of molecular findings with BM morphology and blood counts remains the cornerstone of diagnosis. Importantly, morphologic diagnosis should not only focus on megakaryocytic atypia but has to consider characteristic patterns of other features like age-related cellularity, changes in erythropoiesis, and neutrophil granulopoiesis in context with the grade of BM fibrosis.22 Following the 2016 revision of the WHO classification, an increasing number of investigators were able to validate the diagnostic accuracy of this approach and consequently strongly support the definition of an early/pre-fibrotic stage of PMF (pre-PMF).23-26 In this context, dense clustering of megakaryocytes (3 or more megakaryocytes lying adjacent without other BM cells in between), which is generally accepted as the morphologic hallmark of PMF,22,27 does not exclude the diagnosis of ET, because infrequently small megakaryocytic clusters may be present even in this subtype. Compared with pre-PMF, patients with ET usually present with normal white blood cell counts, no anemia, normal lactate dehydrogenase (LDH) values, less frequently splenomegaly, and lower numbers of CD34-positive progenitor cells in PB and BM.23,24,26 Distinction is important because ET has a lower risk for major hemorrhagic events, a significantly lower risk of myelofibrotic progression (ie, post-ET myelofibrosis) ranging between 0.8% and 4.5% at 10 years, and a very low risk of transformation to BP with more than 20% of PB/BM blasts with a reported 10-year cumulative incidence between 0.7% and 1.9%.28,29


Chronic eosinophilic leukemia, not otherwise specified (CEL, NOS) is an MPN characterized by persistent eosinophilia not meeting the criteria for other genetically defined entities (Table 7). Mutations by NGS have helped to establish clonality in a significant subset of cases with eosinophilic disorders.39-42 However, like other myeloid neoplasms, the application of NGS data in eosinophilic disorders can be challenging because of the prevalence of clonal hematopoiesis of indeterminate potential (CHIP) and technical limitations in using NGS data to define clonality. The BM of CEL, NOS typically shows hypercellularity with dysplastic megakaryocytes, with or without dysplastic features in other lineages, and often significant fibrosis associated with an eosinophilic infiltrate.43,44 Abnormal BM histopathology is now incorporated into the diagnostic criteria for CEL, NOS, allowing for a more definitive confirmation of the neoplastic nature of CEL, NOS and providing a better separation from the related entities idiopathic hypereosinophilic syndromes (iHES) and HE of unknown significance (HEus).45 iHES is characterized by (1) persistent PB hypereosinophilia; (2) organ damage related to infiltration by eosinophils; and (3) no known reactive, familial, or neoplastic etiology, as well as exclusion of lymphocyte-variant HES.46 HEus presents with persistent HE, but has no associated organ damage. Except for increased eosinophils, the BM of iHES and HEus is morphologically unremarkable.43,47 The refined criteria for CEL, NOS and iHES are shown in Tables 7 and 8.


The MDS/MPN category comprises a heterogeneous group of diseases characterized by the co-occurrence of clinical and pathologic features of both myelodysplastic and myeloproliferative neoplasms.81 The 2016 classification included chronic myelomonocytic leukemia (CMML), atypical CML, BCR::ABL1 negative (aCML), juvenile myelomonocytic leukemia (JMML), MDS/MPN with ring sideroblasts and thrombocytosis (MDS/MPN-RS-T), and MDS/MPN unclassifiable (MDS/MPN-U). The ICC now expands on these categories and moves JMML to be grouped with pediatric and/or germline mutation associated disorders. 041b061a72


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