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  • 165.00 lei

    George Henry Falkiner Nuttall (1862–1937) was an American-British bacteriologist who made significant contributions to various aspects of medicine. In this book, which was first published 1904, Nuttall provides a record of investigations carried out in the Pathological Laboratory of the University of Cambridge, chiefly during 1902. The text presents a demonstration of blood relationships among animals by means of the precipitin test for blood. A bibliography is also included. This book will be of value to anyone with an interest in haematology and the history of science.

  • 220.00 lei

     A concise, clinical handbook covering the whole of haematology Reflects current practice with up-to-date investigation and management Easy-to-understand and useful for all grades of medical, nursing, technical, and research staff Includes rare disorders as well as common conditions affecting both adults and children Practically focused, written by a team of experienced, practicing clinicians New to this edition Contains all the latest guidelines and a brand new chapter on rare diseases All sections and protocols on malignant haematology have been completely revised Covers all major advances in the specialty including mlaignant haematology and transfusion medicine The Oxford Handbook of Clinical Haematology provides core and concise information on the entire spectrum of blood disorders affecting both adults and children. Updated for its fourth edition, it includes all major advances in the specialty, including malignant haematology, haemato-oncology, coagulation, transfusion medicine, and red cell disorders, with a brand new chapter on rare diseases. Practically focused, and specifically designed for ease-of-use, and rapid access to the information you need, this handbook is an indispensable resource on all aspects of haematology for all trainee doctors, nurses, technicians, and research professionals. The handbook is divided into clinical approach and disease-specific areas. The clinical approach section outlines various symptoms and signs in patients with blood disease to enable the reader to formulate a sensible differential diagnosis beofre embarking on investigation and treatment. The disease-specific section is written by four authors whose expertise covers the whole breadth of diseases included in the book. All authors have contributed to national guidelines (e. g. British Committee for Standards in Haematology, BCSH) and are experts in the evidence base that exists for each topic. The Oxford Handbook of Clinical Haematology offers a concise and logical approach to caring for patients with diseases of the blood. 1: Clinical approach 2: Red cell disorders 3: White blood cell abnormalities 4: Leukaemia 5: Lymphoma 6: Myelodysplasia 7: Myeloproliferative neoplasms (MPNs) 8: Paraproteinaemias 9: Haematopoietic stem cell transplantation (SCT) 10: Haemostasis and thrombosis 11: Immunodeficiency 12: Paediatric haematology 13: Haematological emergencies 14: Supportive care 15: Protocols and procedures 16: Haematological investigations 17: Blood transfusion 18: Rare diseases A1: Haematology online A2: Charts and nomograms A3: Normal ranges

  • 220.00 lei


    Thrombosis is a deadly malfunctioning of the hemostatic system occurring in numerous conditions and states, from surgery and pregnancy to cancer, sepsis and infarction. Despite availability of antithrombotic agents and vast clinical experience justifying their use, thrombosis is still responsible for a lion's share of mortality and morbidity in the modern world. One of the key reasons behind this is notorious insensitivity of traditional coagulation assays to hypercoagulation and their inability to evaluate thrombotic risks. A possible solution is proposed by use of global assays that aim to mimic and reflect the major physiological aspects of hemostasis process in vitro. Here we review the existing evidence regarding the ability of both established and novel global assays to evaluate thrombotic risk in specific disorders. The biochemical nature of this risk and its detectability by analysis of blood state in principle are also discussed.

  • 220.00 lei


    Bleeding disorders are caused by the defects in the blood vessels, the coagulation mechanism or blood platelets an affected individual may bleed spontaneously for a longer time than a healthy person after an injury or surgery. Hemophilia is a group of inherited disorder in which blood doesn‘t clot properly. Hemophilia is usually not associated with higher incidence or any other congenital abnormality. The incidence is about 1:10000 male‘s birth and all races, religions and socioeconomically groups are affected.Hemophilia is the standard international spelling, also known as haemophilia in the UK, other translations include: hemofilie, haemofili, hemophilie, hemophilia, emofilia. Hemophilia is two types: Haemophilia A: This disease is caused due to deficiency of Factor VIII (FVIII) and Haemophilia B: It is caused due to deficiency of Factor IX*.

  • 27500lei 235.00 lei



    The acclaimed full-color review of the underlying principles of blood diseases and disorders – based on a Harvard Medical School hematology course A Doody's Core Title for 2020! LANGE Pathophysiology of Blood Disorders, Second Edition is a well-illustrated, easy-to-absorb introduction to the physiological principles underlying the regulation and function of blood cells and hemostasis, as well as the pathophysiologic mechanisms responsible for the development of blood disorders. Featuring a strong emphasis on key principles, the book also covers diagnosis and management primarily within a framework of pathogenesis. The organization and content of this book are based on a 3-week hematology course given to students in their second year at Harvard Medical School. All of the authors are lecturers in this course and many of the figures have been taken directly or adapted from their lectures. FEATURES OF THE SECOND EDITION: • NEW summary boxes with high yield points to remember • All figures have been redrawn by a single artist for quality and consistency • A more user-friendly presentation • Each chapter includes learning objectives, and self-assessment questions with detailed explanations • Numerous tables and diagrams encapsulate important information Hailed for its uniformity of style, clarity, brevity, and high level of scientific rigor and clinical relevance, LANGE Pathophysiology of Blood Disorders, Second Edition will prove valuable to medical students, as well as physicians at all stages of their training.


    Table of Contents:


    1. Introduction to Blood and Hematopoietic Tissues

    2. Hematopoiesis

    Part I Anemia and Red Cell Disorders

    3. Overview of the Anemias

    4. Anemias Due to Bone Marrow Failure or Infiltration

    5. Iron Homeostasis: Deficiency and Overload

    6. Megaloblastic Anemias

    7. Anemias Associated With Chronic Illness

    8. Thalassemia

    9. Sickle Cell Disease

    10. Inherited Hemolytic Disorders of the Red Cell Membrane and Red Cell Metabolism

    11. Acquired Hemolytic Anemias

    12. Erythrocytosis

    Part II Hemostasis and Thrombosis

    13. Overview of Hemostasis

    14. Platelet Disorders

    15. Inherited Coagulation Disorders

    16. Acquired Coagulation Disorders

    17. Thrombotic Disorders

    Part III White Blood Cell Disorders

    18. Leukocyte Function and Nonmalignant Leukocyte Disorders

    19. Introduction to Hematologic Malignancies

    20. Myeloproliferative Neoplasms and Myelodysplastic Syndromes

    21. Acute Leukemias

    22. Non-Hodgkin Lymphomas and Chronic Lymphocytic Leukemias

    23. Hodgkin Lymphoma

    24. Multiple Myeloma and Related Disorders

    Part IV Transfusion Medicine

    25. Blood Transfusion

    26. Hematopoietic Stem Cell Transplantation



  • 31000lei 255.00 lei



    The new and fully updated edition of the definitive haematology textbook for undergraduate and postgraduate students and trainees

    Hoffbrand's Essential Haematology is widely regarded as the most authoritative introduction to the subject available, helping medical students and trainee doctors understand the essential principles of modern clinical and laboratory haematology for nearly four decades. Now in its eighth edition, this market-leading textbook introduces the formation and function of blood cells and the diseases that arise from dysfunction and disruption of these processes.

    Beautifully presented with over 300 stunning colour illustrations, the new edition has been thoroughly updated to reflect recent advances in knowledge of the pathogenesis of blood diseases and their diagnosis and treatment. This new text:

    ·         Describes disorders and diseases of the blood such as the various anaemias and white cell disorders, leukaemias, lymphomas and myeloma, as well as bleeding and thrombotic disorders

    ·         Incorporates the latest World Health Organization (WHO) classification of haematological neoplastic diseases

    ·         Reviews contemporary application of multiparameter flow cytometry, DNA sequencing and other technologies in evaluating patients with suspected haematological disease

    ·         Discusses the therapeutic use of chimeric antigen T-cells, mono- and bi-specific monoclonal antibodies, inhibitors of intracellular signalling pathways and direct orally acting anticoagulants

    ·         Includes sections on blood transfusion and the haematological aspects of systemic diseases, pregnancy and the neonate

    Hoffbrand's Essential Haematology is a vital resource for all students and trainees, and a valuable reference for practicing specialists wishing to update their knowledge.




    Preface to the Eighth Edition vi

    Preface to the First Edition vii

    How to use your textbook viii

    About the companion website x

    1 Haemopoiesis 1

    2 Erythropoiesis and general aspects of anaemia 11

    3 Hypochromic anaemias 27

    4 Iron overload 42

    5 Megaloblastic anaemias and other macrocytic anaemias 50

    6 Haemolytic anaemias 64

    7 Genetic disorders of haemoglobin 78

    8 The white cells, part 1: granulocytes, monocytes and their benign disorders 96

    9 The white cells, part 2: lymphocytes and their benign disorders 111

    10 The spleen 126

    11 The aetiology and genetics of haematological neoplasia 132

    12 Management of haematological malignancy 147

    13 Acute myeloid leukaemia 158

    14 Chronic myeloid leukaemia 172

    15 Myeloproliferative neoplasms 182

    16 Myelodysplastic syndromes 196

    17 Acute lymphoblastic leukaemia 206

    18 The chronic lymphocytic leukaemias 219

    19 Hodgkin lymphoma 229

    20 Non-Hodgkin lymphomas 238

    21 Multiple myeloma and related plasma cell neoplasms 255

    22 Aplastic anaemia and bone marrow failure 272

    23 Haemopoietic stem cell transplantation 281

    24 Platelets, blood coagulation and haemostasis 296

    25 Bleeding disorders caused by vascular and platelet abnormalities 312

    26 Coagulation disorders 324

    27 Thrombosis 1: pathogenesis and diagnosis 338

    28 Thrombosis 2: treatment 347

    29 Haematological changes in systemic diseases 360

    30 Blood transfusion 372

    31 Pregnancy and neonatal haematology 386

    Appendix 395

    Index 401


  • Blood Science: Principles and Pathology
    La comanda in aproximativ 4 saptamani
    29700lei 270.00 lei



    An integrated textbook on Blood Science, haematology, clinical biochemistry and immunology, in accordance with the changing educational and training structure for Biomedical Scientists.


    Table of Contents:


    1 Introduction to Blood Science

    Learning objectives

    1.1 What is blood science?

    An historical perspective

    Table 1.1 The biomedical or life sciences

    The reference range

    The normal distribution

    Figure 1.1 The normal distribution.

    The non-normal distribution

    Figure 1.2 The non-normal distribution.

    Variation in reference ranges


    Figure 1.3 Common biochemistry tests. Selected biochemistry results on a presumed healthy middle-aged male. The blood tests themselves are printed out in the first column on the left (headed by urea). The next column is the actual result (in this case, 4.1), and then the units (mmol/L), and finally the reference range on the right (3.0–8.3). Results which are outside the reference range are generally highlighted by an asterisk. The fact that there are no asterisks present means that all results are acceptable and no further testing is required.

    Position statement

    1.2 Biochemistry

    Urea and electrolytes

    Liver function tests

    Lipids, glucose, diabetes and heart disease



    Cardiovascular disease

    Calcium, phosphate, magnesium and bone disease

    Hormones and endocrine disorders

    Other tests

    Table 1.2 Common biochemistry tests

    1.3 Blood transfusion

    Blood groups

    Table 1.3 ABO blood group factors.

    The practice of blood transfusion

    Blood group determination

    Antibody screening


    Blood components (previously blood products)

    Clinical aspects of blood transfusion

    Sources of error

    Table 1.4 Some signs and symptoms of a transfusion reaction.

    Responses to an incompatible transfusion


    1.4 Genetics

    Genetic disease in families


    Genes, chromosomes and DNA

    Chromosomal disorders

    Table 1.5 Chromosome abnormalities.

    Figure 1.4 A normal karyotype: 46 chromosomes arranged in 23 pairs, dependent on the length and the banding patterns, of 22 pairs of autosomes and two sex chromosomes.

    Gene disorders




    Genetics as an independent blood science

    Table 1.6 Molecular genetics across pathology.

    Blood science angle: Haematology and molecular genetics

    1.5 Haematology

    The blood film

    Figure 1.5 A blood film.

    The full blood count

    Red blood cells

    Figure 1.6 The full blood count.

    White blood cells


    Erythrocyte sedimentation rate


    Prothrombin time

    Activated partial thromboplastin time


    Pathology of thrombosis and haemostasis



    Vitamin B12

    The laboratory in micronutrient deficiency

    Haematological disease

    Table 1.7 Common routine haematology blood tests.

    1.6 Immunology


    Figure 1.7 An antibody molecule.



    An inappropriately excessive immune response

    A weak or absent immune response

    Table 1.8 Immunology

    1.7 The role of blood science in modern healthcare

    Blood science in human disease


    Connective tissue disease

    Cardiovascular disease

    Blood scientists: who are they?

    Table 1.9 Blood science and human disease.

    The role of the higher education institutions

    Training in blood science

    Figure 1.8 Training of blood scientists. (

    1.8 What this book will achieve



    Further reading

    Web sites

    2 Analytical Techniques in Blood Science

    Learning objectives

    2.1 Venepuncture

    Figure 2.1 Venepuncture. The process of obtaining a sample of blood, generally from a vein near the surface of the skin on the inside of the elbow. Blood is being drawn into a vacutainer with a yellow top (right-hand side) that has no anticoagulant, but a small piece of gel at the bottom (left-hand side) to help the preparation of serum.

    2.2 Anticoagulants

    Figure 2.2 Vacutainers. Note the different coloured tops, indicating different anticoagulants (blue: sodium citrate; grey: fluoride oxalate) or no anticoagulant (beige). Note also that vacutainers come in different sizes.

    Key anticoagulants

    Ethylenediaminetetraacetic acid

    Sodium citrate

    Fluoride oxalate

    Lithium heparin

    2.3 Sample identification and tracking

    2.4 Technical and analytical confidence

    Assay performance

    Confirming or refuting disease

    Figure 2.3 Concentrations of substance X in the plasma of patients and controls. The thick bar represents the average (mean) value.

    Value in predicting disease

    Confidence in the result

    Example 2.1: Value of a method


    Figure 2.4 The accuracy and reproducibility of a test illustrated by an archery target. In the top figure, the results are spread out (poor reproducibility) but centre on the bull's eye (accurate). In the middle figure, the results are tightly clustered together (good reproducibility) but are far from the bull's eye (inaccurate). The bottom figure shows results that are both tightly clustered and accurate.

    Quality control

    Quality assurance

    Example 2.2: Quality assurance


    Figure 2.5 This Levey–Jennings plot shows sequential results for substance X, which are acceptably stable up to index point 10, then become highly variable, indicating a problem with the method.

    2.5 Major techniques

    An erratic analyser

    The standard operating procedure

    The standard curve

    Figure 2.6 A standard curve. Analyser results from a series of five samples of known concentrations of the analyte (open circles) are plotted on a graph. The analyser result from the patient (perhaps 0.47 units on the vertical axis) drawn across the plot meets the standard curve at point ‘X’. Drawing down from this point to the horizontal axis gives a result of about 120 units.

    Upper and lower limits of sensitivity


    Analysis of metals and nonmetals


    The Beer–Lambert law


    Mass spectrometry



    Enzyme-linked immunosorbent assay

    Figure 2.7 Five common steps in an ELISA, where the amount of an analyte in a sample is converted to colour for analysis. The amounts of the reagents are in excess so that the sole rate-limiting factor in determining the amount of colour being developed is the amount of the analyte.

    Chemiluminesence immunoassay

    Fluorescence immunoassay

    Figure 2.8 A microtitre plate showing results of an ELISA procedure. Samples are loaded in groups of three (triplicates). The three columns (counting from the left: numbers 10–12) of the far right of the plate are the standard curve. The topmost triplet of wells have the highest concentration of a known amount of the analyte (perhaps 100 units/L), and triplets of wells below this have proportionately lower amounts of the known standard (80 units/L, 60 units/L and so on down to maybe 5 units/L). The rest of the plate, to the left of the standard curve, contains triplicates of samples of plasma from different patients. Note that some are highly coloured (such as the three wells in horizontal row F, vertical columns 1–3), and other less so (such as row B, columns 4–6). The standard curve (Figure 2.6) will translate these unknown colours to the concentration (units/L) of the analytes in the plasmas. Columns 7–9 are blank, and so have no colour.

    Immunoturbidimetry and nephelometry




    High-performance liquid chromatography

    Gas–liquid chromatography

    Figure 2.9 HPLC. This compact workstation consists of a series of enclosed units containing the columns, reservoirs for buffers, pumps and (on the far left) the sample area and controls. The Dionex HPLC-DAD offers the separating power of HPLC linked to a photodiode array detector (DAD) for clinical and forensic applications. The DAD records the absorbance spectra of compounds over a range of wavelengths (e.g. 200–595 nm) as they pass through the detector flow cell. This data can then be used to provide definitive identification of a compound, or to select the optimum wavelength for quantitation.


    Counting cells and particles


    Flow cytometry

    Fluorescence-activated cell scanning

    Figure 2.10 Flow cytometry. This technique for counting white cell subpopulations makes use of the size of the nucleus and presence of intracellular granules. The colour coding defined by the analyser's software in this figure makes recognition of each type of cell easier; the cells themselves have no colour. Mono: monocytes; Lymph: lymphocytes; Neut: neutrophils; Baso: basophils; Eo: eosinophils. These cells are described in detail in Chapter 7.


    Figure 2.11 FACS analysis of T lymphocyte subsets. In the upper figure, the scientist has put a ‘gate’ around that region of the plot where they expect lymphocytes to be, and the FACS machine software has coloured these in red. The lower figure shows analysis of those cells which have bound an antibody to CD4 (itself bound to the fluorochrome FITC, lower right (LR) quadrant), an antibody to CD8 (itself bound to fluorochrome phycoerythrin, upper left (UL) quadrant), both antibodies (lower left (LL) quadrant) and neither antibody (upper right (UR) panel).

    Figure 2.12 Immunocytochemistry detecting an abnormal white cell (stained red). Unstained cells are counterstained light blue/grey. The enzyme is alkaline phosphatase.


    Light microscopy

    Figure 2.13 A simple bench light microscope. The top arrow indicates the eyepieces. The three objective lenses are highlighted by the arrow on the left; the stage, where the glass slide is placed, is indicated by the lower right arrow. The lowest arrow on the right points out the light source; the lowest on the left indicates the focusing apparatus.

    Fluorescence microscopy

    Other microscopy


    Figure 2.14 A biochemistry analyser. This substantial item of capital equipment is capable of the simultaneous analysis of several different analytes. However, it still needs to be programmed by scientists, who also need to ensure reagents are kept topped up and that waste is being safely disposed of.

    Figure 2.15 A haematology tracking system. A vacutainer is conducted along a track, and different machines are programmed to perform their own specific analyses as required.

    2.6 Molecular genetics

    Tools in molecular genetics

    Purification and extraction of DNA

    Analysis of DNA

    Figure 2.16 Identification of mutated genes. Two different restriction endonucleases are mixed with the DNA (step 1). One enzyme cuts the DNA strand at nucleotides AB/AB, the other at XY/XY. In a normal situation, this generates two identical small fragments: AB=====XY. The same enzymes applied to the abnormal DNA, with abnormal nucleotides XY/OY but normal AB/AB sequences, which generate only one large fragment because the enzyme specific for XY/XY cannot cut the mutated sequence (step 2). Mixing the fragments with radiolabelled probe AB-----XY will see the probe binding both fragments as both the short normal and longer mutated fragments contain the matching DNA sequence (step 3). When this mixture is run through an electrophoresis gel, the smaller normal fragments will migrate faster than the larger abnormal fragments. The size of the patient's fragments can be assessed by running a series of fragments of known size.

    The application of molecular genetics to human disease

    Molecular genetics in biochemistry

    Figure 2.17 Gene analysis. This is an amplification refractory mutation system PCR used for diagnosis of a β-thalassaemia mutation. Lane 1 (left-hand side) is molecular markers, lanes 2 and 3 patient 1 (normal and mutant primers respectively), lanes 4 and 5 patient 2 (normal and mutant) and lanes 6 and 7 patient 3 (normal and mutant primers). The arrowed bands represent internal control bands that identify a standard region of the DNA regardless of the thalassaemia mutation. This is very useful in confirming that the PCR reaction is optimized as the absence of the specific primer band (normal or mutant), and is diagnostic.

    Molecular genetics in haematology

    Molecular genetics in immunology

    The place of molecular genetics in diagnosis and management


    2.7 Point of care testing



    The advantages of POCT

    Table 2.1 Examples of POCT applications.

    The disadvantages of POCT

    Regulations and guidelines on POCT

    2.8 Health and safety in the laboratory

    Table 2.2 Laboratory hazards.

    The Health and Safety at Work Act

    Duties of employers

    Duties of employees

    The Control of Substances Hazardous to Health (COSHH)

    Figure 2.18 Identification of hazards. All laboratory hazards must be identified. As far as chemicals are concerned, this can be marked on the labels. These include skull and crossbones with ‘toxic’ label on the left, the smaller orange marks on the label of the containers in the middle, and the diamonds on the propylene squeezy bottle on the right.


    Further reading

    Web sites

    3 The Physiology of the Red Blood Cell

    Learning objectives

    3.1 Introduction

    Table 3.1 Red cell aspects of the full blood count and allied tests.a

    3.2 The development of blood cells

    Bone marrow architecture and cellularity

    Models of differentiation

    Figure 3.1 Haemopoiesis. The pluripotent stem cell gives rise to two colony forming units (CFUs: myeloid and lymphoid) that in turn produce lineage-specific stems cells. These ultimately produce mature cells that leave the bone marrow and enter the blood.

    Growth factors

    Bone marrow sampling and analysis

    Figure 3.2 Top: A bone marrow aspirate spread on to a glass slide, dried, and stained as if a sample of peripheral blood. Middle: A trephine sample that retains the architecture of the bone marrow. Lower: For comparison, a sample of peripheral blood at the same low power magnification. Note the markedly fewer number of white cells in the latter.

    Special investigations


    Table 3.2 Commonly used CD markers.a

    Flow cytometry

    Blood science angle: Flow cytometry

    3.3 Erythropoiesis

    Figure 3.3 Erythropoiesis. Stages in the development of the red cell in the bone marrow. Early stages involve the derivation of the lineage-specific CFU for myeloid cells, which develop into proerythroblasts and erythroblasts under the influence of erythropoietin. The nucleated red blood cell loses its nucleus to become a reticulocyte, and then the mature red cell.

    Blood science angle: Erythropoietin

    3.4 The red cell membrane

    Table 3.3 Glycoprotein components of the red cell membrane.

    The organization of the membrane

    Figure 3.4 The red blood cell membrane. Our current view of the red cell membrane can be explained in this cartoon. The ankyrin complex (left) includes transmembrane molecules Band 3 and GpA that span the lipid bilayer. The intracytoplasmic tails link to ankyrin and protein 4.2, and thus the internal cytoskeletom on alpha and beta spectrins. The 4.2 complex (right) also include Band 3, but also GpC. These molecules link to protein 4.1 and tropomyosin and also the spectrins. Not shown for clarity are molecules such as Duffy and Kell.

    Cluster 1

    Cluster 2

    The cytoskeleton and cell volume

    Consequences of membrane specialization

    Blood science angle: Blood groups

    3.5 The cytoplasm of the red cell



    Figure 3.5 Major steps involved in the synthesis of haem in cells such as the erythroblast and nucleated red cell. On the left, within the mitochondrion, glycine and succinyl-coA form aminolevulinic acid, which leaves the mitochondrion and is converted into porphobilinogen, four of which form uroporphyrinogen. The latter enters the mitochondrion, and the enzyme ferrochelatase inserts iron, forming haem.

    Blood science angle: Micronutrients


    Table 3.4 Iron requirements.

    Figure 3.6 Regulation of iron uptake, and its fate. Iron in the diet (1) passes through the enterocyte and is carried in the blood by transferrin (2). In the erythroblast in the bone marrow it is incorporated into haemoglobin (3); in other cells such as the hepatocyte or macrophage, it is stored in ferritin and haemosiderin (3). Tfr: transferrin receptor.

    Blood science angle: Iron genetics



    Embryonic and foetal haemoglobin

    Adult haemoglobin

    Table 3.5 Globin chains in haemoglobin variants.

    Figure 3.7 Haemoglobin (Hb) development. Changes in species of Hb in different stages of development in the embryo (weeks 0–10) where zeta, epsilon and alpha globin molecules are synthesized. As the embryo grows into the foetus the zeta and epsilon chains give way to gamma globin, whilst close to birth the beta globin molecules take over from gamma globin. From perhaps 30 weeks, delta globin genes are active. The gamma globin genes slowly shut down so that after 30 or 40 weeks of age only a trace remains, the dominant molecules alpha and beta chains that form HbA.

    Other haemoglobin species

    Red cell enzymes and metabolism

    Figure 3.8 Red cell metabolic pathways. The major pathway for the anaerobic generation of energy (in the form of adenosine triphosphate (ATP), nicotinamide adenine dinucleotide phosphate (NADH) and nicotinamide adenine dinucleotide phosphate hydrogen (NADPH)) is the Embden–Meyerhof glycolytic pathway (central spine). See text for details.

    Generating energy

    Protection from oxygen

    Clinical aspects of metabolism

    3.6 Oxygen transport

    Figure 3.9 The oxygen saturation curve. The normal relationship between the partial pressure of oxygen in the blood and the degree to which haemoglobin is saturated with oxygen is given by the solid line. It is convenient to refer to the degree of oxygen saturation where 50% of the haemoglobin is saturated (i.e. the P50, where in theory each molecule of haemoglobin carries two molecules of oxygen from a maximum of four molecules). This equates to a partial pressure of oxygen pO2 of approximately 26.8 mmHg.

    Blood science angle: Blood gases

    Factors influencing oxygen metabolism

    Table 3.6 Factors influencing the oxygen dissociation curve.

    3.7 Recycling the red cell

    Figure 3.10 Red cell recycling. When the red cell comes to the end of its life, it is broken up and many of its components are recycled. An exception to this is bilirubin, which is excreted.

    Blood science angle: Jaundice

    3.8 Red cell indices in the full blood count

    Figure 3.11 The RDW. Although both histograms show a roughly symmetrical distribution, values of the MCV in the normal (upper plot) vary from about 60 to 115, giving a mean of 84.9 and a standard deviation of 9.15, so that the RDW is (9.15/84.9) × 100 = 10.8%. Note that in the lower (abnormal) plot, although the mean MCV is a little higher, 86.7, the spread of results is much greater, ranging from 30 to 150, giving a larger standard deviation of 14.99. Hence, the RDW in the lower plot is 17.3%, outside the reference range of 10.3–15.3%.

    Figure 3.12 The ESR. A series of eight ESR tubes, showing a column of cloudy plasma above the column of red cells. Clearly, there is variation in the level of the red cells. In numbers 1–3 and 7 the plasma is less than 10 mm, so the result is normal. In columns 5, 6 and 8 the column of plasma is much greater, being in the region of 70 mm, 80 mm and 105 mm respectively. All these are abnormal. However, in sample 4, the cutoff is not as clear cut, but many would report a result of 30 mm.

    3.9 Morphology of the red cell

    Figure 3.13 Normal red cells with a roughly uniform size and shape. Almost all of them have a small area of pallor right in the centre.

    Figure 3.14 Anisocytosis. This photograph shows variety in the size of the cell; unlike Figure 3.15, there is a great variety in the size of the cells – some are clearly much larger than others; there are both macrocytes and microcytes. Many of the large cells are fully coloured, whereas many of the small cells are coloured only around the outside, with lack of staining in the middle. These small cells may therefore be hypochromic as well as microcytic.


    Figure 3.15 Reticulocytes. This high-magnification photograph is dominated by two reticulocytes (arrowed). They have a more ‘blue’ colour than the other red cells.

    Figure 3.16 The effect of storage. Samples taken into ethylenediaminetetraacetic acid and stored incorrectly or too long will undergo changes resulting in crenation (with lots of ‘spikes’) of the red cells and deterioration of the white cells.

    Figure 3.17 The effect of poor fixation. Poor drying and fixation results in trapped water within the cells and poor morphology.



    Variation in colour

    Other morphological changes

    Inclusion bodies


    Further reading

    4 The Pathology of the Red Blood Cell

    Learning objectives

    4.1 Introduction: diseases of red cells

    Table 4.1 The diverse aetiology of red cell pathology.


    Definitions of anaemia

    Table 4.2 Signs and symptoms of anaemia.a

    A young woman with sickle cell disease

    Classifications of anaemia

    The size of the red cell




    4.2 Anaemia resulting from attack on, or stress to, the bone marrow

    Reduction in red cells alone

    Reduction in red cells and platelets

    Reduction in all blood cells

    Disease arising from the bone marrow itself

    Disease caused by factors originating outside the bone marrow

    Treatment of an anaemia resulting from disease of the bone marrow

    The role of the laboratory in anaemia following bone marrow changes

    Table 4.3 The bone marrow and anaemia.

    4.3 Anaemia due to deficiency


    Blood science angle: The liver

    Figure 4.1 Perls' stain. This process stains iron a blue colour, as illustrated in these two samples of bone marrow: (a) complete lack of blue colour, is from a patient with profound iron deficiency; (b) from a subject with normal iron stores.

    Vitamins B12, B6 and folate

    The role of the laboratory in anaemia following lack of micronutrients

    Microcytic anaemia

    Figure 4.2 Marked microcytic anaemia, in this case due to gross iron deficiency. Almost all of the cells are ‘empty’ of colour, and so of haemoglobin, and almost all are microcytic. Compared with Figure 3.2 and Figure 3.13.

    Macrocytic anaemia

    Figure 4.3 Macrocytic anaemia. These red cells are much larger than those of Figure 4.2, and are also much more heavily stained, and so have more haemoglobin. This macrocytosis is due to deficiency in vitamin B12; an additional factor is the increased number of segments of the nucleus of the neutrophil, the so-called hypersegmented neutrophil, an example of which is shown in this figure. There is also a moderate degree of anisocytosis (variation in the sizes of the red cells).

    Blood science angle: Immunology

    Table 4.4 Deficiency of iron and vitamin B12.

    Iron and vitamin B12 compared and contrasted

    Endocrine disorders

    4.4 Intrinsic defects in the red cell

    Defects in iron metabolism

    Defective synthesis of haem

    Figure 4.4 Ring sideroblast. Perls' stain is also used to define a sideroblast, which in this figure has a large (blue) deposit in the cytoplasm, but there are also some deposits in the nucleus. Ring sideroblasts can be found in sideroblastic anaemia and lead poisoning.

    Iron overload

    The role of the laboratory in iron-related pathology

    Figure 4.5 Basophilic stippling. These inclusion bodies, consisting of over a dozen very small blue or purple dots, can be very hard to detect. Notably, the red cell in which they occur is often larger than other cells.

    Blood science angle: Micronutrients

    Membrane defects

    Hereditary spherocytosis

    Hereditary elliptocytosis

    Figure 4.6 Hereditary spherocytosis. This is manifest as cells which have lost their central pallor. There is also a modest degree of anisocytosis. The bar represents 10 μm.

    Figure 4.7 Hereditary elliptocytosis. Few cells have retained their circular shape, the remainder varying from being slightly oval to grossly elliptical. The bar represents 10 μm.

    Hereditary stomatocytosis

    Paroxysmal nocturnal haemoglobinuria

    Figure 4.8 Hereditary stomatocytosis. This condition is characterized by a slot-shaped area of central pallor, although smaller cells have retained their normal round area of central pallor. The bar represents 10 μm.

    The laboratory in membrane defects

    Other membrane defects

    Figure 4.9 Paroxysmal nocturnal haemoglobinuria. This flow cytometry plot is the result of mixing red cells with one antibody to CD55 and another to CD59, both linked to different fluorescent probes (phycoerythrin and fluorescein isothiocyanate respectively). The machine counts the number of cells binding both antibodies (in the upper right (UR) quadrant), either antibody alone (upper left (UL) and lower right (LR)), or neither antibody (lower left (LL)). In health, all cells would express both CD55 and CD59, and so bind the antibodies, so that the UR quadrant should have almost 100% of the events. However, only 26.34% of the cells express neither CD55 nor CD59, making the diagnosis of PNH.

    The RDW and membrane defects

    Metabolic defects

    G6PD deficiency

    Pyruvate kinase deficiency

    Table 4.5 Defects in the membrane and in enzymes.


    Sickle cell anaemia

    Figure 4.10 The sickle cells are evident. Also present are a nucleated red blood cell and what is likely to be an extruded nucleus. There are also some target cells, so this may be from a patient with a mixed haemoglobinopathy.

    Other qualitative beta globin gene disorders


    Compound and other haemoglobinopathy

    Laboratory definition of haemoglobinopathy

    Table 4.6 Molecular genetics of the haemoglobinopathies.

    Figure 4.11 A wet preparation of whole blood from a patient with sickle cell disease that has been incubated with a buffer to induce hypoxia, and this has resulted in many red cells adopting the sickle shape.

    Figure 4.12 The solubility test. (a) Incubation of red cells in a lysing buffer will indicate those samples likely to come from a patient with sickle cell disease. Of the three tubes, that on the left is the negative control – the black line can easily be seen through the lysed cells. On the right is the positive control – the red cells have not been lysed and so the black line is almost completely obscured. In the middle is the test patient's sample, which clearly gives the same picture as the positive control, thus supporting the diagnosis of sickle cell disease. (b) After centrifugation, a positive result gives a dark red band at the top of clear plasma (middle and right tubes), whereas a negative result is a red column (left tube).

    Figure 4.13 Electrophoresis. (a) At alkaline pH (8.5) together with a commercial control (AFSC) at lane 1. Haemoglobin is a negatively charged protein at alkaline pH and will migrate towards the anode (+) in an electrical field. According to their electrical charges, different Hb variants will separate into different bands. Hb variants can then be identified and compared with known control bands. The results from different patients were as follows: lane 1, AFSC control; lane 2, AS; lane 3, SS + F; lane 4, AC (or A/O-Arab, or A/E); lane 5, SC (or S/O-ARAB, or S/E); lane 6, A; lane 7, SC (or S/O-ARAB or S/E); lane 8, AC (or A/O-Arab or A/E). (b) Haemoglobin electrophoresis results on citrate agar at acidic pH (6.0) together with a commercial control (FASC). The corresponding mobility for the same patients at alkaline pH (8.5) were (from left to right) as follows: lane 1 AC; lane 2, SC + F; lane 3, AS; lane 4, AC; lane 5, A; lane 6, SC + F; lane 7, SS; lane 8, AS + F; lane 9, FASC control.

    Laboratory findings in haemoglobinopathy

    Figure 4.14 HPLC for different haemoglobin species. (a) Normal HPLC scan showing the major peaks of HbA (83.2%) and minor peaks (in red) of HbA2 (2.6%) and HbF (2.2%). (b) The major peak in the middle of the plot, at the HbA position, makes up only 49.3% of total haemoglobin. Note the new large peak to the right, making up 35.2% of all the haemoglobin, and this is HbS. Minor peaks are HbA2 (3.8%) and HbF (1.0%).

    Figure 4.15 Gene analysis by polymerase chain reaction (PCR). BSu 36 I is a restriction enzyme with known restriction sites on the beta globin gene. In sickle cell disease some of these restriction sites disappear and therefore the enzyme cannot digest DNA from PCR products. Accordingly, larger PCR products can be viewed by electrophoresis in sickle cell disease (SS) compared with smaller (digested) bands in normal conditions. In heterozygous conditions (AS) both bands can be seen. Lane 1 is molecular marker, lanes 2 and 3 patient 1 (normal (N) and mutant (M) primers respectively), lanes 4 and 5 patient 2 (normal and mutant), lanes 6 and 7 patient 3 (normal and mutant primers), lane 8 is blank, the arrow points out the DNA variants.

    Figure 4.16 Schistocytes. This figure is from a patient with hereditary pyropoikilocytosis, which leads to a haemolytic anaemia. There are numerous examples of damaged cells and also fragments. However, there are also spherocytes, the cells that are very darkly stained.

    Figure 4.17 Target cells. There are many target cells present, but also microspherocytes, schistocytes, elliptocytes and a nucleated red blood cell. Consequently, the patient will have a complex and severe haemolytic anaemia.

    Figure 4.18 Howell–Jolly bodies. These are small but distinct purple bodies inside six red cells composed of fragments of nuclear material, often found after splenectomy or splenic disease. There are also two white cells (a neutrophil and a lymphocyte).

    Blood science angle: Thalassaemia

    Clinical aspects

    Prenatal diagnosis and prevention of haemoglobinopathy

    4.5 External factors acting on healthy cells


    Autoimmune haemolytic anaemias

    Alloimmune haemolytic anaemia

    The role of the laboratory in antibody-mediated haemolysis

    Blood science angle: Antibodies

    Physical damage

    Drug-induced haemolytic anaemia


    Figure 4.19 Malaria. A marked infection of the ring-form trophozoites of Plasmodium falciparum. Perhaps 20–25% of cells are carrying a parasite.


    Other ‘external’ causes of anaemia

    The anaemia of chronic diseases

    4.6 Erythrocytosis and polycythaemia



    The laboratory in erythrocytosis

    Management of erythrocytosis

    Chuvash polycythaemia



    The laboratory in polycythaemia

    Blood science angle: Polycythaemia and erythrocytosis


    Table 4.7 Erythrocytosis and polycythaemia.

    4.7 Molecular genetics and red cell disease

    Table 4.8 Examples of molecular genetics in red cell pathology.

    4.8 Inclusion bodies

    4.9 Case studies

    Case study 1


    Figure 4.20 Blood film for case study 1.

    Case study 2

    Figure 4.21 Blood film for case study 2.




    Further reading

    5 White Blood Cells in Health and Disease

    Learning objectives

    5.1 Introduction

    Table 5.1 Meaning of common terms.

    CD molecules

    Table 5.2 A white cell differential.

    5.2 Leukopoiesis

    Table 5.3 Selected leukocyte CD molecules


    T lymphocytes (or T cells)

    Figure 5.1 Lymphopoiesis. The process of the development of mature lymphocytes begins in the bone marrow. T lymphocytes must pass through the thymus to become fully functional, but the site of the transformation of pre-B lymphocytes into mature B lymphocytes is unknown.

    B lymphocytes (or B cells)

    Natural killer cells (NK cells)




    Figure 5.2 Myelopoiesis. This process gives rise to red blood cells and platelets, as well as monocytes and granulocytes. As with lymphopoiesis, the key cell is the CFU, which generates the three granulocyte lineages, and the monocyte/macrophage lineage.


    The role of growth factors

    Blasts and malignancy

    5.3 Neutrophils


    Figure 5.3 Three neutrophils. Note the different number and layout of the three or four purple-stained lobes. The fine structure of the cytoplasm is not smooth but irregular, due to the presence of granules.


    5.4 Lymphocytes


    Figure 5.4 The single lymphocyte is characterized by a single, roughly circular (purple) nucleus. Compare the fine details of the cytoplasm (which lacks granules) with the grainy nature of the cytoplasm on neutrophils.

    Figure 5.5 Different lymphocyte groups can be enumerated by the presence of particular CD molecules. This example uses monoclonal antibodies to CD3 and CD19, both linked to different fluorochromes (Pac B and PC 5.5 respectively). Cells binding CD3, but not CD19 are defined as T cells (lower right quadrant), those binding CD19 but not CD3 (upper left quadrant) and B cells, whilst those binding neither antibodies are NK cells (lower left quadrant). There are almost no cells binding both antibodies (upper right quadrant).


    5.5 Monocytes

    Figure 5.6 A monocyte. There are two cells in this figure; the monocyte is the upper cell. Note that about two-thirds to three-quarters of the cell is taken up by the purple nucleus, which has an indent. Contrast this with the lower cell, which is a three-lobed neutrophil.



    5.6 Eosinophils


    Figure 5.7 An eosinophil. The key features are a bilobed nucleus, and a cytoplasm dominated by reddish granules.


    5.7 Basophils


    Figure 5.8 A basophil. The key features are a bilobed nucleus and a cytoplasm dominated by blue–black–purple granules. However, the granules may be so large and numerous that the nucleus becomes obscured.


    Blood science angle: Leukocyte physiology

    5.8 Leukocytes in action


    Recruitment of cells

    Contact of cells with pathogens


    Figure 5.9 Phagocytosis. (a) A monocyte (with its characteristic horseshoe-shaped nucleus) close by a colony of bacteria. The latter have strongly taken up a blue dye. (b) A monocyte that has ingested over a dozen bacteria it has absorbed by the process of phagocytosis. It is tempting to speculate that the bacteria are coated with antibodies and complement opsonins to increase the efficiency of this process.

    Acute inflammation

    Chronic inflammation

    Table 5.4 Location and function of selected lymph nodes.


    Lymph nodes

    Figure 5.10 Anatomy of the activated lymph node. Lymphatic vessels carry lymph fluid (possibly loaded with pathogens and cytokines) from the tissues to the lymph node. A germinal centre is primarily the focus of the activity of T helper cells and antigen-presenting cells in promoting antibody production. Each node is fed by an arterial blood vessel, whilst vein carries effluent blood back to the circulation. A lymphatic vessel may carry cells and lymph fluid to the next node in the chain.

    B lymphocytes

    Figure 5.11 Basic structure of an antibody molecule. Two heavy chains and two light chains come together to form a Y shaped molecule that binds antigens with its Fab sections. The other end of the molecule (the Fc section) has the capacity to dock into special receptors on certain leukocytes. The section of the heavy and light chains that find the antigen are called the variable region – the remainder is the constant region.


    Antibody classes

    Antibody class switch

    Receptors for antibodies

    T lymphocytes

    Figure 5.12 Structure of major antibody classes. The standard ‘Y’-shaped molecule is the prototype, and is typified by IgG, consisting of two heavy chains and two light chains, each with a variable region and a constant region. Two such monomers form an IgA dimer, whilst IgM is composed of five monomers, both being stabilized by J chains.

    Natural killer cells in action

    Antigen recognition and genetics

    5.9 White cells in clinical medicine


    An excessive acute inflammation

    Leukaemoid reaction

    Chronic inflammation

    Blood science angle: The acute-phase response


    Figure 5.13 Activated lymphocytes. The increased white cell count often found in IM is due largely to activated lymphocytes, which are larger than resting lymphocytes and have more cytoplasm. This figure shows four activated and one normal lymphocyte.



    Allergic disease

    Chronic eosinophilic leukaemia

    Hypereosinophilic syndrome

    Other conditions





    Myelodysplasia and myelofibrosis

    Table 5.5 Principal functions of white blood cells.

    5.10 Case studies

    Case study 3


    Case study 4



    Further reading

    6 White Blood Cell Malignancy

    Learning objectives

    6.1 The genetic basis of leukocyte malignancy

    Figure 6.1 Deletions, inversions and translocations. Compared with a normal chromosome (a), a deletion is characterized by a missing nucleotide, gene or larger section of DNA, leading to a shorter chromosome (b). In an inversion (c) the chromosome is of the same length but a section of DNA or part of the chromosome is reversed (d). Most translocations see sections of DNA being reciprocally transferred between different chromosomes (e1 and e2), often resulting in new hybrid chromosomes of different lengths and containing different genes (e3 and e4).




    What this means

    Blood science angle: Cancer genetics

    Genes and chromosomes

    Figure 6.2 Fluorescence in-situ hybridization. Red and green fluorochromes are linked to probes for different genes. Normally, the genes binding the two probes would be on different chromosomes. However, the arrows highlight two chromosomes with both colours, thus defining a reciprocal translocation. Some of the ‘red’ gene has moved to the ‘green’ chromosomes and vice versa.


    Figure 6.3 RNA microarray analysis. The upper panel shows (red colour) binding of patient's mRNA with genes consistent with a diagnosis of acute lymphocytic leukaemia, collected on the left of the array. In the lower panel, the patient's mRNA binds to a different pattern of genes, where the red colour is dominant on the right, suggesting a diagnosis of acute myeloid leukaemia.

    Clinical presentation of white cell malignancies

    6.2 Tissue techniques in haemato-oncology

    Peripheral blood

    Figure 6.4 Use of flow cytometry to quantify the proportion of CD34-bearing blast cells (16.4%; reference range <0.5%) in acute myeloid leukaemia.

    Bone marrow

    Table 6.1 Bone marrow cells in health and malignancy.

    The lymph node

    6.3 Leukaemia


    Chronic myeloid leukaemia

    The Philadelphia chromosome

    Cellular basis of chronic myeloid leukaemia

    Treatment of chronic myeloid leukaemia

    Figure 6.5 Formation of BCR–ABL. This fused gene is generated by part of chromosome 22 joining with part of chromosome 9. The fused product is a variant of a tyrosine kinase that is effectively continuously active. The consequences of this are the activation of several genes involved in cell proliferation and signalling, so that the cell continues to generate abnormal ‘daughter’ progeny – that is, leukaemic cells.

    Figure 6.6 Chronic myeloid leukaemia. This film shows granulocytes at several stages of differentiation. The larger cells are promyelocytes and myelocytes; the smaller cells are metamyelocytes. Note also the degree of granulation in the cytoplasm of the different cells. On the far right is a lymphocyte, with a darker nucleus that occupies almost all of the cell.

    Chronic neutrophil leukaemia

    Table 6.2 Partial FAB classification of AML.

    Acute myeloid leukaemia


    Molecular genetics of acute myeloid leukaemia

    Table 6.3 Prognosis and cytogenetic abnormality.

    A wider view of acute myeloid leukaemia

    Figure 6.7 A blood film in AML. This film shows four large blast cells. That of the top right has an Auer rod.

    Chronic lymphocytic leukaemia

    The blood film

    Figure 6.8 A blood film in CLL. Note that the leukaemic cells in this film are markedly smaller than those of the AML or ALL blasts in Figure 6.7 and Figure 6.9, being only a little larger than the red cells.

    Cytogenetics, prognosis and treatment

    Other laboratory indices

    B-cell chronic lymphocytic leukaemia

    B-cell prolymphocytic leukaemia

    Hairy cell leukaemia

    Abnormal antibodies

    T-cell and NK-cell leukaemias

    Acute lymphoblastic leukaemia

    Other types of leukaemia

    Figure 6.9 A blood film in ALL. These blasts are clearly much larger than nearby red cells, and are also agranular, unlike the AML blasts in Figure 6.7. The presence of CD10 on these cells (as defined by flow cytometry) marks them as malignant B cells.

    Figure 6.10 A blood film in chronic monocytic leukaemia. These blasts are relatively mature, with a low cytoplasm-to-nucleus ratio.

    6.4 Lymphoma

    The natural history of lymphoma

    Aetiology and classification

    Hodgkin lymphoma

    Further classification

    Advanced disease

    Non-Hodgkin lymphoma


    Burkitt's lymphoma

    Lymphoplasmacytoid lymphoma

    T-cell lymphomas

    6.5 Myeloma and related conditions


    The laboratory

    Genetics and pathophysiology

    Blood science angle: Cytogenetics of white cell malignancy

    Myeloma as a systemic disease

    Table 6.4 Protein subsets in health and myeloma.

    Conditions allied to myeloma

    Monoclonal gammopathy of undetermined significance


    Hyperviscosity syndrome


    Lymphoplasmacytoid lymphoma

    Blood science angle: B-cell malignancy

    The paraprotein

    Sub-typing the paraprotein

    Light chain analysis

    Figure 6.11 Immunofixation electrophoresis. Serum protein electrophoresis (SPE). On the left is the densitometer profile showing a large paraprotein peak in the gamma (γ) region. This will have been derived from the SPE trace at the top of the panel on the right. The second aspect of this analysis is the typing of the gamma-globulin band by IFE, which has produced a heavy band in the IgG and the lambda (λ) regions, thereby identifying the paraprotein as an IgGλ.

    Urine analysis

    Figure 6.12 Serum and urine electrophoresis. There are 12 sets of analyses. In each case the urine sample in on the left, and clearly has great deal less ‘blue’ than its paired serum sample to the right. The arrows on the left highlight the albumin band; the arrows on the right point to the gamma globulin region.

    Table 6.5 Major aspects of white malignancies.

    Blood science angle: Urine and serum electrophoresis

    6.6 Myelofibrosis and myelodysplasia

    6.7 Case studies

    Case study 5


    Figure 6.13 Blood film for case study 5. Two abnormal lymphocytes. Note the irregular border of the cytoplasm, best determined with high-magnification lenses.

    Case study 6



    Further reading


    7 The Physiology and Pathology of Haemostasis

    Learning objectives

    Virchow's triad

    Table 7.1 Major indices in haemostasis.

    7.1 The blood vessel wall

    Figure 7.1 Virchow's triad considers different roles for the blood vessel wall, blood flow and the constituents of the blood in the pathogenesis of thrombosis.

    Table 7.2 Involvement of the endothelium in haemostasis.



    Pathophysiology of the endothelium

    7.2 Platelets

    Thrombopoiesis and megakaryocytes

    Figure 7.2 Thrombopoiesis. Platelets are the end cell of this process, intermediates being stem cells, and precursors the megakaryoblast and the megakaryocyte. The leading hormone promoting this process is thrombopoietin.


    Figure 7.3 Platelets in a blood film. This film shows two different white cells (each with a heavy purple nucleus), red cells (coloured pink) and platelets (several small light purple bodies, arrowed).

    Table 7.3 The platelet membrane.

    The platelet membrane

    The platelet cytoplasm

    Figure 7.4 Platelet metabolism. The primary metabolic pathway in the platelet is the generation of thromboxane via arachadonic acid and prostaglandin H2. They key enzyme in this pathway is cyclooxygenase. EC = endothelial cell.

    7.3 The coagulation pathway

    Coagulation factors

    The coagulation pathway


    Table 7.4 Coagulation factors.



    Figure 7.5 The coagulation pathway consists of three overlapping stages, initiation, amplification and propagation, and involves two complex super-enzymes, the tenase complex and the prothrombinase complex. These happen in close proximity to the endothelium and the platelet.

    Table 7.5 Selected functions of thrombin.

    Blood science angle: Anticoagulants



    Tissue factor pathway inhibitor

    Protein C system

    Other inhibitors

    7.4 Haemostasis as the balance between thrombus formation and removal

    Activation of platelets

    Thrombus formation

    Figure 7.6 Platelet activation. A resting platelet undergoes shape change upon stimulation by agonists such as ADP. Further changes include the degranulation, the development of pseudopodia, and the expression of adhesion molecules and phospholipids.


    Figure 7.7 Fibrinolysis. Plasminogen is converted into plasmin by tissue plasminogen activator, itself regulated by an inhibitor. Plasmin, which can be regulated by TAFI, acts on fibrin, generating fragments called d-dimers.

    The dynamics of haemostasis

    Figure 7.8 The dynamics of haemostasis activation. When the forces of coagulation are balanced by those of inhibitors such as antithrombin, and of fibrinolysis, then haemostasis is in balance. However, if the coagulation is dominant then thrombosis is likely. Conversely, if inhibitors and fibrinolysis are stronger, then there is haemorrhage.

    7.5 The haemostasis laboratory


    Platelet aggregation

    Fluorescence flow cytometry

    Platelet microparticles

    Coagulation factors

    Prothrombin time

    Activated partial thromboplastin time

    Thrombin time

    Individual factor assays

    Functional plasma haemostasis

    7.6 The pathology of thrombosis

    Loss of haemostasis

    Arterial thrombosis

    The risk factor hypothesis


    Venous thrombosis

    Risk factors

    Table 7.6 Pathophysiology of arterial and venous thrombosis.


    Contrasting arterial and venous thrombosis

    Blood science angle: Inflammation and haemostasis


    Further reading

    8 The Diagnosis and Management of Disorders of Haemostasis

    Learning objectives

    8.1 Thrombosis 1: overactive platelets and thrombocytosis


    Table 8.1 An overview of major aspects of thrombosis and haemorrhage.

    Qualitative disease

    Quantitative disease: thrombocytosis

    Figure 8.1 The blood film in ET. This blood film shows a remarkably high platelet count, but also an eosinophil (on the left) and a monocyte (to the lower right). There is also a great variation in the size of the platelets (anisocytosis), suggestive of a malignancy, However, before a diagnosis of ET is made, causes of reactive thrombocytosis (e.g. infection, following surgery, post-splenectomy, inflammation, chronic blood loss), chronic myeloid leukaemia, PRV and idiopathic myelofibrosis should be excluded.



    Metabolic inhibitors

    Figure 8.2 Inhibition of platelet function. Platelets may be activated by the occupancy of various receptors (such as the ADP receptor and GpIIb/IIIa) by their particular ligands (ADP and fibrinogen respectively). This leads to the activation of the cyclooxygenase pathway, which in turn initiates platelet shape change, degranulation (releasing ADP, thromboxane and other mediators) and other features that result in the promotion of thrombosis. This includes binding to other platelets (linked by fibrinogen and vWf) and to the subendothelium (via endothelial-derived vWf, collagen, GpVI and GpI//IX/V).

    Adenosine diphosphate receptor blockage

    Preventing platelet–platelet interactions

    Table 8.2 Mechanism for suppressing platelet function.

    Other agents

    8.2 Thrombosis 2: overactive coagulation


    Increased coagulation factors

    Lack of inhibition

    Table 8.3 Stratification of the risk factor for VTE.


    Table 8.4 Increase in the risk of VTE with multiple risk factors.

    Blood science angle: Risk factors for VTE



    Figure 8.3 The risk of a VTE is the sum of individual factors. Suppose that each factor has a particular numerical number: some factors are acquired, others natural. In this model, a score exceeding 15 arbitrary units puts the individual at high risk of a DVT or PE. This may be achieved by a combination of any factors: age 50 plus antithrombin deficiency (12 points plus 5 points equals 17 points) does, whereas age 30 plus hormone replacement therapy (HRT) or oral contraceptive pill (OCP; 3 points plus 9 points equals 12 points) does not. However, this simple model predicts that adding another 40 years (and so 4 points) at age 70 may well precipitate a thrombosis.


    Factor V Leiden and the prothrombin G20210A mutation

    Antiphospholipid syndrome

    Problems and pitfalls in antiphospholipid syndrome and lupus anticoagulant testing

    Testing for thrombophilia



    The drug

    Laboratory management of warfarin

    Pros and cons of warfarin

    Table 8.5 Target INRs and recommended duration of anticoagulation.

    Table 8.6 Patient factors that influence the efficacy of warfarin.

    Patient power – warfarin


    The drug

    Blood science angle: Molecular genetics of antithrombotics and anticoagulants

    Laboratory management of heparin

    Pros and cons of heparin

    Low molecular weight heparin

    The drug

    Laboratory management of low molecular weight heparin

    Table 8.7 Differences between low molecular weight heparin (LMWH) and UFH.

    Table 8.8 Risk factors for VTE for patients about to go on LMWH.

    Table 8.9 Additional risk factors for surgical in-patients.

    Table 8.10 Application of risk assessment for the use of LMWH.

    Important point

    Pros and cons of low molecular weight heparin

    Patient power – low molecular weight heparin

    Use of LMWHs

    Fondaparinux (Arixtra)

    Heparinoids, hirudins and other agents

    New oral anticoagulants

    Direct thrombin inhibition

    Factor Xa inhibition

    An ideal antithrombotic drug

    8.3 Haemorrhage 1: platelet underactivity and thrombocytopenia

    Table 8.11 Features of common anticoagulants.


    The bone marrow

    Intrinsic platelet defects

    Destruction of platelets

    Heparin-induced thrombocytopaenia


    Figure 8.4 A blood film showing microthrombi. To the left and right of the upper leukocyte (a neutrophil) are two microthrombi. The blood scientist needs to ask if these are genuine clots formed in the body by some pathogenic process (such as an autoantibody), or if they have formed in the vacutainer after the blood has been drawn (and so are an artefact of failed anticoagulation).

    Flow cytometry

    Table 8.12 Platelet CD molecules commonly used in flow cytometry.

    Platelet aggregation

    Figure 8.5 Light transmission aggregometry. (upper panel) Changes in light transmission (vertical axis) over 8 min (horizontal axis) when ADP (trace 1), epinephrine (2), collagen (3) and ristocetin (4) are added to platelet-rich plasma. After 4 min, the light transmission to all agonists is greater than 80% of a sample of the subject's platelet-free plasma, indicating the formation of thrombi. (lower panel) Changes in the response of platelet-rich plasma from a 15-year old female whose only symptom was prolonged bleeding from the gums. There were no abnormalities in her coagulation pathway. The aggregation plot shows a normal response to ristocetin (trace 4) of over 90% at 4 min. However, ADP, epinephrine and collagen (traces 1–3, the continuous lines at the top of the printout) have failed to induce any platelet aggregation. This profile supports the diagnosis of Glanzmann's thrombasthenia: the molecular lesion is lack of functioning GpIIb/IIIa.


    The platelet function analyser (PFA-100)

    Other tests of platelet function

    Platelet function and near-patient testing


    8.4 Haemorrhage 2: coagulation underactivity

    Pathophysiology of primary defects

    Insufficient factor VIII

    Insufficient von Willebrand factor

    Insufficient factor IX

    Deficiencies in other factors

    Pathophysiology of secondary defects


    General screening tests

    Factor-specific assays

    Measurement of von Willebrand factor


    Treatment of primary deficiency

    Figure 8.6 vWf multimer analysis. The plasma sample loaded onto the top of an SDS agarose gel, and staining of the resultant electrophoresis plot reveals a series of bands that equate to vWf of different sizes. The topmost are the high molecular weight species that fail to enter the gel, or fail to penetrate very far. Small multimers penetrate further, the smallest being at the bottom. The mass of each band can be estimated by densitometry.

    Treatment of secondary deficiency

    Table 8.13 Action in response to a high INR in an outpatient.

    Table 8.14 Action in response to a high INR in an inpatient.

    Tranexamic acid

    8.5 Disseminated intravascular coagulation




    Blood science angle: DIC

    8.6 Molecular genetics in haemostasis

    Coagulation factors


    Broader value of molecular genetics

    Confirming diagnosis

    8.7 Case studies

    Case study 7

    Interpretation and plan

    Case study 8



    Further reading


    Web sites

    9 Immunopathology

    Cognosce te ipsum: Know thyself

    Learning objectives

    9.1 Introduction



    9.2 Basics of the immune system

    Table 9.1 Principal physiological functions of white blood cells.

    The anatomy of the immune system


    The acute-phase response


    9.3 Humoral immunity


    Figure 9.1 Simplified structure of an immunoglobulin molecule.


    Table 9.2 Complement components.

    Complement pathways

    The regulation of complement

    Blood science angle: Complement, coagulation and blood transfusion

    Figure 9.2 The complement pathway consists of three initial pathways that come together to form different types of C3 convertase. The products of this enzyme, C3a and C3b, go on to have other functions – the former as an inflammatory mediator and the latter as the generator of C5a (another inflammatory mediator) and C5b, the latter coming together with C6–C9 to form the membrane attack complex. MBL = mannose binding lectin, MASP2 = MBL-associated serine protease-2.


    9.4 Immunopathology 1: immunodeficiency

    Quantitative deficiency in white cells

    Bone marrow suppression

    Genetic causes of neutropenia

    Human immunodeficiency virus-1

    DiGeorge syndrome

    Severe combined immunodeficiency

    Qualitative defects in white cells

    Chronic granulomatous disease

    Blood science angle: Leukopenia

    Other neutrophil defects

    Other white cell defects

    Clinical aspects of defective cell-mediated immunity

    Blood science angle: HIV/AIDS

    Leukocyte malignancy

    Defects in humoral immunity



    Clinical aspects of defective humoral immunity

    Table 9.3 Immunodeficiency.

    9.5 Immunopathology 2: hypersensitivity

    Type I hypersensitivity

    Figure 9.3 Cellular basis of type I hypersensitivity. The basis of this process is the sensitization of resting mast cells and basophils by IgE, that itself then binds to the allergen. Cell degranulation releases inflammatory mediators (such as histamine and tryptase) that act on other cells such as smooth muscle cells and endothelial cells to produce the clinical symptoms such as respiratory distress and itching.

    Table 9.4 Common allergens.

    Type II hypersensitivity

    Type III hypersensitivity

    Figure 9.4 Cellular basis of type II hypersensitivity. There are two possible routes: resting cells may become sensitized by the location of IgG into their FcR. The leukocyte may then attack target cells that bear antigens specific for the particular antibody. Alternatively, a leukocyte may directly recognize the FcR of antibodies already bound to a target cell.

    Figure 9.5 Cellular basis of type III hypersensitivity. Antibodies and antigens come together to form soluble or insoluble immune complexes which can bind nonspecifically to innocent cells and tissues. These bound complexes then attract the attention of leukocytes, which proceed to attack the underlying tissues and initiate a local inflammatory response.

    Type IV hypersensitivity

    9.6 Immunopathology 3: autoimmune disease

    Connective tissue disease

    Rheumatoid arthritis


    Figure 9.6 Synovial joint destruction in RA. The affected joint in RA exhibits a number of abnormalities. These include eroded bone and a reduced synovial space (detected by X-ray) and collagen, the presence of leukocytes and inflammatory mediators in the synovial fluid (detected by aspiration of the turbid fluid, and then biochemistry and microscopy), and swollen synovial tissues which have become infiltrated by leukocytes (as detected by histological examination of a biopsy).

    Systemic lupus erythematosus


    Other inflammatory connective tissue disease

    Table 9.5 Major inflammatory connective tissue diseases.

    Blood science angle: Autoimmune connective tissue disease

    Organ-specific disease

    The endocrine system

    The kidney

    The liver

    The intestines

    Table 9.6 Other autoimmune diseases.

    The spectrum of autoimmune disease

    Blood science angle: The haematologist and autoimmunity

    The complex nature of autoantibodies

    Table 9.7 Extractable nuclear antigens.

    Blood science angle: Autoimmune disease and leukaemia

    9.7 Immunotherapy

    Therapeutic antibodies

    Haemolytic disease of the newborn

    Polyclonal antibodies

    Monoclonal antibodies



    Allergy desensitisation

    9.8 The immunology laboratory

    Cellular immunology





    Laboratory assessment of complement

    Table 9.8 Commonly requested autoantibodies.

    Table 9.9 Levels of immunoglobulins.

    Allergy testing

    Clinical testing

    Table 9.10 Defined protein analyses.

    Immunoglobulin E

    Leukocyte testing

    Products of degranulation

    The reference laboratory

    9.9 Case studies

    Case study 9


    Flow cytometry

    Case study 10

    Figure 9.7 Flow cytometry of CD4 and CD8 subsets. The typical four-quadrant result showing 1075 events staining above background for CD8 in the upper left quadrant and 1285 events staining for CD4 in the lower right quadrant. These translate to a CD4/CD8 ratio of 1.2.




    Further reading


    Web sites

    10 Immunogenetics and Histocompatibility

    Cognosce te ipsum etiam meliores: Know thyself even better

    Learning objectives

    10.1 The genetics of antigen recognition

    B lymphocyte responses to antigens

    The B cell receptor

    The genetics of antibody variability

    T lymphocyte responses to antigens

    Figure 10.1 Recombination of immunoglobulin genes. The variability in antibody responses resides in the combined variable regions of heavy and light chains that form the Fab. The VDJ recombinase enzyme selects a J region gene, a D region gene and any one of several variable region genes to form a single combined VDJ-constant gene. This is the template for the RNA polymerase, which generates messenger RNA and ultimately the production of the protein chain by the ribosomes. The inclusion of a membrane region gene traffics the molecule to the cell membrane; without this section it will be exported into the plasma as an antibody molecule.

    The diversity of antigen recognition

    Figure 10.2 Recombination of TcR genes. The antigen recognition site of the TcR is composed of two molecules: an alpha–beta dimer or a gamma–delta dimer, coded for by genes on different chromosomes. Like immunoglobulin genes, the recombination of germ-line V, D and J genes generates a new gene that in turn provides the protein.

    Figure 10.3 The TcR and BcR. The TcR is composed of an alpha–beta dimer or a gamma–delta dimer, and a complex of five molecules that make up CD3. The BcR consists of an immunoglobulin molecule and two CD79 molecules.

    Antigen-presenting cells

    10.2 Human leukocyte antigens

    Class I molecules

    Figure 10.4 The structure of HLA molecules. HLA molecules bear similarities to immunoglobulins, with their globular domain structure. Class I molecules have three domains; each of the two class II molecules (alpha and beta) have two domains. A single-domain-sized molecule of beta-2-microglobulin is associated with the class I molecule. The variation in antigen binding resides in the terminal domains in a manner similar to that of the Fab of antibodies. In class I molecules, the antigen binding site is a groove between domains 1 and 2; in class II molecules, it is formed by the terminal domains of each chain.

    Class II molecules

    Class III molecules

    Figure 10.5 The layout of HLA genes. The HLA genes are arranged in a sequence on chromosome 6 and span some 3600 kilobases. From the 3′ end these are the three class I genes, the class III genes and the three class II gene loci. Between these genes and the centromere is the gene for glyoxylase (GLO).

    The generation of antibodies

    Table 10.1 Molecular recognition systems between antigen presenting cells and T helper lymphocytes.

    Other forms of antigen recognition

    The B-cell co-receptor

    Natural killer cells

    Figure 10.6 T–B interactions generating antibodies. A summary of the interactions between an antigen-presenting cell and a T helper lymphocyte, which receives the antigenic peptide via its TcR. The T cell in turn presents the antigen to the BcR of the ‘early’ B lymphocyte. This is effectively the ‘go’ signal for the B cell to transform into a plasma cell, and so generate antibodies specific for the presented antigen.


    The generation of cytotoxic T lymphocytes

    Figure 10.7 The B-cell co-receptor. B-cells may be activated by the co-recognition of bacterial antigens by the BcR, and by C3d on the surface of the bacteria by CD21.

    Figure 10.8 T cell–antigen-presenting cell interaction. An antigen-presenting cell and a naive T cell interact with HLA class I molecules and the TcR. The T cell CD8 molecule provides assurance that the presenting cell is self. The CD3 complex activates its zeta molecules, which initiates the final maturation of the cell and its clonal proliferation. The resultant cytotoxic T lymphocytes recognize and kill those cells presenting peptide and self-HLA class I molecules, which are therefore altered self.

    10.3 Transplantation

    Polymorphisms in human leukocyte antigen molecules

    Human leukocyte antigen typing

    Serological typing

    Gene typing

    Antibodies to human leukocyte antigen molecules


    The practicalities of transplantation

    Figure 10.9 Inheritance of HLA types. Each individual inherits one HLA haplotype from their mother and a second from their father. In this very simplified example, showing only three HLA loci, sibling A, on the left, requires a transplant. Sibling B, in the middle, has inherited the same maternal haplotype, but a different paternal haplotype, so is a part match. Sibling C, on the right, has inherited a different set of haplotypes, and so is a complete mismatch. All siblings are partially matched with each parent (by definition).

    Solid organ transplantation

    Bone marrow transplantation

    Figure 10.10 Collection of peripheral blood stem cells. The donor undergoes a modified blood transfusion donation using a cell separator. Mononuclear cells are harvested, and red cells, granulocytes and platelets are returned to the donor.


    Figure 10.11 Peripheral blood counts in bone marrow transplantation. Red cell, platelet, total white cell and neutrophil counts before (on the left) and after (the right) transplantation. Note the white cell and neutophil counts fall to zero at conditioning (use of cyclophosphamide). Red cell and platelet numbers are maintained by standard transfusions. Success of the transplanted material is aided by the use of haemopoietic growth factors, such as granulocyte-macrophage colony-stimulating factor, and the use of post-transplant ciclosporin.

    Blood science angle: Transplant rejection

    The ultimate transplant

    Blood science angle: Is transplanation a cure for HIV infection?

    10.4 Autoimmunity and human leukocyte antigens


    Loss of tolerance

    Molecular mimicry

    The scope of human leukocyte antigens and autoimmune disease

    Table 10.2 Autoimmune disease linked with HLA types.

    Blood science angle: HLA, rheumatoid arthritis and cardiovascular disease


    Further reading


    Web sites

    11 Blood Transfusion

    Learning objectives

    Red Book

    What can be transfused?

    The basis of transfusion science

    Blood science angle: Blood transfusion

    11.1 Blood collection and processing

    The blood donor

    Blood processing

    Pathogen screening

    Specialized processing

    Blood components

    Fresh frozen plasma


    Prothrombin complex concentrate




    Blood science angle: Blood components (previously blood products)

    Other blood components

    11.2 Blood groups

    Red cell surface molecules

    Table 11.1 Major red cell surface molecules.

    The ABO system

    Cell surface ABO molecules

    Figure 11.1 Formation of A, B and H blood group structures. The base unit is the substrate for an enzyme coded for by the H gene that adds a molecule of fucose to the terminal galactose molecule. If active, the A enzyme, coded for by the A gene, adds a molecule of N-acetyl galactosamine to the terminal galactose. If active, the enzyme encoded for by the B gene adds another molecule of galactose to the terminal galactose. Whilst most ABH molecules are linked with Band 3 molecule, they are also found elsewhere.


    Table 11.2 ABO blood group structures and antibodies.

    Table 11.3 Racial distribution of ABO groups.

    The secretor phenotype

    The Bombay phenotype

    Subgroups of A and B

    Genetics and the racial distribution of ABO groups

    Implications of ABO blood group

    Blood science angle: von Willebrand factor

    The Rh system

    Molecules of the Rh system

    Genetics of the Rh system

    The Rh-associated glycoprotein

    Table 11.4 Common combination of genotypes of the Rh system.

    Antibodies of the Rh system

    Haemolytic disease of the newborn

    Other blood groups

    Blood science angle: Malaria

    Table 11.5 Human neutrophil antigen determinants.

    White cell antigens


    Clinical consequence of platelet and granulocyte incompatibility

    Table 11.6 Human platelet antigen determinants.

    11.3 Laboratory practice of blood transfusion

    Determination of blood group

    Figure 11.2 Determination of blood group in a single multi-chamber gel agglutination cuvette. Each of the eight compartments is for a separate reaction between the cells and antibody reagents present in the gel. If there is no reaction between the two, the red cells fail to agglutinate and so move to the bottom of the reaction cuvette. However, if there is a reaction, agglutinated cells remain higher up the gel in the particular column. So in this case the cells fail to react with anti-A, anti-B but do react with anti-D and so are group O, RhD positive.

    Antibody screening

    Cross-match/compatibility testing

    Figure 11.3 Principles of a cross-match. In this cross-match, samples of red cells from four packs of blood from potential donors are mixed with plasma from the patient. In three cases, there is no agglutination, so patient lacks antibodies to molecules on cells from the donor packs, which are therefore acceptable for transfusion. However, in one case the patient's plasma has antibodies that react with one of the potential donor cell, causing agglutination, and so these cells are incompatible and cannot be transfused.

    Special investigations

    Antiglobulin testing

    Figure 11.4 Direct antiglobulin testing. Washed cells from the patient are mixed with an antiglobulin reagent to detect antibodies on the red cells. (a) If present, antibodies will be recognized by the antiglobulin reagent, and will cross-link the cells, giving a positive result. (b) In the absence of antibodies, the antiglobulin will have nothing to cross-link, so there will be no agglutination.

    The direct antiglobulin test

    The indirect antiglobulin test

    Figure 11.5 Indirect antiglobulin testing. In step 1, washed cells from the donor are mixed with serum or plasma from the patient. If present, antibodies will bind to the red cells and sensitize them. In step 2, the cells are mixed with an antiglobulin reagent to detect antibodies on the red cells. As in the direct antiglobulin test, the anti-human reagent will cross-link the cells, so that agglutination will mark a positive result.

    Figure 11.6 Antiglobulin testing. Testing for antibodies on red cells by the antiglobulin test can proceed in the same type of plastic cuvette with gel matrix as is used for blood group determination (Figure 11.2). In samples 1 and 2, cells have been agglutinated by the antiglobulin reagent and remain at the top of the column. Unagglutinated cells pass through to the bottom of the column, as in sample 3. The reagent shown here contains antibodies that recognize both IgG and complement component C3d, which may absorb passively onto the surface of the red cell. However, cuvettes are available that detect only the binding of IgG antibodies.

    Immediate spin cross-match

    Electronic issue

    Special cases

    Blood transfusion analysers

    Figure 11.7 A blood transfusion autoanalyser.

    11.4 Clinical practice of blood transfusion

    Indications for transfusion

    Red cell concentrates

    Fresh frozen plasma


    Platelet concentrates

    Alternatives to blood transfusion

    11.5 Hazards of blood transfusion

    The hospital

    Laboratory error

    Post-laboratory error

    Table 11.7 Key features of TRALI and TACO.

    The responses of the body to an incompatible transfusion


    Early reactions

    Table 11.8 Signs and symptoms of a transfusion reaction.

    Late reactions

    Allergic reactions




    Further reading


    Web sites

    12 Waste Products, Electrolytes and Renal Disease

    Learning objectives

    12.1 Renal anatomy and physiology

    Table 12.1 Major renal blood tests.

    The nephron

    12.2 Homeostasis


    Selective reabsorption

    Figure 12.1 The nephron. An afferent blood vessel brings blood to the glomerulus, where ultrafiltration takes place. Filtrate passes into the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule and the collecting duct. The close association between the nephron and blood vessels allows the transfer of substances and water in selective reabsorption, which maintains homeostasis and mediates excretion.

    Local hormones

    Figure 12.2 Hormonal regulation of homeostasis. AVP from the posterior pituitary, and ANP and BNP from atrial cardiomyocytes act directly on the nephron. The juxta-glomerular apparatus secretes renin, which converts angiotensinogen to angiotensin I, which in turn is transformed into angiotensin II by angiotensin-converting enzyme. Angiotensin II acts on the adrenals to synthesize and release aldosterone, which acts on the nephron.

    The electrolytes

    The chemistry of electrolytes

    Table 12.2 Key electrolytes.


    Concentration, mass and volume




    Diabetes insipidus (N.B. unrelated to diabetes mellitus)

    Fluid balance and insensible losses



    Conn's syndrome


    Syndrome of inappropriate antidiuretic hormone (SIADH)



    Addison's disease



    Intravenous fluids

    Blood science angle: Hyperkalaemia and red blood cells

    12.3 Excretion

    Waste products

    Tests of glomerular function


    Creatinine clearance

    Estimated glomerular filtration rate

    Urate/uric acid

    12.4 Renal endocrinology

    Hormones in homeostasis


    Blood science angle: Erythropoietin

    Calcium and vitamin D

    Renal efficiency

    Table 12.3 Constituents of blood, filtrate and urine in health.

    12.5 Renal disease


    Pre-renal disease

    True renal disease

    Post-renal disease

    The perspective of the patient

    Figure 12.3 An anatomical classification of renal disease. We can classify renal disease as being pre-renal, true renal, or post-renal, depending on the particular aetiology. In the first it is a problem with blood entering the kidney, and the last the problem is with urine leaving the kidney. True renal disease is where the nephrons themselves are damaged.

    Acute kidney injury

    Chronic kidney disease

    Table 12.4 Stages of CKD.

    Renal stones (calculi)

    Metabolic renal disease

    Blood science angle: Inflammatory renal disease

    The genetics of renal disease

    12.6 Case studies

    Case study 11


    Case study 12



    Further reading


    Web sites

    13 Hydrogen Ions, pH, and Acid–Base Disorders

    Learning objectives

    13.1 Ions and molecules


    Table 13.1 Major tests in pH and blood gases.

    Water and pH

    Acids and pH



    Other buffers

    13.2 Blood gases


    Figure 13.1 Gases in the air, the lungs and the blood. Partial pressures of oxygen and carbon dioxide in the air, the alveoli, arterial blood, capillary blood and venous blood. As blood passes round the circulation in a clockwise manner, it gradually loses oxygen and gains carbon dioxide.

    Figure 13.2 A blood gas analyser, as is present in an accident and emergency unit. The front left-hand side has two reagent reservoirs; on the right are three reservoirs. The touch-sensitive screen allows programming. Results are printed out on a strip of paper.


    Regulation of blood gases and pH

    At the lung

    At the kidney

    Figure 13.3 Gas exchange at the alveolus. Carbon dioxide generated in the tissues initially forms carbonic acid, which then ionizes to bicarbonate and a hydrogen ion. The latter can be carried by haemoglobin. The constituent parts reform at the alveolar surface, and water and carbon dioxide pass into the exhaled breath.

    Figure 13.4 Regulation at the nephron. A cartoon of five tubule cells and the possible biochemical pathways that may be present. The top three are cells involved in the hormone-controlled regulation of sodium and water. Potassium moves to maintain electrical balance. The lower cells show potential regulation by passive movement of ions across the cell membrane, although some may be actively pumped. Note the sodium can also move passively, but this, like the potassium movement, is also to maintain the electrical balance.


    Total CO2

    Chloride (Cl−)

    Blood science angle: Blood gases and haemoglobin

    13.3 Acidosis (pH <7.3)

    Metabolic acidosis

    The anion gap

    Respiratory acidosis

    13.4 Alkalosis (pH >7.5)

    Metabolic alkalosis

    Respiratory alkalosis

    13.5 Mixed acid–base conditions

    Table 13.2 A summary of acidosis and alkalosis.

    13.6 Clinical interpretation


    13.7 Case studies

    Case study 13


    Case study 14



    Further reading

    Web site

    14 Glucose, Lipids and Atherosclerosis

    Learning objectives

    14.1 Glucose

    Table 14.1 Major blood tests in the pathophysiology of atherosclerosis.

    The metabolism of glucose



    Table 14.2 The effects of insulin and glucagon.

    Somatostatin and incretin hormones

    Insulin resistance and sensitivity

    Impaired lipoprotein regulation

    The laboratory and glycaemia


    Glycated haemoglobin

    Other laboratory tests in glucose pathology

    Figure 14.1 The HPLC trace of a sample of blood. The vertical axis is the percentage of all results attributable to a particular peak, and the horizontal axis is the duration of the analysis. The peak P04 at 1.88 min makes up 11.1%, and is due to glycated haemoglobin, strongly suggestive of a diagnosis of diabetes mellitus.


    The laboratory


    ‘Dad's gone all funny...’


    Impaired fasting glucose

    Impaired glucose tolerance

    The oral glucose tolerance test

    Figure 14.2 In the OGTT, blood glucose concentrations rise, and then fall as insulin mediates the passage of the sugar into cells. The continuous line represents a typical normal profile, the dotted line the profile of IGT and the dashed line the profile as expected in diabetes. The latter two conditions may also have raised fasting glucose (5.6–7.0 mmol/L). N.B. The exact cut-off points vary; refer to your own local service.


    Implications and treatment

    The metabolic syndrome



    Presentation of diabetes

    Epidemiology and economics

    The definition of diabetes

    Type 1 diabetes


    Clinical aspects

    Type 2 diabetes


    Mechanisms of beta cell dysfunction

    Diabetes in pregnancy

    The genetics of glycaemic disease

    Clinical aspects of diabetes

    Diabetic ketoacidosis

    Hyperosmolar hyperglycaemic syndrome

    Impaired lipoprotein regulation

    Long-term complications of diabetes

    Microvascular disease

    Figure 14.3 The biochemistry and clinical aspects of diabetic ketoacidosis. Hyperglycaemia and low insulin lead to physiological changes (left), signs and symptoms (central box) and biochemical changes (right).

    Macrovascular disease

    Other disease

    Treatment of diabetes

    Beta cell stimulation

    Insulin sensitizers


    Other treatments

    Monitoring and management of diabetes

    Diabetes and haematology

    14.2 Dyslipidaemia

    Lipid families

    Fatty acids

    Table 14.3 Common fatty acids.

    Figure 14.4 Structure of fatty acids. The presence of a double bond allows two isomers of a particular molecule: the cis form, when the molecule is effectively straight, and the trans form, where it has a bend of 30° in the middle.



    Figure 14.5 Metabolism of triacylglycerols. Each molecule is synthesized by linking fatty acids to a glycerol by transferase enzymes. If required as a source of energy, the triacylglycerol can be digested back to its component parts by lipase enzymes.

    Figure 14.6 Synthesis of cholesterol. This complex molecule is constructed initially from acetyl groups, which are fused to form hydroxymethylglutatyl-coenzyme A (HMG-CoA). This is converted to mevalonate by the enzyme HMG-CoA reductase, which is inhibited by the statin group of lipid-lowering agents. Later steps see squalene being converted to cholesterol, which can then join with a fatty acid to form cholesterol ester.


    Phospholipid, sphingolipids and glucolipids

    Lipoproteins in the blood and tissues


    Low, intermediate and very low density lipoproteins

    High-density lipoprotein

    Table 14.4 Major features of lipoproteins.

    Lipoprotein (a)

    Cell surface receptors

    Enzymes, transporters and transfer molecules

    Disorders of cholesterol

    Dietary hypercholesterolaemia

    Primary hypercholesterolaemia

    Secondary hypercholesterolaemia

    Increased HDL


    Disorders of triacylglycerols

    Dietary hypertriacylglycerolaemia

    Primary hypertriacylglycerolaemia

    Secondary hypertriacylglycerolaemia

    Combined raised cholesterol and triacylglycerol

    Clinical genetics and dyslipidaemia

    The clinical consequences and treatment of dyslipidaemia

    Treatment of hypercholesterolemia

    Treatment of hypertriacylglycerolaemia

    Treatment of combined hyperlipidaemia

    Other treatments of dyslipidaemia

    The laboratory and lipids

    Total cholesterol

    High-density lipoprotein cholesterol

    Figure 14.7 The enzymatic method for each major lipid has a number of defined steps and requires several different reagents, and notably all conclude with the generation of hydrogen peroxide. Nevertheless, each is amenable to automation and has excellent reproducibility.


    Assay characteristics

    Low-density lipoprotein cholesterol


    Blood science angle: Dyslipidaemia

    14.3 Atherosclerosis

    The risk factors for atherosclerosis

    The pathogenesis of atherosclerosis

    The initial phase

    The development of atheroma

    The late stages

    The consequences of atherosclerosis

    The heart

    Pathophysiology of myocardial infarction

    Cardiac enzymes

    Muscle protein

    The diagnosis and treatment of myocardial infarction

    Table 14.5 Causes of a raised troponin.

    Heart failure

    Peripheral artery disease

    14.4 Case studies

    Case study 15


    Case study 16



    Further reading


    Web sites

    15 Calcium, Phosphate, Magnesium and Bone Disease

    Learning objectives

    Table 15.1 Major blood tests in the biology of bone.

    15.1 Calcium

    The biology of calcium

    Figure 15.1 Distribution and turnover of calcium. Calcium in the diet passes through the intestines into the blood, where some binds to albumin. It may then pass into the bone or be excreted in the urine.

    Parathyroid hormone

    Figure 15.2 Role of PTH in regulating blood calcium. Falling concentrations of free calcium induce the release of PTH from the parathyroid glands, with three major consequences: (1) stimulation of cells within the bone, (2) reabsorption of calcium from urine by the renal tubules and (3) stimulation of the generation of active vitamin D that promotes the absorption of calcium in the intestines.


    Vitamin D

    Figure 15.3 Synthesis of Vitamin D. Various isoforms of vitamin D are metabolized, often by hydroxylation, in the skin, liver and kidney. The most active form of vitamin D is the 1,25-dihydroxy species known as calcitriol.

    15.2 Phosphates

    The biology of phosphate

    Regulation of plasma phosphate

    15.3 Magnesium

    Regulation of magnesium

    15.4 The laboratory

    Laboratory determination of calcium

    The albumin issue

    The effect of pH

    Laboratory measurement of phosphate

    Laboratory measurement of magnesium

    Vitamin D isoforms

    Parathyroid hormone and calcitonin

    15.5 Disorders of calcium homeostasis

    The causes of hypercalcaemia

    The consequences of hypercalcaemia

    Investigation and management of hypercalcaemia

    The causes of hypocalcaemia

    Investigation and management of hypocalcaemia

    15.6 Disorders of phosphate homeostasis

    Table 15.2 Causes of abnormal calcium.

    Causes of hyperphosphataemia

    Consequences of hyperphosphataemia


    Table 15.3 Causes of abnormal phosphates.

    15.7 Disorders of magnesium homeostasis


    Clinical consequences and management of hypermagnesaemia


    Clinical consequences and management of hypomagnesaemia

    15.8 Bone physiology

    The biology of bone

    Figure 15.4 Structure of compact bone. An osteon consists of a series of concentric rings of canaliculi with a Haversian canal at the centre.

    Markers of bone turnover

    Point of nomenclature

    Blood science angle: Bone

    15.9 Bone disease


    Osteomalacia and rickets

    Paget's disease


    Figure 15.5 Pretty as a picture. The National Gallery in London has a portrait, perhaps unkindly titled ‘A Grotesque Old Woman’. Note the increased distance between the upper lip and the base of the nose, and the expanded bone of the front of the skull. The clavicles are also prominent, and it is likely that some fingers are misshapen. On reflection, these are all signs of bone deformity; and indeed, we now recognize that she is likely to have suffered from Paget's disease.


    Renal osteodystrophy

    The scaffolding hypothesis

    Figure 15.6 Bone as scaffolding. If we see bone as simple scaffolding, the long metal poles represent calcium and phosphates, but these poles need to be secured by clamps, which themselves must be place by scaffolders with special tools. The scaffolding will be unsafe if any of these components are defective.

    The genetics of bone, calcium and phosphates

    Familial hypocalciuric hypercalcaemia

    Table 15.4 Blood tests in different bone diseases.

    Familial tumoral calcinosis

    Paget's disease

    15.10 Case studies

    Case study 17


    Case study 18


    Case study 19



    Further reading


    Web sites

    16 Nutrients and Gastrointestinal Disorders

    Learning objectives

    16.1 Nutrients





    Table 16.1 Nutrients.


    Lipid-soluble vitamins

    Water-soluble vitamins

    Other requirements

    Specific nutrients: inorganic micronutrients

    Laboratory assessment of nutrients

    Nutritional disorders

    Table 16.2 Categories of BMI.

    The pathology of underweight

    The pathology of overweight

    Nutritional intervention

    Table 16.3 Components of a typical TPN infusion.

    16.2 The intestines

    Intestinal physiology

    The upper intestines

    The pancreas

    The liver, gall bladder and bile

    The small intestines

    The large intestines

    Other functions of the intestines

    Intestinal disease

    Disease of the mouth, throat and oesophagus

    Diseases of the stomach

    Disease of the biliary tree

    Disease of the pancreas

    Disease of the small Intestine

    Bile acid metabolism

    Disease of the large Intestine

    Cancer of the large and small intestines

    Blood science angle: Nutrition and intestinal disease


    Figure 16.1 Key aspects of intestinal pathology. Different sections of the intestines are host to particular diseases, but some diseases are present in more than one location. Most diseases are inflammatory and neoplastic in nature.


    Table 16.4 Simple tests for initial investigation of malabsorption.

    16.3 Case studies

    Case study 20


    Case study 21



    Further reading


    17 Liver Function Tests and Plasma Proteins

    Learning objectives

    Table 17.1 Major LFTs and plasma proteins.

    17.1 Anatomy and physiology of the liver


    Figure 17.1 The micro-architecture of the liver. (a) The major functional unit of the liver is the lobule, with branches of the hepatic portal vein, the hepatic artery and biliary tree at the periphery, and a branch of the hepatic vein at the centre. (b) Blood passes along sinusoids of merged venous and arterial blood, and perfuses tissues composed of hepatocytes and Kupffer cells, supported by fibroblasts and connective tissues. Bile is generated and passes into the biliary vessels that lead to the gall bladder and bile duct.

    The gall bladder and biliary system



    The acute-phase response

    Excretion of bilirubin and bile

    Table 17.2 Acute-phase reactants.

    Excretion of urea

    Figure 17.2 The metabolism and excretion of bilirubin starts with bilirubin as a breakdown product of the red blood cell. In the plasma it is transported to the liver by albumin, where it is conjugated to glucuronide, becomes part of the bile and passes into the intestines. Some bile metabolites are acted upon by intestinal bacteria, and some may be reabsorbed. The remainder is excreted in the faeces.

    Figure 17.3 The urea/ornithine cycle. This pathway operates partly in the cytoplasm and partly in the mitochondria of hepatocytes.


    Figure 17.4 The liver stores carbohydrate as glycogen (glycogenesis). Glucose can be liberated from the glycogen stores (glycogenolysis) or can be generated from amino acids and glycerol from fatty acids (gluconeogenesis).


    Blood science angle: The liver and the haematologist

    17.2 Liver function tests



    Alkaline phosphatase

    Gamma-glutamyl transpeptidase


    17.3 Diseases of the liver


    Figure 17.5 Jaundice is the yellowing of the skin and mucous membranes due to the deposition of bilirubin. It is often most obvious in the eye, where the white sclera gives good contrast.

    Pre-liver disease

    Figure 17.6 Anatomical classification of liver disease. We can consider liver disease in terms of pre–, true– and post-factors. The principal pre-liver cause of jaundice is excessive haemolysis, whilst most post-liver disease is caused by partial or complete obstruction of the bile duct, leading to cholestasis. True liver disease is characterized by damage to hepatocytes by a defined toxin or condition such as cancer or cirrhosis.

    True liver disease

    Post-liver disease


    Acute liver disease

    A cautionary tale: Acute liver failure

    Chronic liver disease


    Autoimmune hepatitis


    Fatty liver (steatosis)

    Gilbert's syndrome

    Blood science angle: Gilbert's syndrome

    Primary liver cancer

    Secondary liver cancer

    Blood science angle: The genetics of liver disease

    Other liver disease

    Table 17.3 Some selected factors leading to liver disease.

    Disease of the biliary tree

    Primary sclerosing cholangitis

    Primary biliary sclerosis


    Other disease

    Liver function tests in liver disease



    Alkaline phosphatase

    Gamma-glutamyl transpeptidase

    Comparing the liver function tests

    The complexity of liver function tests

    17.4 Plasma proteins

    Table 17.4 A crude synopsis of LFTs.

    Total proteins



    Measurement of proteins

    Protein electrophoresis

    Figure 17.7 Protein electrophoresis. The separation of groups of proteins according to their overall electrical change. Dependent on the pH of the buffers, and their starting point, different molecules migrate towards the anode or cathode. The figure shows four samples of two patients in duplicate. The heavy blue band at the bottom is albumin, the different globulin bands being easily characterized. Note that samples 3 and 4 have a much heavier staining of the gamma-globulin region. This is because of an abnormality, and is called a paraprotein, the origin of which may be malignant.

    Figure 17.8 Quantification of proteins by electrophoresis. These figures are screenshots of densitometer plots. A beam of light passes over the electrophoresis gel (Figure 17.7) and plots the density of the stain, which is proportional to the concentration of protein present in the gel.

    The scope of plasma proteins


    Table 17.5 Major plasma proteins.



    Albumin as a disease marker

    The consequences of hypoalbuminaemia



    Wilson's disease

    Menkes syndrome

    C-reactive protein




    Thyroxine-binding globulin


    Other plasma proteins

    Blood science angle: Plasma proteins

    Analysis of urine

    Bence–Jones protein


    Other analyses

    17.5 Case studies

    Case study 22


    Case study 23



    Further reading

    Web sites

    18 Hormones and Endocrine Disorders

    Learning objectives

    18.1 Endocrine physiology


    Lipid-soluble hormones

    Table 18.1 The endocrine system.

    Water-soluble hormones

    Control of hormone secretion

    The anterior pituitary

    Adrenocorticotrophic hormone

    Figure 18.1 The location of endocrine organs, variously positioned in the skull, then neck, the abdomen and at the base of the trunk.

    Figure 18.2 Feedback inhibition. In almost all cases, the hypothalamus secretes a releasing hormone that stimulates the pituitary, which then releases a second hormone which acts on a target organ. The products of the latter feed back to the hypothalamus and pituitary to suppress this pathway. The target organ may act on a second target organ which itself may release a factor or factors that have a physiological effect.

    Table 18.2 Reference ranges for hormones of the anterior pituitary.

    Growth hormone


    Thyroid stimulating hormone

    Luteinizing hormone and follicle-stimulating hormone

    The posterior pituitary


    Table 18.3 Reference ranges for hormones of the posterior pituitary.

    Arginine vasopressin

    The thyroid

    Table 18.4 Reference ranges for thyroid hormones.

    Thyroid hormones

    Regulation of tri- and tetra-iodothyronine

    Function of thyroid hormones

    Table 18.5 Reference range for parathyroid hormone.

    The parathyroids

    The adrenals

    Table 18.6 The adrenal gland and its hormones.

    Figure 18.3 Functional anatomy of the adrenal gland. The adrenal consists of three areas: the innermost medulla, the cortex and the outer zona glomerulosma. Each has specific functions. CRF: corticotrophin releasing factor; ACTH: adrenocorticotrophic hormone.

    Adrenaline, noradrenaline and dopamine

    Table 18.7 Reference ranges for adrenal hormones.


    Adrenal androgens


    Table 18.8 Reference ranges for testosterone.

    The gonads

    Sex-hormone-binding globulin

    Male sexual development

    Figure 18.4 Fluctuations in concentrations of oestradiol, FSH and testosterone in the life cycle. Concentrations rise in puberty, and change again at the menopause and andropause.

    Female sexual development

    The menstrual cycle

    Table 18.9 Reference ranges for LH, FSH, oestradiol and progesterone according to the menstrual cycle.



    The menopause

    Laboratory issues

    Steroid chemistry

    18.2 The pathology of the endocrine system

    Figure 18.5 Pathways of steroid metabolism. The synthesis of cortisol, aldosterone, testosterone and oestrogens begins with cholesterol, with many complex intermediates which are the substrate for a host of enzymes: (1) desmolase; (2) 17-hydroxylase; (3) 21-hydroxylase; (4) 3-β-hydroxysteroid dehydrogenase; (5) 11-hydroxylase; (6) 17,20-lyase; (7) aldosterone synthase; (8) 17-β-hydroxysteroid dehydrogenase; (9) aromatase; (10) 5-α-reductase. The activity of the enzyme aldosterone synthase is promoted by angiotensin, the end product of a pathway initiated by the kidney, involving angiotensin-converting enzyme and the enzyme renin (Chapter 12). The aromatase enzyme is the objective of inhibitors used to treat breast and ovarian cancer, and also gynaecomastia.

    Figure 18.6 Steroid structure. Very minor differences in the structures of cholesterol and five steroid hormones. N.B. This is very simplified, and with apologies to card-carrying steroid biochemists.

    Abnormalities in adrenocorticotrophic hormone and cortisol

    Cushing's syndrome

    Figure 18.7 Pathogenesis of Cushing's syndrome. On the left, ACTH arising from the pituitary acts on the adrenals, which secrete cortisol. The latter in turn feeds back to the pituitary to regulate ACTH production. In the middle, a pituitary adenoma secretes high levels of ACTH that flood the adrenal, which responds by secreting high concentrations of cortisol. On the right, an adrenal tumour secretes excess cortisol, which feeds back to a normal pituitary so concentrations of ACTH fall. Ectopic production of ACTH and clinical disease caused by steroid therapy are not shown.

    Figure 18.8 Clinical features of Cushing's syndrome. (a) The patient exhibits the round (‘moon’) face characteristic of this disease, a consequence of the high concentrations of cortisol secreted by her adrenocortical adenoma. (b) The same patient 6 months after removal of the tumour.

    Addison's disease

    Investigation of abnormalities in adrenocorticotrophic hormone and cortisol

    Management of Cushing's syndrome

    Abnormalities in growth hormone

    Investigation of acromegaly

    Management of acromegaly

    Low concentrations of growth hormone

    Abnormalities in prolactin


    Investigation of hyperprolactinaemia

    Table 18.10 Increased concentrations of prolactin.


    Thyroid disease


    Figure 18.9 Goitre. An exceptionally large goitre due to profound and chronic iodine deficiency in rural Africa. This case would never develop to such an extent in the UK.

    Pathophysiology of hyperthyroidism

    Clinical features of hyperthyroidism

    Table 18.11 General features of thyroid disease.

    Management of hyperthyroidism


    Pathophysiology of primary hypothyroidism

    Clinical features of hypothyroidism

    Investigation and diagnosis of hypothyroidism

    Management of hypothyroidism

    The laboratory and thyroid disease

    The thyroid and pregnancy

    Thyroid cancer

    Blood science angle: The thyroid

    Anterior pituitary hypofunction

    Posterior pituitary dysfunction

    Decreased levels of arginine vasopressin

    The laboratory in diabetes insipidus

    Increased concentrations of arginine vasopressin

    Parathyroid dysfunction



    Adrenal pathology

    Congenital adrenal hyperplasia

    The laboratory in congenital adrenal hyperplasia

    Conn's syndrome

    Catecholamine abnormalities

    Treatment of adrenal disease

    Abnormalities in male reproductive endocrinology


    Blood science angle: Testosterone

    Testicular cancer

    Male endocrinology as target for therapy

    Abnormalities in female reproductive endocrinology



    Polycystic ovary syndrome

    Investigations in female reproductive endocrinology

    Limitations in assays for steroid and protein hormones

    Multiple endocrine neoplasia

    MEN 1

    MEN 2

    The laboratory in multiple endocrine neoplasia

    Molecular genetics of endocrine disease

    Chromosomal abnormalities

    Genetic mutations

    Figure 18.10 Male precocious puberty. Molecular genetic techniques discovered a gain-of-function mutation in the gene encoding the LH receptor in this patient. The consequences of this are the hyper-reactivity to high testosterone from Leydig cells, and so the development of pubic hair and genitals. The patient is 2 years old but is the size of a 4-year-old.

    The genetics of multiple endocrine neoplasia

    Genetics of steroid production

    18.3 Case studies

    Case study 24


    Case study 25



    Further reading

    Web sites

    19 Cancer and Tumour Markers

    Learning objectives

    19.1 General concepts in cancer biology

    Nomenclature and classification

    Tumour biology

    Table 19.1 Cancer deaths in 2010.

    Clinical oncology

    Tumour markers



    Clinical value

    Figure 19.1 Use of a cancer marker in diagnosis and in monitoring the effect of treatment.

    19.2 Blood science and cancer

    Markers with no clear biological effect

    Blood science angle: Paraproteins

    Markers with a biological effect

    Table 19.2 Bowel cancer.

    Combining markers


    Table 19.3 Selected cancer markers.


    19.3 Molecular genetics


    Blood science angle: Cancer

    19.4 Case studies

    Case study 26


    Case study 27



    Further reading


    Web sites

    20 Inherited Metabolic Disorders

    Learning objectives

    20.1 The genetics of inheritance

    Table 20.1 Examples of IMDs.

    Inherited metabolic disorders

    Figure 20.1 Consequences of an enzyme deficiency in a metabolic pathway. An enzyme deficiency causes reduction of product, together with accumulation of substrate, and minor products of metabolic pathway.

    20.2 Molecular inherited metabolic disorders

    Amino acid disorders

    Methionine and homocysteine

    Figure 20.2 Metabolism of methionine and homocysteine. This grossly simplified metabolic pathway serves as a useful illustration of the interrelationships of certain amino acids, their linked enzymes and vitamin cofactors. The numbers refer to enzymes: (1) methionine synthase (requires vitamin B12), (2) adenosyl transferase, (3) methyl transferase, (4) cystathionine synthase (requires vitamin B6), (5) methylene tetrahydrofolate reductase (MTHFr).

    Ornithine and citrulline

    Phenylalanine and phenylketones

    Figure 20.3 Metabolism of phenylalanine and tyrosine. Phenylalanine is the substrate for phenylalanine hydroxlase, the product being tyrosine, which is the substrate for at least three pathways.


    Organic acid disorders

    Purine and pyrimidine disorders

    Lipid disorders

    Carbohydrate disorders

    Disorders of galactose metabolism

    Disorders of fructose metabolism

    Disorders in glycogen metabolism

    Figure 20.4 Glucose and glycogen metabolism. Maintenance of fasting blood glucose concentrations by glycogenolysis and gluconeogenesis in the liver. Deficiency of the enzyme glucose-6-phosphatase blocks the conversion of glucose-6-phosphate to glucose.

    Cystic fibrosis

    20.3 Organelle inherited metabolic disorders




    20.4 Antenatal diagnosis and neonatal screening

    The laboratory

    20.5 Case studies

    Case study 28


    Figure 20.5 Blood film from case study 29. There is marked anisocytosis with microcytes (possibly some microspherocytes) and many reticulocytes (leading to polychromasia) and some schistocytes. Chapters 3 and 4 have parallel figures of red cell morpohology.

    Case study 29



    Further Reading

    21 Drugs and Poisons

    Learning objectives

    21.1 Toxicology

    General biochemical features of poisoning

    The kidney

    Figure 21.1 Outline of drug metabolism and clinical effect at target sites. This is far from the case that the amount of drug interfacing with cells and tissues is that which is prescribed. Factors such as compliance, absorption, metabolism and excretion all influence drug activity.

    The liver

    Pharmacokinetics and pharmacodynamics

    21.2 Toxicology of specific compounds

    Carbon monoxide

    Table 21.1 Common causes of fatal toxic events.



    Drugs of abuse

    Figure 21.2 Pathways involved in the metabolism of paracetamol. Conjugation to glucuronide, sulphate or glutathione renders the drug nontoxic. However, in their absence, paracetamol causes hepatic and renal cell damage. NAPQI: N-acetyl-p-benzo-quinoneimine.


    Figure 21.3 Metabolism of acetylsalicylic acid. The liver converts acetylsalicylic acid to its active salicylic acid (salicylate) by hydrolysis and deacetylation, and so the generation of a molecule of acetic acid.




    Barbiturates and benzodiazapines


    Heavy metals





    21.3 Therapeutic drug monitoring

    General concepts

    Which drugs to monitor?


    Anticonvulsant drugs

    Antimicrobial drugs

    Cancer chemotherapy

    Blood science angle: Chemotherapy

    Cardiovascular drugs

    Psychoactive drugs

    Table 21.2 Common TDM target ranges.

    Blood science angle: TDM

    21.4 Case studies

    Case study 30


    Case study 31




    Further reading

    22 Case Reports in Blood Science


    Case report 1


    Table 22.1 Case report 1.


    Additional analyses

    Discussion and diagnosis

    Case report 2


    Table 22.2 Case report 2.


    Discussion and diagnosis

    Risk factor management

    Case report 3



    Discussion and diagnosis

    Table 22.3 Case report 3.

    Case report 4

    Part 1


    Table 22.4 Case report 4: part 1.


    Discussion and diagnosis

    Part 2


    Table 22.5 Case report 4: part 2.

    Discussion and diagnosis

    Case report 5

    Part 1



    Discussion and diagnosis

    Table 22.6 Case report 5: part 1.

    Part 2


    Table 22.7 Case report 5: part 2.

    Part 3



    Table 22.8 Case report 5: part 3.

    Discussion and diagnosis

    Case report 6


    Table 22.9 Case report 6.

    Interpretation, discussion and diagnosis

    Case report 7


    Table 22.10 Case report 7.

    Interpretation and discussion


    Case report 8

    Table 22.11 Case report 8.


    Discussion and diagnosis

    Case report 9

    Day 1


    Day 2

    Table 22.12 Case report 9.

    Day 3


    Day 4


    Day 5


    Case report 10

    Day 1

    Table 22.13 Case report 10.

    Interpretation and discussion

    Day 2

    Interpretation and discussion

    Day 3

    Interpretation and discussion

    Case report 11


    Table 22.14 Case report 11.


    Case report 12


    Table 22.15 Case report 12.

    Discussion and diagnosis

    Figure 22.1 Blood film from case report 12

    Case report 13

    Table 22.16 Case report 13.


    Discussion and diagnosis

    Case report 14

    Table 22.17 Case report 14.


    Discussion and diagnosis


    Back Matter

    Appendix Reference Ranges

    Further Reading




  • 31200lei 290.00 lei

    Bridging the gap between science and clinical practice, The Bethesda Handbook of Clinical Hematology, Fourth Edition , provides concise, up-to-date coverage of “need to know” information on the diagnosis and treatment of blood and bone marrow disorders. Written by nationally recognized experts and senior fellows at the National Institutes of Health, and at leading research institutions throughout the United States, this essential pocket reference is logically organized by disease category and features a reader-friendly format that includes tables, algorithms, illustrations, and bulleted lists that highlight key information.

    Discusses the pathophysiology, natural history, risk factors, diagnosis, management, and follow-up of common hematological diseases.

    Contains new information on diagnosis, treatment and management of myelodysplastic and myeloproliferative disorders; leukemias and lymphomas; disorders of hemostasis and thrombosis. Features new diagnostic and treatment strategies, updated references, and revised information throughout.

    Ideal for the student, resident, or fellow on a hematology or oncology service, as well as the internist, hospitalist, family practitioner, and pediatrician who sees patients with blood diseases.

    Perfect as an everyday reference or for board review.

  • 34100lei 300.00 lei



    Hematology Case Studies with Blood Cell Morphology and Pathophysiology compiles specialized case studies with specific information on various hematological disorders with Full Blood Examination (FBE or CBC), blood film images and pathophysiology of each condition. In addition, it provides basic information on how to recognize and diagnose hematological conditions that are frequently observed in the laboratory. Technicians and scientists working in core laboratories such as biochemistry labs or blood banks will find this book to be extremely thorough. Moreover, it can be used as a reference book by technicians, scientists and hematologists in every level of expertise in diagnosing hematological disorders.

    Includes morphology of red cells, white cells and platelets

    Provides images of actual blood slides under the microscope, showing the most important diagnostic features observed in each condition

    Presents details that are considered difficult for beginners or non- hematologists, such as specific tests and techniques

    Covers case studies that finish with the pathophysiology of the condition


    Table of Contents:


    Chapter 1: Introduction


    The Importance of the Blood Film in the Diagnosis of Haematological Disorders

    Microcytic Anaemia, Haemoglobinopathies, and Blood Film Morphology

    Blood Film Morphology and Diagnosis of Macrocytic Anaemia

    Peripheral Blood Film and Diagnosis of Haemolytic Anaemia

    Blood Film Morphology, Thrombocytopenia, and Thrombocytosis

    Blood Film Morphology, Leukaemia, Lymphoma, and Bone Marrow Failure

    Brief About Leukaemia

    Explanations for Some Terms Used in This Booklet



    Myeloperoxidase (MPO)

    Sudan Black B (SBB)

    Chloroacetate Esterase

    Periodic Acid Schiff (PAS)

    Terminal Deoxynucleotidyl Transferase Stain (TdT)

    Neutrophil Alkaline Phosphatase (NAP)

    Tartrate-Resistant Acid Phosphatase Stain (TRAP)

    Acid Phosphatase

    Alpha Naphthyl Acetate Esterase (ANAE)


    Chapter 2: Microcytic Disorders


    Case 1

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 2

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of IDA

    Case 3

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Alpha Thalassemia

    Case 4

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Beta Thalassemia Minor

    Case 5

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Beta Thalassemia Major

    Case 6

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 7

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Haemoglobin E Disease

    Case 8

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Sideroblastic Anaemia

    Congenital Sideroblastic Anaemias

    Acquired Sideroblastic Anaemias

    Chapter 3: Normocytic Disorders


    Case 9A

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Sickle Cell Anaemia

    Case 9B

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Sickle Cell Disease and Thalassaemia

    Case 10

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Anaemia of Chronic Disease

    Case 11

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Aplastic Anaemia

    Case 12

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Final Diagnosis

    Chapter 4: Macrocytic Disorders


    Case 13

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Macrocytosis

    Case 14

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Megaloblastic Anaemia

    Case 15

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Macrocytosis Caused by Liver Disease

    Chapter 5: Nonimmune Haemolytic Disorders (RBC Metabolic Abnormalities)


    Case 16

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of G6PD Deficiency

    Case 17

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of PK Deficiency

    Chapter 6: Nonimmune Haemolytic Disorders (RBC Membrane Abnormalities)


    Case 18

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Hereditary Spherocytosis

    Case 19

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Hereditary Elliptocytosis

    Case 20

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Hereditary Stomatocytosis

    Case 21

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis


    Case 22

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Hereditary Pyropoikilocytosis

    Case 23

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of PNH

    Chapter 7: Immune Haemolytic Disorders


    Case 24

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Drug-Induced Haemolytic Anaemia (DIHA)

    Case 25

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Warm Autoimmune Haemolytic Anaemia (wAIHA)

    Case 26

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Cold Autoimmune Haemolytic Anaemia (cAIHA)

    Case 27

    Clinical presentations

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnosis

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Rh-HDNB

    Chapter 8: Acute Leukaemias


    Case 28

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 29

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 30

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 31

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 32

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 33

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 34

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 35

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of AML

    Case 36

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of ALL

    Chapter 9: Myeloproliferative/Myelodysplastic Disorders


    Case 37

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of CML

    Case 38

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnoses

    Differential Diagnosis

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of PV

    Case 39

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Essential Thrombocythaemia

    Case 40

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of MF

    Case 41

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 42

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 43

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of MDS

    Chapter 10: Chronic Lymphoproliferative Disorders


    Case 44

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of CLL

    Case 45

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 46

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 47

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of HCL

    Chapter 11: Lymphomas


    Case 48

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 49

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Mantle Cell Lymphoma

    Chapter 12: Plasma Cell Disorders


    Case 50

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 51

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Plasma Cell Myeloma

    Chapter 13: Haemostatic Disorders (Microangiopathic Haemolytic Anaemia)


    Case 52

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of DIC

    Case 53

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Haemolytic Uremic Syndrome (HUS)

    Case 54

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of TTP

    Case 55

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Chapter 14: Haematological Infections


    Case 56

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of IM

    Case 57

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 58

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 59

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Case 60

    FBE Results

    RBC Morphology

    WBC Morphology

    Platelet Morphology

    Provisional Diagnosis

    Differential Diagnoses

    Further Tests and Expected Results

    Final Diagnosis

    Pathophysiology of Malarial Infection




  • 33700lei 300.00 lei

    This clinical casebook provides a concise, state-of-the-art review of pediatric bleeding disorders. Presented in a case-based format, each case presents a different variant of bleeding disorder, illustrates the etiology, pathology, genetics, diagnosis, and management of the disorder, and offers clinical pearls. Disorders covered include hemophilia A and B, rare factor deficiencies, von Willebrand disease, immune thrombocytopenia purpura, and platelet dysfunctions. Written by experts in the field, Pediatric Bleeding Disorders: A Clinical Casebook is a valuable resource for clinicians and practitioners treating patients with challenging coagulation issues.

  • 36800lei 320.00 lei



    Learn how to accurately identify cells at the microscope with Clinical Hematology Atlas, 6th Edition. An excellent companion to Rodak's Hematology: Clinical Principles and Applications, this award-winning atlas offers complete coverage of the basics of hematologic morphology, including examination of the peripheral blood smear, maturation of the blood cell lines, and information on a variety of clinical disorders. Vivid photomicrographs, schematic diagrams, and electron micrographs clearly illustrate hematology from normal cell maturation to the development of various pathologies so you can be certain you’re making accurate conclusions in the lab.


    • Schematic diagrams, photomicrographs, and electron micrographs in every chapter visually enhance student understanding of hematologic cellular morphology.
    • Compact size, concise text, and spiral binding make it easy to carry and reference this atlas in the laboratory.
    • Chapter on normal newborn peripheral blood morphology covers the normal cells found in neonatal blood.
    • Chapter on body fluids illustrates the other fluids found in the body besides blood, using images from cytocentrifuged specimens.
    • The most common cytochemical stains, along with a summary chart for interpretation, are featured in the leukemia chapters to assist in the classification of both malignant and benign leukoproliferative disorders.
    • Chapter featuring morphologic changes after myeloid hematopoietic growth factors is included in the text.
    • Morphologic abnormalities coverage in the chapters on erythrocytes and leukocytes, along descriptions of each cell, presents this information in a schematic fashion.
    • Appendix with comparison tables of commonly confused cells includes lymphocytes versus neutrophilic myelocytes and monocytes versus reactive lymphoctyes to help students see the subtle differences between them.
    • Glossary of hematologic terms at the end of the book provides a quick reference to easily look up definitions.

    New To This Edition:

    • NEW! Revised chapters include updates based on extensive reviewer feedback.
    • NEW! Updated photos reflect the most up-to-date information and latest advances in the field.

    Table Of Contents:

    Section 1: Introduction

    1. Introduction to Peripheral Blood Film Examination

    Section 2: Hematopoiesis

    2. Hematopoiesis

    3. Erythrocyte Maturation

    4. Megakaryocyte Maturation

    5. Neutrophil Maturation

    6. Monocyte Maturation

    7. Eosinophil Maturation

    8. Basophil Maturation

    9. Lymphocyte Maturation

    Section 3: Erythrocytes

    10. Variations in Size and Color of Erythrocytes

    11. Variations in Shape and Distribution of Erythrocytes

    12. Inclusions in Erythrocytes

    13. Diseases Affecting Erythrocytes

    Section 4: Leukocytes

    14. Nuclear and Cytoplasmic Changes in Leukocytes

    15. Acute Myeloid Leukemia

    16. Precursor Lymphoid Neoplasms

    17. Myeloproliferative Neoplasms

    18. Myelodysplastic Syndromes

    19. Mature Lymphoproliferative Disorders

    20. Morphologic Changes after Myeloid Hematopoietic Growth Factors

    Section 5: Miscellaneous

    21. Microorganisms

    22. Miscellaneous Cells

    23. Normal Newborn Peripheral Blood Morphology

    24. Body Fluids


    Appendix: Comparison Tables



  • 335.00 lei

    his comprehensive and authoritative text summarizes current evidence and provides experienced perspectives on the etiology, diagnosis, and management of pediatric thrombotic disorders, including arterial ischemic stroke and cerebral sinovenous thrombosis. Authored by leaders in the field, individual chapters are devoted to specific anatomic sites and types of thrombosis. State-of-the-art, pediatric-focused chapters aid in diagnostic evaluation and therapeutic decision making, in settings ranging from the most routine to the most complex and challenging patient scenarios. Topics include: Extremity and Caval Deep Venous Thrombosis; Pulmonary Embolism; Cancer-Associated Thromboembolism; Infection-Associated Thromboembolism; Arterial Ischemic Stroke; Cerebral Sinovenous Thrombosis; Gastrointestinal and Visceral Thrombosis; Developmental Hemostasis; Thrombophilias; Heparin-Induced Thrombocytopenia/Thrombosis Syndrome; Venous Thromboembolism Prevention; Thrombolysis; and Novel Anticoagulants, among others. This text is a 'must-have' for practitioners in pediatric hematology, oncology, hematopoietic stem cell transplantation, neurology, hospital medicine, and intensive care.

  • 370.00 lei

    This is the 13th edition of a book written for students and specialists who are interested in developing a fundamental understanding of pathology and treatment of hematologic diseases. The amount of knowledge required by hematologists to identify the best course of treatment for a patient in this field is changing rapidly and has fueled an explosion of new drugs that target pathways virtually unknown a decade ago. We are now also entering an era of effective immunotherapy for a variety of hematologic malignancies, but the long term outcomes and toxicities of these treatment approaches are still unknown. This first edition in English is a significant novelty in the history of this work. Its underlying goals, however, remain the same of the first Italian edition: to help students and specialists understand the basis, treatment and management of hematologic diseases.

  • 403.00 lei

     Pret: 403 lei 305 lei (pret valabil pana la data de 20 septembrie 2020)


    About this book


    In this book, world-renowned experts in the field of hematopoietic cell transplantation examine a range of issues and controversies relating to apheresis, with the aim of identifying current trends and best practices. Readers will find up-to-date guidance on donor evaluation, CD34+ cell mobilization strategies, options and selection of apheresis device, anticoagulation techniques in apheresis, the role of prediction algorithms in determining procedure eligibility and length, and the prevention and management of complications.

    Applications of apheresis devices in the processing of bone marrow grafts are discussed, and detailed attention is devoted to the indications and rationale for therapeutic apheresis procedures, with individual chapters focusing on therapeutic plasma exchange and immunoadsorption, red cell exchange, and extracorporeal photopheresis. Finally, the applications of apheresis in pediatric donors and in resource-limiting environments are considered. This book, featuring numerous helpful tables, algorithms, and figures, will be of high practical value for residents, fellows, faculty members and other healthcare personnel involved in hematopoietic cell transplantation.


    Table of contents (15 chapters)


    Introduction and Rationale

    Pages 1-3

    Padmanabhan, Anand (et al.)

    Administrative and Regulatory Considerations for Apheresis Collection Facilities

    Pages 5-10

    Schwartz, Joseph (Yossi) (et al.)

    FACT-JACIE Standards: Common Citations and How Best to Avoid Them

    Pages 11-21

    Gastineau, Dennis A. (et al.)

    Donor Evaluation for Hematopoietic Stem and Progenitor Cell Collection

    Pages 23-49

    Connelly-Smith, Laura S.

    Mobilization Strategies: HPC(A) Collections for Autologous Hematopoietic Cell Transplants

    Pages 51-62

    Worel, Nina

    Mobilization Strategies: HPC(A) Collections for Allogeneic Hematopoietic Cell Transplants

    Pages 63-80

    Bhamidipati, Pavan Kumar (et al.)

    Hematopoietic Progenitor Cells, Apheresis and Therapeutic Cells, T-Cells Collection: Instrumentation, Operating Parameters, and Troubleshooting

    Pages 81-100

    Burgstaler, Edwin A. (et al.)

    Anticoagulation and Other Periprocedural Considerations for Apheresis

    Pages 101-107

    Karafin, Matthew S. (et al.)

    Concepts and Rationale for Using Predictive Algorithms for Hematopoietic Progenitor Cell Apheresis Collection

    Pages 109-119

    Cottler-Fox, Michele

    Applications of Apheresis Devices in Processing Bone Marrow Grafts

    Pages 121-134

    Leitner, Gerda C.

    Therapeutic Plasma Exchange and Immunoadsorption: Indications and Implementation

    Pages 135-150

    Handisurya, Ammon (et al.)

    Red Blood Cell Exchange: When and Why?

    Pages 151-160

    Stussi, Georg (et al.)

    Extracorporeal Photopheresis in Hematopoietic Cell Transplantation

    Pages 161-186

    Hölig, Kristina (et al.)

    Prevention and Management of Apheresis Complications

    Pages 187-200

    Neyrinck, Marleen M. (et al.)

    Challenges and Optimization of Apheresis Procedures in Resource-Limiting Environments

    Pages 201-211

    Koh, Mickey B. C. (et al.)



  • 50500lei 430.00 lei




    This book provides a practical guide to the use of novel and conventional anticoagulants for a variety of medical conditions and patients profiled. It reviews data for selecting the most appropriate medication for a given presentation based on a patient’s background while highlighting current best practices. Chapters discuss the choice of agents and optimum duration of therapy while including the relevant literature review and evidence. Specific sections focus on the use of anticoagulants in patients with cardiovascular disease, autoimmune and rheumatologic disorders, antiphospholipid syndrome, cancer, and in the surgical contexts. The book also examines anticoagulation in pregnant and lactating women, pediatric and elderly populations, and patients with extreme weights.  Intended for use in daily practice, Precision Anticoagulation Medicine - A Practical Guide is an essential resource for physicians and related professionals, residents, fellows, and graduate students in hematology, cardiology, rheumatology, oncology, surgery, anesthesiology, and intensive care.      



    Table of contents:


    1. Coagulation and Anticoagulants

    2. Routine Anticoagulation for the Provoked and Unprovoked VTE

    3. Anticoagulation in Cardiac Patients

    4. Thrombosis and Anticoagulation in Children

    5. Cancer-Associated Thrombosis (CAT)

    6. Anticoagulation in Pregnancy and Lactation

    7. Anticoagulation in Autoimmune Rheumatic Diseases

    8. Antiphospholipid Syndrome

    9. Anticoagulation in Patients with Renal Insufficiency

    10. VTE Prophylaxis in General and Orthopedic Surgery

    11. Thromboprophylaxis for Hospitalized Medical Patients

    12. Perioperative Management of Anticoagulation and Antiplatelet Therapy

    13. Anticoagulation Reversal Guide and Reversal Agents


  • 435.00 lei


    The importance of blood to human life has been recognized since prehistorical era. Early man knew that if enough blood leaves the body, then life ceases to function. As a result of this blood has acquired mystic and religious significance throughout the ages. In the classical Greek medicine, blood was associated with air, with springtime, and with a merry and gluttonous (sanguine) personality. It was also believed to be produced exclusively by the liver.In Hippocratic medicine, blood was considered to be one of the four humor, the others being phlegm, yellow bile and black bile.Blood is a specialized bodily fluid that delivers necessary substance and nutrients to the body’s cells and transports waste products away from those some cells. Blood is circulated around the blood vessels by the pumping action of the heart.Medical term related often begins with hemo- or hemato- from the ancient word MA or (haima) for blood.In histological terms, blood is considered a specialized form of connective tissue, given its origin in the bones and the presence of potential molecular fibers in the form of fibrinogen.

  • 54000lei 450.00 lei

    Designed as a practical, succinct guide, for quick reference by clinicians with everyday questions, this title guides the reader through the range of approaches available for diagnosis, management, or prevention of hemorrhagic and thrombotic diseases or disorders. Provides essential practical management for all those working in the field of hemostasis and thrombosis Includes new chapters on direct oral anticoagulants, acquired inhibitors of coagulation, and expanded discussion of thrombotic microangiopathies Covers in a clear and succinct format, the diagnosis, treatment and prevention of thrombotic and haemostatic disorders Follows templated chapter formats for rapid referral, including key points and summary boxes, and further reading Highlights controversial issues and provides advice for everyday questions encountered in the clinic

  • 54300lei 460.00 lei


    Steve Kitchen, Clinical Scientist, Sheffield Haemophilia and Thrombosis Centre, Royal Hallamshire Hospital and Scientific Director, UK National External Quality Assessment Scheme (FQAS) for Blood Coagulation, Scientific Director, WHO and WFH International External Quality Assessment Programs for Blood Coagulation, Sheffield, UK

    John D Olson, Professor and Vice Chair for Clinical Affairs, Department of Pathology, University of Texas Health Sciences Centre, San Antonio, Texas, USA

    F. Eric Preston, Emeritus Professsor of Haematology, University of Sheffield and Director, WHO and WFH International External Quality Assessment Programs for Blood Coagulations, Sheffield, UK

    The hemostasis laboratory has a vital role in the diagnosis and management of patients with familial and acquired hemorrhagic and thrombotic disorders. Rapid changes in the number and complexity of tests in this discipline have presented challenges for laboratories, as they develop quality programs for the oversight of this testing.

    Quality in Laboratory Hemostasis and Thrombosis has been completely revised and updated to reflect the changing process of managing quality. The second edition provides information on all aspects of testing, from pre-analytic to analytic and result reporting, in addition to external quality assurance. Chapters throughout the book include the development of global guidelines for methods, as well as the preparation of international standard plasmas and reagents.

    Designed to capture the elements of quality at all levels of the practice of laboratory hemostasis and thrombosis, this book will guide the reader through the development of a quality program to support all activities in the hemostasis laboratory, both simple and complex.


  • 57000lei 470.00 lei

    The first book on clinical guide to transplantation in lymphoma to present cutting edge knowledge on how to integrate, transplantation and novel therapies in patients with lymphoid malignancies • Provides practical management guidance on how to integrate, transplantation and novel therapies in patients with lymphoid malignancies • Covers an overview of transplantation in lymphoma, and management of the lymphoid malignancies • Discusses organizational aspects of transplant patients and managing a transplant program • Appendices provide practical quick-reference information on follow-up after autologous and allogenic stem cell transplantation in lymphoma

  • 475.00 lei


    In the present study 2ml of blood is sufficient for investigation. Here viscosity and surface tension are measured at stretch. This technique is helpful in quick diagnosis of disease and physical fitness of a patient. This is a potential tool in medical discipline for diagnosis, drug administration and monitoring of a patient suffering from any disease, in general, and thrombosis and cancer in particular.This Technique aided with computer program for data processing may help a physician for quick diagnosis of disease. Biochemical and biophysical perturbation in cell physiology can be mirrored in viscometric data. The rheological parameters such as volumetric flow rate(Q) and velocity(V) are also studied using this technique which are helpful for the understanding of blood circulation on human vascular bed. Using this technique the viscosity and surface tension, velocity and volume flow rates of different diseases thrombasis, bilirubin, diabetes, malaria and cancer. The dielectrical behaviour such as dielectric constant, dielectric loss and conductivity of human blood and human plaama also studied between the frequency in range of 100Hz to 100kHz, which reveals cell properties.

  • 475.00 lei


    Ischemic heart disease is the most common cause of morbidity and mortality worldwide. The hemostatic system is a potentially relevant determinant of these cardiovascular events. Acute arterial thrombosis occurs at the site of a ruptured, lipid-rich atherosclerotic plaque, resulting in arterial occlusion and clinical manifestations such as myocardial infarction. The hemostatic system may be relevant in the initiation and progression of atherosclerosis, as well. The variations in the coagulation and fibrinolytic systems, in the form of hypercoagulable disorders, may predispose carriers to accelerated atherothrombosis, and increased risk of its coronary events. This book will shed light on the role of hereditary thrombophilia in acute coronary syndrome. It is hoped that it will help/guide researchers who have special interests in arterial thrombosis, as well as, in ischemic heart disease.

  • 54600lei 480.00 lei

    This book identifies the various ethical challenges that arise in pediatric hematology/oncology and provides the necessary tools to overcome these challenges. Aiming to expand upon and strengthen providers’ knowledge and experience in pediatric health care ethical issues, the text positions providers to be beneficial resources to faculty, staff, patients, and families within their institution. It presents a multidisciplinary approach to sound ethical practices that is necessary to effectively care for these patients and their families. The book reviews the principles of ethical decision-making, the unique difficulties in using children as research subjects, common ethical conundrums involved in providing end-of-life care, and general moralities of professional practice. 
    Written by experts in their fields, Ethical Issues in Pediatric Hematology/Oncology is an innovative and valuable resource for clinicians, practitioners, and trainees who work in the field of pediatric hematology/oncology. 

  • 59400lei 505.00 lei

    Make sure you are thoroughly prepared to work in a clinical lab. Rodak's Hematology: Clinical Principles and Applications, 6th Edition uses hundreds of full-color photomicrographs to help you understand the essentials of hematology. This new edition shows how to accurately identify cells, simplifies hemostasis and thrombosis concepts, and covers normal hematopoiesis through diseases of erythroid, myeloid, lymphoid, and megakaryocytic origins. Easy to follow and understand, this book also covers key topics including: working in a hematology lab; complementary testing areas such as flow cytometry, cytogenetics, and molecular diagnostics; the parts and functions of the cell; and laboratory testing of blood cells and body fluid cells. UPDATED nearly 700 full-color illustrations and photomicrographs make it easier for you to visualize hematology concepts and show what you'll encounter in the lab, with images appearing near their mentions in the text to minimize flipping pages back and forth. UPDATED content throughout text reflects latest information on hematology. Instructions for lab procedures include sources of possible errors along with comments. Hematology instruments are described, compared, and contrasted. Case studies in each chapter provide opportunities to apply hematology concepts to real-life scenarios. Hematology/hemostasis reference ranges are listed on the inside front and back covers for quick reference. A bulleted summary makes it easy for you to review the important points in every chapter. Learning objectives begin each chapter and indicate what you should achieve, with review questions appearing at the end. A glossary of key terms makes it easy to find and learn definitions. NEW! Additional content on cell structure and receptors helps you learn to identify these organisms. NEW! New chapter on Introduction to Hematology Malignancies provides and overview of diagnostic technology and techniques used in the lab.

  • 505.00 lei

    This book provides the necessary information about not only the clinical aspects of caring for cancer survivors, but also the psychosocial impacts. There are multiple resources available to serve as oncology textbooks, but nothing to provide the necessary information on patient care for the non-MD members of the cancer patient management team. In the post-treatment phase, the management team must go beyond the realm of "conventional" follow-up, helping the patient to intellectually understand and emotionally grasp the path ahead. Cancer Survivorship will prove a vital tool to physicians, nurses, clinical social workers and mental health.

  • 520.00 lei


    Pret: 520 lei 330 lei (pret valabil pana la data de 29 septembrie 2020)

    Reviews the most current and novel treatment strategies for NHL

    Supplemented with numerous color illustrations, photographs, and tables

    Written by worldwide experts in the field


    About this book


    This text provides a state-of-the-art overview on Non-Hodgkin's lymphoma (NHL) in children and adolescents. The volume is divided into seven sections, each of which focuses on a critical component of pediatric NHL, including history and epidemiology, pathology and molecular biology, disease evaluation and response, common and rare sub-types of NHL, and current and novel treatment strategies. The text also comprehensively reviews the late effects of treatment, quality of patient life, and NHL treatment in countries with limited resources.

    Written by experts in the field, Non-Hodgkin's Lymphoma in Childhood and Adolescence is a valuable resource for clinicians and practitioners who treat children and adolescents with NHL.

    Table of contents (28 chapters)

    History of Diagnoses and Treatment Strategies in Pediatric Non-Hodgkin’s Lymphomas

    Pages 3-13

    Mann, Georg

    Epidemiology of Non-Hodgkin Lymphomas in Childhood and Adolescence

    Pages 15-22

    Thacker, Nirav (et al.)

    Diagnosis and Classification

    Pages 23-29

    Molina, Thierry Jo

    Pathogenesis of B-Cell Lymphoma

    Pages 33-50

    Wagener, Rabea (et al.)

    Pathogenesis of T-Non-Hodgkin’s Lymphoma

    Pages 51-56

    Bond, Jonathan (et al.)

    The Pathogenesis of Anaplastic Large Cell Lymphoma

    Pages 57-65

    Turner, Suzanne Dawn


    Pages 67-95

    Kornauth, Christoph (et al.)

    Genetic Predisposition to Non-Hodgkin Lymphoma

    Pages 97-110

    Haas, Oskar A. (et al.)

    Response Assessment in Pediatric Non-Hodgkin Lymphoma

    Pages 113-118

    Truong, Tony H. (et al.)

    Minimal Disseminated and Minimal Residual Disease in Pediatric Non-Hodgkin Lymphoma

    Pages 119-129

    Mussolin, Lara (et al.)

    Prognostic Factors in Childhood and Adolescent Non-Hodgkin Lymphoma

    Pages 131-149

    Pillon, Marta (et al.)

    Lymphoblastic Lymphoma

    Pages 153-164

    Burkhardt, Birgit (et al.)

    Burkitt Lymphoma and Diffuse Large B-Cell Lymphoma

    Pages 167-183

    Egan, Grace (et al.)

    Primary Mediastinal and Gray Zone Lymphomas

    Pages 185-193

    Giulino-Roth, Lisa (et al.)

    Epstein-Barr Virus-Associated Post-Transplantation Lymphoproliferative Disease

    Pages 195-211

    Geerlinks, Ashley V. (et al.)

    Pediatric-Type Follicular Lymphoma (PTFL)

    Pages 213-219

    Attarbaschi, Andishe

    Marginal Zone Lymphoma

    Pages 221-227

    Burkhardt, Birgit

    Primary Central Nervous System Lymphoma

    Pages 229-238

    Abla, Oussama (et al.)

    Rare B-Cell Non-Hodgkin’s Lymphomas in Childhood and Adolescence

    Pages 239-247

    Beishuizen, Auke (et al.)

    Anaplastic Large Cell Lymphoma in Children and Adolescents

    Pages 251-262

    Lowe, Eric J. (et al.)

    Peripheral T-Cell Lymphoma

    Pages 263-269

    Mellgren, Karin (et al.)

    Extranodal NK-/T-Cell Lymphomas and EBV+ Lymphoproliferative Diseases of Childhood

    Pages 271-279

    Wanitpongpun, Chinadol (et al.)

    Cutaneous T-Cell Lymphomas in Childhood and Adolescence

    Pages 281-291

    Willemze, Rein

    Principles of Immunotherapy

    Pages 295-304

    Goldman, Stanton (et al.)

    Hematopoietic Stem Cell Transplantation

    Pages 305-313

    Mori, Tetsuya (et al.)

    Novel Therapies in Paediatric NHL

    Pages 315-335

    Burke, Amos (et al.)

    Childhood and Adolescence Non-Hodgkin Lymphomas in Low- and Middle-Income Countries

    Pages 337-351

    Ozuah, Nmazuo W. (et al.)

    Long-Term Outcomes in Survivors of Childhood and Adolescent Non-Hodgkin Lymphoma

    Pages 353-366

    Nathan, Paul C. (et al.)


  • 55800lei 520.00 lei



    Diagnostic haematology requires the assessment of clinical and laboratory data together with a careful morphological assessment of cells in blood, bone marrow and tissue ­fluids. Subsequent investigations including flow cytometry, immunohistochemistry, cytogenetics and molecular studies are guided by the original morphological findings. These targeted investigations help generate a prompt unifying diagnosis. Haematology: From the Image to the Diagnosis presents a series of cases illustrating how skills in morphology can guide the investigative process. In this book, the authors capture a series of images to illustrate key features to recognize when undertaking a morphological review and show how they can be integrated with supplementary information to reach a final diagnosis.

    Using a novel format of visual case studies, this text mimics ‘real life’ for the practising diagnostic haematologist – using brief clinical details and initial microscopic morphological triage to formulate a differential diagnosis and a plan for efficient and economical confirmatory investigation to deduce the correct final diagnosis. The carefully selected, high-quality photomicrographs and the clear, succinct descriptions of key features, investigations and results will help haematologists, clinical scientists, haematology trainees and haematopathologists to make accurate diagnoses in their day-to-day work.

    Covering a wide range of topics, and including paediatric as well as adult cases, Haematology: From the Image to the Diagnosis is a succinct visual guide which will be welcomed by consultants, trainees and scientists alike.






    1. Haemophagocytic syndrome secondary to anaplastic large cell lymphoma

    2. Bone marrow AL amyloidosis

    3. Cup-like blast morphology in acute myeloid leukaemia

    4. Neutrophil morphology

    5. Primary myelofibrosis

    6. Sarcoidosis

    7. Leishmaniasis

    8. Gelatinous transformation of the bone marrow

    9. Acanthocytic red cell disorders

    10. Large granular lymphocytic leukaemia

    11. Pure erythroid leukaemia

    12. Reactive mesothelial cells

    13. Plasmablastic myeloma

    14. Septicaemia

    15. Unstable haemoglobin (haemoglobin Köln) and a myeloproliferative neoplasm

    16. Sickle cell anaemia in crisis

    17. Acute myeloid leukaemia with t(8;21)(q22;q22.1)

    18. Chronic neutrophilic leukaemia

    19. Essential thrombocythaemia

    20. Hairy cell leukaemia

    21. Mantle cell lymphoma in leukaemic phase

    22. Infantile osteopetrosis

    23. Reactive eosinophilia

    24. Stomatocytic red cell disorders

    25. Reactive lymphocytosis due to viral infection

    26. Therapy-related acute myeloid leukaemia with eosinophilia

    27. Red cell fragmentation syndromes

    28. NK/T-cell lymphoma in leukaemic phase

    29. Myelodysplastic syndrome with del(5q)

    30. Classical Hodgkin lymphoma

    31. Cryoglobulinaemia

    32. Congenital dyserythropoietic anaemia

    33. Acute monoblastic leukaemia with t(9;11)(p21.3;q23.3)

    34. Chronic myeloid leukaemia presenting with myeloid sarcoma and extreme thrombocytosis

    35. Glucose-6-phosphate dehydrogenase deficiency

    36. Leukaemic presentation of hepatosplenic gamma-delta T-cell lymphoma

    37. Myelodysplastic syndromes

    38. Pelger–Huët anomaly

    39. Russell bodies in lymphoplasmacytic lymphoma

    40. T-cell prolymphocytic leukaemia

    41. Myeloid maturation arrest

    42. MDS/MPN with ring sideroblasts and thrombocytosis

    43. Acute myeloid leukaemia with inv(16)(p13.1q22)

    44. Babesiosis

    45. Haemoglobin E disorders

    46. Juvenile myelomonocytic leukaemia

    47. Non-haemopoietic tumours

    48. Richter transformation of chronic lymphocytic leukaemia

    49. Sickle cell-haemoglobin C disease

    50. T cell/histiocyte-rich B-cell lymphoma

    51. Miliary tuberculosis

    52. Pure red cell aplasia

    53. Lymphoblastic transformation of follicular lymphoma

    54. Primary hyperparathyroidism

    55. Gamma heavy chain disease

    56. Acute promyelocytic leukaemia with t(15;17)(q24.1;q21.2)

    57. AA amyloidosis

    58. Acquired sideroblastic anaemia

    59. Diffuse large B-cell lymphoma

    60. Hickman line infection

    61. Monocytes and their precursors

    62. Paroxysmal cold haemoglobinuria

    63. Transient abnormal myelopoiesis

    64. Systemic lupus erythematosus

    65. Granular blast cells in acute lymphoblastic leukaemia

    66. Chronic myelomonocytic leukaemia

    67. Burkitt lymphoma/leukaemia

    68. Gaucher’s disease

    69. Myelodysplastic syndrome with haemophagocytosis

    70. Primary oxalosis

    71. Acute myeloid leukaemia with inv(3)(q21.3q26.2)

    72. Autoimmune haemolytic anaemia

    73. Chronic eosinophilic leukaemia due to FIP1L1-PDGFRA fusion gene

    74. Leukaemic phase of follicular lymphoma

    75. Megaloblastic anaemia

    76. Reactive bone marrow and an abnormal PET scan

    77. Acute megakaryoblastic leukaemia

    78. Erythrophagocytosis and haemophagocytosis

    79. Hyposplenism

    80. Acquired haemoglobin H disease

    81. Cystinosis

    82. Familial platelet disorder with a predisposition to AML

    83. Nodular lymphocyte predominant Hodgkin lymphoma

    84. Acute monocytic leukaemia with NPM1 mutation

    85. Adult T-cell leukaemia/lymphoma

    86. Hereditary elliptocytosis and pyropoikilocytosis

    87. Sézary syndrome

    88. Spherocytic red cell disorders

    89. Acute myeloid leukaemia and metastatic carcinoma

    90. Chédiak-Higashi syndrome

    91. Cortical T-lymphoblastic leukaemia/lymphoma

    92. Trypanosomiasis

    93. Acute myeloid leukaemia with myelodysplasia-related changes

    94. Blastic plasmacytoid dendritic cell neoplasm

    95. Inherited macrothrombocytopenias

    96. Persistent polyclonal B-cell lymphocytosis

    97. Acute myeloid leukaemia with t(6;9)(p23;q34.1)

    98. B-cell prolymphocytic leukaemia

    99. Various red cell enzyme disorders

    100. Sea blue histiocytosis in multiple myeloma

    101. Enteropathy-associated T-cell lymphoma

    Answers to multiple choice questions and further reflections on the theme


  • 61800lei 525.00 lei

    This book provides a unique frame work for examining acute lung syndromes that arise from hematologic disorders or is defined by a hematologic abnormality as a key feature.  Acute lung processes arising from hematologic disorders can present as life-threatening conditions, and as such, the pulmonary physician or critical care physician are often directly involved in care or called upon to provide expertise. Chapters are organized into three sections, each with an emphasis on pathogenesis and current understanding of mechanisms. The text begins with the central theme of the lungs as the direct interface between the external environment and blood, description of individual components of the hematopoietic system, their function and relevance to the lungs. The second section outlines both benign and malignant primary hematologic disorders that can lead to acute pulmonary manifestations. The final section focuses on acute lung syndromes stemming from complications of transfusion and treatment. Chapters are presented in an easy-to-access format, providing information on diagnosis, management, and outcomes. This is a valuable resource for pulmonary fellows in training, pulmonologists, critical care physicians, and physicians involved in caring for patients in the ICU.

  • Blood Cells: A Practical Guide, 5th Edition
    La comanda in aproximativ 4 saptamani
    63700lei 530.00 lei

    • Enables both the haematologist and laboratory scientist to identify blood cell features, from the most common to the more obscure
    • Provides essential information on methods of collection, blood film preparation and staining, together with the principles of manual and automated blood counts
    • Completely revised and updated, incorporating much newly published information: now includes advice on further tests when a specific diagnosis is suspected
    • 400 high quality photographs to aid with blood cell identification • Highlights the purpose and clinical relevance of haematology laboratory tests throughout

  • Hematology in Practice
    La comanda in aproximativ 4 saptamani
    56500lei 540.00 lei


    Basic principles of hematology made memorable. Build a solid understanding of hematology in the context of practical laboratory practice and principles. Visual language, innovative case studies, role-playing troubleshooting cases, and laboratory protocols bring laboratory practice to life.  Superbly organized, this reader-friendly text breaks a complex subject into easy-to-follow, manageable sections. Begin with the basic principles of hematology; discover red and white blood cell disorders; journey through hemostasis and disorders of coagulation; and then explore the procedures needed in the laboratory.

    • “Learning objectives at the beginning of each chapter
    • Special "Troubleshooting: What do you do when...." sections to promote problem solving
    • "Word Key" section that highlights and defines key medical terminology
    • Case studies that illustrate the key principles of each concept in the chapters and encourage practical critical thinking
    • End-of-chapter summaries and review questions



    Current World Health Organization (WHO) categories are reflected in the chapters on acute leukemia and myeloproliferative disorders.

    Thoroughly updated and peer-reviewed to ensure currency and completeness in explanations of theory.



    'Student Alerts' highlight critical values that students must be able to recognize in the laboratory.

    'Deeper Understanding' boxes provide additional theory on specific topics.



    Coverage of hematology automation and flow cell cytometry in a new Chapter 20, Hematology Automation and Flow Cell Cytometry.

    Many new color slides more clearly show normal structures and pathologies.


    Table of Contents:



    Title Page

    Copyright Page







    List of Condensed Cases, Case Studies, and Troubleshootings Cases

    Part I: Basic Hematology Principles

    Chapter 1: Introduction to Hematology and Basic Laboratory Practice

    Introduction to Hematology

    The Microscope

    Significant Parts of the Microscope

    Care of the Microscope

    Corrective Actions in Light Microscopy

    Innovations in Microscopy

    Standard Precautions

    Personal Protective Equipment

    Safety Practices Other Than Personal Protective Equipment

    Chemical and Environmental Hazards

    Basic Concepts of Quality Assurance Plans in the Hematology Laboratory

    Quality Control Monitoring in the Hematology Laboratory

    Reference Intervals

    Delta Checks

    Reflex Testing

    Critical Values

    Preanalytic Variables

    Postanalytic Variables

    Chapter 2: From Hematopoiesis to the Complete Blood Count

    Hematopoiesis: The Origin of Cell Development

    The Spleen as an Indicator Organ of Hematopoietic Health

    Functions of the Spleen

    Potential Risks of Splenectomy

    Bone Marrow and Myeloid:Erythroid Ratio

    Alterations in Myeloid:Erythroid Ratio

    Role of Stem Cells and Cytokines


    Bone Marrow Analysis

    Bone Marrow Procedure

    Bone Marrow Report

    Complete Blood Count

    Morphologic Classification of Anemias

    Calculating Red Blood Cell Indices and Their Role in Indicating Sample Integrity

    Value of Red Blood Cell Distribution Width

    Critical Values

    Clinical Approach to Anemias

    Chapter 3: Red Blood Cell Production, Function, and Relevant Red Blood Cell Morphology

    Basic Red Blood Cell Production

    Red Blood Cell Maturation

    Features of Red Blood Cell Development

    Red Blood Cell Membrane Development and Function

    Composition of Lipids in the Interior and Exterior Layers

    Composition of Proteins in the Lipid Bilayers: Integral Proteins

    Cytoskeleton: Peripheral Proteins

    Red Blood Cell Metabolism

    Abnormal Red Blood Cell Morphology

    Variations in Red Blood Cell Size

    Variations in Red Blood Cell Color

    Variations in Red Blood Cell Shape

    Red Blood Cell Inclusions

    Value of the Reticulocyte Count

    Chapter 4: Hemoglobin Function and Principles of Hemolysis

    Hemoglobin Structure and Synthesis

    Genetics and Chain Formation of Hemoglobin

    Hemoglobin Function

    Oxygen Dissociation Curve

    Abnormal Hemoglobins


    Types and Physiology of Hemolysis

    Laboratory Evidence of Hemolysis

    Classifications Relevant to the Hemolytic Anemias

    Part II: Red Blood Cell Disorders

    Chapter 5: The Microcytic Anemias


    Iron Intake and Iron Absorption

    Iron Storage and Recycled Iron

    Iron Deficiency Anemia

    Pathophysiology and Symptoms

    Tests Used to Help Diagnose Iron Deficiency

    Treatment for Iron Deficiency

    Anemia of Chronic Disease and Inflammation: Pathophysiology, Diagnosis, and Treatment

    Sideroblastic Anemias

    Hereditary Hemochromatosis (Congenital Iron Overload)

    Thalassemia Syndromes

    Pathophysiology of Thalassemias

    Alpha Thalassemia

    Beta Thalassemia Major: Cooley’s Anemia, Mediterranean Anemia

    Thalassemia Intermedia and Beta Thalassemia Trait

    Chapter 6: The Macrocytic Anemias

    Macrocytic Anemias and the Megaloblastic Process

    Red Blood Cell Precursors in Megaloblastic Anemia

    Ineffective Erythropoiesis in Megaloblastic Anemia

    Pernicious Anemia as a Subset of Megaloblastic Anemias

    Vitamin B12 and Folic Acid: Nutritional Requirements and Metabolism

    Vitamin B12 and Folic Acid Deficiency

    Vitamin B12 Transport Into the Bone Marrow

    Clinical Features of Patients With Megaloblastic Anemia

    Hematologic Features of Megaloblastic Anemias

    Laboratory Diagnosis of Megaloblastic Anemias

    Serum Vitamin B12 Levels and Folic Acid Levels

    Serum Methylmalonic Acid and Homocysteine

    Intrinsic Factor and Parietal Cell Antibodies

    Treatment and Response of Patients With Megaloblastic Anemia

    Macrocytic Anemias That Are Not Megaloblastic

    Chapter 7: Normochromic Anemias: Biochemical, Membrane, and Miscellaneous Red Blood Cell Disorders

    Role of the Spleen in Red Blood Cell Membrane Disorders

    Hereditary Spherocytosis

    Genetics and Pathophysiology of Hereditary Spherocytosis

    Clinical Presentation in Hereditary Spherocytosis

    Laboratory Diagnosis of Hereditary Spherocytosis

    Treatment and Management of Hereditary Spherocytosis

    Hereditary Elliptocytosis

    Common Hereditary Elliptocytosis

    Southeast Asian Ovalocytosis

    Spherocytic Hereditary Elliptocytosis

    Hereditary Pyropoikilocytosis

    Hereditary Stomatocytosis and Hereditary Xerocytosis

    Glucose-6-Phosphate Dehydrogenase Deficiency

    Genetics of Glucose-6-Phosphate Dehydrogenase Deficiency

    Clinical Manifestations of Glucose-6-Phosphate Dehydrogenase Deficiency

    Acute Hemolytic Anemia

    Diagnosis of Glucose-6-Phosphate Dehydrogenase Deficiency

    Pyruvate Kinase Deficiency

    Miscellaneous Red Blood Cell Disorders

    Aplastic Anemia

    Fanconi’s Anemia

    Diamond-Blackfan Anemia

    Paroxysmal Nocturnal Hemoglobinuria

    Cold Agglutinin Syndrome

    Paroxysmal Cold Hemoglobinuria

    Congenital Dyserythropoietic Anemias

    Acquired Anemias of Variable External Causes

    Chapter 8: The Normochromic Anemias Caused by Hemoglobinopathies

    General Description of Hemoglobinopathies

    Sickle Cell Anemia

    Genetics and Incidence of Sickle Cell Anemia

    Pathophysiology of Sickling Process

    Clinical Considerations for Sickle Cell Anemia

    Laboratory Diagnosis

    Sickle Cell Trait

    Hemoglobin C Disease and Trait and Hemoglobin SC

    Variant Hemoglobins

    Hemoglobin S–Beta Thalassemia

    Hemoglobin E

    Hemoglobin DPunjab and Hemoglobin GPhila

    Hemoglobin OArab

    Part III: White Blood Cell Disorders

    Chapter 9: Leukopoiesis, WBC Differential, and Lymphocyte Function


    Stages of Leukocyte Maturation

    Features of Cell Identification

    Lymphocyte Origin and Function

    Lymphocyte Populations

    Travel Path of Lymphocytes

    Lymphocytes and Development of Immunocompetence

    Response of Lymphocytes to Antigenic Stimulation

    Lymphocyte Cell Markers and Cluster of Differentiation

    Leukocyte Count From Complete Blood Cell Count to Differential

    Manual Differential Versus Differential Scan

    Relative Versus Absolute Values

    Chapter 10: Abnormalities of White Blood Cells: Quantitative, Qualitative, and the Lipid Storage Diseases

    Introduction to White Blood Cell Disorders

    Quantitative Changes in White Blood Cells

    Specific Terminology Relating to Quantitative White Blood Cell Changes

    Stages of White Blood Cell Phagocytosis

    Qualitative Defects of White Blood Cells

    Toxic Changes in White Blood Cells

    Human Ehrlichiosis

    Nuclear Abnormalities: Hypersegmentation

    Hereditary White Blood Cell Disorders

    May-Hegglin Anomaly

    Alder’s Anomaly

    Pelger-Huët Anomaly

    Chédiak-Higashi Syndrome

    Reactive Lymphocytosis in Common Disease States

    Other Viral Sources of Reactive Lymphocytosis

    Effect of HIV/AIDS on Hematology Parameters

    Lipid Storage Diseases

    Common Features of a Few Lipid Storage Diseases

    Bone Marrow Cells in Lipid Storage Disorders

    Bacteria and Other Unexpected White Blood Cell Changes

    Chapter 11: Acute Leukemias

    Definition of Leukemia

    Comparing Acute and Chronic Leukemia

    Leukemia History

    Acute Myeloid Leukemia


    Clinical Features

    Laboratory Features


    Acute Leukemias of Ambiguous Lineage

    Important Acute Myeloid Leukemia Prognostic Factors

    Acute Lymphoblastic Leukemia


    Clinical Features


    Prognosis in Acute Lymphoblastic Leukemia

    Chapter 12: Myeloproliferative Neoplasms

    Introduction to Myeloproliferative Neoplasms

    World Health Organization Classifications

    Chronic Myeloid Leukemia BCR-ABL1+


    Clinical Features and Symptoms

    Peripheral Blood and Bone Marrow




    Chronic Neutrophilic Leukemia

    Chronic Eosinophilic Leukemia Not Otherwise Specified

    Polycythemia Vera


    Clinical Features and Symptoms

    Peripheral Blood and Bone Marrow Findings




    Primary Myelofibrosis


    Clinical Features and Symptoms

    Peripheral Blood and Bone Marrow Findings




    Essential Thrombocythemia


    Clinical Features and Symptoms

    Peripheral Blood and Bone Marrow Findings





    Chapter 13: Lymphoproliferative Disorders and Related Plasma Cell Disorders

    Lymphoid Malignancies

    Chronic Lymphocytic Leukemia

    Prolymphocytic Leukemia

    Hairy Cell Leukemia

    Hodgkin’s Lymphoma and Non-Hodgkin’s Lymphoma

    Sézary Syndrome

    Plasma Cell Disorders

    Plasma Cell Structure and Function

    Multiple Myeloma

    Waldenström’s Macroglobulinemia

    Chapter 14: The Myelodysplastic Syndromes

    Introduction to Myelodysplastic Syndromes


    Chromosomal Abnormalities

    Common Features and Clinical Symptoms

    How to Recognize Dysplasia

    Classification of Myelodysplastic Syndromes

    Specific Features of 2016 World Health Organization Classification

    Prognostic Factors and Clinical Management

    Part IV: Hemostasis and Disorders of Coagulation

    Chapter 15: Overview of Hemostasis and Platelet Physiology

    Normal Hemostasis: Overview

    Vascular System


    Contribution of Endothelial Cells

    Evaluation of Endothelial Cells

    Platelets and Primary Hemostasis

    Platelet Structure and Physiology

    Platelet Function in Primary Hemostasis

    Platelet Properties

    Evaluation of Platelets

    Hemostatic Proteins and Secondary Hemostasis

    Coagulation Factors (Coagulation Cascade)

    Regulatory Inhibitors

    Hemostatic Protein Groups

    Fibrinolytic System

    Screening Tests for Evaluation of Bleeding Disorders

    Chapter 16: Quantitative and Qualitative Platelet Disorders

    Quantitative Disorders of Platelets

    Thrombocytopenia Related to Sample Integrity and Preanalytic Variables

    Thrombocytopenia Related to Decreased Production

    Thrombocytopenia Related to Altered Distribution of Platelets

    Thrombocytopenia Related to Immune Effect of Specific Drugs or Antibody Formation

    Thrombocytopenia Related to Consumption of Platelets


    Inherited Qualitative Disorders of Platelets

    Disorders of Adhesion

    Platelet Release Defects

    Acquired Defects of Platelet Function

    Vascular Disorders Leading to Platelet Dysfunction

    Chapter 17: Defects of Plasma Clotting Factors

    Plasma Clotting Factors and Hemophilias

    Evaluation of a Bleeding Disorder

    Treatment of Hemophilia A Patients

    Quality-of-Life Issues for Hemophilia A Patients

    Factor VIII Inhibitors

    Hemophilia B (Christmas Disease)

    Congenital Factor Deficiencies

    Congenital Factor Deficiencies With Bleeding Manifestations

    Congenital Factor Deficiencies in Which Bleeding Is Mild or Absent

    Factor XIII Deficiency

    Bleeding Secondary to a Chronic Disease Process

    Role of Vitamin K in Hemostasis

    Vitamin K Deficiency and Subsequent Treatment

    Chapter 18: Fibrinogen, Thrombin, and the Fibrinolytic System

    Overview of Fibrinogen in Clot Formation and Lysis

    Disorders of Fibrinogen




    Multiple Roles of Thrombin in Hemostasis


    Clot Dissolution

    Naturally Occurring Inhibitors of Fibrinolysis

    Measurable Products of the Fibrinolytic System

    Disseminated Intravascular Coagulation

    Mechanism of Acute Disseminated Intravascular Coagulation

    Primary Fibrinolysis

    Clinical Symptoms and Laboratory Results in Acute Disseminated Intravascular Coagulation

    Treatment of Acute Disseminated Intravascular Coagulation

    Chapter 19: Introduction to Thrombosis and Anticoagulant Therapy

    Thrombophilia and Thrombosis—an Overview

    Physiologic and Pathologic Thrombosis

    Pathophysiology of Thrombosis

    Laboratory Diagnosis of Thrombotic Disorders

    Inherited Thrombotic Disorders

    Acquired Thrombotic Disorders

    The Laboratory’s Role in Diagnosing Thrombophilia

    Anticoagulant Therapy

    Antiplatelet Drugs

    Anticoagulant Drugs

    Alternative Anticoagulant Drugs

    Thrombolytic Drugs

    Part V: Hematology Automation, Flow Cell Cytometry, and Laboratory Procedures

    Chapter 20: Hematology Automation and Flow Cell Cytometry

    Hematology Automation

    Electrical Impedance





    Optical Scatter

    VCS Technology

    Hydrodynamic Focusing

    Flow Cytometry

    Optical Platelet Counting and Flow Cytometry


    Data Reporting

    Beckman-Coulter Instrumentation

    Sysmex Instrumentation

    CellaVision Automated Digital Cell Morphology

    Abbott CELL-DYN Instrumentation

    Siemens Healthcare Advia Instrumentation

    Cerebrospinal Fluid Analysis on the Advia 120/2120

    Quality Assurance and Quality Control

    Coagulation Automation and Instruments

    Coagulation Automation

    Coagulation Instruments

    Flow Cytometry Instrumentation

    Principles of Operation





    Quality Control

    Applications of Flow Cytometry

    Chapter 21: Basic Procedures in a Hematology Laboratory


    Modified Westergren Sedimentation Rate

    Manual Reticulocyte Procedure

    Peripheral Smear Procedure

    Performing a Manual Differential and Assessing Red Blood Cell Morphology

    Leukochek White Blood Cell and Platelet Manual Count

    Sickle Cell Screening Procedure

    Cerebrospinal Fluid and Body Fluid Cell Count and Differential

    Body Fluid Analysis on the Sysmex XE-5000

    Prothrombin Time and Activated Partial Thromboplastin Time: Automated Procedure

    Quantitative D-Dimer—Innovance on Sysmex CA7000

    Appendix A: Answers to Review Questions

    Appendix B: List of Abbreviations


  • 63500lei 565.00 lei

    Managing patients with thrombotic vascular disease is complex and challenging:

    • Ischemic vascular disease remains a complicated interplay of atherosclerosis and thrombosis—even with the evolution in our understanding of the pathobiology of thrombosis.
    • There has been tremendous growth in therapeutic options which are quickly finding their place in daily practice, including a remarkable expansion in the number of intravenous and oral antithrombotic agents and new antiplatelet agents

    Now more than ever, all cardiologists, hematologists, and specialists in vascular medicine, as well as other professionals, such as hospital pharmacists, who deal with prognosis and intervention in preventing thrombosis, need a resource that distills current knowledge of this important subject.

    Written and edited by today’s leading international, Therapeutic Advances in Thrombosis, 2e provides physicians with the very latest in medical and surgical advances in antithrombotic therapies. With this comprehensively updated edition you get:

    • Coverage of virtually all aspects of venous and arterial thrombotic disease and the corresponding therapies
    • Strategies to manage specific clinical conditions and how to tailor treatment to individual patient needs
    • Updated chapters covering thrombolysis in ST-elevated myocardial infarctions; thrombosis in patients with diabetes, pregnancy, and renal dysfunction
    • Special emphasis on the pharmacology of novel anticoagulants and their practical use in venous thromboembolism and atrial fibrillation.

    Plus, all chapters fully explore clinical trial designs and outcomes for particular treatment therapies, as well as contain the relevant ACC/AHA/ESC guidelines, so you can confidently apply what you learn.

  • 63000lei 570.00 lei



    This book focuses on hematopoietic and lymphoid neoplasms that initially present as peripheral blood abnormalities, with either cytopenias or elevated peripheral blood counts, as well as non-neoplastic conditions that may raise concern for a hematologic malignancy. The scope of the book includes myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), mixed myelodysplastic/myeloproliferative neoplasms (MDS/MPN), as well as lymphomas and lymphoid leukemias that typically present initially with peripheral blood abnormalities.  Within each category, a comprehensive list of differential diagnoses is discussed. For each disease entity, the reader is updated with new molecular genetic data, biomarkers, and recent applications of immunophenotyping, and how to incorporate the new information in disease diagnosis and classifications is illustrated, including the use of diagnostic algorithms where appropriate. The book employs the revised WHO Classification of Hematopoietic Neoplasms for all disease entities.   Diagnosis of Blood and Bone Marrow Disorders will serve as a very useful resource for pathologists, pathologists in training, hematologists and medical technologists who are involved in the clinical work-up of patients with bone marrow and blood neoplasms.  It will provide a practical and concise yet comprehensive review.


    Table of Contents:


    1. Identifying Blood and Bone Marrow Abnormalities in the Laboratory

    2. Cytopenias: Reactive and Neoplastic

    3. Inherited Bone Marrow Failure Syndromes, Myeloid Neoplasms with Germline Predisposition and Myeloid Proliferations Associated with Down Syndrome

    4. Cytopenias: Acquired Bone Marrow Failure

    5. Leukocytosis: Neutrophilia, Basophilia, and Blasts

    6. Leukocytosis: Eosinophilia

    7. Monocytosis

    8. Thrombocytosis

    9. Erythrocytosis

    10. Mixed Cytoses and Cytopenias

    11. T- and NK-Cell Lymphocytosis

    12. B-Cell Lymphocytosis

    13. Multiple Myeloma and Other Plasma Cell Neoplasms


  • 67400lei 580.00 lei


    • Provides up-to-date knowledge on the pathogenesis and management of the syndrome
    • Presents and discusses innovative treatments in addition to standard treatment options
    • Describes the involvement of other organs or organ systems

    About this book

    This book, part of the series Rare Diseases of the Immune System, offers comprehensive, up-to-date coverage of the pathophysiology and management of the antiphospholipid syndrome (APS). Immunologic and genetic aspects are discussed and the pathogenic mechanisms responsible for such phenomena as APS-mediated thrombosis and pregnancy loss/complications are explained.

    The main clinical manifestations, classification criteria and diagnostic tools are identified, and close attention is paid to the nature of the involvement of various organs or organ systems in APS. Specific chapters describe the treatment of the different symptoms, therapies of value in avoiding recurrences, and innovative treatment approaches. The authors are senior experts in the field who are aided by younger fellows, ensuring that the book is also educationally oriented. This handy volume will be a valuable tool for postgraduates in training and professionals wishing to extend their knowledge of this specific syndrome.


    From the book reviews:

    “The purpose is to provide an overview of this very difficult subject that will benefit bench researchers as well as bedside clinicians. The book would serve any audience who wants to know more about antiphospholipid syndrome. … This is an excellent, up-to-date overview of antiphospholipid syndrome. It will serve as a handy tool to get more information on the topic.” (Dany V. Thekkemuriyil, Doody’s Book Reviews, February, 2015)


    Table of contents (20 chapters)

    ·         Genetics and Origin of Antiphospholipid Syndrome

    Soriano, Alessandra (et al.)

    Pages 1-12

    ·         The Paradox of Lupus Anticoagulant

    Banzato, Alessandra (et al.)