SEED Haematology Sysmex Educational Enhancement and Development October 2012
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Blood, Lymph, and Immunity Joann Colville
Blood, Lymph, and Immunity Joann Colville CHAPTER OUTLINE .»: BLOOD Function Introduction Lymphatic Structures Plasma THE IMMUNE SYSTEM Cellular Components of Blood Function Red Blood Cells Immune Reactions Platelets Immunization: Protection Against Disease White Blood Cells THE LYMPHATICSYSTEM Lymph Formation Characteristics LEARNING OBJECTIVES • List and describe the functions of blood • List the functions of the lymphatic system • Describe the composition of blood plasma • Describe the structure and functions of the lymph nodes, • Describe the characteristics of mature erythrocytes spleen, thymus, tonsils, and GALT Describe the structure of the hemoglobin molecule and • List the functions of the immune system explain the fate of hemoglobin following intravascular and • Differentiate between specific and nonspecific immune extravascular hemolysis reactions • Give the origin of thrombocytes and describe their • Differentiate between cell-mediated and humoral immunity characteristics and functions • List the components involved in cell-mediated immunity • Listthe types of leukocytes and describe the functions of each and explain the role of each • Describe the formation of lymph fluid and its circulation List and describe the classes of immunoglobulins through the lymphatic system • Differentiate between active and passive immunity BLOOD vessels of the cardiovascular system. It has three main func- tions: transportation, regulation, and defense. INTRODUCTION Blood. Say the word, and some people cringe, others faint, Function and if you believe authors Bram Stoker, Stephen King, and 1. Blood is a transport system. Christopher Moore (all authors of vampire books), others • It carries oxygen, nutrients, and other essential com- drool. But no matter what you think about blood, animals pounds to every living cell in the body. -
The Diagnosis of Paroxysmal Nocturnal Hemoglobinuria: Role of Flow Cytometry
THE DIAGNOSIS OF PAROXYSMAL NOCTURNAL HEMOGLOBINURIA: ROLE OF FLOW CYTOMETRY Alberto Orfao Department of Medicine, Cancer Research Centre (IBMCC-CSIC/USAL), University of Salamanca, Salamanca, Spain Paroxysmal nocturnal hemoglobinuria (PNH) on one or multiple populations of peripheral blood is an acquired clonal disorder typically affecting red cells and/or leucocytes of PNH patients, this young adults, which involves the phosphatidylino- translating into a new diagnostic test. Because sitol glycan anchor biosynthesis class A gene of this flow cytometry became an essential tool (PIGA) coded in chromosome X, in virtually every in the diagnosis of PNH. In turn, it could be also case. The altered gene encodes for a defective pro- demonstrated that investigation of the presence of tein product, the pig-a enzyme which is involved GPI-deficient cells among circulating mature neu- in the early steps of the synthesis of glycosylphos- trophils and monocytes, increases the sensitivity phatidylinositol (GPI). This later molecule (GPI) of red blood cell screening because of the shorter acts as an anchor of a wide range of proteins to lifetime of both populations of leucocytes. Despite the cell surface. At present a large number of GPI- all the above, routine assessment of CD55 and anchor associated proteins have been described CD59 is also associated with several limitations which are expressed by one or multiple distinct due to distinct patterns of expression among dif- compartments of hematopoietic cells. The altered ferent cell populations, dim and heterogeneous PIGA gene leads to an altered GPI anchor which expression among normal individuals and the lack leads to defective expression of GPI-AP on the of experience in many labs as regards the normal cytoplasmic membrane, on the cell surface. -
Hemolytic Disease of the Newborn
Intensive Care Nursery House Staff Manual Hemolytic Disease of the Newborn INTRODUCTION and DEFINITION: Hemolytic Disease of the Newborn (HDN), also known as erythroblastosis fetalis, isoimmunization, or blood group incompatibility, occurs when fetal red blood cells (RBCs), which possess an antigen that the mother lacks, cross the placenta into the maternal circulation, where they stimulate antibody production. The antibodies return to the fetal circulation and result in RBC destruction. DIFFERENTIAL DIAGNOSIS of hemolytic anemia in a newborn infant: -Isoimmunization -RBC enzyme disorders (e.g., G6PD, pyruvate kinase deficiency) -Hemoglobin synthesis disorders (e.g., alpha-thalassemias) -RBC membrane abnormalities (e.g., hereditary spherocytosis, elliptocytosis) -Hemangiomas (Kasabach Merritt syndrome) -Acquired conditions, such as sepsis, infections with TORCH or Parvovirus B19 (anemia due to RBC aplasia) and hemolysis secondary to drugs. ISOIMMUNIZATION A. Rh disease (Rh = Rhesus factor) (1) Genetics: Rh positive (+) denotes presence of D antigen. The number of antigenic sites on RBCs varies with genotype. Prevalence of genotype varies with the population. Rh negative (d/d) individuals comprise 15% of Caucasians, 5.5% of African Americans, and <1% of Asians. A sensitized Rh negative mother produces anti-Rh IgG antibodies that cross the placenta. Risk factors for antibody production include 2nd (or later) pregnancies*, maternal toxemia, paternal zygosity (D/D rather than D/d), feto-maternal compatibility in ABO system and antigen load. (2) Clinical presentation of HDN varies from mild jaundice and anemia to hydrops fetalis (with ascites, pleural and pericardial effusions). Because the placenta clears bilirubin, the chief risk to the fetus is anemia. Extramedullary hematopoiesis (due to anemia) results in hepatosplenomegaly. -
Evaluation of Anemia Survey (NHANES III) Data- 9 10-28% of Patients Over 65 Years Are Anemic Mark Wurster, M.D., F.A.C.P
Anemia - Definition • National Health and Nutrition Examination Evaluation of Anemia Survey (NHANES III) data- 9 10-28% of patients over 65 years are anemic Mark Wurster, M.D., F.A.C.P. 9 One third of these are due to iron, folate, B12 The Ohio State University deficiency alone or in combination 9 One third are due to renal disease, or other chronic inflammatory response 9 One third are due to various primary marrow disorders, malignancies or other disorders Anemia Anemia - Definition Classification Schemes • A simplified approach to anemia, • Most common hematologic disorder emphasizing information already included • Decrease from normal levels of Hgb, Hct, RBC: in the CBC: 9 FlFemales – MHb14/dlMean Hgb = 14 g/dl; -2SD = 12 g /dl • Mean Cellular Volume (MCV) 9 Males – Mean Hgb = 15.5 g/dl; -2SD = 13.5 g/dl • Red Cell Distribution Width (RDW) • Caveat – Anemia is a syndrome, not a disease. • Retic count An abnormal Hgb or Hct should ALWAYS be investigated if confirmed on repeat testing. 1 Anemia Anemia Classification Schemes Classification Schemes • Mean Cellular Volume (MCV) • Red blood cell Distribution Width (RDW) • Decreased MCV (microcytic); < 80 fL 9 A numerical expression of • Normal MCV (normocytic); 80 – 99 fL anisocytosis, or variation in RBC size • Increased MCV (macrocytic); > 100 fL Anemia Anemia Classification Schemes Classification Schemes • Red blood cell Distribution Width (RDW) 9 Normal RDW - representing a uniform population • Red blood cell Distribution Width (RDW) of RBCs with respect to size (actually the standard deviation of red blood cell volume divided by the mean volume) 9 Normal; < or = to app. -
Clinical Pathology Interpretation Barbara Horney
CLINICAL PATHOLOGY PATHOLOGIE CLINIQUE Clinical pathology interpretation Barbara Horney History, physical examination, and Table 1. Hematologic findings from a lethargic, laboratory findings 4-year-old schipperke 4-year-old, spayed female, schipperke was pre- Blood cell count Reference range A sented because of mild lethargy. Pale mucous mem- White blood cells branes were observed on physical examination. Table 1 (WBC) gives the results of the hematological examination of Total 6.0 X 109/L 6.0-17.1 X 109/L blood at Differential samples taken this time. No significant abnor- segmented 65% 3.85 X 109/L 3.6-11.5 X 109/L malities were identified on the serum biochemical neutrophils profile. eosinophils 2% 0.12 X 109/L 0.01-1.25 X 109/L lymphocytes 27% 1.59 X 109/L 1.0-4.8 X 109/L Interpretation and discussion monocytes 6% 0.35 X 109/L 0.15-1.35 X 109/L Red blood cells The hematology results can be summarized as severe, Total 1.2 X 1012/L 5.5-8.5 X 109/L microcytic, normochromic, nonregenerative anemia nucleated 1/100 WBC <1-2 per 100 WBC associated with marked spherocytosis. spherocytes 4+ microcytosis 2+ The presence of spherocytes is often associated with immune-mediated hemolytic disease [1,2], although Platelets estimated normal hereditary membrane defects [3] and zinc toxicosis [4] in number can also result in spherocyte formation. A direct antibody Reticulocytes 0 X 109/L up to 120 X 109/L test (Coomb's test) was weakly positive. This finding can Hemoglobin 22 g/L 120-180 g/L support the tentative diagnosis of anemia of immune- Hematocrit 0.068 L/L 0.37-0.55 L/L mediated etiology, although this test is subject to both Mean corpuscular false positive and false negative results [2,5]. -
Anemia and the QT Interval in Hypertensive Patients
2084 International Journal of Collaborative Research on Internal Medicine & Public Health Anemia and the QT interval in hypertensive patients Ioana Mozos 1*, Corina Serban 2, Rodica Mihaescu 3 1 Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania 2 Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania 3 1st Department of Internal Medicine, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania * Corresponding Author ; Email: [email protected] Abstract Introduction: A prolonged ECG QT interval duration and an increased QT dispersion (QTd) are predictors of sudden cardiac death. Anemia is known as a marker of adverse outcome in cardiovascular disease. Objective: The aim was to assess the relationship between anemia and QT intervals in hypertensive patients. Method: A total of 72 hypertensive patients underwent standard 12-lead ECG. QT intervals and QT dispersions were manually measured. Complete blood count was also assessed. Result: Linear regression analysis revealed significant associations between prolonged QTc and increased QTd and anemia and macrocytosis, respectively. Multiple regression analysis revealed a significant association between red cell distribution width (RDW) >15% and prolonged heart rate corrected maximal QT interval duration (QTc) and QT interval in lead DII (QTIIc). The most sensitive and specific predictor of prolonged QTc and QTIIc was anisocytosis. Anemia was the most sensitive predictor of -
Chapter 06 Lecture Outline
Chapter 06 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright © 2016 McGraw-Hill Education. Permission required for reproduction or display. 1 Cardiovascular System: Blood © SPL/Science Source, (inset) © Andrew Syred/Science Source 2 Points to ponder • What type of tissue is blood and what are its components? • What is found in plasma? • Name the three formed elements in blood and their functions. • How does the structure of red blood cells relate to their function? • Describe the structure and function of each white blood cell. • What are disorders of red blood cells, white blood cells, and platelets? • What do you need to know before donating blood? • What are antigens and antibodies? • How are ABO blood types determined? • What blood types are compatible for blood transfusions? • What is the Rh factor and how is this important to pregnancy? • How does the cardiovascular system interact with other systems to maintain homeostasis? 3 6.1 Blood: An Overview What are the functions of blood? • Transportation: oxygen, nutrients, wastes, carbon dioxide, and hormones • Defense: against invasion by pathogens • Regulatory functions: body temperature, water- salt balance, and body pH 4 6.1 Blood: An Overview What is the composition of blood? • Remember: blood is a fluid connective tissue. • Formed elements are produced in red bone marrow. – Red blood cells/erythrocytes (RBCs) – White blood cells/leukocytes (WBCs) – Platelets/thrombocytes 5 6.1 Blood: An Overview What is the composition of blood? • Plasma – It consists of 91% water and 9% salts (ions) and organic molecules. – Plasma proteins are the most abundant organic molecules. -
20 Hemolytic Anemias Due to Abnormal Red Cell Enzymes
Hemolytic Anemias Due to Abnormal Red Cell Enzymes MODULE Hematology and Blood Bank Technique 20 HEMOLYTIC ANEMIAS DUE TO Notes ABNORMAL RED CELL ENZYMES 20.1 INTRODUCTION The main metabolic substrate for the RBCs is glucose. It is metabolized by two pathways: approximately 90% of the glucose is metabolized through the Embden Meyerhoff (glycolytic) pathway and the rest by the hexose monophosphate (HMP) pathway. In the Embden Meyerhoff (glycolytic) pathway glucose is metabolized to lactate through a series of enzymatic steps. Each molecule of glucose gives rise to 2 molecules of ATP. The ATP provides energy to maintain red cell volume, shape and flexibility. An ATP dependent pump in the red cell membrane actively keeps sodium out of the cell and potassium inside. The red cell has the enzymes that are needed for the glycolytic pathway. These enzymes help break down glucose to generate ATP which is the source of energy. About 10% of the glucose is diverted to the Hexose Monophosphate shunt pathway and this is essential for protection of red cells from oxidative stress. This pathway is necessary for the generation of NADPH which then reduces oxidized glutathione (GSSG) to reduced glutathione (GSH). GSH prevents the accumulation of H2O2 and the oxidation of hemoglobin to methemoglobin. When the level of GSH falls, H2O2 accumulates in the cell and oxidizes the hemoglobin to methemoglobin which becomes denatured and precipitates as Heinz bodies. These inclusions are rigid and attached to the red cell membrane and make the red cell susceptible to hemolysis. The NADPH required in this pathway is generated by the enzyme Glucose 6 phosphate dehydrogenase (G6PD). -
Hematology Unit Lab 1 Review Material
Hematology Unit Lab 1 Review Material Objectives Laboratory instructors: 1. Facilitate lab discussion and answer questions Students: 1. Review the introductory material below 2. Study and review the assigned cases and questions in small groups before the Lab. This includes the pathological material using Virtual Microscopy 3. Be prepared to present your cases, questions and answers to the rest of your Lab class during the Lab Erythropoiesis: The process of red blood cell (RBC) production • Characterized by: − Increasing hemoglobin synthesis Erythroid maturation stages (Below): − Decreasing cell size - Average of 4 cell divisions during maturation − Decreasing cytoplasmic basophilia [One pronormoblast gives rise to 16 red cells] (increasing pink color) - pronormoblast → reticulocyte = 7 days − Progressive chromatin condensation of the - reticulocytes → mature RBC =1-2 days nuclei − Extrusion of nucleus (orthochromatic stage) − Extruded nuclei are subsequently phagocytized − Loss of mitotic capability after the early stage of polychromatophilic normoblast • Picture below: Erythroid progenitors (normoblasts) cluster around macrophages (arrows) in the bone marrow and spleen • Macrophages store iron • Iron is transferred from macrophages to erythroid precursor cells • Iron is used by normoblasts for hemoglobin synthesis aka nucleated rbc aka reticulocyte 1 Mature Red Blood Cell 7-8 microns; round / ovoid biconcave disc with orange-red cytoplasm, no RNA, no nucleus; survives ~120 days in circulation Classification of Anemia by Morphology 1. -
CD59: a Long-Known Complement Inhibitor Has Advanced to a Blood Group System
B LOOD G ROUP R EVIEW CD59: A long-known complement inhibitor has advanced to a blood group system C. Weinstock, M. Anliker, and I. von Zabern The blood group system number 35 is based on CD59, a 20-kDa by Zalman et al.1 from the group of H.J. Muller-Eberhard in La membrane glycoprotein present on a large number of different Jolla, California, and in 1988 by Schönermark et al. from the cells, including erythrocytes. The major function of CD59 is to group of G.M. Hänsch in Heidelberg (Germany).2 This inhibitor protect cells from complement attack. CD59 binds to complement components C8 and C9 and prevents the polymerization of C9, was published under the designations “HRF (homologous which is required for the formation of the membrane attack restriction factor)” and “C8bp (C8 binding protein),” complex (MAC). Other functions of CD59 in cellular immunity respectively, to describe its properties.1,2 “C8bp” indicates the are less well defined. CD59 is inserted into the membrane by a glycosylphosphatidylinositol (GPI) anchor. A defect of this anchor binding capacity for C8. The name “HRF” points to a species causes lack of this protein from the cell membrane, which leads to incompatibility of this “factor” that provides protection from an enhanced sensitivity towards complement attack. Patients with complement attack more effectively in a homologous (e.g., paroxysmal nocturnal hemoglobinuria (PNH) harbor a varying human erythrocytes as a target of human complement) than in percentage of red blood cell clones with a defect in GPI-anchored proteins, including CD59. The most characteristic symptoms of a heterologous system (e.g., human erythrocytes as a target of this disease are episodes of hemolysis and thromboses. -
The Widespread Application of Red Cell Survival Sive Red
CLINICAL DETERMINATION OF THE SITES OF RED CELL SEQUESTRATION IN HEMOLYTIC ANEMIAS1 By JAMES H. JANDL, MORTIMER S. GREENBERG, ROBERT H. YONEMOTO, AND WILLIAM B. CASTLE (From the Thorndike Memorial Laboratory and Second and Fourth (Harvard), Medical Services Boston City Hospital, and the Department of Medicine, Harvard Medical School, Boston, Mass.) (Submitted for publication January 30, 1956; accepted April 3, 1956) The widespread application of red cell survival greater than that of other tissues even when cor- techniques has revealed the importance of exces- rection was made for the Cr5l activity of the re- sive red cell destruction in the pathologic physi- sidual red cells. Moreover, the radioactivity of ology of many of the anemias. An increasing ar- the packed red cells removed from the spleen ex- ray of in vitro methods for detecting red cell or ceeded that of a comparable sample of packed red serum abnormalities has provided insight into the cells from the peripheral blood. In order to in- in vivo mechanisms underlying some of these proc- vestigate the possibility that Cr51-labelled red cell esses. In certain disease states the presence of deposition could be determined by measuring body visible or physically measurable alterations of the surface radioactivity, several questions required red cells has permitted detection of the sites and exploration: 1) Are the emanations of Cr5 suit- to some extent of the mechanisms of sequestration able for external body scanning at safe dosage of these cells. Such valuable observations have levels? 2) Does the site of tissue deposition of been made upon pathologic material from patients Cr65 following the intravenous injection of Cr51- with congenital hemolytic anemia (1-5) and labelled red cells necessarily indicate the site of sickle cell anemia (1, 5-7). -
Acoi Board Review 2019 Text
CHERYL KOVALSKI, DO FACOI NO DISCLOSURES ACOI BOARD REVIEW 2019 TEXT ANEMIA ‣ Hemoglobin <13 grams or ‣ Hematocrit<39% TEXT ANEMIA MCV RETICULOCYTE COUNT Corrected retic ct = hematocrit/45 x retic % (45 considered normal hematocrit) >2%: blood loss or hemolysis <2%: hypoproliferative process TEXT ANEMIA ‣ MICROCYTIC ‣ Obtain and interpret iron studies ‣ Serum iron ‣ Total iron binding capacity (TIBC) ‣ Transferrin saturation ‣ Ferritin-correlates with total iron stores ‣ can be normal or increased if co-existent inflammation TEXT IRON DEFICIENCY ‣ Most common nutritional problem in the world ‣ Absorbed in small bowel, enhanced by gastric acid ‣ Absorption inhibited by inflammation, phytates (bran) & tannins (tea) TEXT CAUSES OF IRON DEFICIENCY ‣ Blood loss – most common etiology ‣ Decreased intake ‣ Increased utilization-EPO therapy, chronic hemolysis ‣ Malabsorption – gastrectomy, sprue ‣ ‣ ‣ TEXT CLINICAL MANIFESTATIONS OF IRON DEFICIENCY ‣ Impaired psychomotor development ‣ Fatigue, Irritability ‣ PICA ‣ Koilonychiae, Glossitis, Angular stomatitis ‣ Dysphagia TEXT IRON DEFICIENCY LAB FINDINGS ‣ Low serum iron, increased TIBC ‣ % sat <20 TEXT MANAGEMENT OF IRON DEFICIENCY ‣ MUST LOOK FOR SOURCE OF BLEED: ie: GI, GU, Regular blood donor ‣ Replacement: 1. Oral: Ferrous sulfate 325 mg TID until serum iron, % sat, and ferritin mid-range normal, 6-12 months 2. IV TEXT SIDEROBLASTIC ANEMIAS Diverse group of disorders of RBC production characterized by: 1. Defect involving incorporation of iron into heme molecule 2. Ringed sideroblasts in