Diagnostic Cells in the Peripheral Blood Smear
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Tareq Al-Adaily Ibrahim Elhaj Ayah Fraihat Dana Alnasra Sheet
Anemia of decreased production II Sheet 3 – + Hemolytic anemia Dana Alnasra Ayah Fraihat Ibrahim Elhaj Tareq Al-adaily 0 **Flashback to previous lectures: − Anemia is the reduction of oxygen carrying capacity of blood secondary to a decrease in red cell mass. − We classified anemia according to cause into: 1. Anemia of blood loss (chronic and acute) 2. Anemia of decreased production 3. Hemolytic anemia − Then, we mentioned general causes for the anemia of decreased production, which are: nutritional deficiency, chronic inflammation, and bone marrow failure. We’ve already discussed the first two and now we will proceed to the last one. Anemias resulting from bone marrow failure: 1. Aplastic anemia 2. Pure red cell aplasia 3. Myelophthisic anemia 4. Myelodysplastic syndrome Other anemias of decreased production: 1. Anemia of renal failure 2. Anemia of liver disease 3. Anemia of hypothyroidism 00:00 1. Aplastic anemia Is a condition where the multipotent myeloid stem cells produced by the bone marrow are damaged. Remember: the bone marrow has stem cells called myeloid stem cells which eventually differentiate into erythrocytes, megakaryocytes (platelets), and myeloblasts (white blood cells). Notice that lymphocytes are not produced from the myeloid progenitor, therefore, they are not affected. depleted normal 1 | P a g e As a result, the bone marrow becomes depleted of hematopoietic cells. And this is reflected as peripheral blood pancytopenia (all blood cells -including reticulocytes- are decreased, with the exception of lymphocytes). Pathogenesis There are two forms of aplastic anemia according to pathogenesis: a. Acquired aplastic anemia It happens because of an extrinsic factor e.g. -
Molecular Basis of Spectrin Deficiency in Beta Spectrin Durham. a Deletion
Molecular basis of spectrin deficiency in beta spectrin Durham. A deletion within beta spectrin adjacent to the ankyrin-binding site precludes spectrin attachment to the membrane in hereditary spherocytosis. H Hassoun, … , S S Chiou, J Palek J Clin Invest. 1995;96(6):2623-2629. https://doi.org/10.1172/JCI118327. Research Article We describe a spectrin variant characterized by a truncated beta chain and associated with hereditary spherocytosis. The clinical phenotype consists of a moderate hemolytic anemia with striking spherocytosis and mild spiculation of the red cells. We describe the biochemical characteristics of this truncated protein which constitutes only 10% of the total beta spectrin present on the membrane, resulting in spectrin deficiency. Analysis of reticulocyte cDNA revealed the deletion of exons 22 and 23. We show, using Southern blot analysis, that this truncation results from a 4.6-kb genomic deletion. To elucidate the basis for the decreased amount of the truncated protein on the membrane and the overall spectrin deficiency, we show that (a) the mutated gene is efficiently transcribed and its mRNA abundant in reticulocytes, (b) the mutant protein is normally synthesized in erythroid progenitor cells, (c) the stability of the mutant protein in the cytoplasm of erythroblasts parallels that of the normal beta spectrin, and (d) the abnormal protein is inefficiently incorporated into the membrane of erythroblasts. We conclude that the truncation within the beta spectrin leads to inefficient incorporation of the mutant protein into the skeleton despite its normal synthesis and stability. We postulate that this misincorporation results from conformational changes of the beta spectrin subunit affecting the binding of the abnormal heterodimer to ankyrin, and we provide evidence […] Find the latest version: https://jci.me/118327/pdf Molecular Basis of Spectrin Deficiency in p8 Spectrin Durham A Deletion within .3 Spectrin Adjacent to the Ankyrin-binding Site Precludes Spectrin Attachment to the Membrane in Hereditary Spherocytosis Hani Hassoun,* John N. -
Erythrocytes: Overview, Morphology, Quantity by AH Rebar Et
In: A Guide to Hematology in Dogs and Cats, Rebar A.H., MacWilliams P.S., Feldman B.F., Metzger F.L., Pollock R.V.H. and Roche J. (Eds.). Publisher: Teton NewMedia, Jackson WY (www.veterinarywire.com). Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org), 8-Feb-2005; A3304.0205 Erythrocytes: Overview, Morphology, Quantity A.H. Rebar1, P.S. MacWilliams2, B.F. Feldman 3, F.L. Metzger 4, R.V.H. Pollock 5 and J. Roche 6 1Dept of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, IN,USA. 2Dept of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, WI, USA. 3Dept of Biomedical Sciences & Pathobiology, VA-MD - Regional College of Veterinary Medicine, Virginia Tech, VA, USA. 4Metzger Animal Hospital,State College,PA, USA. 5Fort Hill Company, Montchanin, DE, USA. 6 Hematology Systems, IDEXX Laboratories, Westbrook, ME, USA. Overview Production Red blood cells (RBC) are produced in the bone marrow. Numbers of circulating RBCs are affected by changes in plasma volume, rate of RBC destruction or loss, splenic contraction, erythropoietin (EPO) secretion, and the rate of bone marrow production. A normal PCV is maintained by an endocrine loop that involves generation and release of erythropoietin (EPO) from the kidney in response to renal hypoxia. Erythropoietin stimulates platelet production as well as red cell production. However, erythropoietin does not stimulate white blood cell (WBC) production. Erythropoiesis and RBC numbers are also affected by hormones from the adrenal cortex, thyroid, ovary, testis, and anterior pituitary. Destruction Red cells have a finite circulating lifespan. In dogs, the average normal red cell circulates approximately 100 days. -
Hereditary Spherocytosis: Clinical Features
Title Overview: Hereditary Hematological Disorders of red cell shape. Disorders Red cell Enzyme disorders Disorders of Hemoglobin Inherited bleeding disorders- platelet disorders, coagulation factor Anthea Greenway MBBS FRACP FRCPA Visiting Associate deficiencies Division of Pediatric Hematology-Oncology Duke University Health Service Inherited Thrombophilia Hereditary Disorders of red cell Disorders of red cell shape (cytoskeleton): cytoskeleton: • Mutations of 5 proteins connect cytoskeleton of red cell to red cell membrane • Hereditary Spherocytosis- sphere – Spectrin (composed of alpha, beta heterodimers) –Ankyrin • Hereditary Elliptocytosis-ellipse, elongated forms – Pallidin (band 4.2) – Band 4.1 (protein 4.1) • Hereditary Pyropoikilocytosis-bizarre red cell forms – Band 3 protein (the anion exchanger, AE1) – RhAG (the Rh-associated glycoprotein) Normal red blood cell- discoid, with membrane flexibility Hereditary Spherocytosis: Clinical features: • Most common hereditary hemolytic disorder (red cell • Neonatal jaundice- severe (phototherapy), +/- anaemia membrane) • Hemolytic anemia- moderate in 60-75% cases • Mutations of one of 5 genes (chromosome 8) for • Severe hemolytic anaemia in 5% (AR, parents ASx) cytoskeletal proteins, overall effect is spectrin • fatigue, jaundice, dark urine deficiency, severity dependant on spectrin deficiency • SplenomegalSplenomegaly • 200-300:million births, most common in Northern • Chronic complications- growth impairment, gallstones European countries • Often follows clinical course of affected -
Thrombotic Microangiopathy Score As a New Predictor for Neurologic Outcome in Patients Undergoing Targeted Temperature Management After Out-Of-Hospital Cardiac Arrest
Thrombotic Microangiopathy Score as a New Predictor for Neurologic Outcome in Patients Undergoing Targeted Temperature Management After Out-of-hospital Cardiac Arrest Taeyoung Kong Yonsei University College of Medicine Hye Sun Lee Yonsei University College of Medicine Soyoung Jeon Yonsei University College of Medicine Jong Wook Lee Konyang University Hospital Hyun Soo Chung Yonsei University College of Medicine Sung Phil Chung Yonsei University College of Medicine Je Sung You ( [email protected] ) Yonsei University College of MedicineGangnam Severance Hospital https://orcid.org/0000-0002-2074- 6745 Original research Keywords: Out-of-hospital cardiac arrest, Targeted temperature management, Thrombotic microangiopathy score, Mortality, Predictor, Schistocytes Posted Date: July 8th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-40096/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/21 Abstract Background: Given the morphological characteristics of schistocytes, thrombotic microangiopathy (TMA) score can be benecial as it can be quickly and serially measured without additional effort or costs. This study aimed to investigate whether the serial TMA scores until 48 h post admission are associated with clinical outcomes in patients undergoing targeted temperature management (TTM) after out-of-hospital cardiac arrest (OHCA). Methods:We retrospectively evaluated a cohort of 185 patients using a prospective registry. We analyzed the TMA score at admission and after 12, 24, and -
Rbcs) in Both the Sinus and Cord, Histiocytes Werc Swollen by a Granu}Ar Substance in the Cytoplasm and Also Many Secondary Lysosomes
The UOEHAssociationUOEH Association ofofHealth Health Sciences JUOEH20(1)!11-19 (1998) 11 [Original) Pathological Study Splenomegaly Associated with Cadmium-inducedof Anemia in Rats Tetsuo HAMADA', Akihide TANIMOT02, Nobuyuki ARIMA!, Yoshihiro IDEL, Takakazu SASAGURI2, Shohei SHIMiVIRI2, Yoshitaka MURATA', Ke-Yong WANG2 and Yasuyuki SASAGURIL' 'Dopartment of'Surgical Pathotogy, University llosPital ?Dopartment qf Palhology and Cell Biotogy, Scheol of' Adlrdicine, (1itib'ersity of Occapational and Environmental Health., .lapan. }'dhatanishi-ku, Kiialp,ztshu 807-8imr, .1apan Ahstract : Splenomegaly was observcd both in male and R)malc Spraguc-Dawley rats after 1 week of exposure to CdC12 (O,6 mg (:d/kg/day), Sp]een weight reached about double that in controls by 8 weeks of Cd exposure. Histopathologica] cxamination of the enlargcd spleen rcvcaled that iron- and lipid-laden histiocytes were clustered in tha periarterial lymphatic sheath, and the red pulp appeared to be expanded. It is noteworthy that electron microscopy rcvealed markcd poikilocytosis and Hcinz body formation in red blood cells (RBCs) in both the sinus and cord, Histiocytes werc swollen by a granu}ar substance in the cytoplasm and also many secondary lysosomes. Thesc morphological findings indicatc that degradation of damagcd RBCs induced by exposure to Cd might bc promoted in the splccn and possibly cause splenomcgaly, This RBC damage-hcmolysis-splcnomegaly sequence is also considered to be associated with the etioiogy of Cd-induced anemia, In addition to the abnormal RBC degradation, nuclel of ]ymphocytes in thc Cd-cxposcd spleen exhibited high elcctron density, consistent with a preapoptotic statc suggesting the immunosupprcssive effhct ofCd. Kay woralf :spienomegaly, poiki]ocytosis, Heinz body, cadmiurn, anemia, (Received 18 November 1997, accepted I9January 1998) Introduction Cd was reported to cause anemia in dogs as early as 1896 [1], and subsequently, anemia was found in humans after Cd exposure [2]. -
Hereditary Spherocytosis
Hereditary Spherocytosis o RBC band 3 protein testing is a very sensitive and Indications for Ordering specific test for the diagnosis of hereditary Use to confirm diagnosis of hereditary spherocytosis when spherocytosis hemolytic anemia and spherocytes are present Physiology • RBC band 3 protein is a major structural protein of RBCs Test Description o Reduction in the amount of band 3 fluorescence after Test Methodology binding with EMA correlates with spherocytosis • Red blood cell (RBC) surface protein band 3 staining with Genetics eosin-5-maleimide (EMA) analyzed by flow cytometry Clinical Validation Genes: ANK1, EPB42, SLC4A1, SPTA1, SPTB • Validated against the clinical diagnosis of hereditary Inheritance spherocytosis supported by osmotic fragility and/or • Autosomal dominant: 75% molecular testing • Autosomal recessive: 25% Tests to Consider Penetrance: variable Structure/Function Primary Test • Chromosomal location: 17q21.31 RBC Band 3 Protein Reduction in Hereditary Spherocytosis • Provides structure for the red cell cytoskeleton 2008460 • Use to confirm diagnosis of hereditary spherocytosis Test Interpretation when hemolytic anemia and spherocytes are present Sensitivity/Specificity Related Test • Clinical sensitivity: 93% Osmotic Fragility, Erythrocyte 2002257 • Analytical sensitivity/specificity: unknown • Functional testing of RBC sensitivity to osmotic stress Results Disease Overview • Normal o Normal staining of band 3 protein with EMA does not Prevalence: 1/2,000 in northern Europeans suggest hereditary spherocytosis -
Hereditary Spherocytosis (HS)
Hereditary Spherocytosis (HS) Hereditary spherocytosis (HS) is a medical term for a condition What are the symptoms of HS? which affects the red blood cells. Symptoms of HS are due to 2 processes: hemolysis and anemia. What are red blood cells? When red blood cells break down (hemolysis), they release biliruin Blood contains 3 types of cells: red blood cells (RBC), white blood into the bloodstream, which causes yellowing of the skin (jaundice) cells (WBC), and platelets. Red blood cells are the most common and eyes. Hemolysis causes different problems depending on the type of blood cell, and are responsible for delivering oxygen to all age: parts of the body. • Newborns – may need light therapy or further measures Red blood cells, like white cells and platelets, are continuously made • Children – increasing size of the spleen in the bone marrow. When released into the bloodstream, the average lifespan of a red cell is 120 days. • Teens/adults – gallstones that may require surgery Under the microscope, normal red cells are shaped like discs or If enough red cells are destroyed, the red cell count will be low donuts with the centers partially scooped out. This shape makes (anemia). Symptoms of anemia include looking pale, being tired or them very soft and flexible, so they can easily squeeze through even weak, headaches, poor concentration, and challenges with behavior very small blood vessels. and school. Sometimes there is a problem with the wall of the red cell, and they How is HS treated? change shape to look like spheres or balls. These cells are called ‘spherocytes’. -
Morphological Study of Human Blood for Different Diseases
Research Article ISSN: 2574 -1241 DOI: 10.26717/BJSTR.2020.30.004893 Morphological Study of Human Blood for Different Diseases Muzafar Shah1*, Haseena1, Kainat1, Noor Shaba1, Sania1, Sadia1, Akhtar Rasool2, Fazal Akbar2 and Muhammad Israr3 1Centre for Animal Sciences & Fisheries, University of Swat, Pakistan 2Centre for Biotechnology and Microbiology, University of Swat, Pakistan 3Department of Forensic Sciences, University of Swat, Pakistan *Corresponding author: Muzafar Shah, Centre for Animal Sciences & Fisheries, University of Swat, Pakistan ARTICLE INFO ABSTRACT Received: August 25, 2020 The aim of our study was the screening of blood cells on the basis of morphology for different diseased with Morphogenetic characters I e. ear lobe attachment, clinodactyly Published: September 07, 2020 and tongue rolling. For this purpose, 318 blood samples were collected randomly. Samples were examined under the compound microscopic by using 100x with standard Citation: Muzafar Shah, Haseena, method. The results show 63 samples were found normal while in 255 samples, different Kainat, Noor Shaba, Sania, Sadia, et al. types of morphological changes were observed which was 68.5%, in which Bite cell 36%, Morphological Study of Human Blood for Elliptocyte 34%, Tear drop cell 30%, Schistocyte 26%, Hypochromic cell 22.5%, Irregular Different Diseases. Biomed J Sci & Tech Res contracted cell 16%, Echinocytes 15.5%, Roleaux 8%, Boat shape 6.5%, Sickle cell 5%, Keratocyte 4% and Acanthocytes 1.5%. During the screening of slides, bite cell, elliptocyte, tear drop cell, schistocytes, hypochromic cell, irregular contracted cells were found 30(1)-2020.Keywords: BJSTR.Human MS.ID.004893. blood; Diseases; frequently while echinocytes, boat shape cell, acanthocytes, sickle cells and keratocytes Morphological; Acanthocytes; Keratocyte were found rarely. -
Chapter 03- Diseases of the Blood and Certain Disorders Involving The
Chapter 3 Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism (D50- D89) Excludes2: autoimmune disease (systemic) NOS (M35.9) certain conditions originating in the perinatal period (P00-P96) complications of pregnancy, childbirth and the puerperium (O00-O9A) congenital malformations, deformations and chromosomal abnormalities (Q00-Q99) endocrine, nutritional and metabolic diseases (E00-E88) human immunodeficiency virus [HIV] disease (B20) injury, poisoning and certain other consequences of external causes (S00-T88) neoplasms (C00-D49) symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified (R00-R94) This chapter contains the following blocks: D50-D53 Nutritional anemias D55-D59 Hemolytic anemias D60-D64 Aplastic and other anemias and other bone marrow failure syndromes D65-D69 Coagulation defects, purpura and other hemorrhagic conditions D70-D77 Other disorders of blood and blood-forming organs D78 Intraoperative and postprocedural complications of the spleen D80-D89 Certain disorders involving the immune mechanism Nutritional anemias (D50-D53) D50 Iron deficiency anemia Includes: asiderotic anemia hypochromic anemia D50.0 Iron deficiency anemia secondary to blood loss (chronic) Posthemorrhagic anemia (chronic) Excludes1: acute posthemorrhagic anemia (D62) congenital anemia from fetal blood loss (P61.3) D50.1 Sideropenic dysphagia Kelly-Paterson syndrome Plummer-Vinson syndrome D50.8 Other iron deficiency anemias Iron deficiency anemia due to inadequate dietary -
Congenital Heinz-Body Haemolytic Anaemia Due to Haemoglobin Hammersmith
Postgrad Med J: first published as 10.1136/pgmj.45.527.629 on 1 September 1969. Downloaded from Case reports 629 TABLE 1 After transfusion Before transfusion 24 hr 72 hr 6 days Haemoglobin (g) ND 7-5 7-6 7-6 PCV 20 29 23 29 Plasma free Hb (mg/100 ml) 241 141 5 6 Bleeding time 14 6 4 1 Clotting time No clot 8 5-5 2 Haemolysins 3±+ - - Serum bilirubin (mg/100 ml) 4-0 4-8 1-3 0-6 Urine volume/24 hr (ml) 970 1750 1500 1300 Haemoglobinuria 4+ 1 + - - Urobilin 2+ 3+ 3 + 1+ Blood urea (mg/100 ml) 30 148 75 32 Serum Na (mEq/l) 128 132 136 140 Serum K (mEq/l) 3-8 4-2 4-6 4-6 Serum HCO3 (mEq/l) 21-2 27-6 28-4 30 0 SGOT Frankel Units ND 110 84 36 SGPT Frankel Units 94 96 68 Acknowledgment Reference We are greatly indebted to Dr P. E. Gunawardena, REID, H.A. (1968) Snake bite in the tropics. Brit. med. J. 3, Superintendent of the National Blood Transfusion Service 359. for his help in this case. Protected by copyright. Congenital Heinz-body haemolytic anaemia due to Haemoglobin Hammersmith N. K. SHINTON D. C. THURSBY-PELHAM M.D., M.R.C.P., M.C.Path. M.D., M.R.C.P., D.C.H. H. PARRY WILLIAMS M.R.C.S., F.R.C.P. Coventry and Warwickshire Hospital and City General Hospital, Stoke-on-Trent http://pmj.bmj.com/ THE ASSOCIATION of haemolytic anaemia with red shown by Zinkham & Lenhard (1959) to be associ- cell inclusion bodies was well recognized at the end ated with an hereditary deficiency of the red cell ofthe Nineteenth Century in workers exposed to coal enzyme glucose-6-phosphate dehydrogenase. -
TOPIC 5 Lab – B: Diagnostic Tools & Therapies – Blood & Lymphatic
TOPIC 5 Lab – B: Diagnostic Tools & Therapies – Blood & Lymphatic Disorders Refer to chapter 17 and selected online sources. Refer to the front cover of Gould & Dyer for normal blood test values. Complete and internet search for videos from reliable sources on blood donations and blood tests. Topic 5 Lab - A: Blood and Lymphatic Disorders You’ll need to refer to an anatomy & physiology textbook or lab manual to complete many of these objectives. Blood Lab Materials Prepared slides of normal blood Prepared slides of specific blood pathologies Models of formed elements Plaque models of formed elements Blood typing model kits Blood Lab Objectives – by the end of this lab, students should be able to: 1. Describe the physical characteristics of blood. 2. Differentiate between the plasma and serum. 3. Identify the formed elements on prepared slides, diagrams and models and state their main functions. You may wish to draw what you see in the space provided. Formed Element Description / Function Drawing Erythrocyte Neutrophil s e t y c Eosinophils o l u n a r Basophils Leukocytes G e Monocytes t y c o l u n Lymphocytes a r g A Thrombocytes 4. Define differential white blood cell count. State the major function and expected range (percentage) of each type of white blood cell in normal blood. WBC Type Function Expected % Neutrophils Eosinophils Basophils Monocytes Lymphocytes 5. Calculation of the differential count? 6. Define and use in proper context: 1. achlorhydria 5. amyloidosis 2. acute leukemia 6. anemia 3. agnogenic myeloid metaplasia 7. autosplenectomy 4. aleukemic leukemia 8. basophilic stippling 9.