Weathered MC252 Crude Oil-Induced Anemia and Abnormal Erythroid
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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. -
Section 8: Hematology CHAPTER 47: ANEMIA
Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited. -
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]. -
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. -
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]. -
Vitamin D Insufficiency Is a Frequent Finding in Pediatric and Adult
al Dis ion ord rit e t rs u N & f T o h l e a r n a Winters et al., J Nutr Disorders Ther 2014, 4:2 r p u y o Journal of Nutritional Disorders & Therapy J DOI: 10.4172/2161-0509.1000140 ISSN: 2161-0509 Research Article Open Access Vitamin D Insufficiency is a Frequent Finding in Pediatric and Adult Patients with Sickle Cell Disease and Correlates with Markers of Cell Turnover Winters AC1, Kethman W2, Kruse-Jarres R3 and Kanter J4* 1Cincinnati Children's Hospital, Burnet Ave, Cincinnati, OH 45229, USA 2Stanford University, Serra Mall, Stanford, CA 94305, USA 3Tulane University, St Charles Ave, New Orleans, LA 70118, USA 4Medical University of South Carolina, Charleston, SC, USA *Corresponding author: Julie Kanter, Director, Sickle Cell Disease Research, MUSC, 135 Rutledge Avenue, MSC 558, Charleston, SC, 29425, USA, Tel: (843) 876-8483; E-mail: [email protected] Rec Date: April 14, 2014, Acc Date: Jun 16, 2014, Pub Date: Jun 18, 2014 Copyright: © 2014 Winters AC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Vitamin D insufficiency affects 33%-78% of children and 60-100% of adults with sickle cell disease (SCD). There are no previous reports demonstrating a correlation between vitamin D insufficiency and cell turnover in patients with SCD. We hypothesized that vitamin D insufficiency was prevalent in our SCD population (ages 0-60 years) and would correlate with reticulocyte counts in these patients. -
A Study of the Neonatal Haematology of Children with Down Syndrome
A study of the neonatal haematology of children with Down syndrome Rebecca James submitted in accordance with the requirements for the degree of Doctor of Philosophy Department of Health Sciences University of York, March 2011 Abstract This thesis describes the establishment and initial findings of the Children with Down Syndrome Study, a birth cohort of children with DS. The Children with Down Syndrome Study was set up in order to characterise the haematology of neonates with Down syndrome and specifically to test the hypothesis that that this differed in this population. The study was carried out with the support of the Down Syndrome Association and the Down Syndrome Medical Interest Group, and through consultation with clinicians and families. Following a pilot study in the Yorkshire region it was established in over 60 hospitals across the north of England. The Children with Down Syndrome Study is the largest birth cohort of children with Down syndrome established to date, and this is the largest reported analysis of the haematology of neonates with Down syndrome. The results confirm that neonates with Down syndrome have a distinct haematological profile. Means and ranges for haematological parameters throughout the neonatal period are provided. The effects of gestational age, birth weight, postnatal age and the venepuncture to processing interval on the neonatal full blood count were examined, and this is the first report of factors that influence the haematological parameters in neonates with Down syndrome. In order to analyse the blood cell morphology a new approach to morphology was developed and validated. Morphological review of samples from neonates with Down syndrome demonstrated that blasts were common. -
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. -
A New Familial Disorder with Abnormal Ervthrocvte Morphology and Increased Permeability of the Erythrocytes to Sodium and Potassium
Pediat. Res. 5:159-166 (1971) cation permeability ion transport cell lysis osmosis erythrocyte potassium g1ucose sodium hemolysis A New Familial Disorder with Abnormal Ervthrocvte Morphology and Increased Permeability of the Erythrocytes to Sodium and Potassium GEORGE R. HONIG1351, PERPETUA s. LACSON, AND HELEN s. MAURER The Department of Pediatrics, The Abraham Lincoln School of Medicine, University of Illinois, Chicago, Illinois, and The Departments of Pediatrics and of Laboratories, University of the East, Ramon Magsaysay Memorial Medical Center, Quezon City, Philippines Extract A newborn infant of Philippine parents was found to have a morphological abnor- mality of his erythrocytes consisting of an elliptical shape of the cells and one or more transverse slitlike areas of decreased density. These changes were also present in eryth- rocytes of the patient's father, a half-sister of the father, and four of the patient's six siblings. None of the affected family members had anemia or evidence of abnormal hemolysis, and erythrocyte survival by the radiochromium method was normal in three of the individuals studied. Erythrocytes from the affected family members had an increased degree of autohemolysis after incubation for 48 hr, but this was pre- vented almost entirely by addition of glucose. Glucose consumption in vitro by erythro- cytes of the propositus occurred at a rate approximately 60% greater than that of normal controls. The intracellular sodium concentration of the erythrocytes was not different from that of erythrocytes from normal individuals, but a moderate decrease in intracellular potassium was found. When washed cells were incubated in a glucose- free medium, sodium gain and potassium loss were significantly greater than from cells of normal controls. -
Hereditary Spherocytosis in a 27-Year-Old Woman:Case Report
Annals of African Medicine Vol. 8, No. 1; 2009: 61 - 63 CASE REPORT HEREDITARY SPHEROCYTOSIS IN A 27-YEAR-OLD WOMAN: CASE REPORT A. Hassan, A. A. Babadoko, A. H. Isa and P. Abunimye Departments of Haematology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria Reprint requests to: Dr. A. Hassan, Department of Haematology, Ahmadu Bello University Teaching Hospital, P. O. BOX 06, Shika, Zaria, Nigeria. E-mail: [email protected] Accepted: 14th August 2008 Abstract Hereditary spherocytosis (HS) is a familial hemolytic disorder with marked heterogeneity of clinical features, ranging from an asymptomatic condition to a fulminant hemolytic anemia. Although a positive family history of spherocytosis increases the risk for this disorder, it may be sporadic in some cases. In severe cases the disorder may be detected in early childhood, but in mild cases it may go unnoticed until later in adult life. A 27-year-old Nigerian woman presented with mild anemia, jaundice, splenomegaly and a history of multiple blood transfusion. Blood film showed about 70% spherocytes, reticulocytosis of 6.5%, increased osmotic fragility test and a negative direct antiglobulin test. She was managed conservatively on nutritional supplements and a significant regression of symptoms after 6 months was achieved. Keywords: Anaemia, jaundice, splenomegaly, hereditary, spherocytosis Résumé Le spherocytosis héréditaire (HS) est un désordre hémolytique familial avec l'hétérogénéité marquée des dispositifs cliniques, s'étendant d'un état asymptomatique à une anémie hémolytique fulminante. Bien que des antécédents familiaux positifs de spherocytosis augmentent le risque pour ce désordre, ils peuvent être sporadiques dans quelques cas. Dans des cas graves le désordre peut être détecté dans l'enfance tôt, mais dans des cas doux il peut entrer inaperçu jusque postérieur à la vie d'adulte. -
Erythronoclastic) Anaemias of Later Infancy and Childhood: with Special Reference to the Acute Heemolytic Anemia of Lederer and the Anvemia of Von Jaksch
Arch Dis Child: first published as 10.1136/adc.8.45.184 on 1 June 1933. Downloaded from Part V.-The hamolytic (erythronoclastic) anaemias of later infancy and childhood: with special reference to the acute heemolytic anemia of Lederer and the anvemia of von Jaksch BY LEONARD G. PARSONS, M.D., F.R.C.P., AND J. C. HAWKSLEY, M.D., M.R.C.P. The destructive diseases of the erythron which fall for consideration under this heading show many points of general similarity although individual variations are frequent. In Part IV emphasis has been laid upon the fact that the erythron may be affected adversely either in the bone marrow or in the circulation; further, that for this reason the term haemolytic anaemia was probably incorrect because it stressed the destruction of red blood cells, but that the title of erythronoclastic ansemia was more correct http://adc.bmj.com/ because it indicated that the erythron may be affected in the circulation or in the marrow or in both situations. Moreover, this is not the whole story, because not only may the erythron itself be affected in either the circulation, the marrow or both, but also the other elements of the blood, the thrombocyte system and the myeloid leucocyte system, may suffer damage. in child's of iron Again, the latter months of the lactation period the supply on September 27, 2021 by guest. Protected copyright. for haemoglobin-building is somewhat precarious; a disturbance of the erythron is therefore likely to render manifest any iron deficiency and thus a deficiency anaemia may develop in the course of a haemolytic ansemia.