Hematology, Peripheral Blood Abnormalities
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Digitalcommons@UNMC Agranulocytosis
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Agranulocytosis Gordon A. Gunn University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Gunn, Gordon A., "Agranulocytosis" (1935). MD Theses. 386. https://digitalcommons.unmc.edu/mdtheses/386 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. AGRANULOOYTOSIS ,- Senior Thesis by GOrdon .M.. Gunn INTRODUCTION Fifteen years ago the medioal profession new nothing of the disease spoken of in this paper as agranulocytosis. Since Schultz, in 1922, gave an accurate description of a fulminat ing case, agranulocytosis has oomettoClOCo.'UPy more and more prominence in the medical field. Today, the literature is fairly teeming with accounts of isolated cases of all descriptions. Added to this a confus ing nomenclature, varied classifications, and heterogeneous forms of treatment; and the large question of whether it is a disease entity, a group of diseases, or only a symptom complex, and some idea may be garnered as to the progress made. Time is a most important factor in diagnosis of this disease, and the prognosis at best is grave. The treatment has gone through the maze of trials as that of any other new disease; there must be a cause and so there must be some specific treatment. -
Leukocyte Adhesion Deficiency-I
Clinical Communications Leukocyte adhesion deficiency-I: A this article’s Online Repository at www.jaci-inpractice.org for a comprehensive review of all published comprehensive listing of publications and patient numbers by cases country and Table E2 for a comprehensive listing of references). Elena Almarza Novoa, PhDa,b,*, Per investigator assessment, 113 patients were considered to have severe LAD-I, 63 moderate, and 147 not classified. Sanchali Kasbekar, PharmDc,*, d e Neutrophil CD18 expression was reported for 265 cases and was Adrian J. Thrasher, MD, PhD , Donald B. Kohn, MD , less than 2% in 135 patients (51%) and 2% or more in 130 Julian Sevilla, MD, PhDf, Tony Nguyen, MBAg, patients (49%). Four patients with CD18 greater than or equal Jonathan D. Schwartz, MDc,z, and to 2% were considered to have severe LAD-I (CD18% range, Juan A. Bueren, PhDa,b,z 2.4-17.3). Sex information was available for 282 patients, of which 148 (52%) were males. Clinical Implications Age at presentation was reported for 146 cases. For 63 patients with CD18 less than 2%, median presentation was at age 1 Leukocyte adhesion deficiency-I (LAD-I) is a rare, serious month (range, 0.03-18 months); for 62 patients with CD18 of disorder with severity determined by defective CD18 2% or more, median presentation was at age 6 months (range, expression. LAD-I is characterized by umbilical 0.03-192 months). HSCT was performed for 125 patients; 198 complications, granulocytosis, and diverse infections. patients did not undergo HSCT. Severe LAD-I is frequently fatal before the age of 2 years Infections were described for 248 (77%) of the 323 cases; fi without allogeneic transplant. -
University of Illinois College of Medicine at Urbana-Champaign
UNIVERSITY OF ILLINOIS COLLEGE OF MEDICINE AT URBANA-CHAMPAIGN PATHOLOGY - VOLUME I 2014 - 2015 PATHOLOGY TEACHING FACULTY LIST Jerome Anderson, MD Farah Gaudier, MD Richard Tapping, PhD Department of Pathology Dept. of Pathology Associate Professor. McDonough District Hosp. Carle Physician Group Dept. of Microbiology McComb, IL 61455 [email protected] [email protected] Phone: (309) 837-2368 [email protected] Teaching Assistant Nasser Gayed, MD Lindsey Burnett, PhD Brett Bartlett, MD Dept. of Med. Info. Sciences [email protected] Dept. of Pathology 190 Medical Sciences Bldg SBL Health Centre 506 South Mathews Avenue Mattoon, IL 61938 Urbana, IL 61801 Pathology Office [email protected] [email protected] Jackie Newman Phone: (217) 244-2265 Frank Bellafiore, MD Nicole Howell, MD [email protected] Dept. of Pathology Dept. of Pathology Carle Physician Group Carle Physician Group 602 West University Avenue [email protected] Urbana, IL 61801 [email protected] Zheng George Liu, MD Dept. of Pathology Allan Campbell, MD Carle Physician Group Dept. Of Pathology 602 West University Avenue UICOM Peoria IL Urbana, IL 61801 [email protected] [email protected] Gregory Freund, MD Steve Nandkumar, M.D. Head, Dept. of Pathology Pathology Course Director 190 Medical Sciences Building 249 Medical Sciences Building 506 South Mathews Avenue 506 South Mathews Avenue Urbana, IL 61801 Urbana, IL 61801 [email protected] [email protected] Page 2 Pathology M-2 Introduction INTRODUCTION Pathology – study of the essential nature of diseases and the structural and functional changes produced by them. ( Pathos= suffering; ologos = study) Pathology consists of two major subdivisions. -
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. -
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. -
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]. -
Modelling of Red Blood Cell Morphological and Deformability Changes During In-Vitro Storage
applied sciences Article Modelling of Red Blood Cell Morphological and Deformability Changes during In-Vitro Storage Nadeeshani Geekiyanage 1 , Emilie Sauret 1,*, Suvash Saha 2 , Robert Flower 3 and YuanTong Gu 1 1 School of Mechanical, Medical and Process Engineering, Science and Engineering Faculty, Queensland University of Technology (QUT), Brisbane City, QLD 4000, Australia; [email protected] (N.G.); [email protected] (Y.G.) 2 School of Mechanical and Mechatronic Engineering, University of Technology Sydney (UTS), Ultimo, NSW 2007, Australia; [email protected] 3 Research and Development, Australian Red Cross Lifeblood, Kelvin Grove, QLD 4059, Australia; [email protected] * Correspondence: [email protected] Received: 28 February 2020; Accepted: 27 April 2020; Published: 4 May 2020 Featured Application: Red blood cell (RBC) storage lesion is a critical issue facing transfusion treatments, and significant changes in RBC morphology and deformability are observed due to the storage lesion. RBCs require high deformability to sustain in-vivo circulation, and impaired deformability leads to several post-transfusion adverse outcomes. Therefore, improved understanding of the interrelation between the morphological and deformability changes and the quality and viability of the stored RBCs is essential to prevent or reduce the transfusion related adverse outcomes. To support this requisite, the influence on RBC deformability due to several aspects of the storage lesion, namely, the changes in cell morphology, surface area and volume, RBC membrane biomechanics, and cytoskeletal structural integrity are explored numerically in this study. Abstract: Storage lesion is a critical issue facing transfusion treatments, and it adversely affects the quality and viability of stored red blood cells (RBCs). -
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 -
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. -
Anormal Rbc in Peripheral Blood. [Repaired].Pdf
1. Acanthocyte 2. Burr-cell 3. Microcyte 1. Basophilic Normoblast 2. Polychromatic Normoblast 3. Pycnotic Normoblast 4. Plasmocyte 5. Eosinophil 6. Promyelocyte 1. Macrocyte 2. Elliptocyte 1. Microcyte 2. Normocyte 1. Polychromatic Erythrocyte 2. Acanthocyte 3. Elliptocyte 1. Polychromatic Normoblast 2. Pycnotic Normoblast 3. Neutrophil Myelocyte 4. Neutrophil Metamyelocyte 1. Schistocyte 2. Microcyte BASOPHILIC ( EARLY ) NORMOBLASTS Basophilic Erythroblast Basophilic Stippling, Blood smear, May-Giemsa stain, (×1000) CABOT'S RINGS Drepanocyte Elliptocyte Erythroblast ERYTHROBLAST in the blood Howell-jolly body Hypo chromic LACRYMOCYTES Leptocyte Malaria, Blood smear, May-Giemsa stain, ×1000 MICROCYTES Orthochromatic erythroblast Pappen heimer Bodies & 1. Schistocyte 2. Elliptocyte 3. Acanthocyte POIKILOCYTOSIS Polychromatic Erythroblast Pro Erytroblast Proerythroblasts Reticulocyte Rouleaux SICKLE CELLS Sickle cell Spherocyte Spherocyte Spherocyte SPHEROCYTES STOMATOCYTES Target Cells Tear Drop Cell, Blood smear, May-Giemsa stain, x1000 Anulocyte 1. Burr-cell 2. Elliptocyte 1. Macrocyte 2. Microcyte 3. Elliptocyte 4. Schistocyte 1. Ovalocyte 2. Lacrymocyte 3. Target cell 1. Polychromatic Erythrocyte 2. Basophilic Stippling 1. Proerythroblast 2. Basophilic Erythroblast 3. Intermediate Erythroblast 4. Late Erythroblast 5. Monocyte 6. Lymphocyte 1. Target-cell 2. Elliptocyte 3. Acanthocyte 4. Stomatocyte 5. Schistocyte 6. Polychromatophilic erythrocyte. 1.Pro erythroblast 2.Basophilic normoblast 3.Polychromatic normoblast 4.Pycnotic normoblast -
SEED Haematology Sysmex Educational Enhancement and Development October 2012
SEED Haematology Sysmex Educational Enhancement and Development October 2012 The red blood cell indices The full blood count has been used in conjunction with the traditional red The complete blood count (CBC) is central to clinical deci- cell indices in order to narrow down the possible causes sion making. This makes it one of the commonest laboratory of anaemia in an individual patient. investigations performed worldwide. Whilst the definition of what constitutes an CBC is influenced by the number Impedance technology and type of parameters measured by different haematology The RBC, HCT and MCV are all closely interrelated as they analysers, the traditional red cell indices that are widely are derived from information obtained from the passage used to classify anaemias are common to all. of cells through the aperture of the impedance channel of an automated haematology analyser. The impedance The laboratory approach to anaemia technology is based on the principle that an electrical field, Anaemia is an extremely common global healthcare prob- created between two electrodes of opposite charge, can lem. However, anaemia is merely a symptom which can be used to count and determine the size of cells. Blood result from a multitude of causes. Effective treatment is cells are poor conductors of electricity. The diluent in which only possible if the underlying cause is correctly identified. they are suspended as they pass through the aperture To this end, several classification systems have been devis- during counting is an isotonic solution which is a good ed. The most useful and widely used classification system conductor of electricity.