Causes Anemia Workup - Exaggerated

Total Page:16

File Type:pdf, Size:1020Kb

Causes Anemia Workup - Exaggerated Anemia - Definition Update on (Approach to) Anemia • Decrease in the number of circulating red blood cells How to efficiently and accurately • Most common hematologic disorder by far work up the anemic patient • Almost always a secondary disorder • As such, critical for internist to know how David L. Diuguid, MD Associate Professor of Clinical Medicine to evaluate/determine cause College of Physicians & Surgeons of Columbia University Anemia - Causes Anemia Workup - Exaggerated • Iron/TIBC/Ferritin •Acid hemolysis • Folate/B • Blood loss 12 • Osmotic fragility • LDH/Bilirubin • Rx iron/folate/B • Decreased production of red blood cells 12 • Haptoglobin/Urine for •Type & Cross (Marrow failure) hemosiderin • Transfuse 2-4 units • Increased destruction of red blood cells • Coombs Test – Direct & indirect • GI Consult –Hemolysis • Hemoglobin • Hematology Consult – electrophoresis Bone Marrow ANEMIA ANEMIA Decreased Production Increased Destruction 1 Anemia Anemia Workup - 1st Test • History and Exam • Reticulocyte count RETICULOCYTE • Blood film COUNT •MCV • Ferritin • WBC, diff, platelets Reticulocyte Count - Absolute Value • = Retic % x RBC Count – eg 0.01 x 5,000,000 = 50,000 • Normal up to 120,000/µl • More accurate way to assess body’s response to anemia Anemia - Peripheral Blood Smear Anemia Workup Findings • If retic count is elevated, following • Look for size and shape of RBC’s - esp for tests not needed: variability in sizes & shapes – Iron/Iron Binding Capacity/Ferritin • Is there polychromasia present? (Often implies reticulocytosis) – Folate/Vitamin B12 • Is there a dimorphic population of RBCs? –Acid Hemolysis • Are there platelet and WBC abnormalities? – GI Consult – Bone Marrow 2 Mean Corpuscular Volume Anemia Workup - MCV MCV Anemia Macrocytic >100 fl Microcytic Normocytic Macrocytic Normocytic 80-100 fl Iron Deficiency Anemia of chronic disease Megaloblastic anemias Anemia of Chronic Disease Early iron deficiency Liver disease/alcohol Microcytic < 80 fl Thalassemias Hemoglobinopathies Hemoglobinopathies Hemoglobinopathies Primary marrow disorders Metabolic disorders Sideroblastic Anemia Combined deficiencies Primary marrow disorders Increased destruction Increased destruction Anemia – Normocytic (MCV 80-100) Anemia of Chronic Disease •Common • Most commonly caused by anemia of chronic disease • Develops over 1 to 2 months • Early iron deficiency often causes • Non-progressive normocytic anemia as well • Usually mild to moderate • Anemia of chronic investigation – particular – but hematocrit < 0.20 occasionally hazard of ICU patients • 30% mildly microcytic • Combined deficiencies • WBC, platelets normal or increased 3 Anemia of Chronic Disease - Pathophysiology Effects of Interleukin-1 (IL-1) Cytokine effects (eg, IL-1, TNF) Stimulates Inhibits DNA & RNA iron-response elements ↓ erythropoietin responsiveness (& production) fever erythropoiesis granulopoiesis ↓ transferrin synthesis thrombopoiesis ↓ Fe mobilization from macrophages synthesis of: ↓ Fe re-utilization in erythropoiesis ferritin synthesis of: ↓ serum Fe despite adequate stores Ig transferrin ↑ serum ferritin fibrinogen, VIII albumin Reticulocytopenia CRP Anemia IL-2, IL-6 Marrow Failure ANEMIA OF CHRONIC DISEASE - Causes Normocytic Anemia (MCV 80-100 fl) • Thyroid disease Type of Marrow • Collagen Vascular Disease anemia Blood film Ferritin Fe TIBC Fe stores – Rheumatoid Arthritis – Systemic Lupus Erythematosus – Polymyositis Chronic Normochromic, Nl or ↑ ↓ ↓ Nl or ↑, – Polyarteritis Nodosa disease* normocytic • Inflammatory Bowel Disease clumped – Ulcerative Colitis – Crohn’s Disease • Malignancy Early Fe Mild anisocytosis, Nl or ↓ ↓ ↑ absent • Chronic Infectious Diseases deficiency hypochromia – Osteomyelitis – Tuberculosis • Familial Mediterranean Fever *including anemia due to renal disease and AIDS • Renal Failure Anemia Workup - MCV ANEMIA - Microcytic (MCV < 80) • Iron Deficiency - High RDW (Red cell Anemia distribution width) • Thalassemia minor - Normal RDW Normocytic Macrocytic Microcytic •Rare – Sideroblastic anemia Iron Deficiency Anemia of chronic disease Megaloblastic anemias Anemia of Chronic Disease Early iron deficiency Liver disease/alcohol – Metal poisoning (esp lead, aluminum) Thalassemias Hemoglobinopathies Hemoglobinopathies – Occasional hemoglobinopathies Hemoglobinopathies Primary marrow disorders Metabolic disorders – Thalassemia major Sideroblastic Anemia Combined deficiencies Primary marrow disorders Increased destruction Increased destruction 4 Anemia MCV, Retics, Blood film Ferritin Ferritin < Ferritin ≥ 120 15 Ferritin 15-120 TIBC High Normal or low trial of Fe Rx anemia anemia corrected not corrected examine marrow Fe stores Fe absent Fe present Fe deficiency anemia Fe deficiency excluded Anemia Workup - MCV Anemia - Macrocytic (MCV > 100) Anemia Microcytic Normocytic Macrocytic • If MCV 100-110 fl, must look for other causes of macrocytosis Iron Deficiency Anemia of chronic disease Megaloblastic anemias • If MCV > 110 fl, almost always folate or Anemia of Chronic Disease Early iron deficiency Liver disease/alcohol cobalamin deficiency Thalassemias Hemoglobinopathies Hemoglobinopathies Hemoglobinopathies Primary marrow disorders Metabolic disorders Sideroblastic Anemia Combined deficiencies Primary marrow disorders Increased destruction Increased destruction 5 Macrocytosis (MCV > 100 fl) Macrocytosis of Alcoholism •Common – Drugs (cytotoxics, immunosuppressants, AZT, anticonvulsants) • 25-96% of alcoholics – Alcohol – Liver disease • MCV elevation usually slight (100-110 fl) – Reticulocytosis • Minimal or no anemia –B12/folate deficiency – Myelodysplastic syndrome • Macrocytes round (not oval) – Marrow infiltration (malignancy, fibrosis) • Less common • Neutrophil hypersegmentation absent –Aplasia • ‘Artifactual’ • Folate stores normal – Cold agglutinins – Hyperglycemia – Hyperleukocytosis Megaloblastic Hematopoiesis Evolving Cobalamin Deficiency • Marrow failure due to: disrupted DNA synthesis • Usual sequence: & ineffective hematopoiesis – Serum Cobalamin falls • Giant precursors and nuclear:cytoplasmic – Serum methylmalonic acid & homocysteine rise dyssynchrony in marrow – MCV rises within the normal range, with • Neutrophil hypersegmentation & macroovalocytes hypersegmentation of neutrophils in blood – MCV rises above normal • Anemia (and often leukopenia & – Anemia and/or neuropathy thrombocytopenia) –Symptoms • Almost always due to Cbl or folate deficiency 6 ‘Dimorphic’ Anemias • Folate & Fe deficiency (eg, pregnancy, alcoholism) •B12 & Fe deficiency (eg, pernicious anemia with atrophic gastritis) • Thalassemia minor & B12 or folate deficiency • Fe deficiency & hemolysis (eg, prosthetic valve) • Folate deficiency & hemolysis (eg, HgbSS disease) • Blood smear critical to assess these Tests Used to Diagnose Hemolytic Anemia Hemolysis • Reticulocyte count (combined with serial Hb) • Anemia of increased destruction • Haptoglobin – Normochromic, normochromic anemia • Urine hemosiderin – Shortened RBC survival • Also helpful: – Reticulocytosis - Response to increased RBC – Serum bilirubin destruction –Serum LDH – Hemoglobinuria Blood morphology in hemolytic Findings Consistent with Hemolysis anemias Serum unconjugated bilirubin Increased Sickle cells Sickle cell anemia Serum LDH (and LDH1:LDH2) Increased Hb crystals Hb CC disease Serum haptoglobin Decreased Urine hemoglobin Present Fragments, helmets Microangiopathic hemolysis Urine hemosiderin Present Microspherocytes Hereditary spherocytosis Urine urobilinogen Increased Immune hemolysis 51 Cr -RBC lifespan Decreased Elliptocytes Hereditary elliptocytosis Reticulocyte count Increased (problems with sensitivity and specificity; none define cause) N.B., hemolysis is not excluded by a normal blood smear. 7 Tests to define the cause of Anemia hemolysis Summary • Hemoglobin electrophoresis • Check reticulocyte count 1st • Hemoglobin A (beta-thalassemia trait) – If elevated, look for causes of increased 2 destruction or bleeding • RBC enzymes (G6PD, PK, etc) – If normal or decreased, look for causes of • Direct & indirect antiglobulin tests (immune) marrow failure • Workup for marrow failure tailored by MCV, RDW, • Cold agglutinins and peripheral blood smear • Osmotic fragility (spherocytosis) – If low, iron problems or globin problems – If high, megaloblastic or DNA problems • Acid hemolysis test (PNH) – If normal, need to look for combined anemias • Clotting profile (DIC) NB: These tests do not demonstrate the presence of hemolysis 8.
Recommended publications
  • Viral Hepatitis with Acute Hemoglobinuria
    22 Case Report Viral Hepatitis with Acute Hemoglobinuria Jagabandhu Ghosh1 Joydeep Ghosh2 1 Department of Paediatrics, I.P.G.M.E.R and S.S.K.M Hospital, Kolkata, Address for correspondence Jagabandhu Ghosh, MD (PAED), Ushashi West Bengal, India Housing Society, 245 Vivekananda Road, Kolkata 700006, India 2 Department of Biotechnology, Heritage Institute of Technology, (e-mail: [email protected]). Kolkata, West Bengal, India J Pediatr Infect Dis 2015;10:22–24. Abstract A 7-year-old male child presented with moderate degree fever, yellowish discoloration of eyes and urine. Examination on admission revealed severe anemia, jaundice, hepato- Keywords megaly, and splenomegaly. On the day following admission, the child showed evidence ► hepatitis of blackish discoloration of urine. The diagnosis was established as viral A hepatitis with ► G6PD glucose-6-phosphate dehydrogenase (G6PD) deficiency. The child recovered with ► viral supportive therapy. We suggest that either universal immunization against hepatitis ► hemolysis A, or routine newborn screening for G6PD deficiency, could prevent the serious ► intravascular morbidity or mortality that can occur when these two conditions coexist. Introduction of eyes, and urine for the past 5 days before admission. There was no history of hematemesis, melena, or any other bleed- Acute viral hepatitis A is widely prevalent in India.1 Viral ing, swelling of body, convulsion, and drug ingestion just hepatitis is the leading of acute hepatitis in children in our before present illness or any previous blood transfusion. His country, and hepatitis A is the most common type of viral urine volume was satisfactory. On examination, the child was hepatitis. Hepatitis A does not commonly present with severe deeply icteric, severely anemic, and drowsy.
    [Show full text]
  • Hematopoiesis/RBC Disorders
    Neonatal Hematopoiesis and RBC Disorders Vandy Black, MD, MSc Pediatric Hematology June 2, 2016 Objectives • Review normal erytHropoiesis in tHe fetus and neonate and regulation of fetal hemoglobin • Outline tHe differential diagnosis of neonatal RBC disorders witH a focus on tHe clinical and laboratory findings • Discuss common presentations of intrinsic red cell disorders in neonates WhicH of tHe following infants is most likely to be diagnosed with a primary hematologic disorder (i.e. need ongoing follow-up in my office)? A. A full-term male with a Hb of 7.5 gm/dL at birth (MCV 108) B. A one week old witH a newborn screen tHat shows Hb FAS C. A full-term Caucasian male with a peak bilirubin of 21 mg/dL whose mom is AB+ D. A 26 week AA female wHose fatHer Has a history of G6PD deficiency RBC Disorders in tHe NICU • Anemia is a common finding in tHe NICU • Differential is broad • Hospitalized preterm infants receive more PRBC transfusions tHan any otHer patient group • >80% of ELBW infants receive at least one PRBC transfusion How RBC Disorders Present? • Anemia on a CBC – May be an expected or incidental finding • Abnormal RBC indices • Abnormal newborn screens • Hyperbilirubinemia • Screening because of family History What is Normal? CHristensen et al, Semin Perinatol 2009 What is Normal? CHristensen et al, Semin Perinatol 2009 Hemoglobin SwitcHing How to ApproacH Anemia • Are otHer cell lines involved? • What is tHe MCV? • What is tHe reticulocyte count? • What does tHe peripHeral blood smear sHow? Microcytic Anemia • Iron Deficiency – Iron supplementation for preterm infants • Thalassemia – Beta-thalassemia less likely in the neonatal period • Chronic Inflammation – Disorders of iron transport (e.g.
    [Show full text]
  • Simultaneous Pure Red Cell Aplasia and Auto-Immune Hemolytic Anemia in a Previously Healthy Infant
    Simultaneous Pure Red Cell Aplasia and Auto-immune Hemolytic Anemia in a Previously Healthy Infant Robert P. Sanders, MD July 16, 2002 Case Presentation Patient Z.H. • Previously Healthy 7 month old WM • Presented to local ER 6/30 with 1 wk of decreased activity and appetite, low grade temp, 2 day h/o pallor. • Noted to have severe anemia, transferred to LeBonheur • Review of Systems – ? Single episode of dark urine – 4 yo sister diagnosed with Fifth disease 1 wk prior to onset of symptoms, cousin later also diagnosed with Fifth disease – Otherwise negative ROS •PMH – Term, no complications – Normal Newborn Screen – Hospitalized 12/01 with RSV • Medications - None • Allergies - NKDA • FH - Both parents have Hepatitis C (pt negative) • SH - Lives with Mom, 4 yo sister • Development Normal Physical Exam • 37.2 167 33 84/19 9.3kg • Gen - Alert, pale, sl yellow skin tone, NAD •HEENT -No scleral icterus • CHEST - Clear • CV - RRR, II/VI SEM at LLSB • ABD - Soft, BS+, no HSM • SKIN - No Rash • NEURO - No Focal Deficits Labs •CBC – WBC 20,400 • 58% PMN 37% Lymph 4% Mono 1 % Eo – Hgb 3.4 • MCV 75 MCHC 38.0 MCH 28.4 – Platelets 409,000 • Retic 0.5% • Smear - Sl anisocytosis, Sl hypochromia, Mod microcytes, Sl toxic granulation • G6PD Assay 16.6 U/g Hb (nl 4.6-13.5) • DAT, Broad Spectrum Positive – IgG negative – C3b, C3d weakly positive • Chemistries – Total Bili 2.0 – Uric Acid 4.8 –LDH 949 • Urinalysis Negative, Urobilinogen 0.2 • Blood and Urine cultures negative What is your differential diagnosis? Differential Diagnosis • Transient Erythroblastopenia of Childhood • Diamond-Blackfan syndrome • Underlying red cell disorder with Parvovirus induced Transient Aplastic Crisis • Immunohemolytic anemia with reticulocytopenia Hospital Course • Admitted to ICU for observation, transferred to floor 7/1.
    [Show full text]
  • The Lower Urinary Tract & Male Reproductive System
    Chapter 21 Hematopathology Nam Deuk Kim, Ph.D. Pusan National University 1 Contents I. Red blood cells II. Hemostasis III. White blood cells IV. Disorders of the lymphopoietic system V. Spleen VI. Thymus 2 THE HEMATOPOIETIC SYSTEM Composition of Human Blood Blood • Transports oxygen, nutrients, hormones, leukocytes (white cells), red cells, platelets and antibodies to tissues in the body and carbon dioxide and other waste products of cell metabolism to the excretory organs of the body • Volume of blood: Represents about 8% of total body weight • approximately 5 quarts, but it varies according to size of individual (5 liters in women; 5.5 liters in men) • Almost half of the blood consists of cellular elements suspended in plasma (viscous fluid) 3 4 Hemopoiesis Cellular differentiation and maturation of the lymphoid and myeloid components of the hematopoietic system. Only the precursor cells (blasts and maturing cells) are identifiable by light microscopic evaluation of the bone marrow. BFU = burst-forming unit; CFU = colony-forming unit (Ba = basophils; E = erythroid; Eo = eosinophils; G = polymorphonuclear leukocytes; GM = granulocyte-monocyte; M = monocyte/macrophages; Meg = megakaryocytic); EPO = erythropoietin; Gm-CSF = granulocyte-macrophage colony-stimulating factor; IL = interleukin; NK = natural killer; SCF = stem cell factor; TPO = thrombopoietin. 5 Composition of Human Blood • All blood cells arise from precursor cells within the bone marrow, called stem cells • These undergo further differentiation to form red cells, white cells,
    [Show full text]
  • 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.
    [Show full text]
  • Hemophagocytic Lymphohistiocytosis in a Child with Sickle Cell Disease
    Hematology & Transfusion International Journal Case Report Open Access Hemophagocytic lymphohistiocytosis in a child with sickle cell disease Keywords: hemophagocytic lymphohistiocytosis, FHL, EBV, hemoglobin S, sickle cell disease, X-ray Volume 6 Issue 5 - 2018 Introduction Walaa Shoman,1 Yasmine El Chazli,2 Asmaa Elsharkawy,2 Neveen Mikhael,3 Akram Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening deghaidy,3 Abeer Al-Battashi,4 Yasser Wali2 hyper-inflammatory syndrome which represents the extreme end of 1Department of Pediatrics, Immunology/Rheumatology unit, a severe uncontrolled hyperinflammatory reaction that can occur in Alexandria University, Egypt many underlying conditions.1 HLH can be divided into primary and 2Department of Pediatrics, Hematology/Oncology unit, secondary HLH. Primary HLH is caused by gene mutation, either at Alexandria University, Egypt 3 one of the Familial HLH (FHL) loci or in a gene responsible for one Department of Clinical pathology, Alexandria University, Egypt 4Department of Child Health, Royal Hospital, Oman of several immunodeficiency syndromes.2 The most common form of secondary HLH is infection associated HLH. Infectious triggers Correspondence: Yasser Wali, Department of Pediatrics, include viruses (as EBV, cytomegalovirus, HHV8, HIV), bacteria (as Hematology/Oncology unit, Alexandria University, Egypt, mycobacteria, mycoplasma), parasites (as leishmania, plasmodium), Email [email protected] 3,4 and fungi (as candida, cryptococcus). Sickle cell disease (SCD) Received: September 02, 2018 | Published: September 27, and its variants are genetic disorders resulting from the presence 2018 of a mutated form of hemoglobin, hemoglobin S (HbS), which can be detected by hemoglobin electrophoresis. SCD is suggested by a high-grade unremitting fever, grunting, marked pallor, jaundice, the typical clinical picture of chronic hemolytic anemia and vaso- and marked re-enlargement of both liver and spleen despite improved occlusive crisis.5,6 We present a case of HLH in an Egyptian boy who chest condition and radiogram.
    [Show full text]
  • Hereditary Spherocytosis with Gilbert's Syndrome
    IOSR Journal of Dental and Medical Sciences (IOSR-JDMS) e-ISSN: 2279-0853, p-ISSN: 2279-0861.Volume 20, Issue 4 Ser.6 (April. 2021), PP 25-28 www.iosrjournals.org Hereditary Spherocytosis with Gilbert’s Syndrome – a case report. Dr Deepan Panneerselvam Intern, Department of Internal Medicine. Dr Thabuna Sivaprakasam Intern, Department of Internal Medicine. Dr Raja sekar PGY2 Internal Medicine Resident. Dr Govindarajulu Ethirajulu Chief, Department of Internal Medicine. Government Kilpauk Medical College and Hospital. Abstract: A 23 year old previously diagnosed female with Gilbert’s syndrome on treatment with Prednisone, presented with a lower respiratory tract infection for the past 4 days with additional complaints of significant lethargy and fatigue, palpitation and intermittent yellowish discolouration of sclera since 9 years old. The patient’s mother and elder sister also had similar history of intermittent jaundice. Routine investigations of the patient revealed normal values except a hemoglobin level of 6.0 g/dl, HCT of 19.5%, MCV of 75.6 fL, serum total bilirubin of 6.3 mg/dl ( Direct: 1.3mgdl, Indirect: 5.0 mg/dl ). This made us suspect another basic hematologic abnormality that contributed to such elevated indirect bilirubin levels. Further investigations revealed a peripheral smear with moderate microcytic hypochromic anemia, anisopoikilocytosis, leucopenia and a reticulocyte count of 2.3%, negative Direct coombs test and a serum LDH of 345U/L. Ultrasound sound abdomen revealed multiple calculi in gall bladder largest measuring 3mm and splenomegaly. Peripheral smear was repeated only to reveal a dimorphic blood picture with eosinophilia, normocytic normochromic anemia with a few fragmented RBCs and spherocytes.
    [Show full text]
  • Approach to Anemia
    APPROACH TO ANEMIA Mahsa Mohebtash, MD Medstar Union Memorial Hospital Definition of Anemia • Reduced red blood mass • RBC measurements: RBC mass, Hgb, Hct or RBC count • Hgb, Hct and RBC count typically decrease in parallel except in severe microcytosis (like thalassemia) Normal Range of Hgb/Hct • NL range: many different values: • 2 SD below mean: < Hgb13.5 or Hct 41 in men and Hgb 12 or Hct of 36 in women • WHO: Hgb: <13 in men, <12 in women • Revised WHO/NCI: Hgb <14 in men, <12 in women • Scrpps-Kaiser based on race and age: based on 5th percentiles of the population in question • African-Americans: Hgb 0.5-1 lower than Caucasians Approach to Anemia • Setting: • Acute vs chronic • Isolated vs combined with leukopenia/thrombocytopenia • Pathophysiologic approach • Morphologic approach Reticulocytes • Reticulocytes life span: 3 days in bone marrow and 1 day in peripheral blood • Mature RBC life span: 110-120 days • 1% of RBCs are removed from circulation each day • Reticulocyte production index (RPI): Reticulocytes (percent) x (HCT ÷ 45) x (1 ÷ RMT): • <2 low Pathophysiologic approach • Decreased RBC production • Reduced effective production of red cells: low retic production index • Destruction of red cell precursors in marrow (ineffective erythropoiesis) • Increased RBC destruction • Blood loss Reduced RBC precursors • Low retic production index • Lack of nutrients (B12, Fe) • Bone marrow disorder => reduced RBC precursors (aplastic anemia, pure RBC aplasia, marrow infiltration) • Bone marrow suppression (drugs, chemotherapy, radiation)
    [Show full text]
  • Laboratory Approach to Anemia Laboratory Approach to Anemia
    DOI: 10.5772/intechopen.70359 Provisional chapter Chapter 12 Laboratory Approach to Anemia Laboratory Approach to Anemia Ebru Dündar Yenilmez and Abdullah Tuli Ebru Dündar Yenilmez and Abdullah Tuli Additional information is available at the end of the chapter Additional information is available at the end of the chapter http://dx.doi.org/10.5772/intechopen.70359 Abstract Anemia is a major cause of morbidity and mortality worldwide and can be defined as a decreased quantity of circulating red blood cells (RBCs). The epidemiological studies suggested that one-third of the world’s population is affected with anemia. Anemia is not a disease, but it is instead the sign of an underlying basic pathological process. However, the sign may function as a compass in the search for the cause. Therefore, the prediag- nosis revealed by thorough investigation of this sign should be supported by laboratory parameters according to the underlying pathological process. We expect that this review will provide guidance to clinicians with findings and laboratory tests that can be followed from the initial stage in the anemia search. Keywords: anemia, complete blood count, red blood cell indices, reticulocyte 1. Introduction Anemia, the meaning of which in Greek is “without blood,” is a relatively common sign and symptom of various medical conditions. Anemia is defined as a significant decrease in the count of total erythrocyte [red blood cell (RBC)] mass, although this definition is rarely used in clinical settings. According to the World Health Organization, anemia is a condition in which the number of red blood cells (RBCs, and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiologic needs [1, 2].
    [Show full text]
  • Anemic Syndrome and White Blood Cells Disorders
    27. 11. 2020 Anemic syndrome and white blood cells disorders Kristína Repová, M.D., PhD. [email protected] Institute of Pathophysiology, Faculty of Medicine, Bratislava Prepared exclusively for the purposes of distance education at the Faculty of Medicine, Comenius University in Bratislava in 2020/21 Hematopoeisis • Hematopoietic organs: • Bone marrow: • forming of erythrocytes, granulocytes, monocytes, thrombocytes, partially lymphocytes • Thymus: • forming of T-lymphocytes • Lymphatic nodes, tonsils, spleen: • forming of B-lymphocytes lymphoid multipotent stem cell pluripotent progenitor cell precursor cell stem cell myleoid multipotent stem cell 1 27. 11. 2020 Hematopoeisis 3 Pluripotent hematopoietic stem cell (self-renewal) Myeloid multipotent Lymphoid multipotent stem cell stem cell Megacaryocyte and Granulocyte and T-cell and NK B-cell erythroid progenitor Macrophage progenitor cell progenitor progenitor Megacaryocyte Erythrocyte Granulocyte Monocyte progenitor progenitor progenitor progenitor (CFU-Meg) (CFU-E) (CFU-G) (CFU-M) Myeloblast NK-cell Proerythroblast Monoblast Lymphoblast Lymphoblast Promyelocyte Megacaryoblast Erythroblast Myelocyte Promonocyte Prolymphocyte Prolymphocyte Megacaryocyte Reticulocyte Metamyelocyte Monocyte T-cell B-cell Thrombocyte Erythrocyte Band cell Basophil Eosinophil Macrophage Dendritic cell Neutrophil 2 27. 11. 2020 I. Disorders of red blood cells II. Disorders of white blood cells III. Myeloproliferative and lymphoproliferative disorders I. Disorders of red blood cells 1. Anemia 2.
    [Show full text]
  • Hemolytic Anemia Presenting As Hemoglobinuria from Intentional Paradichlorobenzene Mothball Ingestion
    Hemolytic Anemia from Intentional ParadichlorobenzeneCASE Mothball REPORT Ingestion Hemolytic Anemia Presenting as Hemoglobinuria from Intentional Paradichlorobenzene Mothball Ingestion Mary Ondinee U. Manalo,1 Cherie Grace G. Quingking2 and Carissa Paz C.Dioquino2 1Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila 2National Poison Management and Control Center, University of the Philippines-Philippine General Hospital less acutely toxic of the two. However, like naphthalene, it has also been known to induce hemolytic anemia because it possesses one benzene ring.1 We report a case of a man who intentionally ingested three mothballs made of paradicholorobenzene who experienced severe hemolytic anemia that necessitated blood transfusion. Case A 24-year-old male inmate from Manila was admitted for persistent vomiting three days after ingestion of three crushed mothballs. Three days prior to admission, the patient intentionally swallowed three crushed mothballs. After an hour, he experienced nausea and vague abdominal pain. A day prior to admission, he presented with persistent vomiting and passed out dark stools. Eight hours prior to admission, Introduction vomiting became more frequent and was now associated Mothballs could be made of naphthalene, with coffee-ground material. Abdominal pain became more paradichlorobenzene, or camphor. Differentiation among intense as well. He was then brought to the Emergency mothballs is difficult because they may have similar odors Room of the Philippine General Hospital for consultation. and are all white, crystalline solids at room temperature. The patient presented at the emergency room awake but Paradichlorobenzene is commonly found here in the weak-looking, tachypneic but with otherwise stable vital Philippines as a component of toilet deodorant blocks, but signs.
    [Show full text]
  • General Refugee Health Guidelines
    GENERAL REFUGEE HEALTH GUIDELINES U.S. Department of Health and Human Services Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases Division of Global Migration and Quarantine August 6, 2012 Background On average, more than 50,000 refugees relocate to the United States annually. 1 They come from diverse regions of the world and bring with them health risks and diseases common to all refugee populations as well as some that may be unique to specific populations. The purpose of this document is to describe general and optional testing components that do not fall into the specific disease categories of these guidelines. These guidelines are based upon principles of best practices, with references to primary published reports when available. This document differs from others in the guidelines, which recommend screening for specific disorders. The guidelines in this document include testing for abnormalities or clinical conditions that are not specific disorders but are suggestive of underlying disorders. The tests in this document may indicate either acute or chronic disorders and generally indicate the need for further testing and evaluation to identify the condition causing the abnormality. Testing for chronic health conditions is important, since these conditions are common in newly arriving refugees, both children and adults. 2 Since refugee populations are diverse and are predisposed to diseases that may differ from those found in the U.S. population, the differential diagnosis and initial evaluation of abnormalities are discussed to assist the clinician. General and Optional Tests Many disorders may be detected by using general, nonspecific testing modalities.
    [Show full text]