Rouleaux Formation of White Blood Cells and Platelets in Leukemia

Total Page:16

File Type:pdf, Size:1020Kb

Rouleaux Formation of White Blood Cells and Platelets in Leukemia 410 Original Article ROULEAUX FORMATION OF WHITE BLOOD CELLS AND PLATELETS IN LEUKEMIA FORMAÇÃO DE ROULEAUX DE GLÓBULOS BRANCOS E PLAQUETAS EM LEUCEMIA 1 2 2 2 3 Hafeez ULLAH ; Khalid NAEEM ; Munir AKHTAR ; Fayyaz HUSSAIN ; Mukhtar AHMAD 1. Biohotonics Research laboratory, Department of Physics, The Islamia University of Bahawalpur, Bahawalpur, Pakistan; 2. Laser and Optronics Laboratory, Department of Physics, Bahauddin Zakariya University, Unive Bosan Road, Multan, Pakistan; 3. Department of Physics, COMSATS Institute of Information Technology, Lahore, Pakistan. ABSTRACT: The objective of this study was to measure the effects of glucose and salt level on white blood cells, red blood cells and platelets (PLTs) in the blood of a leukemic patient by using a white light microscope. Different concentrations of glucose and salt in the range of 0 mM to 500 mM were admixed in the blood sample to prepare blood smear. We revealed that shape of erythrocytes, leukocytes and platelets changes and form aggregates. Increasing concentrations of glucose cause to increases aggregation process of white blood cells, red blood cells and platelets. And the increasing concentration of sodium chloride causes to increase rouleaux formation and aggregation of platelets but dehydration due to increased sodium chloride concentration causes to break the aggregation of white blood cells. Comparison of CBC reports of these samples with and without analytes shows that total leukocyte count (TLC) decreases gradually towards normal ranges of leukocytes which is favorable in the treatment of leukemia but at the same time decreasing level of hemoglobin HGB, mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and increasing level of red blood cell (RBCs) causes to reduce oxygen supply which is in favor of cancer growth and anemia. This work provides us the base for translation this in vitro study towards the in vivo case of blood microvasculature as a non-invasive methodology. KEYWORDS: White light microscopy. Complete blood count (CBC). Total leukocyte count (TLC). Red blood cell (RBC). White blood cell (WBC). Mean corpuscular hemoglobin (MCH). Mean corpuscular hemoglobin concentration (MCHC). INTRODUCTION ARDEKANI, 2007) so when we eat sugar it directly fills the place of vitamin C in white blood Blood is a connective fluid tissue which cell and as a result, the active quantity of vitamin C constitutes about 7% of our total body weight. It is in white blood cell decreases. As sugar is empty composed of 45% of blood cells and 55% plasma. calories so it does not help the white blood cells to In living animals, like the human body, blood destroy pathogens (JANJUA et al., 2016). High transport salts, minerals, oxygen, carbon dioxide consumption of sugar suppresses the immune and ingredients of foods to all parts of the body system causes to decrease the phagocytic capacity (JANJUA et al., 2016). A disease in which cells of neutrophils. Thus, weaken the immune system. violates normal rules of cell division and continue According to the scientist Otto Warburg an uncontrolled growth is called cancer. The (ANNIBALDI; WIDMANN, 2010) increased spreading of cancerous cells to other parts of the levels of sugar cause to increase the production of body is called metastasis and if cancerous cells cancer cells. Tumor cells consume more glucose form a clump it is called tumor (HEJMADI, 2009). than normal cells. Tumor cells convert glucose into Leukemia is a non-solid tumor and causes by the lactic acid even in the normal supply of oxygen. abnormal production of WBCs (LAM, 2003). Tumor cells produce and release many cytokines Cancer of leukocytes arises by the mutation in the that increase the accumulation of leukocytes hematopoietic stem cell. Malignant cells replace (PRANDONI et al., 2005). As we know that and turn off the normal marrow elements, causing glucose is a form of carbohydrates and is a anemia, thrombocytopenia, and a deficiency of compound of carbon, oxygen, and hydrogen. Its normally functioning leukocytes. The leukemic concentration is controlled by two hormone insulin cells infiltrate other organs, destroying normal & glucagon to keep the normal concentration of tissue. glucose in the blood. Any disruption in these Leukemia is caused by abnormal hormones leads to hypoglycemia or hyperglycemia production of white blood cells. Vitamin C and which is known as diabetes. All tumor cells have glucose have the same chemical structure the ability to activate clotting process thus causes (AFKHAMI-ARDEKANI; SHOJAODDINY- the accumulation of different cells like red blood Received: 18/01/17 Biosci. J., Uberlândia, v. 34, n. 2, p. 410-422, Mar./Apr. 2018 Accepted: 05/12/17 411 Rouleaux formation of white blood… ULLAH, H. et al. cells (RBCs), platelets (PLTs) & and white blood Our sample set 1 consists of six different cells (WBCs)(De Cicco, 2004). concentrations i.e. 0 mM, 100 mM, 200 mM, 300 Salt is one of the important gradients of mM, 400 mM and 500 mM of glucose (C 6H12 O6) in diet to maintain homeostasis in the body. The cancerous blood i.e. leukemia. The corresponding normal value of NaCl is 135-145 mM/L. The concentrations of glucose were weighed with concentration of sodium chloride affects the blood Sartorius digital balance (least count 0.0001g). pressure. Hypernatremia causes high blood Each concentration was prepared in 2 ml blood of pressure. Due to the nucleus and sensitive leukemia patient with blood group A+ve and membrane effect of salt is clear in white blood aforementioned concentrations of glucose were cells. Increased level of sodium in the blood causes admixed gently to prepare blood smear of each dehydration (ADROGUÉ; MADIAS, 2000) and concentration. The smear of each concentration was increase the production of immune cells that cause examined under a microscope with the objective of the autoimmune diseases i.e. they destroy healthy 100X and images were saved with the help of CCD cells (WU et al., 2013, KLEINEWIETFELD et al., camera. 2013). Dysfunction of kidneys, drugs, and excess of water intake causes hyponatremia. In cancer, Sample set 2 (Effects of Salt [NaCl] on hyponatremia is more dangerous than cancerous blood) hypernatremia (JANJUA et al., 2016). Tumor cells Our sample set 2 was prepared with the have a higher concentration of sodium inside them same protocol as sample set 1 except the analyte than a healthy one. was replaced with salt (NaCl) having same Accumulation of sodium in blood vessels concentrations. Here, 0 mM means there is no extra results in high blood pressure that causes many salt is added i.e. inherent salt is present. A problems like cardiovascular, renal dysfunction, centrifuge machine for five minutes at 800 rpm was heart strokes, and stiffness of arteries. Platelet used to prepare platelet-rich plasma (PRP). The reactivity increases due to the accumulation of prepared smears were covered with coverslips and sodium, so high intake of sodium chloride results in examined one by one under the microscope at 40X clumping of platelets and causes high blood in dark field to analyze the effect of sodium pressure. chloride on platelets. The blood was drawn after Different techniques and instruments have signing a written consent by the donor for the been used to observe the effects of two analytes purpose of experimentations. (glucose and Table salt) on blood cells including photoacoustic spectroscopy, mid-infrared RESULTS spectroscopy, optical coherence tomography, microscopy, computed tomography, optical diffuse For Glucose analyte reflectance, and light polarimetry etc (JANJUA et 2-D images of each concentration in whole al., 2016). The objective of this work was to measure blood of leukemia of WBCs and PLTs under the effects of glucose and salt level on white blood cells, glucose analyte are shown in Figures 1 and 2 red blood cells and platelets (PLTs) in the blood of a respectively. Table 1 gives CBC reports of glucose leukemic patient by using a white light microscope. containing samples. MATERIAL AND METHODS For Salt analyte 2-D images of each concentration in whole We have used white light digital blood of leukemia of WBCs and PLTs under salt microscopy (Optika, Italy) and dark field analyte are shown in Figures 3 and 4 respectively. microscopy with CCD camera and have recorded Table 2 gives CBC reports of NaCl containing the 2D images in transmission mode. In light samples. microscopy, intense beam of light is used to make sample visible, objective lens magnify the cells up to many times to analyze cells bodies. Sample set 1: (Effect of glucose (C 6H12 O6) on cells in cancerous blood) Biosci. J., Uberlândia, v. 34, n. 2, p. 410-422, Mar./Apr. 2018 412 Rouleaux formation of white blood… ULLAH, H. et al. (a) (b) (c) (d) (e) (f) Figure 1: 2D images of leukocytes and erythrocytes in whole blood of 40 years old leukemic patient obtained with light microscope in transmission mode of glucose concentrations of (a) 0 mM, (b) 100 mM, (c) 200 mM, (d) 300 mM, (e) 400 mM and (f) 500 mM. Biosci. J., Uberlândia, v. 34, n. 2, p. 410-422, Mar./Apr. 2018 413 Rouleaux formation of white blood… ULLAH, H. et al. (a) (b) (c) (d) (e) (f) Figure 2: 2D images of PRP ( platelet-rich plasma) of leukemic patient with 40X magnification in transmission mode for glucose concentrations (a) 0 mM, (b) 100 mM, (c) 200 mM, (d) 300 mM, (e) 400 mM, (f) 500 mM Biosci. J., Uberlândia, v. 34, n. 2, p. 410-422, Mar./Apr. 2018 414 Rouleaux formation of white blood… ULLAH, H. et al. (a) (b) (c) (d) (e) (f) Figure 3: 2D images of leukemia patient with light microscope 100X magnification in transmission mode for NaCl concentrations (a) 0 mM, (b) 100 mM, (c) 200 mM, (d) 300 mM, (e) 400 mM and (f) 500 mM.
Recommended publications
  • Red Blood Cell Rheology in Sepsis K
    M. Piagnerelli Red blood cell rheology in sepsis K. Zouaoui Boudjeltia M. Vanhaeverbeek J.-L. Vincent Abstract Changes in red blood cell membrane components such as sialic (RBC) function can contribute to acid, and an increase in others such alterations in microcirculatory blood as 2,3 diphosphoglycerate. Other flow and cellular dysoxia in sepsis. factors include interactions with Decreases in RBC and neutrophil white blood cells and their products deformability impair the passage of (reactive oxygen species), or the these cells through the microcircula- effects of temperature variations. tion. While the role of leukocytes Understanding the mechanisms of has been the focus of many studies altered RBC rheology in sepsis, and in sepsis, the role of erythrocyte the effects on blood flow and oxygen rheological alterations in this syn- transport, may lead to improved drome has only recently been inves- patient management and reductions tigated. RBC rheology can be influ- in morbidity and mortality. enced by many factors, including alterations in intracellular calcium Keywords Erythrocyte · and adenosine triphosphate (ATP) Deformability · Nitric oxide · concentrations, the effects of nitric Sialic acid · Multiple organ failure · oxide, a decrease in some RBC Oxygen transport Introduction ogy of microcirculatory alterations and, perhaps, the treatment of sepsis. Severe sepsis and septic shock are the commonest causes This review evaluates alterations occurring in RBC of death in intensive care units (ICUs), with associated rheology during sepsis and possible underlying mecha- mortality rates of 30–50% [1]. Sepsis is a complex nisms. The potential implications of blood transfusion pathophysiological process that involves both alterations and erythropoietin administration in sepsis will not be in the microcirculation and changes in the biochemical discussed.
    [Show full text]
  • Canine Immune-Mediated Hemolytic Anemia – Brief Review
    TRADITION AND MODERNITY IN VETERINARY MEDICINE, 2018, vol. 3, No 1(4): 59–64 CANINE IMMUNE-MEDIATED HEMOLYTIC ANEMIA – BRIEF REVIEW Iliyan Manev1, Victoria Marincheva2 1University of Forestry, Faculty of Veterinary Medicine, Sofia, Bulgaria 2Animal Rescue, Sofia, Bulgaria E-mail: [email protected] ABSTRACT Immune-mediated hemolytic anemia (IMHA) is a common autoimmune disorder in dogs. It affects both sexes but occurs more often in female, middle-aged animals. IMHA can be idiopathic (primary) or secondary to infectious, neoplastic and autoimmune disorders. There is an acute regenerative anemia with accompanying hypoxia. Destruction of erythrocytes can be intravascular (as a result of complement system activation) or extravascular (removal of antibody-coated red blood cells by the macrophages in the liver and spleen). Diag- nosis is based on the presence of anemia, in vitro autoagglutination, positive direct antiglobulin test (Coomb`s test), detection of spherocytes. It is crucial to exclude possible secondary causes. The treatment protocol aims to cease cell destruction by high doses of corticosteroids, aggressive supportive care and long-term application of immunosuppressive drug combinations. Still lethality is high because of complications (pulmonary throm- boembolism, DIC), medication resistance, relapses. Key words: immune-mediated, anemia, canine, hemolysis, immunosuppressive drugs. Immune-mediated hemolytic anemia is one of the commonly diagnosed canine autoimmune diseases and a model of acute and clinically relevant anemia. Impaired
    [Show full text]
  • Canine Multiple Myeloma
    Canine Multiple Myeloma Meredith Maczuzak, DVM; Kenneth S. Latimer, DVM, PhD; Paula M. Krimer, DVM, DVSc; and Perry J. Bain, DVM, PhD Class of 2003 (Maczuzak) and Department of Pathology (Latimer, Krimer, Bain), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388 Introduction Multiple myeloma or plasma cell myeloma, is a neoplasm of well- differentiated B cell lymphocytes typically originating from the bone marrow. Neoplastic cells can metastasize widely, having a predilection for bone and resulting in osteolysis. The malignant transformation of a single B cell can secrete a homogenous immunoglobulin product known as paraprotein, which will mimic the structure of normal immunoglobulins. Overabundant production of paraprotein, consisting of any of the immunoglobulin classes, will appear as a sharp, well-defined peak or monoclonal gammopathy on serum electrophoresis. The most frequently encountered multiple myelomas secrete IgG or IgA paraproteins, however IgM myelomas (macroglobulinemia) have also been diagnosed in companion animals. Light chain disease is caused by plasma cell overproduction of the light chain segment of the immunoglobulin complex, consisting of either the lambda or kappa light chain. These proteins are referred to as Bence-Jones proteins and are the most commonly observed immunoglobulin fragments in the monoclonal gammopathies.2 There are rare instances where a malignant plasma cell neoplasm will be nonsecretory. These tumors occur in approximately 1% of all cases of multiple myeloma and are referred
    [Show full text]
  • Complete Blood Count in Primary Care
    Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document.
    [Show full text]
  • 8 Erythrocyte Sedimentation Rate (Esr)
    MODULE Erythrocyte Sedimentation Rate (ESR) Hematology and Blood Bank Technique 8 Notes ERYTHROCYTE SEDIMENTATION RATE (ESR) 8.1 INTRODUCTION Erythryocyte Sedimentation Rate (ESR) is the measurement after 1hour of the sedimentation of red cells when blood is allowed to stand in an open ended glass tube mounted vertically on a stand. OBJECTIVES After reading this lesson, you will be able to: z describe the methods used for measuring ESR z enlist the factors influencing the sedimentation of red cells z discuss the significance of measuring ESR z describe the reticulocyte count and it’s significance 8.2 METHODS OF MEASURING ESR ESR can be measured in the laboratory by two methods z Westergren method z Automated ESR analyser The International Council for Standardization in Hematology recommends the use of Westergren method as the standard method for measuring ESR. Westergren method The Westergren pipette is a glass pipette 30 cm in length and 2.5mm in diameter. The bore is uniform to within 5% throughout. A graduated scale in mm extends over the lower 20 cm. 62 HEMATOLOGY AND BLOOD BANK TECHNIQUE Erythrocyte Sedimentation Rate (ESR) MODULE Sample: Venous blood collected in EDTA. Four volumes of blood is diluted in Hematology and Blood 1 volume of citrate. Alternatively, 2ml blood is directly collected in 0.5ml of Bank Technique 3.8% trisodium citrate. Equipment required 1. Westergren pipette 2. Stainless steel rack for holding pipette Notes 3. Timer Method 1. Mix the blood sample well and draw in the Westergren pipette to the 0mm mark with a rubber teat. 2. Place the tube exactly vertical in the rack which has a rubber cork at the bottom.
    [Show full text]
  • Successful Autologous Peripheral Blood Stem Cell Harvest and ­Transplantation After Splenectomy in a Patient with Multiple ­Myeloma with Hereditary Spherocytosis
    International Journal of Myeloma 8(3): 11–15, 2018 CASE REPORT ©Japanese Society of Myeloma Successful autologous peripheral blood stem cell harvest and transplantation after splenectomy in a patient with multiple myeloma with hereditary spherocytosis Daisuke FURUYA1,4, Rikio SUZUKI1,4, Jun AMAKI1, Daisuke OGIYA1, Hiromichi MURAYAMA1,2, Hidetsugu KAWAI1, Akifumi ICHIKI1,3, Sawako SHIRAIWA1, Shohei KAWAKAMI1, Kaito HARADA1, Yoshiaki OGAWA1, Hiroshi KAWADA1 and Kiyoshi ANDO1 Hereditary spherocytosis (HS) is the most common inherited red cell membrane disorder worldwide. We herein report a 58-year-old male HS patient with mild splenomegaly who developed symptomatic multiple myeloma (MM). Autologous stem cell transplantation (ASCT) was considered to be adopted against MM, although there was a possibility of splenic rupture following stem cell mobilization. Therefore, splenectomy was performed prior to stem cell harvest, and he was able to safely mobilize sufficient CD34+ cells with G-CSF and plerixafor and undergo ASCT. This case suggests that stem cell mobilization after splenectomy is safe and effective in HS patients complicated with malignancies. Key words: multiple myeloma, hereditary spherocytosis, splenectomy, autologous peripheral blood stem cell harvest Introduction Consolidation with melphalan-based HDT followed by ASCT is still the standard treatment option for transplant-eligible Multiple myeloma (MM) is characterized by clonal prolifera- patients with MM, leading to higher complete response rates tion of abnormal plasma cells in the bone marrow (BM) micro- and increased progression-free survival and overall survival environment, monoclonal protein in the blood and/or urine, compared with conventional chemotherapy regimens [2]. bone lesions, and immunodeficiency [1]. In recent years, the Importantly, the emergence of novel agent-based therapy introduction of high-dose chemotherapy (HDT) and autol- combined with ASCT has revolutionized MM therapy [2].
    [Show full text]
  • 10 11 Cyto Slides 81-85
    NEW YORK STATE CYTOHEMATOLOGY PROFICIENCY TESTING PROGRAM Glass Slide Critique ~ November 2010 Slide 081 Diagnosis: MDS to AML 9 WBC 51.0 x 10 /L 12 Available data: RBC 3.39 x 10 /L 72 year-old female Hemoglobin 9.6 g/dL Hematocrit 29.1 % MCV 86.0 fL Platelet count 16 x 109 /L The significant finding in this case of Acute Myelogenous Leukemia (AML) was the presence of many blast forms. The participant median for blasts, all types was 88. The blast cells in this case (Image 081) are large, irregular in shape and contain large prominent nucleoli. It is difficult to identify a blast cell as a myeloblast without the presence of an Auer rod in the cytoplasm. Auer rods were reported by three participants. Two systems are used to classify AML into subtypes, the French- American-British (FAB) and the World Health Organization (WHO). Most are familiar with the FAB classification. The WHO classification system takes into consideration prognostic factors in classifying AML. These factors include cytogenetic test results, patient’s age, white blood cell count, pre-existing blood disorders and a history of treatment with chemotherapy and/or radiation therapy for a prior cancer. The platelet count in this case was 16,000. Reduced number of platelets was correctly reported by 346 (94%) of participants. Approximately eight percent of participants commented that the red blood cells in this case were difficult to evaluate due to the presence of a bluish hue around the red blood cells. Comments received included, “On slide 081 the morphology was difficult to evaluate since there was a large amount of protein surrounding RBC’s”, “Slide 081 unable to distinguish red cell morphology due to protein” and “Unable to adequately assess morphology on slide 081 due to poor stain”.
    [Show full text]
  • Hyperviscosity Syndrome Complicating Rheumatoid Arthritis: Report of Two Additional Cases and Review of the Literature
    Henry Ford Hospital Medical Journal Volume 30 Number 4 Article 3 12-1982 Hyperviscosity Syndrome Complicating Rheumatoid Arthritis: Report of Two Additional Cases and Review of the Literature Michael R. Lovy Mark C. Kranc Gilbert B. Bluhm Jeanne M. Riddle Paul D. Stein Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Lovy, Michael R.; Kranc, Mark C.; Bluhm, Gilbert B.; Riddle, Jeanne M.; and Stein, Paul D. (1982) "Hyperviscosity Syndrome Complicating Rheumatoid Arthritis: Report of Two Additional Cases and Review of the Literature," Henry Ford Hospital Medical Journal : Vol. 30 : No. 4 , 189-198. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol30/iss4/3 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med J Vol 30, No 4,1982 Clinical Reports Hyperviscosity Syndrome Complicating Rheumatoid Arthritis: Report of Two Additional Cases and Review of the Literature Michael R. Lovy, MD,* Mark C. Krane, MD,** Gilbert B. Bluhm, MD, *** Jeanne M. Riddle, PhD,*** and Paul D. Stein, MD**** A hyperviscosity syndrome developed in two patients ity caused by the presence ofthe high molecular weight with rheumatoid arthritis. Analytic ultracentrifugation complexes. These abnormalities, as well as the clinical of the sera from one patient demonstrated 225 com­ bleeding, whole blood, and plasma viscosity, became plexes. Intermediate, 22S, and 375 complexes were normal after treatment.
    [Show full text]
  • Red Blood Cell Aggregation in Preterm and Term Neonates and Adults
    1356 LINDERKAMP ET AL. 003 1-3998/84/18 12-1356$02.00/0 PEDIATRIC RESEARCH Vol. 18, No. 12, 1984 Copyright O 1984 International Pediatric Research Foundation, Inc. Printed in U.S. A. Red Blood Cell Aggregation in Preterm and Term Neonates and Adults OTWIN LINDERKAMP, PATRICK OZANNE, PAUL Y. K. WU, AND HERBERT J. MEISELMAN Department of Pediatrics, University of Heidelberg, Federal Republic of Germany and Department of Physiology and Biophysics and Department of Pediatrics, University of Southern California, Los Angeles, California 90024 ABSTRACT. Aggregation of red blood cells (RBC) is a only during stasis or at low shear stresses (5, 22, 23). ~t high major determinant of blood viscosity and of blood circula- shear stresses (about 3 dynes/cm2 or more), RBC aggregates are tion through vessels with slow flow (i.e. veins). RBC ag- rapidly dispersed (23). Thus, RBC aggregation usually takes place gregation and plasma fibrinogen were studied in placental only in the venous portion of the circulation where the blood blood samples from 25 neonates with 24 to 41 wk of flow rate is slow and the fluid shear stresses are low. RBC gestation and in blood from 13 normal adults. The rate and aggregation may occur in other sections of the circulation, how- final extent of RBC aggregation were measured by means ever, under pathophysiological situations of reduced blood flow of a rheoscope (increase in light transmission during blood (i.e. shock). Conversely, increased RBC aggregation (e.g. as a stasis). Both the rate and extent of RBC aggregation were result of high fibrinogen level) can cause lower blood flow rates, low in the premature infants, increased with gestational and this latter mechanism has been suggested as a possible factor age, and reached the highest values in the adults.
    [Show full text]
  • Blood Lab First Week
    Blood Lab First Week This is a self propelled powerpoint study atlas of blood cells encountered in examination of the peripheral blood smear. It is a requirement of this course that you begin review of these slides with the first day of class in order to familiarize yourself with terms used in describing peripheral blood morphology. Laboratory final exam questions are derived directly from these slides. The content of these slides may duplicate slides (1-37) listed on the Hematopathology Website. You must familiarize yourself with both sets of slides in order to have the best learning opportunity. Before Beginning This Slide Review • Please read the Laboratory information PDF under Laboratory Resources file to learn about – Preparation of a blood smear – How to select an area of the blood smear for review of morphology and how to perform a white blood cell differential – Platelet estimation – RBC morphology descriptors • Anisocytosis • Poikilocytosis • Hypochromia • Polychromatophilia Normal blood smear. Red blood cells display normal orange pink cytoplasm with central pallor 1/3-1/2 the diameter of the red cell. There is mild variation in size (anisocytosis) but no real variation in shape (poikilocytosis). To the left is a lymphocyte. To the right is a typical neutrophil with the usual 3 segmentations of the nucleus. Med. Utah pathology Normal blood: thin area Ref 2 Normal peripheral blood smear. This field is good for exam of cell morphology, although there are a few minor areas of overlap of red cells. Note that most cells are well dispersed and the normal red blood cell central pallor is noted throughout the smear.
    [Show full text]
  • Life Is in the Blood
    Scholars Crossing Faculty Publications and Presentations Department of Biology and Chemistry 8-2-2019 Life Is in the Blood Alan L. Gillen Liberty University, [email protected] Jason Conrad Follow this and additional works at: https://digitalcommons.liberty.edu/bio_chem_fac_pubs Part of the Biology Commons Recommended Citation Gillen, Alan L. and Conrad, Jason, "Life Is in the Blood" (2019). Faculty Publications and Presentations. 148. https://digitalcommons.liberty.edu/bio_chem_fac_pubs/148 This Article is brought to you for free and open access by the Department of Biology and Chemistry at Scholars Crossing. It has been accepted for inclusion in Faculty Publications and Presentations by an authorized administrator of Scholars Crossing. For more information, please contact [email protected]. Life Is in the Blood by Dr. Alan L. Gillen and Jason Conrad on August 2, 2019 Keywords: Blood, Circulation, Leeuwenhoek, red blood cells, white blood cells, capillary, life is in the blood, erythrocyte, leukocyte, rouleaux Abstract It takes about 60 seconds for all the blood in your body to complete its journey. It travels from your heart to your extremities and returns, there and back again. Blood moves with the rapid current of the great arterial rivers and through the smallest capillary creeks. William Harvey first noticed circulation (1628) through the heart into arteries and veins; however, he could not see how they connected since he did not have a microscope. The man who first described this was Anton van Leeuwenhoek about 46 years later (1674). Then, J. J. Lister and Thomas Hodgkin described the rouleaux formation or stacking of RBCs through a capillary bed.
    [Show full text]
  • BLOOD CELL IDENTIFICATION Educational Commentary Is
    EDUCATIONAL COMMENTARY – BLOOD CELL IDENTIFICATION Educational commentary is provided through our affiliation with the American Society for Clinical Pathology (ASCP). To obtain FREE CME/CMLE credits click on Continuing Education on the left side of the screen. Learning Objectives: After completion of this testing event, the participant will be able to: • Describe morphologic features of normal peripheral blood leukocytes and platelets. • Identify morphologic abnormalities in erythrocytes and leukocytes associated with Waldenström's macroglobulinemia. The patient presented in the case study for this testing event has been diagnosed with Waldenström's macroglobulinemia. The images for review represent not only normal leukocytes and platelets, but also several abnormalities in red blood cells that may be seen in this condition. The photographs also include a leukocyte (plasma cell) that is not normally viewed in the peripheral blood. BCI-15 depicts a band (stab) neutrophil. Band cells are the earliest precursors of neutrophil maturation that can be normally visualized in the peripheral blood. They characteristically have a nucleus that is shaped like the letters “C” or “U”. The chromatin is clumped and dense. The cytoplasm in band cells contains many specific granules that stain tan, pink, or violet. Picture BCI-16 shows a polychromatophilic erythrocyte. This cell actually represents the stage of red blood cell maturation just prior to the mature erythrocyte, the reticulocyte. The reticulocyte stage begins just after the nucleus has been extruded by the erythrocyte. A small amount of RNA (ribonucleic acid) is still present in the cells and therefore the cell appears blue-gray when Wright’s stain is used.
    [Show full text]