DOCSLIB.ORG

Lab Test Results to Albertans

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Lab Test Results to Albertans Available Lab Tests 0-9 Apolipoprotein A1 Calcium, Stool 17-Hydroxyprogesterone Apolipoprotein B100 Calcium, Urine (Random and 24 Hr) 5-Hydroxyindoleacetic Acid (HIAA), Urine (Random And 24 Hour) Arginine Provocation Panel Calculus (Renal Stone) Arsenic Level, Blood Calprotectin, Stool Arsenic Level, Inorganic, Urine (Occupational) Canadian Blood Services Prenatal Testing A Arsenic Level, Urine (Random and 24 Hr) Cancer Antigen 125, Serum Acetaminophen Ascaris Serology Cancer Antigen 125 (CA 125), Body Fluid Acanthamoeba Culture ASO Titre Cancer Antigen 19-9 (CA 19-9), Body Fluid Acetylcholine Receptor Antibody Aspartate Aminotransferase (AST) Cancer Antigen 19-9, Serum Acetylcholinesterase Aspartate Aminotransferase (AST), Body Fluid Carbamazepine ACTH (Cortrosyn) Stimulation Selective Adrenal Vein Sampling Aspergillus Galactomannan Serology (Blood and Fluid) Carbapenemase Producing Organisms Screen ACTH (Cortrosyn) Stimulation, (1 And 250 Microgram Panels) Carbon Dioxide Content, Fluid Actin Antibody B Carboxyhemoglobin Activated Clotting Time Babesia Examinaon Carcinoembryonic Antigen (CEA), Body Fluid Activated Protein C Resistance Babesia Serology Carcinoembryonic Antigen (CEA), Serum Acylcarnitine Profile, Blood Bacterial Enteric Panel Carotene, Serum Acylcarnitine Profile, Dried Blood Spot Bacterial Vaginosis/Yeast Screen Catecholamines, Urine, Random And 24 Hour Adrenal Cortex Antibody Barium Level, Serum Catheter Tip Culture Adrenal Receptors Panel Barium Level, Urine (Random adnd 24 Hr) CBC and Differential Adrenal Vein Bleed Bartonella Serology CBC No Differential Adrenocorticotropic Hormone (ACTH) Beryllium Level, Serum Centromere B Antibody Alanine Aminotransferase (ALT) Beryllium Level, Urine (Random and 24 Hr) Cerebrospinal Fluid Culture Albumin Beta Cross Laps Ceruloplasmin Albumin Urine/Creatinine (Random and 24 Hour) Beta HCG, Quantitative, CSF Chikungunya Virus Serology Albumin, Body Fluid Beta Streptococcus Test, Throat Chlamydia Trachomatis Serology Albumin, CSF Beta Trace Protein, Body Fluid Chloride, Body Fluid Alcohols (Serum) (methanol, ethylene glycol, isopropanol, Beta-2 Microglobulin Chloride, Stool Aldosteroneacetone) Beta-Hydroxybutyrate Chloride, Sweat Aldosterone, 24H Urine bHCG POCT Cholesterol Aldosterone/Renin Ratio Bile Acids Cholesterol, Body Fluid Alkali Denaturation Test (APT) Bile Acids, Body Fluid Chromium Level, Serum Alkaline Phosphatase (ALP) Bile Acids, Stool Chromium Level, Urine (Occupational) Alkaline Phosphatase, Fluid Bilirubin, Body Fluid Chromium Level, Urine (Random and 24 Hr) Allergies Bilirubin, Total & Conjugated Chromogranin A Alpha 1 Microglobulin, Urine Biotinidase Chylomicrons Alpha Feto Protein Bismuth Level, Urine (Random and 24 Hr) Chylomicrons, Body Fluid Alpha Fetoprotein, CSF Blastomyces Serology Citrate, Urine (Random And 24 Hour) Alpha-1 Antitrypsin Blood Culture For Mycobacteria (AFB) Clobazam And Metabolite Level Alpha-1 Antitrypsin Phenotype Blood Culture, Routine And Fungal Clomipramine And Metabolite Level ALT, Body Fluid Blood Gases Clonazepam Level Aluminum Level, Serum Blood Group Type Clonidine Stimulation Panel Aluminum Level, Urine (Random and 24 Hour) Blood Review For Malaria Parasites Clonidine Suppression Test Amikacin (Pre, Post, Other) BNP, NT-Pro BNP Clostridium Difficile Culture Amino Acids Quantitation, CSF Body Fluid Culture Clostridium Difficile Test Amino Acids Quantitation, Plasma Bone Culture Closure Time Amino Acids Quantitation, Urine, Random Bone Marrow Culture Clozapine Level Amiodarone Bordetella Culture CMV Ab IgG Antibody Amitriptyline And Metabolite Level Borrelia hermsii Serology CMV Ab IgM Antibody Ammonia Branched Chain Amino Acid Monitoring, Dried Blood Spot Cobalt Level, Blood Amoeba Serology Bronchial Culture, Routine Cobalt Level, Urine (Occupational) Amylase Bronchial Wash, Cystic Fibrosis Culture Cobalt Level, Urine (Random and 24 Hr) Amylase (Random And 24 Hr Urine) Bronchoalveolar Lavage Culture Cocaine Metabolite (Benzoylecgonine) Confirmation, Urine Amylase, Body Fluid Brucella Antibody Coccidioides Serology Amylase, CSF Cold Antibody Agglutinin And Titre Anaerobic Culture C Complement (C3) Anaplasma Serology C1 Esterase Inhibitor Quantitation Complement (C4) Androstenedione C1 Esterase Inhibitor, Functional And Pediatric) Angiotensin Converting Enzyme Cadmium Level, Blood Copper Level, Serum Angiotensin Converting Enzyme (ACE), CSF Cadmium Level, Blood(Occupational) Copper Level, Tissue Anti Nuclear Antibody Cadmium Level, Urine (Occupational) Copper Level, Urine (Random and 24 Hr) Anti Nuclear Antibody, Body Fluid Cadmium Level, Urine (Random and 24 Hr) Cord Blood Testing, Post Natal Antibiotic Resistant Culture Calcitonin Antimony Level, Urine (Random and 24 Hour) Calcium Antiretroviral Drug Levels Calcium Infusion Panel Antithrombin Activity Calcium, Body Fluid Anti-Xa Heparin Level Calcium, Ionized #Classification: Protected A Available Lab Tests C Continued Erythropoietin Glucose Tolerance, Gestational, 2 hr Corticotropin Releasing Hormone (CRH) Stimulation Panel Estradiol Glucose Tolerance, Postprandial Hypoglycemia Panel Cortisol (Random, AM and PM) Ethanol Glucose, 2 Hr PC Cortisol, Saliva Ethanol (blood) Glucose, Body Fluid Cortisol, Urine 24 Hr Ethanol Screen, Urine Glucose, Random COVID-19 testing (PCR NAT) Ethosuximide Glucose, Random Urine Coxiella burnetii Serology Ethyl Glucuronide Screen, Urine Glutamic Acid Decarboxylase (Gad65) Antibody C-Peptide Extended Spectrum Beta-lactamase (ESBL) Screen Glutamic Acid Decarboxylase (Gad65) Antibody, CSF C-Peptide, Urine, Random Extractable Nuclear Antibody (ENA) Gnathostoma Serology C-Reactive Protein (CRP) Eye Bacterial Culture Gonadotropin Releasing Hormone Stimulation Panel Creatine Kinase (CK) Gonococcus Culture Creatine Kinase, Body Fluid F Group B Strept Serotyping Creatinine (Random and 24 Hr) Factor II Activity Group B Streptococcus Screen Creatinine (eGFR) Factor IX Activity (Chromogenic And Clot Based) Growth Hormone Suppression Panel Creatinine Clearance Factor IX Inhibitor Creatinine POCT Factor V Activity H Creatinine, Body Fluid Factor V Leiden Mutation Haptoglobin CRRT - Post Filter Ionized Calcium POCT Factor VII Activity Haemophilus Serotyping Cryofibrinogen Factor VIII Activity (Chromogenic And Clot Based) Hantavirus Serology Cryoglobulin Factor VIII Inhibitor HCG, Serum (Quantitative) Cryptococcal Antigen Factor X Activity Heinz Bodies CSF, Cell Count & Differential Factor XI Activity Homocysteine Total CSF, Glucose Factor XII Activity Homovanillic Acid (Hva) And Vanillylmandelic Acid (VMA), Urine CSF, Total Protein Factor XIII Activity (Random And 24 Hr) CVD Risk Assessment: Framingham Risk Score Fasciola Serology HSV IgG Antibody Cyclic Citrullinated Peptide Antibody Fat, Stool, 72 Hour Human Growth Hormone Cyclosporine (Pre and 2 hr post dose) Fat, Stool, Qualitative Hydrogen Breath Test Cystatin C Fecal Alpha-1 Antitrypsin, Stool Hypoglycemia Fasting Panel Cysticercosis Ferritin Helicobacter Pylori Culture Cystinuria / Homocystinuria Screen Fetal Cells, Blood Helicobacter Pylori Stool Test Cystinuria Investigation Fibrinogen Hemoglobin Cytomegalovirus IgG Avidity Fibrinogen Heparin Neutralization Hemoglobin A1C Filaria Blood Smear Hemoglobin A1c D Filaria Serology Hemoglobin And Hematocrit Fluid D-dimer FIT Colorectal Cancer Screening Hemoglobin, Free (Plasma and Body Fluid) Dengue Virus Serology Fluid Cell Count Hemoglobinopathy Evaluation Desipramine Level Fluid Cell Differential Count Heparin Induced Thrombocytopenia Desmopressin Stimulation Panel Fluid Crystal Analysis Hepatitis A Virus Acute Serology – IgM Antibody Device Culture Fluorescent Treponemal Antibody Hepatitis A Virus Immunity Serology – IgG Antibody Dexamethasone Suppression Test Follicle Stimulating Hormone (FSH) Hepatitis B Core Antibody (Total and IgM) DHEA-S Foreign Body Culture Hepatitis B e Antibody Provincial Lab Digoxin Francisella Tularensis Serology Hepatitis B e Antigen Provincial Lab Diphtheria Antitoxin Free Androgen Index Hepatitis B Surface Antibody Diphtheria Culture Fructosamine Hepatitis B Surface Antigen Diphtheria Screen Fungal Culture Hepatitis C Virus Antibody Direct Antiglobulin Test (DAT) Hepatitis Delta Serology Donath Landsteiner Test (Paroxysmal Cold Hemoglobinuria) G Hepatitis E Serology Double Stranded DNA Antibody Galactosemia Screen Herpes Type Specific Serology Doxepin And Metabolite Level Gamma Glutamyl Transferase (GGT) Histone Antibody Gamma Glutamyl Transferase, Body Fluid Histoplasma Antigen E Gastrin HIV 1 and 2 Serology (Antigen and Antibody) Echinococcus General Toxicology Panel-Urine HIV by Rapid Assay Ear Bacterial Culture Genital Culture, Bacterial HIV Serology Confirmation Ehrlichia Serology Gentamicin (Pre, Post, Interval, Other) HTLV I and II Serology Elastase, Stool Giardia Cryptosporidia Assay Electrolyte Panel (Sodium, Potassium, Chloride, Bicarbonate) Glomerular Basement Membrane Antibody I Electrolyte Panel, Urine (Sodium, Potassium, Chloride), Random Glucagon Imipramine And Metabolite Level and 24 Hr Glucagon Stimulation Panel Immunoglobulin D Endomysial Antibodies Glucose Fasting Immunoglobulin Free Light Chains Eosinophil Count, Fluid Glucose Gestational Diabetes Screen (GDS) Immunoglobulin G Subclasses Eosinophil Count, Smear Glucose Meter Check Immunoglobulin G, CSF Eosinophil Count, Stool Glucose Meter POCT Immunoglobulin G4 Eosinophil Count, Urine Glucose Suppression Panel Epstein Barr Serology Panel Glucose Tolerance, 2 hr Erythrocyte Sedimentation Rate Glucose Tolerance, 3 Hours #Classification: Protected
Load more

Recommended publications
  • Supplementary Information Changes in the Plasma Proteome At
    Supplementary Information Changes in the plasma proteome at asymptomatic and symptomatic stages of autosomal dominant Alzheimer’s disease Julia Muenchhoff1, Anne Poljak1,2,3, Anbupalam Thalamuthu1, Veer B. Gupta4,5, Pratishtha Chatterjee4,5,6, Mark Raftery2, Colin L. Masters7, John C. Morris8,9,10, Randall J. Bateman8,9, Anne M. Fagan8,9, Ralph N. Martins4,5,6, Perminder S. Sachdev1,11,* Supplementary Figure S1. Ratios of proteins differentially abundant in asymptomatic carriers of PSEN1 and APP Dutch mutations. Mean ratios and standard deviations of plasma proteins from asymptomatic PSEN1 mutation carriers (PSEN1) and APP Dutch mutation carriers (APP) relative to reference masterpool as quantified by iTRAQ. Ratios that significantly differed are marked with asterisks (* p < 0.05; ** p < 0.01). C4A, complement C4-A; AZGP1, zinc-α-2-glycoprotein; HPX, hemopexin; PGLYPR2, N-acetylmuramoyl-L-alanine amidase isoform 2; α2AP, α-2-antiplasmin; APOL1, apolipoprotein L1; C1 inhibitor, plasma protease C1 inhibitor; ITIH2, inter-α-trypsin inhibitor heavy chain H2. 2 A) ADAD)CSF) ADAD)plasma) B) ADAD)CSF) ADAD)plasma) (Ringman)et)al)2015)) (current)study)) (Ringman)et)al)2015)) (current)study)) ATRN↓,%%AHSG↑% 32028% 49% %%%%%%%%HC2↑,%%ApoM↓% 24367% 31% 10083%% %%%%TBG↑,%%LUM↑% 24256% ApoC1↓↑% 16565% %%AMBP↑% 11738%%% SERPINA3↓↑% 24373% C6↓↑% ITIH2% 10574%% %%%%%%%CPN2↓%% ↓↑% %%%%%TTR↑% 11977% 10970% %SERPINF2↓↑% CFH↓% C5↑% CP↓↑% 16566% 11412%% 10127%% %%ITIH4↓↑% SerpinG1↓% 11967% %%ORM1↓↑% SerpinC1↓% 10612% %%%A1BG↑%%% %%%%FN1↓% 11461% %%%%ITIH1↑% C3↓↑% 11027% 19325% 10395%% %%%%%%HPR↓↑% HRG↓% %%% 13814%% 10338%% %%% %ApoA1 % %%%%%%%%%GSN↑% ↓↑ %%%%%%%%%%%%ApoD↓% 11385% C4BPA↓↑% 18976%% %%%%%%%%%%%%%%%%%ApoJ↓↑% 23266%%%% %%%%%%%%%%%%%%%%%%%%%%ApoA2↓↑% %%%%%%%%%%%%%%%%%%%%%%%%%%%%A2M↓↑% IGHM↑,%%GC↓↑,%%ApoB↓↑% 13769% % FGA↓↑,%%FGB↓↑,%%FGG↓↑% AFM↓↑,%%CFB↓↑,%% 19143%% ApoH↓↑,%%C4BPA↓↑% ApoA4↓↑%%% LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) Supplementary Figure S2.
    [Show full text]
  • Human Plasma and Recombinant Hemopexins: Heme Binding Revisited
    International Journal of Molecular Sciences Article Human Plasma and Recombinant Hemopexins: Heme Binding Revisited Elena Karnaukhova 1,*, Catherine Owczarek 2, Peter Schmidt 2, Dominik J. Schaer 3 and Paul W. Buehler 4,5,* 1 Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA 2 CSL Limited, Bio21 Institute, Parkville, Victoria 3010, Australia; [email protected] (C.O.); [email protected] (P.S.) 3 Division of Internal Medicine, University Hospital of Zurich, 8091 Zurich, Switzerland; [email protected] 4 Department of Pathology, The University of Maryland School of Medicine, Baltimore, MD 21201, USA 5 The Center for Blood Oxygen Transport and Hemostasis, Department of Pediatrics, The University of Maryland School of Medicine, Baltimore, MD 21201, USA * Correspondence: [email protected] (E.K.); [email protected] (P.W.B.) Abstract: Plasma hemopexin (HPX) is the key antioxidant protein of the endogenous clearance pathway that limits the deleterious effects of heme released from hemoglobin and myoglobin (the term “heme” is used in this article to denote both the ferrous and ferric forms). During intra-vascular hemolysis, heme partitioning to protein and lipid increases as the plasma concentration of HPX declines. Therefore, the development of HPX as a replacement therapy during high heme stress could be a relevant intervention for hemolytic disorders. A logical approach to enhance HPX yield involves recombinant production strategies from human cell lines. The present study focuses on a biophysical assessment of heme binding to recombinant human HPX (rhHPX) produced in the Expi293FTM (HEK293) cell system.
    [Show full text]
  • 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.
    [Show full text]
  • Method Development and Validation of Vitamin D2 and Vitamin D3 Using Mass Spectrometry
    Method Development and Validation of Vitamin D2 and Vitamin D3 Using Mass Spectrometry Devon Victoria Riley A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science University of Washington 2016 Committee: Andrew Hoofnagle Geoffrey Baird Dina Greene Program Authorized to Offer Degree: Laboratory Medicine ©Copyright 2016 Devon V. Riley ii University of Washington Abstract Method Development and Validation of Vitamin D2 and Vitamin D3 Using Mass Spectrometry Devon V. Riley Chair of the Supervisory Committee: Associate Professor Andrew Hoofnagle, MD, PhD Vitamin D has long been known to maintain bone health by regulating calcium and phosphorous homeostasis. In recent years, scientists have discovered additional physiological roles for vitamin D. The complex interaction between the active vitamin D hormone and its metabolic precursors continues to be a rich area of research. Fundamental to this research is the availability of accurate and precise assays. Few published assays for vitamins D2 and D3 have contained sufficient details on method validation or performance characteristics. The liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay developed for this thesis has undergone a rigorous validation and proven to yield a sensitive and specific method that exceeds the capabilities of all previously published methods. Developing and validating a novel assay is often complicated by the lack of established acceptability standards. This thesis explores this challenge, specifically for establishing meaningful interpretations and qualification standards of the lower limit of the measuring interval. Altogether, future research focused on vitamins D2, D3 and the Vitamin D pathway can benefit from this robust LC-MS/MS assay and the associated quality parameters outlined in this thesis.
    [Show full text]
  • Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
    Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder.
    [Show full text]
  • Toxicology and Environmental Teaching Tue 1St Oct 2019
    TOXICOLOGY AND ENVIRONMENTAL TEACHING TUE 1ST OCT 2019 CASE ONE The ambulance bring in a 50 year old woman who has been found confused at her home by friends. There is no history available, but she was last seen well around dinner yesterday. She has no known past history and her medications are unknown. Initial Obs: - GCS M 5, E4, V4 pupils large and reactive - SBP 110 - HR 120 - Sats 99% o/a - Afebrile - BSL 8 1. She is confused and denies any ingestion or overdose. She dose state she only took some sleeping medication. What investigations would you do and how would you manage her presentation? Look up NHI: prior hx, community dispensing etc Investigations: Bloods, VBG, ECG Consider differential diagnoses : sepsis, trauma, metabolic 2. You note a community dispensing for 60 x 20mg amitriptyline tablets a few days ago. Her ECG and VBG are shown, please describe and discuss the findings: Potential toxic dose > 10mg/kg onset, toxicity usually rapid onset in 1- 2hrs VBG pH 7.35 PCO2 4.0 HCO3 15 Na 143 K 4.2 Lactate 3.5 - Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2). - Broad QRS complexes. - Positive R’ wave in aVR. ECG Features of Sodium-Channel Blockade Interventricular conduction delay — QRS > 100 ms in lead II Right axis deviation of the terminal QRS: o Terminal R wave > 3 mm in aVR o R/S ratio > 0.7 in aVR Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1) receptor blockade.
    [Show full text]
  • Serious Hazards of Transfusion (SHOT) Annual Report 2017
    ANNUAL SHOT REPORT 2017 working with Affiliated to the Royal College of Pathologists DS OF ZAR TR A AN H S S F U U O S I I R O E N S A Y N R N A U S A R L E S YEARS IV H N O N T A RE T PORT 21S ANNUAL SHOT REPORT 2017 Serious Hazards of Transfusion (SHOT) Steering Group Chair Professor Mark Bellamy SHOT Medical Director Dr Paula Bolton-Maggs Operations Manager Ms Alison Watt Research Analyst Ms Debbi Poles Patient Blood Management Practitioner Mrs Jayne Addison Clinical Incidents Specialist Mr Simon Carter-Graham Mrs Ann Fogg Laboratory Incidents Specialist Mrs Hema Mistry National Coordinator for Mrs Rachael Morrison (Ms Dory Kovacs in 2018) Transfusion-Transmitted Infections (Public Health England) Working Expert Group (WEG) & Writing Group, on behalf of the SHOT Steering Group Chair: Dr Paula Bolton-Maggs Professor Mark Bellamy, Ms Alison Watt, Ms Debbi Poles, Mrs Hema Mistry, Mr Simon Carter-Graham, Mrs Ann Fogg, Mrs Jayne Addison, Mrs Rachael Morrison, Dr Tom Latham, Mrs Diane Sydney, Dr Helen New, Dr Megan Rowley, Dr Fiona Regan, Mr Chris Robbie, Dr Peter Baker, Dr Janet Birchall, Dr Jane Keidan, Mrs Terrie Perry, Mrs Katy Cowan, Dr Sharran Grey, Mrs Clare Denison, Dr Catherine Ralph, Dr Sarah Haynes, Mrs Pamela Diamond, Dr Anicee Danaee, Ms Tracey Tomlinson, Dr Shruthi Narayan, Mrs Heather Clarke. Steering Group (SG) during 2017 Chair: Professor Mark Bellamy Dr Shubha Allard British Society for Haematology Guidelines National Blood Transfusion Committee Dr Ganesh Suntharalingam Intensive Care Society, Faculty of Intensive Care Medicine
    [Show full text]
  • Evaluation of Prolonged Surface Activated Coagulation Time
    Biomedical Science Faculty of Health and Society Malm¨oUniversity SE-205 06 Malm¨o Sweden Master programme in Biomedical Surface Science http://edu.mah.se/en/Program/VABSE Evaluation of prolonged surface activated coagulation time Master degree thesis, 30 ECTS Author: Amalie Jesting Supervisors: Sebastian Bj¨orklund,PhD, Lecturer, Malm¨oUniversity Jens Peter Gøtze, MD, DMSc Professor, Chief-Physician, Rigshospitalet Søren Frank Jørgensen, MSc, Senior Lecturer, Metropolitan University College August 2018 MALMO¨ UNIVERSITY Abstract Faculty of Health and Society Master programme in Biomedical Surface Science Evaluation of prolonged surface activated coagulation time by Amalie Jesting Background: Blood coagulation is an essential defense mechanism to prevent bleeding. Disorders in the coagulation system can be severe and blood tests measuring the blood's ability to coagulate are important. Activated partial thromboplastin time (APTT) is a blood test that measures blood coagulation time. An abnormal prolonged APTT can both be associated with a bleeding tendency or a risk of thrombosis. Additional blood tests are needed to discover the cause of a prolonged APTT. One potential test is the APTT mixing study, which can separate samples with and without inhibitors. The aim of this project is to investigate how the cause of a prolonged APTT is evaluated today and to examine if it is possible to indicate the cause of a prolonged APTT using the APTT mixing study performed on routine samples. The goal is to be able to indicate the cause of a prolonged APTT immediately when is it first discovered. This will save time and help guide the physicians in their work with the patient.
    [Show full text]
  • HEMATOLOGY for THE.Pdf
    HEMATOLOGY FOR THE UNDERGRADUATES By: Dr. Muhammad Saboor, PhD Assistant Professor, Baqai Institute of Hematology Director, Baqai Institute of Medical Technology Baqai Medical University and Dr. Moinuddin, FRCP(C), FRCP (E), PhD (Hons.) Professor of Hematology Director, Baqai Institute of Hematology Baqai Medical University HIGHER EDUCATION COMMISSION ISLAMABAD 1 Copyrights @ Higher Education Commission Islamabad Lahore Karachi Peshawar Quetta All rights are reserved. No part of this publication may be reproduced, or transmitted, in any form or by any means – including, but not limited to, electronic, mechanical, photocopying, recording, or, otherwise or used for any commercial purpose what so ever without the prior written permission of the publisher and, if publisher considers necessary, formal license agreement with publisher may be executed. Project: “Monograph and Textbook Writing Scheme” aims to develop a culture of writing and to develop authorship cadre among teaching and researcher community of higher education institutions in the country. For information please visit: www.hec.gov.pk HEC – Cataloging in Publication (CIP Data): Muhammad Saboor, Dr. Hematolog for Undergraduate I. Hematology 616.15 – dc23 2015 ISBN: 978-969-417-181-4 First Edition: 2015 Copies Printed: 500 Published By: Higher Education Commission – Pakistan Disclaimer: The publisher has used its best efforts for this publication through a rigorous system of evaluation and quality standards, but does not assume, and hereby disclaims, any liability to any person for any loss or damage caused by the errors or omissions in this publication, whether such errors or emissions result from negligence, accident, or any other cause. 2 PREFACE Hematology is one of the oldest specialties in conception yet it is the youngest in its inception.
    [Show full text]
  • MASSHEALTH TRANSMITTAL LETTER LAB-22 July 2002 TO
    Commonwealth of Massachusetts Executive Office of Health and Human Services Division of Medical Assistance 600 Washington Street Boston, MA 02111 www.mass.gov/dma MASSHEALTH TRANSMITTAL LETTER LAB-22 July 2002 TO: Independent Clinical Laboratories Participating in MassHealth FROM: Wendy E. Warring, Commissioner RE: Independent Clinical Laboratory Manual (Laboratory HCPCS) The federal government has revised the HCFA Common Procedure Coding System (HCPCS) for MassHealth billing. This letter transmits changes for your provider manual that contain the new and revised codes. The revised Subchapter 6 is effective for dates of service on or after April 30, 2002. The codes introduced under the 2002 HCPCS code book are effective for dates of service on or after April 30, 2002. We will accept either the new or the old codes for dates of service through July 28, 2002. For dates of service on or after July 29, 2002, you must use the new codes to receive payment. If you wish to obtain a fee schedule, you may purchase Division of Health Care Finance and Policy regulations from either the Massachusetts State Bookstore or from the Division of Health Care Finance and Policy (see addresses and telephone numbers below). You must contact them first to find out the price of the publication. The Division of Health Care Finance and Policy also has the regulations available on disk. The regulation title for laboratory is 114.3 CMR 20.00: Laboratory. Massachusetts State Bookstore Division of Health Care Finance and Policy State House, Room 116 Two Boylston Street
    [Show full text]
  • A Life-Threatening Case of Pregnancy-Related Atypical
    Puri et al. BMC Nephrology (2020) 21:488 https://doi.org/10.1186/s12882-020-02100-4 CASE REPORT Open Access A life-threatening case of pregnancy- related atypical Haemolytic uremic syndrome and successful treatment with Eculizumab Prianka Puri1,2* , Anida Hanxhiu1, Daniel V. O’Hara1,3, Danny Hsu4 and Mirna Vucak-Dzumhur1,5 Abstract Background: Pregnancy-related Atypical Haemolytic Uremic Syndrome (P-aHUS) is a rare condition affecting genetically predisposed women during pregnancy. It is often difficult to diagnose and has a significant impact on maternal and foetal outcomes. It is characterised by microangiopathic haemolytic anaemia and kidney injury from thrombotic microangiopathy. Case presentation: A 27-year-old female of Lebanese descent presented at 36 weeks’ gestation with foetal death in-utero (FDIU) with placental abruption on a background of previously normal antenatal visits. She was coagulopathic and anaemic with anuric acute kidney injury, requiring emergency Caesarean section, intubation and dialysis. Her coagulopathy rapidly resolved, however, her anaemia and renal dysfunction persisted. A diagnosis of P-aHUS was made, and she was empirically treated with Eculizumab. Her ADAMTS13 level was normal, effectively excluding thrombotic thrombocytopenic purpura. Within 2 weeks of treatment her haematological parameters improved, and her renal function began to recover and within 2 months she became dialysis independent. Conclusion: This case highlights the challenges of a timely diagnosis of P-aHUS from other pregnancy-related diseases. Although our patient is dialysis-independent, her risk of relapse remains high with subsequent pregnancies. Currently we are awaiting her genetic sequencing to complete her assessment for underlying mutations and are determining the safest approach to a future planned pregnancy.
    [Show full text]
  • Tests for the Evaluation of Preterm Labor and Premature Rupture of Membranes
    Medical Coverage Policy Effective Date ............................................. 7/15/2021 Next Review Date ....................................... 7/15/2022 Coverage Policy Number .................................. 0099 Tests for the Evaluation of Preterm Labor and Premature Rupture of Membranes Table of Contents Related Coverage Resources Overview .............................................................. 1 Recurrent Pregnancy Loss: Diagnosis and Treatment Coverage Policy ................................................... 1 Ultrasound in Pregnancy (including 3D, 4D and 5D General Background ............................................ 2 Ultrasound) Medicare Coverage Determinations .................. 13 Coding/Billing Information .................................. 13 References ........................................................ 15 INSTRUCTIONS FOR USE The following Coverage Policy applies to health benefit plans administered by Cigna Companies. Certain Cigna Companies and/or lines of business only provide utilization review services to clients and do not make coverage determinations. References to standard benefit plan language and coverage determinations do not apply to those clients. Coverage Policies are intended to provide guidance in interpreting certain standard benefit plans administered by Cigna Companies. Please note, the terms of a customer’s particular benefit plan document [Group Service Agreement, Evidence of Coverage, Certificate of Coverage, Summary Plan Description (SPD) or similar plan document] may differ
    [Show full text]