Basic Skills in Interpreting Laboratory Data

Total Page:16

File Type:pdf, Size:1020Kb

Basic Skills in Interpreting Laboratory Data INDEX 4K score, 612 determining respiratory versus rheumatoid arthritis, 505 4Ts score, 399 metabolic, 307 systemic lupus erythematosus, 509 5-alpha reductase enzyme, 593–594 metabolic acidosis, 308–309, 309, 310. Acute phase response, 500 See also Metabolic acidosis 5' nucleotidase, 334, 335, 636 Acute type B hepatitis (minicase), 349 metabolic alkalosis, 309, 310. See also 6-mercaptopurine (6-MP), 138 ADAM Questionnaire, 596 Metabolic alkalosis 13C- and 14C-labeled urea, 353 Addison disease, 219 respiratory acidosis, 310, 311 15/15 rule, 208 Adenocarcinoma of lung respiratory alkalosis, 311, 311 17-OHP, 578 anaplastic lymphoma kinase, 526 Acid-base homeostasis, 270–271 21-hydroxylase deficiency, 526 EGFR and, 525 Acid-base homeostasis, regulation of, 99m Tc-sestamibi imaging, 165 306–307, 307 Adenosine, 164 201 TI perfusion imaging, 165 Acid-base physiology, 306 Adenosine diphosphate (ADP), 394, Acidemia, 303 394 A Acid-fast bacilli and stains, 470 Adenoviridae, 456 A1c. See Glycated hemoglobin (A1c) Acidosis. See also Metabolic acidosis ADME (absorption, distribution, metabolism, and excretion), 136 Abacavir, 468–469 defined, 303 Adnexal tumors, hirsutism secondary to Absolute neutropenia, 387 lactic, 308, 309 (minicase), 577 Absorbance optical system, 28 respiratory, 310, 311 Adolescents Absorption, distribution, metabolism, and Activated clotting time (ACT), 408 excretion (ADME), 136 categories of substances abused by, 70 Activated partial thromboplastin time prerequisite drug testing of, 82–83 Accu Check Compact Plus, 200 (aPTT), 406–408, 418 Adrenal disorders, 218–219 Accuracy, 3, 55, 59, 61 Activated protein (APC) resistance, 403 Adrenal glands, 218 Acetaminophen Active metabolites, 99–100, 106 nomogram for, 79 Acute blood loss anemia, 374, 379 Adrenal insufficiency, 210 overview of, 106 Acute coronary syndrome (ACS), 152 ADVIA Centaur, 163 serum concentration of, in poisoning electrocardiographic findings in, 154, Afatinib, EGFR and, 140–141, 143 (minicase), 80 154, 154–155 Affinity chromatography in measuring toxicity from, 79 imaging studies and, 163–164 HgbA1c, 57 Acetoacetate, 204, 206, 240 laboratory tests used in evaluation of, Agar dilution, 430, 432–433 Acetone, 204, 206 155 Agarose gel electrophoresis, 27 Acid, defined, 303 biochemical cardiac markers, Agar proportion method, 471 Acid-base chemistry 155–160, 156 Agars, 423, 425 ABG assessments in, 307–308 minicase on, 155 Age-related differences. See also anion gap in, 305 Acute hepatitis, 342, 343, 349 Hematology; Kidney function tests; Liver function tests; Pediatrics arterial bicarbonate in, 304 Acute homeostasis, 271 in laboratory test results, 10–11, 11 arterial blood gas interpretation and, Acute kernicterus, 566 307 Acute liver failure (minicase), 350 in total blood volume, 548–549, 549 arterial oxygen saturation in, 305 Acute lymphoblastic leukemia (ALL), Agglutination, 31–32, 32 arterial partial pressure of carbon 387 Aging Males’ Symptom Scale, 596 dioxide in, 304 Acute myeloblastic leukemia (AML), Agranulocytosis, 387 arterial partial pressure of oxygen in, 387 AHFS Drug Information, 47 304 Acute myocardial infarction (AMI), 152 Alanine aminotransferase (ALT) arterial pH in, 304 Acute pancreatitis, 352 as category of liver function tests, 330, serum lactate in, 305 Acute pharyngitis, 479 330 terminology in, 303 Acute phase reactants (proteins) omega-3 fatty acids and, 187 venous oxygen saturation in, 305 defined, 373 in pediatric patients, 565 venous total carbon dioxide (serum infection and, 484–485 Quickview Chart on, 366 bicarbonate) in, 305 in rheumatic diseases reference range for, in traditional and SI Acid-base disorders juvenile idiopathic arthritis, 507 units, 636 classifications for, 307 overview, 500–501 statins and, 186 Note: Page numbers in italics indicate a figure; page numbers in boldface indicate a list, a Quickview Chart, or a table. Unauthenticated | Downloaded 09/30/21 04:04 PM UTC 640 BASIC SKILLS IN INTERPRETING LABORATORY DATA Albumin American College of Cardiology/ Androgen deficiency in aging males as category of liver function tests, 330, American Heart Association (ACC/ (ADAM), 594–595, 595 330 AHA) Androgen Deficiency in Aging Males liver function testing and, 331 Guideline on Treatment of Blood (ADAM) questionnaire, 596 Quickview Chart on, 362 Cholesterol, 179, 182 Andropause, 594–595, 595 reference range for, in traditional and SI Guidelines for Assessment Androstenedione, 593 units, 636 of Cardiovascular Risk in Anelloviridae, 456 Asymptomatic Adults, 185 serum, in pediatric patients, 564–565 Anemia(s) guidelines for C-reactive protein in urinalysis, 250 measurement, 501 acute blood loss, 374, 379 Albumin-bound testosterone, 594, 598 lipid guidelines, 208 aplastic, 387 Albuminuria, 250 American College of Chest Physicians causes of, 57, 373 Alcohol Evidence-Based Clinical Practice of chronic disease, 374, 379, 381 driving under influence of, 70 Guidelines, 400, 404, 405, 411 drug-induced hemolytic, 380, 380 HDL and, 179 American Society of Health-System erythrocyte morphology for differential Aldosterone Pharmacists, AHFS Drug Information, diagnosis of, 373, 374 47 potassium and effects of, 263, 269, 270, glucose-6-phosphate dehydrogenase, 272 American Urological Association System 11, 380 Index (AUA-SI), 603–604 sodium and effects of, 264–265 hemolytic, 374, 379–380 Amikacin, 99 Alkalemia, 303 hereditary, 11 Amino acid chains, 493–494, 494 Alkaline phosphatase (ALP) with increased MCV (minicase), 375 Aminoglycosides, 112–113 as category of liver function tests, 330, 330 iron deficiency and, 377–379 Aminophylline, 106–107 evaluation of elevated concentrations iron stores and (minicase), 378 of, 334, 334 Aminotransferases, 330, 338–339 laboratory assessment of, 373–381 liver function and, 334 Amiodarone, 118 low platelet count and (minicase), 379 nonhepatic causes of elevated, 334, 335 Amitriptyline, 122–123 lymphopenia and (minicase), 386 in pediatric patients, 565 Ammonia macrocytic, 373, 375–377 Quickview Chart on, 364 hepatic encephalopathy and, 339–340 macrocytic, megaloblastic, 376 reference range for, in traditional and SI Quickview Chart on, 368 microcytic, 377–379 units, 636 reference range for, in traditional and SI myeloblast crisis (minicase), 382 Alkaline picrate assay, 240 units, 636 myelodysplastic, 387 Alkalosis. See also Metabolic alkalosis Ammonium sulfate precipitation assay, 599 normochromic, normocytic, 379–381 defined, 303 AmpC beta-lactamases, 436 overview of, 373 respiratory, 311, 311 Amperometry, 200 in pediatric patients, 567 ALK inhibitor, 141–142 Amphetamine pernicious, 376 Alpha-fetoprotein (AFP), 518, 523, 535 Quickview Chart on urine drug screen physiologic, of infancy, 568 for, 88 Alpha-glucosidase inhibitors, 224 rheumatologic diseases and, 503 reliability of drug screening (minicase), Altered serum binding, 104–106 juvenile idiopathic arthritis, 507 72 Altitude, laboratory test results and, 12 rheumatoid arthritis, 506 Amphotericin B, 271 Amenorrhea systemic lupus erythematosus, 509 AmpliChip® microarray, 143 defined, 572 sickle cell, 11, 381 Amylase, pancreatitis and, 351–352 differential diagnosis of, 574 signs and symptoms of, 373 Amylin estrogen status and, 577 typical laboratory findings for types of, analog of, 226 functional, 573–574 374 effect of, on glucose concentrations, Angiocardiography, 165 hyperandrogenism and, 576–577 193–194 Angiotensin II, 264 hyperprolactinemia and, 573 levels of, 195–196 Angiotensinogen, 264 hypothyroidism and, 573, 574 Anaerobic bacteria, susceptibility testing ovarian failure and, 574–576 of, 438–439 Angiotension-converting enzyme (ACE) inhibitors, 209 physical examination findings Analgesic/anti-inflammatory drugs, 244. associated with, 572–573, 573 See also Acetaminophen Angiotension receptor blockers (ARBs), 209 polycystic ovary syndrome and, 576, Analytes, 3–4, 52 Anion gap, 305 576, 577 Analytical reliability, 144 Anion gap acidosis, 308, 309 primary and secondary, 572 Analytic specificity (interference), 56. See symptoms associated with, 572, 572 also Drug interferences Anisocytosis, 371, 372 uterine outflow obstruction and, 573 Anaplastic lymphoma kinase (ALK), 519, Anterior pituitary dysfunction, 573 American Association of Clinical 526, 543 Antiasthmatics Endocrinologists (AACE), guideline on Anaplastic lymphoma kinase (ALK) caffeine as, 107 LDL, 182 inhibitor, 141–142 theophylline as, 99 Note: Page numbers in italics indicate a figure; page numbers in boldface indicate a list, a Quickview Chart, or a table. Unauthenticated | Downloaded 09/30/21 04:04 PM UTC INDEX 641 Antibiotic concentration gradient pregabalin as, 112 Antineutrophil cytoplasmic antibodies, methods, 433–434, 434 tiagabine as, 112 498–499, 499 Antibiotics topiramate as, 112 Antinuclear antibodies (ANAs) detecting presence of resistance unbound serum concentrations and characteristics of, 496 mechanisms, 435–439 (minicase), 105 defined, 495 direct measure of activity, 429–435 valproic acid as, 110–111 in juvenile idiopathic arthritis, 507 interaction between sulfonylureas and zonisamide as, 112 in rheumatoid arthritis, 505 sulfa-type, 208 Antifungals in systemic lupus erythematosis, 507 pseudomembranous colitis induced by azole, 115–116 tests for (minicase), 357 data to aid interpretation of, 100 algorithm, 497 tests for bactericidal activity of, 434–435 flucytosine as, 115 overview, 495, 497–498 Antibiotic therapy Antifungal susceptibility testing, qualitative results, 498 empiric, 441 454, 455 quantitative results, 497–498 hospital-acquired pneumonia and Antigen
Recommended publications
  • Point-Of-Care Testing for Anticoagulation Monitoring In
    Point-of-Care Testing for Anticoagulation PATIENT SAFETY Monitoring in Neuroendovascular Procedures H.M. Hussein SUMMARY: POC testing is defined as diagnostic testing at or near the site of patient care. Rapid A.L. Georgiadis measurement of the intensity of anticoagulation and, more recently, platelet inhibition allows dose titration of adjuvant medications such a heparin and antiplatelet agents during neuroendovascular A.I. Qureshi procedures. However, knowledge among practicing physicians regarding the pathophysiologic basis of these measurements and variations in knowledge about the differences among devices is often limited. This review discusses the role of anticoagulation in endovascular procedures and the currently available POC tests for anticoagulation monitoring. ABBREVIATIONS: ACT ϭ activated clotting time; Anti-Xa ϭ quantitative chromogenic heparin assay; aPTT ϭ activated partial thromboplastin time; AT ϭ antithrombin; CI ϭ confidence interval; GP IIb/IIIa ϭ glycoprotein IIb/IIIa; Hemonox-CT ϭ Hemonox clotting time; HIT ϭ heparin-induced thrombocytopenia; HMT ϭ Heparin Management Test; IV ϭ intravenous; LMWH ϭ low-molecular- weight heparin; MI ϭ myocardial infarction; OR ϭ odds ratio; PCI ϭ percutaneous coronary intervention; POC ϭ point of care; UFH ϭ unfractionated heparin hromboembolism ensues from activation of platelets and Brief Overview of Anticoagulant Medications Tthe coagulation cascade and is a major source of compli- Anticoagulants reduce the activity of proteases in the coagula- cations during endovascular procedures. Multiple studies tion cascade. On the basis of their mechanism of action (Fig 1), have demonstrated accelerated platelet activation during cor- anticoagulants can be divided into 4 major groups: vitamin K onary and cerebral angioplasty.1,2 The coagulation cascade antagonists (warfarin), heparins (UFH and LMWH), direct (Fig 1) consists of a sequential conversion of a series of proen- thrombin inhibitors, and direct factor Xa inhibitors.
    [Show full text]
  • Syllabus: Page 23
    The University of Texas at El Paso College of Health Sciences Clinical Laboratory Science Program CLSC 3364 Hematology II Course Outline Spring What do you see? What is in your Head? Video or audio recordings will not be permitted. Instructor M. Lorraine Torres, Ed. D, MT (ASCP) College of Health Sciences Room 423 Phone: 747-7282 E-Mail: [email protected] Office Hours TR 3:00 – 4:00 p.m., Friday 2 – 3 p.m. or by appointment Class Schedule Monday and Wednesday 11:00 – 12:30 A.M. HSCI 135 Course Description This course is a sequel to Hematology I. It will include but is not limited to the study of the white blood cells with emphasis on white cell formation and function and the etiology and treatment of white blood cell disorders. This course will also encompass an introduction to hemostasis and laboratory determination of hemostatic disorders. Prerequisite; CLSC 3356 & CLSC 3257. Topical Outline 1. Maturation series and biology of white blood cells 2. Disorders of neutrophils 3. Reactive lymphocytes and Infectious Mononucleosis 4. Acute and chronic leukemias 5. Myelodysplastic syndromes 6. Myeloproliferative disorders 7. Multiple Myeloma and related plasma cell disorders 8. Lymphomas 9. Lipid (lysosomal) storage diseased and histiosytosis 10. Hemostatic mechanisms, platelet biology 11. Coagulation pathways 12. Quantitative and qualitative vascular and platelet disorders (congenital and acquired) 13. Disorders of plasma clotting factors 14. Interaction of the fibrinolytic, coagulation and kinin systems 15. Laboratory methods REQUIRED TEXTBOOKS: same books used for Hematology I Keohane, E.M., Smith, L.J. and Walenga, J.M. 2016. Rodak’s Hematology: Clinical Principles and applications.
    [Show full text]
  • The Role of the Laboratory in Treatment with New Oral Anticoagulants
    Journal of Thrombosis and Haemostasis, 11 (Suppl. 1): 122–128 DOI: 10.1111/jth.12227 INVITED REVIEW The role of the laboratory in treatment with new oral anticoagulants T. BAGLIN Department of Haematology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Trust, Cambridge, UK To cite this article: Baglin T. The role of the laboratory in treatment with new oral anticoagulants. J Thromb Haemost 2013; 11 (Suppl. 1): 122–8. tion of thromboembolism in patients with atrial fibrilla- Summary. Orally active small molecules that selectively tion. For some patients, these drugs offer substantial and specifically inhibit coagulation serine proteases have benefits over oral vitamin K antagonists (VKAs). For the been developed for clinical use. Dabigatran etexilate, majority of patients, these drugs are prescribed at fixed rivaroxaban and apixaban are given at fixed doses and doses without the need for monitoring or dose adjustment. do not require monitoring. In most circumstances, these There are no food interactions and very limited drug inter- drugs have predictable bioavailability, pharmacokinetic actions. The rapid onset of anticoagulation and short half- effects, and pharmacodynamic effects. However, there life make the initiation and interruption of anticoagulant will be clinical circumstances when assessment of the therapy considerably easier than with VKAs. As with all anticoagulant effect of these drugs will be required. The anticoagulants produced so far, there is a correlation effect of these drugs on laboratory tests has been deter- between intensity of anticoagulation and bleeding. Conse- mined in vitro by spiking normal samples with a known quently, the need to consider the balance of benefit and risk concentration of active compound, or ex vivo by using in each individual patient is no less important than with plasma samples from volunteers and patients.
    [Show full text]
  • Approach to Coagulopathy in the Icu Dic and Thrombotic Emergencies
    APPROACH TO COAGULOPATHY IN THE ICU DIC AND THROMBOTIC EMERGENCIES NEIL KUMAR, MD UNIVERSITY OF ROCHESTER MEDICAL CENTER Disclosures u I have no financial disclosures u I am NOT A HEMATOLOGIST Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies Coagulation u Coagulation is the process in which blood clots u Fibrinolysis is the process in which clot dissolves u Hemostasis is the stopping of bleeding or hemorrhage. u Ideally, hemostasis is a balance between coagulation and fibrinolysis Coagulation (classic pathways) Michael G. Crooks Simon P. Hart Eur Respir Rev 2015;24:392-399 Coagulation (another view) Gando, S. et al. (2016) Disseminated intravascular coagulation Nat. Rev. Dis. Primers doi:10.1038/nrdp.2016.37 Coagulation (yet another view) u Inflammation and coagulation intersect with platelets in the middle u An example of this is Disseminated Intravascular Coagulation. Gando, S. et al. (2016) Disseminated intravascular coagulation Nat. Rev. Dis. Primers doi:10.1038/nrdp.2016.37 Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies PT / INR u Prothrombin Time u Test of Extrinsic Pathway u Take plasma (blood without cells) and re-add calcium u Calcium was removed with citrate in tube u Add tissue factor u See how long it takes to clot and normalize PT to get INR Coagulation (classic pathways) Michael G.
    [Show full text]
  • Essential Trace Elements in Human Health: a Physician's View
    Margarita G. Skalnaya, Anatoly V. Skalny ESSENTIAL TRACE ELEMENTS IN HUMAN HEALTH: A PHYSICIAN'S VIEW Reviewers: Philippe Collery, M.D., Ph.D. Ivan V. Radysh, M.D., Ph.D., D.Sc. Tomsk Publishing House of Tomsk State University 2018 2 Essential trace elements in human health UDK 612:577.1 LBC 52.57 S66 Skalnaya Margarita G., Skalny Anatoly V. S66 Essential trace elements in human health: a physician's view. – Tomsk : Publishing House of Tomsk State University, 2018. – 224 p. ISBN 978-5-94621-683-8 Disturbances in trace element homeostasis may result in the development of pathologic states and diseases. The most characteristic patterns of a modern human being are deficiency of essential and excess of toxic trace elements. Such a deficiency frequently occurs due to insufficient trace element content in diets or increased requirements of an organism. All these changes of trace element homeostasis form an individual trace element portrait of a person. Consequently, impaired balance of every trace element should be analyzed in the view of other patterns of trace element portrait. Only personalized approach to diagnosis can meet these requirements and result in successful treatment. Effective management and timely diagnosis of trace element deficiency and toxicity may occur only in the case of adequate assessment of trace element status of every individual based on recent data on trace element metabolism. Therefore, the most recent basic data on participation of essential trace elements in physiological processes, metabolism, routes and volumes of entering to the body, relation to various diseases, medical applications with a special focus on iron (Fe), copper (Cu), manganese (Mn), zinc (Zn), selenium (Se), iodine (I), cobalt (Co), chromium, and molybdenum (Mo) are reviewed.
    [Show full text]
  • Anticoagulation of Children Undergoing Cardiopulmonary Bypass Is Overestimated by Current Monitoring Techniques
    PAPER Anticoagulation of Children Undergoing Cardiopulmonary Bypass Is Overestimated by Current Monitoring Techniques John T. Owings, MD; Marc E. Pollock, MD; Robert C. Gosselin, MT; Kevin Ireland, RN, CCP; Jonathan S. Jahr, MD; Edward C. Larkin, MD Hypothesis: Children who undergo cardiopulmonary reserve, fibrinogen; the natural antithrombotic, anti- bypass (CPB) are proportionally more hemodiluted than thrombin; and heparin concentration. adults who undergo CPB. Current methods of monitor- ing high-dose heparin sulfate anticoagulation are depen- Results: Ten children and 10 adults completed the study. dent on fibrinogen level. Because of the decreased fi- Children had lower fibrinogen levels than adults through- brinogen levels in children, current methods of monitoring out CPB (P,.05). All adults had both therapeutic ACT and heparin anticoagulation overestimate their level of anti- Heparin Management Test levels measured throughout coagulation. CPB. Although children had therapeutic ACT levels, their Heparin Management Test levels were subtherapeutic while Design: Prospective controlled trial. undergoing CPB. The children had significantly higher thrombin-antithrombin complexes and prothrombin Main Outcome Measure: Production of thrombin (ad- fragment F1.2 than adults, indicating ongoing thrombin equacy of anticoagulation). production (P,.01). The increases in thrombin- antithrombin complexes and prothrombin fragment F1.2 Methods: Children and adults undergoing cardiac sur- in children were inversely proportional to their weight. gery who received CPB were anticoagulated in the stan- dard fashion as directed by activated clotting time Conclusions: Children undergoing CPB with heparin (ACT) results. Each subject had blood sampled at base- dosing adjusted to optimize the ACT manifest inad- line; heparinization; start of the CPB; CPB at 30, 60, equate anticoagulation (ongoing thrombin formation).
    [Show full text]
  • Chromium, Vanadium and Ascorbate Effects on Lipids, Cortisol
    CHROMIUM, VANADIUM AND ASCORBATE EFFECTS ON LIPIDS, CORTISOL, GLUCOSE AND TISSUE ASCORBATE OF GUINEA PIGS by WOLE KOLA OLADUT, B.S., M.S. A DISSERTATION IN HOME ECONOMICS Submitted to the Graduate Faculty of Texas Tech University in Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY Approved áxigust. tq^ 11;^ ACKNOWLEDGMENTS - <"-^ f/K^ 1 would like to express my sincere gratitude and respect to Dr. Barbara J. Stoecker for her patience, encouragment and direction throughout my graduate program and research project. I am also grateful to other members of my committee, Professors Elizabeth Fox, Donald Oberleas, Marvin Shetlar and Shiang P. Yang. My appreciation is extended to my colleagues, Dr. Reza Zolfaghari for his technical advice, Ms. Gay Riggan, my typist and my coworkers at Methodist Hospital Laboratory. Special thanks are extended to my mother, Mrs. Comfort Oladutemu, my brother, Jide Oladutemu, Dr. Bayode Lasekan and all other family members and friends for their love, help and encouragement during the completion of my graduate education. 11 CONTENTS Page ACKNOWLEDGMENTS il LIST OF TABLES v LIST OF FIGURES viii LIST OF ABBREVIATIONS Ix I. INTRODUCTION 1 II. REVIEW OF LITERATURE 4 Ascorbate and Carbohydrate Metabolism 4 Ascorbate and Lipid Metabolism 6 Chromium and Carbohydrate Metabolism 12 Chromium and Lipid Metabolism 15 Vanadium and Carbohydrate Metabolism 19 Vanadium and Lipid Metabolism 20 Cholesterol-fed Guinea Pigs 22 Conclusion 27 III. ADRENAL ASCORBATE AND CORTISOL CONCENTRATIONS OF GUINEA PIGS SUPPLEMENTED WITH CHROMIUM AND/OR VANADIUM .... 29 Abstract 29 Introduction 30 Materials and Methods 32 Results and Discussion 36 IV.
    [Show full text]
  • Vitamins and Minerals for the Gastroenterologist
    VitaminsVitamins andand MineralsMinerals forfor thethe GastroenterologistGastroenterologist AmyAmy Tiu,Tiu, MDMD Feb.Feb. 9,9, 20062006 7:00AM7:00AM conferenceconference ObjectivesObjectives DescriptionDescription fatfat--solublesoluble andand waterwater solublesoluble vitaminsvitamins TraceTrace mineralsminerals (zinc,(zinc, selenium,selenium, iodide,iodide, copper,copper, chromium)chromium) DeficiencyDeficiency andand ToxicityToxicity SourcesSources andand RecommendationsRecommendations ClinicalClinical implicationimplication HistoryHistory 18351835 BritishBritish ParliamentParliament passedpassed thethe MerchantMerchant SeamanSeaman’’ss ActAct thatthat requiredrequired lemonlemon juicejuice toto bebe includedincluded inin thethe rationsrations ofof sailorssailors toto preventprevent scurvyscurvy 19121912 CasimirCasimir FunkFunk coinedcoined thethe termterm vitaminevitamine DailyDaily ValuesValues (DV(DV waswas RDA)RDA) establishedestablished byby thethe NationalNational AcademyAcademy ofof SciencesSciences andand NationalNational ResearchResearch CouncilCouncil asas thethe amountamount toto preventprevent grossgross deficiencydeficiency syndromessyndromes WhichWhich foodfood hashas thethe mostmost vitaminvitamin A?A? Sweet potatoes Beef liver Cantoloupe 1 RE = 10 IU MVI = 3500 IU TPN = 3300 IU VitaminVitamin AA Prevents xerophthalmia (abnormalities in corneal and conjunctival development) Phototransduction Cellular differentiation and integrity of the eye Ancient Egyptians used liver to treat night blindness VitaminVitamin AA
    [Show full text]
  • Vitamin and Minerals and Neurologic Disease
    Vitamin and Minerals and Neurologic Disease Steven L. Lewis, MD World Congress of Neurology October 2019 Dubai, UAE [email protected] Disclosures . Dr. Lewis has received personal compensation from the American Academy of Neurology for serving as Editor-in-Chief of Continuum: Lifelong Learning in Neurology and for activities related to his role as a director of the American Board of Psychiatry and Neurology, and has received royalty payments from the publishers Wolters Kluwer and Wiley-Blackwell for book authorship. He has no disclosures related to the content or topic of this talk. Objective . Discuss the association of trace mineral deficiencies and vitamin deficiencies (and excess) with neuropathy and myeloneuropathy and other peripheral neurologic syndromes Outline of Presentation . List minerals relevant to neuropathy or myeloneuropathy . Proceed through each mineral and its associated clinical syndrome . List vitamins relevant to neuropathy or myeloneuropathy . Proceed through each vitamin and its associated clinical syndrome Minerals . Naturally occurring nonorganic homogeneous substances . Elements . Required for optimal metabolic and structural processes . Both cations and anions . Essential trace minerals: must be supplied in the diet . Some have recommended daily allowances (RDA) Macrominerals . Sodium . Potassium . Calcium . Magnesium . Phosphorus . Sulfur Macrominerals . Sodium . Potassium . Calcium . Magnesium . Phosphorus . Sulfur Trace Minerals . Chromium . Cobalt . Copper . Iodine . Iron . Manganese . Molybdenum . Selenium . Zinc Trace Minerals . Chromium . Cobalt . Copper . Iodine . Iron . Manganese . Molybdenum . Selenium . Zinc Generalized dose-reponse curve for an essential nutrient Howd and Fan, 2007 Copper . Essential trace element . Human body contains approximately 100 mg Cu . Cofactor of many redox enzymes . Ceruloplasmin most abundant of the cuproenzymes . Involved in antioxidant defense, neuropeptide and blood cell synthesis, and immune function1 1 Bost, J Trace Elements 2016 Copper Deficiency .
    [Show full text]
  • P R O G R a M Guide
    2015 PROGRAM GUIDE APPROVED BY CLIA, COLA, JCAHO ACCEPTED BY THE COLLEGE OF AMERICAN PATHOLOGISTS 2015 Program Guide Cover - 14831PTS.indd 3 12/18/14 2:18 PM GENERAL TABLE OF CONTENTS 2015 Schedule…......................…………………………………………………………….…………….....................................................................................3 General Instructions……………………………………………………………………………….............................................................................................4-7 Online Reporting Instructions………………………………………………………………………………...............................................................................7-8 Reporting Form Instructions......................................................................................................................................................................9 Chemistry............................................................................................................................................................................................10-20 Specialty Programs…………………………………………………………………………..…………………………………………………………..………………………………19-20 Clinical Microscopy & Urinalysis.........................................................................................................................................................20-21 Coagulation.........................................................................................................................................................................................21-24 General Hematology Instructions............................................................................................................................................................24
    [Show full text]
  • Nutrition Journal of Parenteral and Enteral
    Journal of Parenteral and Enteral Nutrition http://pen.sagepub.com/ Micronutrient Supplementation in Adult Nutrition Therapy: Practical Considerations Krishnan Sriram and Vassyl A. Lonchyna JPEN J Parenter Enteral Nutr 2009 33: 548 originally published online 19 May 2009 DOI: 10.1177/0148607108328470 The online version of this article can be found at: http://pen.sagepub.com/content/33/5/548 Published by: http://www.sagepublications.com On behalf of: The American Society for Parenteral & Enteral Nutrition Additional services and information for Journal of Parenteral and Enteral Nutrition can be found at: Email Alerts: http://pen.sagepub.com/cgi/alerts Subscriptions: http://pen.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav >> Version of Record - Aug 27, 2009 OnlineFirst Version of Record - May 19, 2009 What is This? Downloaded from pen.sagepub.com by Karrie Derenski on April 1, 2013 Review Journal of Parenteral and Enteral Nutrition Volume 33 Number 5 September/October 2009 548-562 Micronutrient Supplementation in © 2009 American Society for Parenteral and Enteral Nutrition 10.1177/0148607108328470 Adult Nutrition Therapy: http://jpen.sagepub.com hosted at Practical Considerations http://online.sagepub.com Krishnan Sriram, MD, FRCS(C) FACS1; and Vassyl A. Lonchyna, MD, FACS2 Financial disclosure: none declared. Preexisting micronutrient (vitamins and trace elements) defi- for selenium (Se) and zinc (Zn). In practice, a multivitamin ciencies are often present in hospitalized patients. Deficiencies preparation and a multiple trace element admixture (containing occur due to inadequate or inappropriate administration, Zn, Se, copper, chromium, and manganese) are added to par- increased or altered requirements, and increased losses, affect- enteral nutrition formulations.
    [Show full text]
  • Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants
    biomedicines Review Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants Osamu Kumano 1,2,* , Kohei Akatsuchi 3 and Jean Amiral 1 1 Research Department, HYPHEN BioMed, 155 Rue d’Eragny, 95000 Neuville sur Oise, France; [email protected] 2 Protein Technology, Engineering 1, Sysmex Corporation, Kobe 651-2271, Japan 3 R&D Division, Sysmex R&D Center Americas, Inc., Mundelein, IL 60060, USA; [email protected] * Correspondence: [email protected]; Tel.: +81-78-991-2203 Abstract: Anticoagulant drugs have been used to prevent and treat thrombosis. However, they are associated with risk of hemorrhage. Therefore, prior to their clinical use, it is important to assess the risk of bleeding and thrombosis. In case of older anticoagulant drugs like heparin and warfarin, dose adjustment is required owing to narrow therapeutic ranges. The established monitoring methods for heparin and warfarin are activated partial thromboplastin time (APTT)/anti-Xa assay and pro- thrombin time – international normalized ratio (PT-INR), respectively. Since 2008, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), have been widely prescribed to prevent and treat several thromboembolic diseases. Although the use of DOACs without routine monitoring and frequent dose adjustment has been shown to be safe and effective, there may be clinical circumstances in specific patients when measurement of the anticoagulant effects of DOACs Citation: Kumano, O.; Akatsuchi, K.; is required. Recently, anticoagulation therapy has received attention when treating patients with Amiral, J. Updates on Anticoagulation coronavirus disease 2019 (COVID-19). In this review, we discuss the mechanisms of anticoagulant and Laboratory Tools for Therapy drugs—heparin, warfarin, and DOACs and describe the methods used for the measurement of Monitoring of Heparin, Vitamin K their effects.
    [Show full text]