DOCSLIB.ORG

The Basics of Pharmacology

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Basics of Pharmacology THE BASICS OF PHARMACOLOGY An Overview Jassin M. Jouria, MD Dr. Jassin M. Jouria is a practicing Emergency Medicine physician, professor of academic medicine, and medical author. He graduated from Ross University School of Medicine and has completed his clinical clerkship training in various teaching hospitals throughout New York, including King’s County Hospital Center and Brookdale Medical Center, among others. Dr. Jouria has passed all USMLE medical board exams, and has served as a test prep tutor and instructor for Kaplan. He has developed several medical courses and curricula for a variety of educational institutions. Dr. Jouria has also served on multiple levels in the academic field including faculty member and Department Chair. Dr. Jouria continues to serve as a Subject Matter Expert for several continuing education organizations covering multiple basic medical sciences. He has also developed several continuing medical education courses covering various topics in clinical medicine. Recently, Dr. Jouria has been contracted by the University of Miami/Jackson Memorial Hospital’s Department of Surgery to develop an e- module training series for trauma patient management. Dr. Jouria is currently authoring an academic textbook on Human Anatomy & Physiology. ABSTRACT The science of pharmacology and the responsibility relationship building with patients are important elements of a health professional’s clinical knowledge and skills to provide safe and appropriate pharmacotherapeutic regimens in everyday practice. Interdisciplinary members of the health team are required to continually interpret specific patient health data to implement and evaluate outcomes of medication treatment. All health clinicians are increasingly relying on practice guidelines and the applied specialized training of health team members when obtaining the patient health history 1 nursece4less.com nursece4less.com nursece4less.com nursece4less.com to improve therapeutic medication regimens, avoid adverse effects, and to safely and effectively treat a disease state. Policy Statement This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities. Continuing Education Credit Designation This educational activity is credited for 3 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity. Pharmacology content is 3 hours. Statement of Learning Need Online pharmacology continuous learning has become a highly satisfying method for interdisciplinary health clinicians to increase and maintain proficiency in medication prescribing and administration. Pharmacotherapy education tailored to enhance clinical knowledge in the treatment of specific disease states are expected to lead to improved collaborative practice among health professionals and patient care outcomes. Course Purpose 2 nursece4less.com nursece4less.com nursece4less.com nursece4less.com To improve knowledge for health clinicians at all levels of experience in basic pharmacology of medication prescribing, administration and monitoring of medication treatment outcomes. Target Audience Advanced Practice Registered Nurses and Registered Nurses (Interdisciplinary Health Team Members, including Vocational Nurses and Medical Assistants may obtain a Certificate of Completion) Course Author & Planning Team Conflict of Interest Disclosures Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA Susan DePasquale, MSN, FPMHNP-BC - all have no disclosures Acknowledgement of Commercial Support There is no commercial support for this course. Please take time to complete a self-assessment of knowledge, on 3 nursece4less.com nursece4less.com nursece4less.com nursece4less.com page 4, sample questions before reading the article. Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course. 1. The process of drug absorption, distribution in the body, metabolism and excretion is called a. pharmacodynamics. b. pharmacokinetics. c. therapeutic pharmacology. d. pharmacogenomics. 2. The relationship determined by a drugs concentration and time at the preferred action site, along with the drug's effects, both therapeutic and adverse, are referred to as a. pharmacodynamics. b. pharmacokinetics. c. therapeutic pharmacology. d. pharmacogenomics. 3. The deciding factor in choosing which medication may be a more effective treatment for a patient is the drug with an EC50 that has a. a higher EC50. b. a lower EC50. c. the EC50 has no impact on this type of decision. d. the EC50 is the same for both drugs. 4. Therapeutic levels of a drug a. are best monitored with tissue samples. b. cannot cause toxicity. c. are not altered by diversity of medical conditions. d. give the best medication therapy with minimized side effects. 5. If normal dose of a medication is 10 milligrams/kilogram (10 mg/kg), an individual weighing 110 pounds (50 kilograms) would be given _______ mg. a. 50 4 nursece4less.com nursece4less.com nursece4less.com nursece4less.com b. 250 c. 500 d. 1000 Introduction There are two distinct sets of responsibilities that health clinicians must fulfill relative to pharmacology. One is a social responsibility to engage and inform patients of their medication and the second is a scientific responsibility that involves understanding the benefits and risks of medication. Drug prescribing and administration falls squarely at the intersection of these two responsibilities. Not only do all health clinicians need to understand the scientific elements of pharmacology but the social component, as well. Clinicians need to build relationships in order to glean important information from their patients and to educate both patients and their families. This first part of a 3-part series on pharmacology will provide basic definitions and discussion on pharmacokinetics and pharmacodynamics to prepare clinicians in a medical and therapeutic milieu where medication selection and ongoing treatment becomes indicated. Advancements In Medication Treatments The field of pharmacology is the most vital and extensively researched field of the medical sciences. There now exists a seemingly unlimited variety of medications. The rapid advancement in medication has brought forward new cures, therapies and treatments for diseases and medical conditions that previously were incurable. These advancements in pharmacology involve the study of drug actions on living organisms. Health clinicians need to be aware 5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com of both the widely used pharmaceuticals as well as any advancements in the current research and new medications that may influence medical treatment. A medication suitable for one patient might not necessarily be suitable to another even if that patient is exhibiting a similar condition. The information that clinicians obtain from their patients is critical to avoid drug-drug interactions and drug-food interactions, allergic reactions, and other adverse effects. Without a strong background in the scientific elements of pharmacokinetics and pharmacodynamics1, this information is not as useful. The study of drugs and their mechanisms of action (MOAs) should not be neglected in clinical practice. A comprehensive understanding regarding drug usage and precautionary measures that need to be considered while giving patients different drugs is required so that drug benefits can be maximized and harmful side effects minimized.2 The science of pharmacology has existed for millennia. The application and usage of pharmacologic products to relieve adverse conditions and suffering has been accepted practice in almost every country throughout the world. Modern trends and advancement in medical science have greatly enhanced pharmacology.2,3 Drugs have historically been a fundamental component of the treatment of various diseases from the earliest existence of humankind, where various materials found in nature were used, such as from tree bark, roots, herbs, animal parts, plant seeds, etc. The MOA was unknown and, as such, usages of these substances were based solely on the observed therapeutic benefits or the lack thereof. With the passage of time, through trial and error, knowledge was developed to distinguish between harmful and beneficial substances to be used as medication. 6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com Modern pharmacology started in the mid 19th century through scientific study of the chemical separation of particular active agents from their complicated and complex mixtures, often plant extracts. It began with scientists predicting the impacts of the medicine on the human patient. This developed into further investigations of the effects of specific agents on isolated organs; an example among many of this development in modern pharmacology is the studied effect of ergometrine on strips of uterine muscle. The origin of experimental pharmacology is usually linked with the work of the French physiologist, Francois Magendie, at the start of the 19th century. Magendie’s research was based on strychnine-containing plants that clearly established the action site of these substances. The sites of action were
Load more

Recommended publications
  • Principle of Pharmacodynamics
    Principle of pharmacodynamics Dr. M. Emamghoreishi Full Professor Department of Pharmacology Medical School Shiraz University of Medical Sciences Email:[email protected] Reference: Basic & Clinical Pharmacology: Bertrum G. Katzung and Anthony J. Treveror, 13th edition, 2015, chapter 20, p. 336-351 Learning Objectives: At the end of sessions, students should be able to: 1. Define pharmacology and explain its importance for a clinician. 2. Define ―drug receptor‖. 3. Explain the nature of drug receptors. 4. Describe other sites of drug actions. 5. Explain the drug-receptor interaction. 6. Define the terms ―affinity‖, ―intrinsic activity‖ and ―Kd‖. 7. Explain the terms ―agonist‖ and ―antagonist‖ and their different types. 8. Explain chemical and physiological antagonists. 9. Explain the differences in drug responsiveness. 10. Explain tolerance, tachyphylaxis, and overshoot. 11. Define different dose-response curves. 12. Explain the information that can be obtained from a graded dose-response curve. 13. Describe the potency and efficacy of drugs. 14. Explain shift of dose-response curves in the presence of competitive and irreversible antagonists and its importance in clinical application of antagonists. 15. Explain the information that can be obtained from a quantal dose-response curve. 16. Define the terms ED50, TD50, LD50, therapeutic index and certain safety factor. What is Pharmacology?It is defined as the study of drugs (substances used to prevent, diagnose, and treat disease). Pharmacology is the science that deals with the interactions betweena drug and the bodyor living systems. The interactions between a drug and the body are conveniently divided into two classes. The actions of the drug on the body are termed pharmacodynamicprocesses.These properties determine the group in which the drug is classified, and they play the major role in deciding whether that group is appropriate therapy for a particular symptom or disease.
    [Show full text]
  • Prof. Hanan Hagar Quantitative Aspects of Drugs
    Quantitative aspects of drugs Prof. hanan Hagar Ilos Determine quantitative aspects of drug receptor binding. Recognize concentration binding curves. Identify dose response curves and the therapeutic utility of these curves. Classify different types of antagonism QUANTIFY ASPECTS OF DRUG ACTION Bind Initiate Occupy Activate D + R D R DR* RESPONSE[R] Relate concentration [C] of D used (x- axis) Relate concentration [C] of D used (x- to the binding capacity at receptors (y-axis) axis) to response produced (y-axis) Concentration-Binding Curve Dose Response Curves AFFINITY EFFICACY POTENCY Concentration binding curves Is a correlation between drug concentration [C] used (x- axis) and drug binding capacity at receptors [B] (y-axis). i.e. relation between concentration & drug binding Concentration-Binding curves are used to determine: oBmax (the binding capacity) is the total density of receptors in the tissues. oKD50 is the concentration of drug required to occupy 50% of receptors at equilibrium. oThe affinity of drug for receptor The higher the affinity of D for receptor the lower is the KD i.e. inverse relation Concentration-Binding Curve (Bmax): Total density of receptors in the tissue K D KD (kD )= [C] of D required to occupy 50% of receptors at equilibrium Dose -response curves o Used to study how response varies with the concentration or dose. o Is a correlation between drug concentration [D] used (x- axis) and drug response [R] (y-axis). o i.e. relation between concentration & Response TYPES of Dose -response curves Graded dose-response curve Quantal dose-response curve (all or none). Graded Dose-response Curve o Response is gradual o Gradual increase in response by increasing the dose (continuous response).
    [Show full text]
  • Factors Affecting Drug Response2
    Types of drug concentration– response relationship A. Graded drug concentration-Response Relationships As the dose of a drug is increased, the response (effect) of the tissue or organ is also increased. The efficacy (Emax) and potency (ED50) parameters are derived from these data. 112 GRADED DOSE- RESPONSE CURVE QUANTAL DOSE- RESPONSE CURVE 113 B. Quantal or all or none dose response relation ship. The Plot of the fraction of the population that responds at each dose of the drug versus the log of the dose administered. responses follow all or none phenomenon – that means the individual of the responding system either respond to their maximum limit or not at all to a dose of drug and there is no gradation of response. population studies. relates dose to frequency of effect . The median effective (ED50), median toxic (TD50) ,and median lethal doses (LD50) are extracted from experiments carried out in this manner. 114 Median effective dose (ED50):the dose at which 50% of individuals exhibit the specified quantal effect. Median toxic dose (TD50) :the dose required to produce a particular toxic effect in 50% of animals. Median lethal dose (LD50): is the lethal dose that causes death in 50% animal under experiment. 115 119 1. Excretion - Alteration of urine PH. e.g. Phanobarbitone + NaHCo3 - Alteration of active tubular secretion e.g. Probenecid + peincillin. II – Pharmcodynamic interaction - It occurs by modification of pharmacological response of one drug by another without altering the concentration of the drug in the tissue or tissue fluid. 1. Additive – Occurs when the combined effect of two drugs is equal to the sum of the effects of each agent given alone.
    [Show full text]
  • Pharmacokinetics of Pancreatic Polypeptide in Man
    Gut: first published as 10.1136/gut.19.10.907 on 1 October 1978. Downloaded from Gut, 1978, 19, 907-909 Pharmacokinetics of pancreatic polypeptide in man T. E. ADRIAN, G. R. GREENBERG, H. S. BESTERMAN, AND S. R. BLOOM From the Department ofMedicine, Royal Postgraduate Medical School, Hammersmith Hospital, London SUMMARY Pure bovine pancreatic polypeptide (PP) was infused into 23 healthy subjects at doses of 1, 3, and 5 pmol/kg/min over 60 minutes and plasma PP was measured by radioimmunoassay. During the infusions mean plasma levels of 203 + 34, 575 + 73, and 930 ± 48 pmol/l respectively were achieved. Mean disappearance half time on stopping the infusion was 6-9 + 0 3 min (mean + SEM). The metabolic clearance rate was 5-1 + 0-2 ml/kg/min (mean + SEM) and the apparent volume of distribution was calculated to be 51 ± 3 ml/kg (mean ± SEM). This study provides for the first time pharmacokinetic data for PP in man. Pancreatic polypeptide (PP) is a recently discovered syringe ram pump for a basal period of 30 minutes. hormonal 36 amino acid peptide localised in an BPP was then added to the infusion at nominal endocrine cell of the mammalian and avian pancreas doses of 1 (n = 6), 3 (n = 9), and 5 (n = 8) pmol/ (Kimmel et al., 1968; Lin and Chance, 1972). PP cir- kg/min. culates in plasma and levels rise substantially on the Blood samples were collected in chilled tubes with ingestion of a meal and remain raised for several 10 units heparin and 400 KIU aprotinin (Trasylol) hours (Adrian et al., 1976; Floyd et al., 1976; per ml, centrifuged, and the plasma frozen within 15 Schwartz et al., 1976).
    [Show full text]
  • PHARMACOLOGY the HISTORY of PHARMACOLOGY Prehistoric People Recognized the Beneficial Or Toxic Effects of Many Plant and Animal Materials
    Lecture 1_2 Dr.Labeeb PHARMACOLOGY THE HISTORY OF PHARMACOLOGY Prehistoric people recognized the beneficial or toxic effects of many plant and animal materials. Early written records from Iraq, China and from Egypt list remedies of many types, including a few still recognized as useful drugs today. Most, however, were worthless or actually harmful . In the 1500 years ago introduced rational methods into medicine, but none was successful owing to the dominance of systems of thought that purported to explain all of biology and disease without the need for experimentation and observation, This idea that disease was caused by excesses of bile or blood in the body, that wounds could be healed by applying a salve to the weapon that caused the wound, and so on. Around the end of the 17th century, reliance on observation and experimentation began to replace theorizing in medicine. As the value of these methods in the study of disease became clear, physicians began to apply them to the effects of traditional drugs used in their own practices. In the late 18th and early 19th centuries, began to develop the methods of experimental animal physiology and pharmacology. Advances in chemistry and the further development of physiology therapeutics only about 50 years ago it become possible to accurately evaluate therapeutic claims. Around the same time, a major expansion of research efforts in all areas of biology began. As new concepts and new techniques were introduced, information accumulated about drug action. Two general principles that the student should always remember are, first, that all substances can under certain circumstances be toxic; and second, that all dietary supplements and all therapies promoted as health-enhancing should meet the same standards of efficacy and safety,.
    [Show full text]
  • Estimation of Nizatidine Gastric Nitrosatability and Product Toxicity Via an Integrated Approach Combining HILIC, in Silico Toxicology, and Molecular Docking
    journal of food and drug analysis 27 (2019) 915e925 Available online at www.sciencedirect.com ScienceDirect journal homepage: www.jfda-online.com Original Article Estimation of nizatidine gastric nitrosatability and product toxicity via an integrated approach combining HILIC, in silico toxicology, and molecular docking * ** Rania El-Shaheny a,b, , Mohamed Radwan c,d,e, Koji Yamada f, , Mahmoud El-Maghrabey a,g a Department of Pharmaceutical Analytical Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt b Department of Hygienic Chemistry and Toxicology, Course of Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan c Department of Drug Discovery, Science Farm Ltd., 1-7-30 Kuhonji, Chuo-ku, Kumamoto 862-0976, Japan d Department of Bioorganic Medicinal Chemistry, Faculty of Life Sciences, Kumamoto University, 5e1 Oehonmachi, Chuo-ku, Kumamoto 862e0973, Japan e Chemistry of Natural Compounds Department, Pharmaceutical and Drug Industries Research Division, National Research Centre, Dokki 12622, Cairo, Egypt f Medical Plant Laboratory, Course of Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan g Department of Analytical Chemistry for Pharmaceuticals, Course of Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan article info abstract Article history: The liability of the H2-receptor antagonist nizatidine (NZ) to nitrosation in simulated Received 24 June 2019 gastric juice (SGJ) and under WHO-suggested conditions was investigated for the first time. Received in revised form For monitoring the nitrosatability of NZ, a hydrophilic interaction liquid chromatography 29 July 2019 (HILIC) method was optimized and validated according to FDA guidance.
    [Show full text]
  • Provisional Peer Reviewed Toxicity Values for 4-Amino-2,6-Dinitrotoluene
    EPA/690/R-20/002F | June 2020 | FINAL Provisional Peer-Reviewed Toxicity Values for 4-Amino-2,6-dinitrotoluene (CASRN 19406-51-0) U.S. EPA Office of Research and Development Center for Public Health and Environmental Assessment EPA/690/R-20/002F June 2020 https://www.epa.gov/pprtv Provisional Peer-Reviewed Toxicity Values for 4-Amino-2,6-dinitrotoluene (CASRN 19406-51-0) Center for Public Health and Environmental Assessment Office of Research and Development U.S. Environmental Protection Agency Cincinnati, OH 45268 ii 4-Amino-2,6-dinitrotoluene AUTHORS, CONTRIBUTORS, AND REVIEWERS CHEMICAL MANAGER Daniel D. Petersen, MS, PhD, DABT, ATS, ERT Center for Public Health and Environmental Assessment, Cincinnati, OH DRAFT DOCUMENT PREPARED BY SRC, Inc. 7502 Round Pond Road North Syracuse, NY 13212 PRIMARY INTERNAL REVIEWERS Jeffry L. Dean II, PhD Center for Public Health and Environmental Assessment, Cincinnati, OH Michelle M. Angrish, PhD Center for Public Health and Environmental Assessment, Research Triangle Park, NC This document was externally peer reviewed under contract to Eastern Research Group, Inc. 110 Hartwell Avenue Lexington, MA 02421-3136 Questions regarding the content of this PPRTV assessment should be directed to the U.S. EPA Office of Research and Development’s Center for Public Health and Environmental Assessment. iii 4-Amino-2,6-dinitrotoluene TABLE OF CONTENTS COMMONLY USED ABBREVIATIONS AND ACRONYMS ................................................... v BACKGROUND ...........................................................................................................................
    [Show full text]
  • Mechanism of Drug Action
    Compiled and circulated by Dr. Parimal Dua, Assistant Professor, Dept. of Physiology, Narajole Raj college Unit IV: Pharmacodynamics: Concept of LD50, LC50, TD50 and therapeutic index Quantal dose-response graphs can be characterised by the median effective dose (ED50). The median effective dose is the dose at which 50% of individuals exhibit the specified quantal effect. The median toxic dose is the dose required to produce a defined toxic effect in 50% of subjects. The median lethal dose is the dose required to kill 50% of subjects. The therapeutic index is the ratio of the TD50 to the ED50, a parameter which reflects the selectivity of a drug to elicit a desired effect rather than toxicity. The therapeutic window is the range between the minimum toxic dose and the minimum therapeutic dose, or the range of doses over which the drug is effective for most of the popuation and the toxicity is accceptable. Anatomy of the quantal dose-response graph contain the following elements: Three sigmoid curves The median effective dose (ED50) The median toxic dose (TD50) The median lethal dose (LD50) The therapeutic window The end result should look something like this: Page | 1 SEC-4: Pharmacology and Toxicology Compiled and circulated by Dr. Parimal Dua, Assistant Professor, Dept. of Physiology, Narajole Raj college Median effective dose, ED50 This thing is distinct from the identical ED50 in graded dose-response curves, where it corresponds to a measure of the potency of a drug, being the dose of a drug required to produce 50% of that drug’s maximal effect.
    [Show full text]
  • QUESTION 1 (Principle: the Graded Dose-Response Curve)
    Pharmacology and Therapeutics Pharmacodynamics Small Group IV August 15, 2019, 10:30am-12:00 PM FACILITATORS GUIDE QUESTION 1 (Principle: The Graded Dose-Response Curve) A 34-year old man is brought to the emergency room in a disheveled and unresponsive state. His vital signs reveal a heart rate of 26 bpm and he is apneic. He has no palpable blood pressure, but has a palpable slow pulse in his femoral artery. Fresh needle track marks, consistent with recent injections, are present in his left antecubital fossa (elbow pit). He is suspected to be a victim of the epidemic of superpotent heroin, “China White”. Heroin overdose is typically treated by I.V. administration of naloxone (a drug that binds to the same site on the mu-opioid receptors as heroin, but without the narcotic effects of heroin). Despite oral intubation, mechanical ventilation, advanced cardiac life support measures, and large intravenous doses of naloxone, the patient died. Part 1 (Teaching Point: Graded Dose Response Curves for Various Opiate Receptor Agonists) China white is the street name for 3-methyl-fentanyl, a short-acting synthetic opioid agonist estimated to have 10,000 times the potency of heroin at mu-opioid receptors. Pharmaceutical fentanyl has a potency of 100 times that of heroin, while the commonly used opioid analgesic morphine is approximately 5 times less potent than heroin. All four drugs are equally efficacious with respect to the effects produced by their activation of m opioid receptors. If the potency of heroin at mu-opioid receptors is 10 mg/kg, using the axes below, draw semi-logarithmic dose- response curves to show the expected relative relationships between heroin, fentanyl, morphine and China White (3-methyl fentanyl), indicate their respective ED50’s and show in the figure how these are values are determined.
    [Show full text]
  • 7. Calculation of Doses- General Considerations.Ppt [相容模式]
    Calculation of Doses: General considerations 劑量計算：一般考量 Objectives 1 Dose definitions n The dose of a drug: q is the quantitative amount administered or taken by a patient for the intended medicinal effect. q may be expressed as: n a single dose, the amount taken at one time; n a daily dose; n a total dose, the amount taken during the time-course of therapy. n A daily dose： q may be subdivided and taken in divided doses, q two or more times per day depending on the characteristics of the drug and the illness. n The schedule of dosing {e.g., four times per day for 10 days) is referred to as the dosage regimen. 2 n Drug dosesvary greatly between drug substances; some drugs have small doses, other drugs have relatively large doses. n The dose of a drug is based on: q its biochemical and pharmacologic activity, q its physical and chemical properties, q the dosage form used, q the route of administration, q various patient factors. n The dose of a drug for a particular patient may be determined in part on the basis of the patient's age, weight, body surface area, general physical health, liver and kidney function (for drug metabolism and elimination), and the severity of the illness being treated. n The usual adult dose of a drug is the amount that ordinarily produces the medicinal effect intended in adults. n The usual pediatric dose is similarly defined for the infant-or child-patient. n The usual dosage range for a drug indicates the quantitative range or amounts of the drug that may be prescribed within the guidelines of usual medical practice.
    [Show full text]
  • Borax by the Forest Service from 2000 to 2004
    SERA TR-056-15-03c Sporax® and Cellu-Treat® (Selected Borate Salts) Human Health and Ecological Risk Assessment FINAL REPORT Submitted to: Dr. Harold Thistle USDA Forest Service Forest Health Technology Enterprise Team 180 Canfield St. Morgantown, WV 26505 Email: [email protected] USDA Forest Service Contract: AG-3187-C-12-0009 USDA Forest Order Number: AG-3187-D-15-0074 SERA Internal Task No. 56-15 Submitted by: Patrick R. Durkin Syracuse Environmental Research Associates, Inc. 8125 Solomon Seal Manlius, New York 13104 E-Mail: [email protected] Home Page: www.sera-inc.com October 17, 2016 Table of Contents LIST OF TABLES ......................................................................................................................... vi LIST OF FIGURES ....................................................................................................................... vi LIST OF APPENDICES ................................................................................................................ vi LIST OF ATTACHMENTS .......................................................................................................... vi ACRONYMS, ABBREVIATIONS, AND SYMBOLS .............................................................. viii COMMON UNIT CONVERSIONS AND ABBREVIATIONS ................................................... xi CONVERSION OF SCIENTIFIC NOTATION .......................................................................... xii EXECUTIVE SUMMARY ........................................................................................................
    [Show full text]
  • 7 X 11.5 Long Title.P65
    Cambridge University Press 978-0-521-51781-2 - Small Molecule Therapy for Genetic Disease Edited by Jess G. Thoene Index More information Index Abderhalden, Emil, 101 long-term therapy results, 147–149 absolute oral bioavailability, 37 side effects, 147 acquired copper deficiency, 202–203 antagonists, 46 active tubular secretion, 43 apomorphine, 12 acute hereditary tyrosinemia, 115 apoptosis, in cysteamine treatment, for adenosine triphosphate (ATP) nephropathic cystinosis, 103 ATP7A, 203 apparent first-order kinetics, 40–41 distal hereditary motor neuropathy, apparent volume of distribution, 39 206–207 argininosuccinate lyase (AL) deficiency, Menkes disease, 203 135 OHS, 206 argininosuccinate synthetase (AS) nephropathic cystinosis, 103 deficiency, 135 agonists, 46 AS deficiency. See argininosuccinate AKU. See alkaptonuria synthetase deficiency AL deficiency. See argininosuccinate lyase ATP. See adenosine triphosphate deficiency ATP7A, 203 ALA. See aminolevulinic acid distal hereditary motor neuropathy, alkaptonuria (AKU), 114, 118–121 206–207 cardiac involvement, 119–120 Menkes disease, 203 clinical presentation, 119 OHS, 206 arthritis as, 119 diagnosis, 121 basal ganglion diseases, 60 dietary therapies, 120 biotin therapy, 66 genetic factors, 121 inheritance factors, 63 HGA, 118–119 Bench-To-Bedside Research Program, HPPD inhibition, 124 25 incidence rates, 118–119 betaine, in homocystinuria treatment, nitisinone therapy, 125 176–179 future developments, 130 clinical evidence of, 176–177 side effects, 127 development, 176–177 tyrosine levels,
    [Show full text]