Uniform Classification Guidelines for Foreign Substances and Recommended Penalties Model Rule
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The Pharmacology of Amiodarone and Digoxin As Antiarrhythmic Agents
Part I Anaesthesia Refresher Course – 2017 University of Cape Town The Pharmacology of Amiodarone and Digoxin as Antiarrhythmic Agents Dr Adri Vorster UCT Department of Anaesthesia & Perioperative Medicine The heart contains pacemaker, conduction and contractile tissue. Cardiac arrhythmias are caused by either enhancement or depression of cardiac action potential generation by pacemaker cells, or by abnormal conduction of the action potential. The pharmacological treatment of arrhythmias aims to achieve restoration of a normal rhythm and rate. The resting membrane potential of myocytes is around -90 mV, with the inside of the membrane more negative than the outside. The main extracellular ions are Na+ and Cl−, with K+ the main intracellular ion. The cardiac action potential involves a change in voltage across the cell membrane of myocytes, caused by movement of charged ions across the membrane. This voltage change is triggered by pacemaker cells. The action potential is divided into 5 phases (figure 1). Phase 0: Rapid depolarisation Duration < 2ms Threshold potential must be reached (-70 mV) for propagation to occur Rapid positive charge achieved as a result of increased Na+ conductance through voltage-gated Na+ channels in the cell membrane Phase 1: Partial repolarisation Closure of Na+ channels K+ channels open and close, resulting in brief outflow of K+ and a more negative membrane potential Phase 2: Plateau Duration up to 150 ms Absolute refractory period – prevents further depolarisation and myocardial tetany Result of Ca++ influx -
New Rules Pertaining to the Banning of Anabolic Steroids in the Western Australian Harness Racing Industry to Be Introduced 1St September 2014
NEW RULES PERTAINING TO THE BANNING OF ANABOLIC STEROIDS IN THE WESTERN AUSTRALIAN HARNESS RACING INDUSTRY TO BE INTRODUCED 1ST SEPTEMBER 2014 Notice is hereby given that the Board of Racing and Wagering WA have resolved that the RWWA Rules of Harness Racing 2004 be amended. In accordance with section 45 (1) (b) of the Racing and Wagering Western Australia Act 2003 the Board of Racing and Wagering WA on the 10th April 2014 resolved that these amendments be adopted accordingly into the RWWA Rules of Harness Racing. The Harness Racing Board had advised of these amendments and the RWWA Board has determined that these amendments will come into effect on 1st September 2014. The details of the relevant rules pertaining to this ban of anabolic steroids for reference can be found following this advice. There are many implications arising from the introduction of these rules, and to assist trainers and veterinarians to comply with the new rules the following explanatory statement has been prepared. Which steroids are banned under these rules? The new rules ban the use of "anabolic androgenic steroids" in Standardbred horses at any time from birth until retirement. "Anabolic androgenic steroids" include those that are currently registered in Australia by the APVMA for use in horses, such as boldenone, ethylestrenol (in Nitrotain), methandriol, nandrolone, stanozolol and testosterone. Exogenous anabolic androgenic steroids that are banned also include but are not limited to those listed in the WADA prohibited list, such as 1-androstenediol; 1-androstenedione; -
Tricyclic Antidepressant
Princess Margaret Hospital for Children Emergency Department Guideline PAEDIATRIC ACUTE CARE GUIDELINE Poisoning – Tricyclic Antidepressant Scope (Staff): All Emergency Department Clinicians Scope (Area): Emergency Department This document should be read in conjunction with this DISCLAIMER http://kidshealthwa.com/about/disclaimer/ Poisoning – Tricyclic Antidepressant This guideline is a general approach to tricyclic antidepressant poisoning. For specific details please contact Poisons Information: 131126 or refer to the Toxicology Handbook. Agents: Amitriptyline Clomipramine Dothiepin Doxepin Imipramine Nortriptyline Trimipramine Background Tricyclic antidepressants (TCAs) act on a variety of receptors whose actions include: Noradrenaline reuptake inhibition Central and peripheral anticholinergic effect Fast sodium channel blockade in the myocardium Peripheral alpha1-adrenergic receptor blockade The life threatening effects of acute tricyclic antidepressant (TCA) overdose are: Rapid onset of coma Seizures Cardiac dysrhythmias Page 1 of 6 Emergency Department Guideline Poisoning – Tricyclic Antidepressant Hypotension and central and peripheral anticholinergic effects may also be seen Risk Assessment Most acute accidental paediatric exposures do not result in life threatening toxicity A 10kg child can develop life threatening poisoning with the ingestion of a single tablet (e.g. 150mg amitriptyline) Patients who ingest a large dose of TCA usually develop evidence of intoxication within 2-4 hours, and always within 6 hours If their is suspicion -
This Table Summarizes Changes to the HF Qxq As of 10/11/2019 Question
Updated HFS Instructions (QxQs) This table summarizes changes to the HF QxQ as of 10/11/2019 Question in HF QxQ Description of Changes in HF QXQ General Instructions, pg. 3 Clarification added to rules for history Q29.d.10., pg. 40 Clarification made on how to record pulmonary hypertention Q29.d.14., pg. 41 Clarification made on how to record diastolic dysfunction Q42., pg. 42 Clarification made on how to record troponin I Section VII: Medication, pg. 54 Clarificaiton made on how to record medications Appendix A, pg. 61 Updated list of medications Edoxaban (ACOAG, Generic) Lixiana (ACOAG, Trade) Prexxartan (ARB, Trade) INSTRUCTIONS FOR COMPLETING HEART FAILURE HOSPITAL RECORD ABSTRACTION FORM HFS Version C, 10/1/2015 HFA Version D, 10/1/2015 HF QxQ, 10/11/2019 Table of Contents Page General Instructions……………………………………………………………….. 2 Specific Items………………………………………………………………………. 3 Section l: Screening for Decompensation………………………………….. 5 Section ll: History of Heart Failure…………………………………………... 10 Section lll: Medical History ………………………………………………….. 13 Section lV: Physical Exam - Vital Signs…………………………………….. 24 Section V: Physical Exam - Findings……………………………………….. 26 Section Vl: Diagnostic Tests…………………………………………………. 31 Section Vll: Biochemical Analyses………………………………………….. 48 Section Vlll: Interventions…………………………………………………….. 51 Section lX: Medications………………………………………………………. 54 Section X: Complications Following Events………………………………… 59 Section Xl: Administrative……………………………………………………. 60 Appendix A: ARIC Heart Failure/Cardiac Drugs: ………………………………. 61 Alphabetical Sort Appendix B: Potential Scenarios of the Onset of Heart………………………. 73 Failure Event or Decompensation HF QxQ 10/11/2019 Page 1 of 73 General Instructions The HFAA form was initially used for all discharges selected for HF surveillance. It was replaced by the HFAB and HFSA forms and then updated June 2012 with HFAC and HFSB. -
Withdrawing Benzodiazepines in Primary Care
PC\/ICU/ ADTiriC • CNS Drugs 2009,-23(1): 19-34 KtVltW MKIIWLC 1172-7047/I»/O(X)1«119/S4W5/C1 © 2009 Adis Dato Intocmation BV. All rights reserved. Withdrawing Benzodiazepines in Primary Care Malcolm Luder} Andre Tylee^ and ]ohn Donoghue^ 1 Institute of Psychiatry, King's College London, London, England 2 John Moores University, Liverpool, Scotland Contents Abstract ' 19 1. Benzodiazepine Usage 22 2. Interventions 23 2.1 Simple interventions 23 2.2 Piiarmacoiogicai interventions 25 2.3 Psychoiogical Interventions 26 2.4 Meta-Anaiysis ot Various interventions 27 3. Outcomes 28 4. Practicai Issues 29 5. Otiier Medications 30 5.1 Antidepressants 30 5.2 Symptomatic Treatments 30 6. Conciusions 31 Abstract The use of benzodiazepine anxiolytics and hypnotics continues to excite controversy. Views differ from expert to expert and from country to country as to the extent of the problem, or even whether long-term benzodiazepine use actually constitutes a problem. The adverse effects of these drugs have been extensively documented and their effectiveness is being increasingly questioned. Discontinua- tion is usually beneficial as it is followed by improved psychomotor and cognitive functioning, particularly in the elderly. The potential for dependence and addic- tion have also become more apparent. The licensing of SSRIs for anxiety disorders has widened the prescdbers' therapeutic choices (although this group of medications also have their own adverse effects). Melatonin agonists show promise in some forms of insomnia. Accordingly, it is now even more imperative that long-term benzodiazepine users be reviewed with respect to possible discon- tinuation. Strategies for discontinuation start with primary-care practitioners, who are still the main prescdbers. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
United States Patent (10) Patent No.: US 8,916,581 B2 Boyd Et Al
USOO891 6581 B2 (12) United States Patent (10) Patent No.: US 8,916,581 B2 Boyd et al. (45) Date of Patent: *Dec. 23, 2014 (54) (S)-N-METHYLNALTREXONE 4,194,045 A 3, 1980 Adelstein 4,203,920 A 5, 1980 Diamond et al. (75) Inventors: Thomas A. Boyd, Grandview, NY (US); 4,241,066 A 12, 1980 Kobylecki et al. H OW d Wagoner,goner, Warwick,s NY (US);s 4,311,833.4,277,605 A T.1/1982 1981 NamikoshiBuyniski et etal. al. Suketu P. Sanghvi, Kendall Park, NJ 4.322,426 A 3/1982 Hermann et al. (US); Christopher Verbicky, 4.326,074 A 4, 1982 Diamond et al. Broadalbin, NY (US); Stephen 4.326,075 A 4, 1982 Diamond et al. “. s 4,377.568 A 3/1983 Chopra et al. Andruski, Clifton Park, NY (US) 4.385,078 A 5/1983 Onda et al. 4.427,676 A 1/1984 White et al. (73) Assignee: Progenics Pharmaceuticals, Inc., 4,430,327 A 2, 1984 Frederickson et al. Tarrytown, NY (US) 4,452,775 A 6/1984 Kent 4,457,907 A 7/1984 Porteret al. (*) Notice: Subject to any disclaimer, the term of this 4,462.839 A 7/1984 McGinley et al. patent is extended or adjusted under 35 4,518.4334,466,968 A 5/19858, 1984 McGinleyBernstein et al. U.S.C. 154(b) by 344 days. 4,533,739 A 8/1985 Pitzele et al. This patent is Subject to a terminal dis- 4,606,9094,556,552 A 12/19858/1986 PorterBechgaard et al. -
)&F1y3x PHARMACEUTICAL APPENDIX to THE
)&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ACTODIGIN 36983-69-4 ABANOQUIL 90402-40-7 ADAFENOXATE 82168-26-1 ABCIXIMAB 143653-53-6 ADAMEXINE 54785-02-3 ABECARNIL 111841-85-1 ADAPALENE 106685-40-9 ABITESARTAN 137882-98-5 ADAPROLOL 101479-70-3 ABLUKAST 96566-25-5 ADATANSERIN 127266-56-2 ABUNIDAZOLE 91017-58-2 ADEFOVIR 106941-25-7 ACADESINE 2627-69-2 ADELMIDROL 1675-66-7 ACAMPROSATE 77337-76-9 ADEMETIONINE 17176-17-9 ACAPRAZINE 55485-20-6 ADENOSINE PHOSPHATE 61-19-8 ACARBOSE 56180-94-0 ADIBENDAN 100510-33-6 ACEBROCHOL 514-50-1 ADICILLIN 525-94-0 ACEBURIC ACID 26976-72-7 ADIMOLOL 78459-19-5 ACEBUTOLOL 37517-30-9 ADINAZOLAM 37115-32-5 ACECAINIDE 32795-44-1 ADIPHENINE 64-95-9 ACECARBROMAL 77-66-7 ADIPIODONE 606-17-7 ACECLIDINE 827-61-2 ADITEREN 56066-19-4 ACECLOFENAC 89796-99-6 ADITOPRIM 56066-63-8 ACEDAPSONE 77-46-3 ADOSOPINE 88124-26-9 ACEDIASULFONE SODIUM 127-60-6 ADOZELESIN 110314-48-2 ACEDOBEN 556-08-1 ADRAFINIL 63547-13-7 ACEFLURANOL 80595-73-9 ADRENALONE -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
The Effects of Antipsychotic Treatment on Metabolic Function: a Systematic Review and Network Meta-Analysis
The effects of antipsychotic treatment on metabolic function: a systematic review and network meta-analysis Toby Pillinger, Robert McCutcheon, Luke Vano, Katherine Beck, Guy Hindley, Atheeshaan Arumuham, Yuya Mizuno, Sridhar Natesan, Orestis Efthimiou, Andrea Cipriani, Oliver Howes ****PROTOCOL**** Review questions 1. What is the magnitude of metabolic dysregulation (defined as alterations in fasting glucose, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, and triglyceride levels) and alterations in body weight and body mass index associated with short-term (‘acute’) antipsychotic treatment in individuals with schizophrenia? 2. Does baseline physiology (e.g. body weight) and demographics (e.g. age) of patients predict magnitude of antipsychotic-associated metabolic dysregulation? 3. Are alterations in metabolic parameters over time associated with alterations in degree of psychopathology? 1 Searches We plan to search EMBASE, PsycINFO, and MEDLINE from inception using the following terms: 1 (Acepromazine or Acetophenazine or Amisulpride or Aripiprazole or Asenapine or Benperidol or Blonanserin or Bromperidol or Butaperazine or Carpipramine or Chlorproethazine or Chlorpromazine or Chlorprothixene or Clocapramine or Clopenthixol or Clopentixol or Clothiapine or Clotiapine or Clozapine or Cyamemazine or Cyamepromazine or Dixyrazine or Droperidol or Fluanisone or Flupehenazine or Flupenthixol or Flupentixol or Fluphenazine or Fluspirilen or Fluspirilene or Haloperidol or Iloperidone -
Treatment of Schizophrenia Course Director: Philip Janicak, M.D
S6735- Treatment of Schizophrenia Course Director: Philip Janicak, M.D. #APAAM2016 Saturday, May 14, 2016 Marriott Marquis - Marquis Ballroom D psychiatry.org/ annualmeetingS4637 ANNUAL MEETING May 14-18, 2016 • Atlanta Reference • Janicak PG, Marder SR, Tandon R, Goldman M (Eds.). Schizophrenia: Recent Advances in Diagnosis and Treatment. New York, NY: Springer; 2014. Schizophrenia: Recent Diagnostic Advances, Neurobiology, and the Neuropharmacology of Antipsychotic Drug Therapy Rajiv Tandon, MD Professor of Psychiatry University of Florida College of Medicine Gainesville, Florida Annual Meeting of the American Psychiatric Association New York, New York May 3–7, 2014 Disclosure Information MEMBER, WPA PHARMACOPSYCHIATRY SECTION MEMBER, DSM-5 WORKGROUP ON PSYCHOTIC DISORDERS A CLINICIAN AND CLINICAL RESEARCHER Pharmacological Treatment of Any Disease • Know the Disease that you are treating • Nature; Treatment targets; Treatment goals; • Know the Treatments at your disposal • What they do; How they compare; Costs; • Principles of Treatment • Measurement-based; Targeted; Individualized Program Outline • Nature and Definition of psychosis? • Clinical description • What is wrong in psychotic illness • Dimensions of Psychopathology • Neurobiological Abnormalities • Mechanisms underlying antipsychotic effects? • What contributes to Efficacy • Basis of Side-effect differences 5 Challenges in DSM-IV Construct of Psychotic Disorders ♦ Indistinct Boundaries ♦ With Other Disorders (eg., with OCD) ♦ Within Group of Psychotic Disorders (eg. between -
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Cr
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Crizotinib (PF-02341066) 1 4 55 Docetaxel 1 5 98 Anastrozole 1 6 25 Cladribine 1 7 23 Methotrexate 1 8 -187 Letrozole 1 9 65 Entecavir Hydrate 1 10 48 Roxadustat (FG-4592) 1 11 19 Imatinib Mesylate (STI571) 1 12 0 Sunitinib Malate 1 13 34 Vismodegib (GDC-0449) 1 14 64 Paclitaxel 1 15 89 Aprepitant 1 16 94 Decitabine 1 17 -79 Bendamustine HCl 1 18 19 Temozolomide 1 19 -111 Nepafenac 1 20 24 Nintedanib (BIBF 1120) 1 21 -43 Lapatinib (GW-572016) Ditosylate 1 22 88 Temsirolimus (CCI-779, NSC 683864) 1 23 96 Belinostat (PXD101) 1 24 46 Capecitabine 1 25 19 Bicalutamide 1 26 83 Dutasteride 1 27 68 Epirubicin HCl 1 28 -59 Tamoxifen 1 29 30 Rufinamide 1 30 96 Afatinib (BIBW2992) 1 31 -54 Lenalidomide (CC-5013) 1 32 19 Vorinostat (SAHA, MK0683) 1 33 38 Rucaparib (AG-014699,PF-01367338) phosphate1 34 14 Lenvatinib (E7080) 1 35 80 Fulvestrant 1 36 76 Melatonin 1 37 15 Etoposide 1 38 -69 Vincristine sulfate 1 39 61 Posaconazole 1 40 97 Bortezomib (PS-341) 1 41 71 Panobinostat (LBH589) 1 42 41 Entinostat (MS-275) 1 43 26 Cabozantinib (XL184, BMS-907351) 1 44 79 Valproic acid sodium salt (Sodium valproate) 1 45 7 Raltitrexed 1 46 39 Bisoprolol fumarate 1 47 -23 Raloxifene HCl 1 48 97 Agomelatine 1 49 35 Prasugrel 1 50 -24 Bosutinib (SKI-606) 1 51 85 Nilotinib (AMN-107) 1 52 99 Enzastaurin (LY317615) 1 53 -12 Everolimus (RAD001) 1 54 94 Regorafenib (BAY 73-4506) 1 55 24 Thalidomide 1 56 40 Tivozanib (AV-951) 1 57 86 Fludarabine