ENLON-PLUS (Edrophonium Chloride, USP and Atropine Sulfate, USP) Injection
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Severe Organophosphate Poisoning with Delayed Cholinergic Crisis, Intermediate Syndrome and Organophosphate Induced Delayed Polyneuropathy on Succession
Organophosphate Poisoning… Aklilu A 203 CASE REPORT SEVERE ORGANOPHOSPHATE POISONING WITH DELAYED CHOLINERGIC CRISIS, INTERMEDIATE SYNDROME AND ORGANOPHOSPHATE INDUCED DELAYED POLYNEUROPATHY ON SUCCESSION Aklilu Azazh ABSTRACT Organophosphate compounds are the organic derivatives of Phosphorous containing acids and their effect on neuromuscular junction and Autonomic Synapses is clinically important. After exposure these agents cause acute and sub acute manifestations depending on the type and severity of the agents like Acute Cholinergic Manifestations, Intermediate Syndrome with Nicotinic features and Delayed Central Nervous System Complications. The patient reported here had severe Organophosphate Poisoning with various rare complications on a succession. This is the first report of Organophosphates Poisoning complicated by Intermediate Syndrome and Organophosphate Induced Delayed Polyneuropathy in Ethiopia and it is reported to increase awareness of health care workers on these rare complications of a common problem. INTRODUCTION phosphorylated by the Phosphate end of Organophosphates; then the net result is Organophosphate compounds are the organic accumulation of excessive Acetyl Chlorine with derivatives of Phosphorous containing acids and resultant effect on Muscarinic, Nicotinic and their effect on Neuromuscular Junction and central nervous system (Figure 2). Autonomic synapses is clinically important. In the Neuromuscular Junction Acetylcholine is released Following classical OP poisoning, three well when a nerve impulse reaches -
Non-Steroidal Drug-Induced Glaucoma MR Razeghinejad Et Al 972
Eye (2011) 25, 971–980 & 2011 Macmillan Publishers Limited All rights reserved 0950-222X/11 www.nature.com/eye 1,2 1 1 Non-steroidal drug- MR Razeghinejad , MJ Pro and LJ Katz REVIEW induced glaucoma Abstract vision. The majority of drugs listed as contraindicated in glaucoma are concerned with Numerous systemically used drugs are CAG. These medications may incite an attack in involved in drug-induced glaucoma. Most those individuals with narrow iridocorneal reported cases of non-steroidal drug-induced angle.3 At least one-third of acute closed-angle glaucoma are closed-angle glaucoma (CAG). glaucoma (ACAG) cases are related to an Indeed, many routinely used drugs that have over-the-counter or prescription drug.1 Prevalence sympathomimetic or parasympatholytic of narrow angles in whites from the Framingham properties can cause pupillary block CAG in study was 3.8%. Narrow angles are more individuals with narrow iridocorneal angle. The resulting acute glaucoma occurs much common in the Asian population. A study of a more commonly unilaterally and only rarely Vietnamese population estimated a prevalence 4 bilaterally. CAG secondary to sulfa drugs is a of occludable angles at 8.5%. The reported bilateral non-pupillary block type and is due prevalence of elevated IOP months to years to forward movement of iris–lens diaphragm, after controlling ACAG with laser iridotomy 5,6 which occurs in individuals with narrow or ranges from 24 to 72%. Additionally, a open iridocorneal angle. A few agents, significant decrease in retinal nerve fiber layer including antineoplastics, may induce thickness and an increase in the cup/disc ratio open-angle glaucoma. -
Cardiovascular Monitoring with Acetylcholinesterase Inhibitors: a Clinical Protocol† Jeremy P
Advances in Psychiatric Treatment (2007), vol. 13, 178–184 doi: 10.1192/apt.bp.106.002725 Cardiovascular monitoring with acetylcholinesterase inhibitors: a clinical protocol† Jeremy P. Rowland, John Rigby, Adam C. Harper & Rosalind Rowland Abstract There has been significant anxiety among prescribers regarding the potential for cardiac adverse effects associated with acetylcholinesterase (AChE) inhibitors in Alzheimer’s disease. There is no consensus on how to manage this cardiovascular risk, and memory clinics vary widely in their practice. Review of published evidence reveals that the incidence of cardiovascular side-effects is low, and that serious adverse events are rare. Intensive cardiovascular screening such as pre-treatment electrocardiograms or 24 h cardiac monitoring is not justified. Furthermore, there are no high-risk groups to target. This article suggests pragmatic guidelines for managing cardiovascular risk in patients receiving AChE inhibitors. The guidelines are intended to be easy to incorporate into routine clinical practice in a memory clinic. A few years ago it was estimated that almost 18 thus followed some uncertainty as to how treatment million people worldwide had dementia (Alzheimer’s should be properly managed. Society, 2004), with Alzheimer’s disease accounting Since the manufacturers’ cautions remain (see the for over half of cases (Fratiglioni, 2000). The second- relevant entries in http://emc.medicines.org.uk) and generation acetylcholinesterase (AChE) inhibitors guidance has been unforthcoming, services now vary donepezil, rivastigmine and galantamine were widely in their practice: some, for example, require introduced into clinical practice from 1997 for the electrocardiograms (ECGs) before use and during symptomatic treatment of Alzheimer’s disease, and treatment, whereas others do not. -
Abcd (Ipratropium Bromide and Albuterol Sulfate) Inhalation Aerosol
ATTENTION PHARMACIST: Detach “Patient’s Instructions for Use” from package insert and dispense with the product. Combivent® abcd (ipratropium bromide and albuterol sulfate) Inhalation Aerosol Bronchodilator Aerosol For Oral Inhalation Only Rx only Prescribing Information DESCRIPTION COMBIVENT Inhalation Aerosol is a combination of ipratropium bromide (as the monohydrate) and albuterol sulfate. Ipratropium bromide is an anticholinergic bronchodilator chemically described as 8-azoniabicyclo[3.2.1] octane, 3-(3-hydroxy-1-oxo-2-phenylpropoxy)-8-methyl 8-(1-methylethyl)-, bromide monohydrate, (3-endo, 8-syn)-: a synthetic quaternary ammonium compound chemically related to atropine. Ipratropium bromide is a white to off-white crystalline substance, freely soluble in water and methanol, sparingly soluble in ethanol, and insoluble in lipophilic solvents such as ether, chloroform, and fluorocarbons. The structural formula is: + N OH Br . H O H 2 O O C20H30BrNO3•H2O ipratropium bromide Mol. Wt. 430.4 Albuterol sulfate, chemically known as (1,3-benzenedimethanol, α'-[[(1,1dimethylethyl) amino] methyl]-4-hydroxy, sulfate (2:1)(salt), (±)- is a relatively selective beta2-adrenergic bronchodilator. Albuterol is the official generic name in the United States. The World Health Organization recommended name for the drug is salbutamol. Albuterol sulfate is a white to off-white crystalline powder, freely soluble in water and slightly soluble in alcohol, chloroform, and ether. The structural formula is: Reference ID: 2927161 OH NH * . H2SO4 OH OH 2 (C13H21NO3)2•H2SO4 albuterol sulfate Mol. Wt. 576.7 Combivent® (ipratropium bromide and albuterol sulfate) Inhalation Aerosol contains a microcrystalline suspension of ipratropium bromide and albuterol sulfate in a pressurized metered-dose aerosol unit for oral inhalation administration. -
Malathion Human Health and Ecological Risk Assessment Final Report
SERA TR-052-02-02c Malathion Human Health and Ecological Risk Assessment Final Report Submitted to: Paul Mistretta, COR USDA/Forest Service, Southern Region 1720 Peachtree RD, NW Atlanta, Georgia 30309 USDA Forest Service Contract: AG-3187-C-06-0010 USDA Forest Order Number: AG-43ZP-D-06-0012 SERA Internal Task No. 52-02 Submitted by: Patrick R. Durkin Syracuse Environmental Research Associates, Inc. 5100 Highbridge St., 42C Fayetteville, New York 13066-0950 Fax: (315) 637-0445 E-Mail: [email protected] Home Page: www.sera-inc.com May 12, 2008 Table of Contents Table of Contents............................................................................................................................ ii List of Figures................................................................................................................................. v List of Tables ................................................................................................................................. vi List of Appendices ......................................................................................................................... vi List of Attachments........................................................................................................................ vi ACRONYMS, ABBREVIATIONS, AND SYMBOLS ............................................................... vii COMMON UNIT CONVERSIONS AND ABBREVIATIONS.................................................... x CONVERSION OF SCIENTIFIC NOTATION .......................................................................... -
Beyond the Cholinergic Crisis Galle Medical Association Oration 2015
Reviews Beyond the cholinergic crisis Galle Medical Association Oration 2015 Jayasinghe S S Department of Pharmacology, Faculty of Medicine, University of Ruhuna, Galle, Sri Lanka. South Asian Clinical Toxicology Research Collaboration, Department of Medicine, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. Correspondence: Dr. Sudheera S Jayasinghe e-mail: [email protected] ABSTRACT Introduction: Organophosphates (OP) are the most frequently involved pesticides in acute poisoning. In Sri Lanka it has been ranked as the sixth or seventh leading cause of hospital deaths for many years. Neurotoxic effects of acute OP have been hitherto under-explored. The aims of the studies were to assess the effects of acute OP poisoning on somatic, autonomic nerves, neuro- muscular junction (NMJ), brain stem and cognitive function. Methods: Patients following self-ingestion of OP were recruited to cohort studies to evaluated the function of somatic, autonomic nerves, NMJ, brain stem and cognition. Motor and sensory nerve function was tested with nerve conduction studies. Cardiovascular reflexes based autonomic function tests and sympathetic skin response (SSR) was used to evaluate autonomic function. NMJ function was assessed with slow repetitive supramaximal stimulation of the median nerve of the dominant upper limb. Brain stem function and cognitive function were assessed with Brain Stem Evoked Response Audiometry (BERA) and Mini Mental State Examination (MMSE) respectively. The data of the patients were compared with age, gender and occupation matched controls. Results: There were 60-70 patients and equal number of controls in each study. Motor nerve conduction velocity, amplitude and area of compound muscle action potential on distal stimulation, sensory nerve conduction velocity and F-wave occurrence were significantly reduced. -
Pharmacology of Ophthalmic Agents
Ophthalmic Pharmacology Richard Alan Lewis M.D., M.S., PHARMACOLOGY FOPS PHARMACOKINETICS OF Professor, Departments of Ophthalmology, • The study of the absorption, OPHTHALMIC Medicine, Pediatrics, and Molecular distribution, metabolism, AGENTS and Human Genetics and excretion of a drug or and the National School of Tropical agent Introduction and Review Medicine Houston, Texas PHARMACOKINETICS Factors Affecting Drug Penetration Factors Affecting Drug Penetration into Ocular Tissues • A drug can be delivered to ocular tissue: into Ocular Tissues – Locally: • Drug concentration and solubility: The higher the concentration the better the penetration, • Surfactants: The preservatives in ocular • Eye drop but limited by reflex tearing. preparations alter cell membrane in the cornea • Ointment and increase drug permeability, e.g., • Viscosity: Addition of methylcellulose and benzalkonium and thiomersal • Periocular injection polyvinyl alcohol increases drug penetration by • pH: The normal tear pH is 7.4; if the drug pH is • Intraocular injection increasing the contact time with the cornea and altering corneal epithelium. much different, it will cause reflex tearing. – Systemically: • Lipid solubility: Because of the lipid rich • Drug tonicity: When an alkaloid drug is put in • Orally environment of the epithelial cell membranes, relatively alkaloid medium, the proportion of the uncharged form will increase, thus more • IM the higher lipid solubility, the more the penetration. • IV penetration. FLUORESCEIN FLUORESCEIN Chemistry Dosage ● C20H1205, brown crystal ● Adults: 500-750 mg IV ● M.W. 322.3 e.g., 3 cc 25% solution ● Peak absorption 485-500 nm. 5 cc 10% solution ● Peak emission 520-530 nm. ● Children: 1.5-2.5 mg/kg IV Richard Alan Lewis, M.D., M.S. -
On Tardive Dyskinesia'
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.37.8.941 on 1 August 1974. Downloaded from Journial of Neurology, Neurosurgery, alid Psychiatry, 1974, 27, 941-947 Effect of cholinergic and anticholinergic agents on tardive dyskinesia' H. L. KLAWANS2 AND R. RUBOVITS Fr-om the Divisioni of Neurology, Michael Reese Medical Center, Chicago, Illinois anid the Departmentt ofPsychiatry, University of Maryland, Baltimore, Maryland, U.S.A. SYNOPSIS Tardive dyskinesia, like several other choreiform disorders, is felt to be primarily related to dopaminergic activity within the striatum. Physostigmine has been demonstrated to improve the abnormal movements in patients with tardive dyskinesia while scopolamine tends to aggravate abnormal movements and in some cases elicits abnormal movement not previously observed. This evidence supports the hypothesis that anticholinergic therapy in patients prone to develop tardive dyskinesia may increase the incidence of this disorder the threshold for the by lowering appearance guest. Protected by copyright. of these movements. Tardive dyskinesia is a well-recognized side- been fully elucidated. However, there is evidence effect of long-term neuroleptic therapy (Crane, which suggests that dopamine acting at striatal 1968). The most prominent manifestation dopaminergic receptor sites may be closely is lingual-facial-buccal dyskinesia. Limb and related to the initiation of these choreiform trunkal chorea may accompany the facial move- movements in several clinical settings. Drugs ments (Paulson, 1968). The syndrome is most which alter the availability of dopamine at often seen in patients ranging in age from 50 to dopaminergic receptor sites alter choreiform 70 years who are most often diagnosed as symptomatology. Huntington's chorea is re- suffering chronic deteriorating schizophrenia. -
Pharmacology for Respiratory Care 1
RESP-1340: Pharmacology for Respiratory Care 1 RESP-1340: PHARMACOLOGY FOR RESPIRATORY CARE Cuyahoga Community College Viewing: RESP-1340 : Pharmacology for Respiratory Care Board of Trustees: March 2020 Academic Term: Fall 2020 Subject Code RESP - Respiratory Care Course Number: 1340 Title: Pharmacology for Respiratory Care Catalog Description: General principles of pharmacology and calculations of drug dosages. Discussion of pharmacologic principles and agents used in treatment of cardiopulmonary disorders. Credit Hour(s): 2 Lecture Hour(s): 2 Lab Hour(s): 0 Other Hour(s): 0 Requisites Prerequisite and Corequisite RESP-1300 Respiratory Care Equipment and RESP-1310 Cardiopulmonary Physiology. Outcomes Course Outcome(s): A. Evaluate specific information on various categories of drugs. Objective(s): 1. Demonstrate an understanding of basic terminology for respiratory care pharmacology. 2. Identify the official drug publication in the U.S. 3. Identify four common sources of drug information. Course Outcome(s): B. Describe the basic principles of drug action emphasizing the pharmaceutical phase, pharmacokinetic phase and pharmacodynamic phase. Objective(s): 1. Identify the three phases involved in drug action. 2. Identify five different routes of administration and give advantages and disadvantages of each route. 3. Identify the four processes involved in the pharmacokinetics phase. 4. Identify the essential concepts involved with the interaction of a drug molecule with its target receptor site. 2 RESP-1340: Pharmacology for Respiratory Care Course Outcome(s): C. Calculate and interpret adult dosages for medications given by respiratory care practitioners. Objective(s): 1. Calculate dosages from percentage strength solutions. 2. Calculate the amount of solute per ml of solution given a ratio. -
Pharmaceuticals As Environmental Contaminants
PharmaceuticalsPharmaceuticals asas EnvironmentalEnvironmental Contaminants:Contaminants: anan OverviewOverview ofof thethe ScienceScience Christian G. Daughton, Ph.D. Chief, Environmental Chemistry Branch Environmental Sciences Division National Exposure Research Laboratory Office of Research and Development Environmental Protection Agency Las Vegas, Nevada 89119 [email protected] Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada Why and how do drugs contaminate the environment? What might it all mean? How do we prevent it? Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada This talk presents only a cursory overview of some of the many science issues surrounding the topic of pharmaceuticals as environmental contaminants Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada A Clarification We sometimes loosely (but incorrectly) refer to drugs, medicines, medications, or pharmaceuticals as being the substances that contaminant the environment. The actual environmental contaminants, however, are the active pharmaceutical ingredients – APIs. These terms are all often used interchangeably Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada Office of Research and Development Available: http://www.epa.gov/nerlesd1/chemistry/pharma/image/drawing.pdfNational -
Integrated Approach for Identifying the Molecular, Cellular, and Host Responses to Chemical Insults
Integrated Approach for Identifying the Molecular, Cellular, and Host Responses to Chemical Insults Audrey E. Fischer, Emily P. English, Julia B. Patrone, Kathlyn Santos, Jody B. G. Proescher, Rachel S. Quizon, Kelly A. Van Houten, Robert S. Pilato, Eric J. Van Gieson, and Lucy M. Carruth e performed a pilot study to characterize the molecular, cellular, and whole-organism response to nonlethal chemical agent exposure in the central nervous system. Multiple methodologies were applied to measure in vitro enzyme inhibition, neuronal cell pathway signaling, and in vivo zebrafish neural development in response to challenge with two different classes of chemical compounds. While all compounds tested exhibited expected enzyme inhibitory activity against acetylcholinesterase (AChE), a well-characterized target of chemical agents, distinct differences between chemical exposures were detected in cellular toxicity and pathway target responses and were tested in a zebrafish model. Some of these differences have not been detected using conventional chemical toxicity screening methods. Taken together, the data demonstrate the potential value of an integrated, multimethodological approach for improved target and pathway identification for subsequent diagnostic and therapeutic biomarker development. INTRODUCTION To build capability and leverage new and growing cell models to complete living organisms. Regardless of biology and chemistry expertise at APL, a collabora- the model selected, challenges exist in sample collection, tive, cross-departmental effort was established through a dose determination, and biases inherent in each assay/ series of related independent research and development technology. Therefore, multiple experimental methodol- (IR&D) projects. The focus of this effort was on mitiga- ogies brought to bear on a particular biological question tion of chemical and biological threat agents. -
Indirect Acting Cholinergic Drugs
Editing File Indirect acting cholinergic drugs Objectives: ✓ Classification of indirect acting cholinomimetics ✓ Mechanism of action, kinetics, dynamics and uses of anticholinesterases ✓ Adverse effects & contraindications of anticholinesterases ✓ Symptoms and treatment of organophosphates toxicity. Important Notes Extra ❖ Also called Anticholinesterases Anticholinesterases prevent hydrolysis of Ach by inhibiting acetyl cholinesterase thus, increase Ach concentrations and actions at the cholinergic receptors (both nicotinic and muscarinic). Acetylcholine binds to acetylcholinesterase at M.O. two sites, anionic site and esteric site, then A the enzyme somehow breakdown the acetylcholine into acetic acid and choline. In order to inhibit this enzyme we need to create a substance that is similar to acetylcholine either in both sites or even one site. (Similar structure) Reversible anticholinesterases Irreversible anticholinesterases Durat Short Acting Intermediate Long Acting ion of actio acting n (Alcohols) (Carbamates (Phosphates esters) e.g. esters) e.g. e.g. insecticides, gas war e.g. Physostigmine, Drug edrophonium. Ecothiophate & Isoflurophate. s Neostigmine, Classi Using those drugs leads to death ficati Pyridostigmine. on Forms weak Binds to two sites used as insecticides(malathion) or hydrogen bond of cholinesterase nerve gases (sarin) . with enzyme. Form very stable covalent bond with All polar and cholinesterase . Feat acetylcholineste ures synthetic except All phosphates are lipid soluble except rase enzyme physostigmine. Ecothiophate