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Symptom Management in the Last Days of Life This Is About Managing Symptoms in the Last Days of Life Where the Dying Process Has Set In
Symptom management in the last days of life This is about managing symptoms in the last days of life where the dying process has set in. It assumes that the therapeutic aims are therefore: To allow the patient to die comfortably To support the family/carers and to start to prepare them for bereavement To discontinue any burdensome or irrelevant clinical procedures Key Prescribing Questions in the last days of life 1. Ahead of time Page a. Pre-emptive prescribing 1 b. Differences in specific circumstances 1 2. Once the oral route is lost a. What can be stopped? – managing co-morbidities at the end of life 2 (insulin; anti-epileptics; steroids; cardiac medicines) b. How to prescribe a syringe pump 3 i. Opioid conversion 4 ii. Combining drugs in a syringe – what can and can’t be mixed? 5 iii. Dosing other drugs 6 c. What can and can’t be given subcutaneously 7 3. Problems a. Uncontrolled symptoms (pain; restlessness; secretions; breathlessness; nausea; thirst) 8 b. Obtaining medicines out of hours 11 c. References and contact phone numbers 12 Pre-emptive prescribing The pre-emptive prescribing of p.r.n. medication for anticipated symptoms can avoid great distress. The cost is negligible and it saves time on the part of both families and out-of-hours health professionals. Typical maximum doses are described on page 22, but the doses needed by individuals vary widely: it is more important to assess the effectiveness of each p.r.n. before repeating or increasing doses – if a p.r.n. is ineffective, try a different approach or seek advice (see flow diagrams) A typical “pre-emptive p.r.n.” regimen for patients approaching the end of life might include: Morphine sulphate 2.5-5mg 1-4 hourly p.r.n. -
Early Protective Effects of Tiotropium Bromide in Patients with Airways Hyperres P O N S I V E N E S S
European Review for Medical and Pharmacological Sciences 2004; 8: 259-264 Early protective effects of tiotropium bromide in patients with airways hyperres p o n s i v e n e s s C. TERZANO, A. PETROIANNI, A. RICCI, L. D’ANTONI, L. ALLEGRA* Department of Cardiovascular and Respiratory Sciences, Respiratory Diseases Unit, Fondazione E. Lorillard Spencer Cenci, “La Sapienza” University - Rome (Italy) *Institute of Respiratory Diseases, University of Milan, Ospedale Maggiore IRCCS – Milan (Italy) Abstract. – Tiotropium is an anticholiner- Introduction gic drug for Ch ronic Obstructive Pulmonary Di sease (COPD) patients, with a peak b ron- Ti o t rop ium is a qu atern a ry amm o niu m chodilator effect observed after 1.5 to 2 hours and a long duration of action. The aim of our co ngener of atropine. It has been developed study was to quantify the early protection of a as a lon g-acting an ticho linergic bro n c h o d i l a- single dose of inhaled tiotropium against metha- tor for inhalation by patients with chronic ob- choline-induced bronchoconstriction in asthmat- s t ructive pu lmon ary d isease (COPD). Dru g ic patients with airway hyperresponsiveness. p ro p e rties o f ant icho lin ergic agent s have Ten subjects (7M, 3F), with history of asthma been well-kno wn to man y cultures for many and a baseline FEV (Forced Expiratory Volume 1 1 1 c e n t u r i e s . In the 1920s the d iscovery o f the sec) >80% of pred icted, were enrolled in the s t u d y. -
Future Directions for Intrathecal Pain Management 93
NEUROMODULATION: TECHNOLOGY AT THE NEURAL INTERFACE Volume 11 • Number 2 • 2008 http://www.blackwell-synergy.com/loi/ner ORIGINAL ARTICLE FBlackwell uturePublishing Inc Directions for Intrathecal Pain Management: A Review and Update From the Interdisciplinary Polyanalgesic Consensus Conference 2007 Timothy Deer, MD* • Elliot S. Krames, MD† • Samuel Hassenbusch, MD, PhD‡ • Allen Burton, MD§ • David Caraway, MD¶ • Stuart Dupen, MD** • James Eisenach, MD†† • Michael Erdek, MD‡‡ • Eric Grigsby, MD§§ • Phillip Kim, MD¶¶ • Robert Levy, MD, PhD*** • Gladstone McDowell, MD††† • Nagy Mekhail, MD‡‡‡ • Sunil Panchal, MD§§§ • Joshua Prager, MD¶¶¶ • Richard Rauck, MD**** • Michael Saulino, MD†††† •Todd Sitzman, MD‡‡‡‡ • Peter Staats, MD§§§§ • Michael Stanton-Hicks, MD¶¶¶¶ • Lisa Stearns, MD***** • K. Dean Willis, MD††††† • William Witt, MD‡‡‡‡‡ • Kenneth Follett, MD, PhD§§§§§ • Mark Huntoon, MD¶¶¶¶¶ • Leong Liem, MD****** • James Rathmell, MD†††††† • Mark Wallace, MD‡‡‡‡‡‡ • Eric Buchser, MD§§§§§§ • Michael Cousins, MD¶¶¶¶¶¶ • Ann Ver Donck, MD******* *Charleston, WV; †San Francisco, CA; ‡Houston, TX; §Houston, TX; ¶Huntington, WV; **Bellevue, WA; ††Winston Salem, NC; ‡‡Baltimore, MD; §§Napa, CA; ¶¶Wilmington, DE; ***Chicago, IL; †††Columbus, OH; ‡‡‡Cleveland, OH; §§§Tampa, FL; ¶¶¶Los Angeles, CA; ****Winston Salem, NC; ††††Elkings Park, PA; ‡‡‡‡Hattiesburg, MS; §§§§Colts Neck, NJ; ¶¶¶¶Cleveland, OH; *****Scottsdale, AZ; †††††Huntsville, AL; ‡‡‡‡‡Lexington, KY; §§§§§Iowa City, IA; ¶¶¶¶¶Rochester, NY; ******Nieuwegein, The Netherlands; ††††††Boston, MA; ‡‡‡‡‡‡La Jolla, CA; §§§§§§Switzerland; ¶¶¶¶¶¶Australia; and *******Brugge, Belgium ABSTRACT Background. Expert panels of physicians and nonphysicians, all expert in intrathecal (IT) therapies, convened in the years 2000 and 2003 to make recommendations for the rational use of IT analgesics, based on the preclinical and clinical literature known up to those times, presentations of the expert panels, discussions on current practice and standards, and the result of surveys of physicians using IT agents. -
Dopamine: a Role in the Pathogenesis and Treatment of Hypertension
Journal of Human Hypertension (2000) 14, Suppl 1, S47–S50 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00 www.nature.com/jhh Dopamine: a role in the pathogenesis and treatment of hypertension MB Murphy Department of Pharmacology and Therapeutics, National University of Ireland, Cork, Ireland The catecholamine dopamine (DA), activates two dis- (largely nausea and orthostasis) have precluded wide tinct classes of DA-specific receptors in the cardio- use of D2 agonists. In contrast, the D1 selective agonist vascular system and kidney—each capable of influenc- fenoldopam has been licensed for the parenteral treat- ing systemic blood pressure. D1 receptors on vascular ment of severe hypertension. Apart from inducing sys- smooth muscle cells mediate vasodilation, while on temic vasodilation it induces a diuresis and natriuresis, renal tubular cells they modulate sodium excretion. D2 enhanced renal blood flow, and a small increment in receptors on pre-synaptic nerve terminals influence nor- glomerular filtration rate. Evidence is emerging that adrenaline release and, consequently, heart rate and abnormalities in DA production, or in signal transduc- vascular resistance. Activation of both, by low dose DA tion of the D1 receptor in renal proximal tubules, may lowers blood pressure. While DA also binds to alpha- result in salt retention and high blood pressure in some and beta-adrenoceptors, selective agonists at both DA humans and in several animal models of hypertension. receptor classes have been studied in the treatment of -
Hyoscine Butylbromide, Levomepromazine, Metoclopramide, Midazolam, Ondansetron
TRUST WIDE/DIVISIONAL DOCUMENT Delete as appropriate Policy/Standard Operating Procedure/ Clinical Guideline Policy and Procedure for the T34 Ambulatory Syringe Pump DOCUMENT TITLE: in adults (Palliative Care) DOCUMENT ELHT/CP22 Version 5.3 NUMBER: DOCUMENT REPLACES Which ELHT/CP22 Version 5.2 Version LEAD EXECUTIVE DIRECTOR DGM AUTHOR(S): Note Syringe pump policy task and finish group chaired by should not include Palliative Medicine Consultant names TARGET AUDIENCE: Medical and Nursing Staff 1 To provide a clear governance framework to ensure a safe and consistent approach to the use of the T34 Ambulatory Syringe Pump DOCUMENT 2 To provide details of how to set up and administer PURPOSE: medication by a T34 Ambulatory Syringe Pump 3 To provide easily accessible information about the common medicines used in a Syringe Pump Clinical Practice Summary. Guidance on consensus approaches To be read in to managing palliative care symptoms. Lancashire and South conjunction with Cumbria consensus guidance – August 2017 (identify which internal C064 V5 Medicines Management Policy documents) IC24 V4 Aseptic non touch technique (ANTT) policy East Lancashire Hospital NHS Trust – Policies & Procedures, Protocols, Guidelines ELHT/CP22 v5.2 May 2020 Page 1 of 77 Nursing and Midwifery Council - Standards for Medicines Management 2015 Dickman et al (2016) The Syringe Driver, 4th edition, Oxford Press T. Mitten, (2000) Subcutaneous drug infusions, a review of problems and solutions. International Journal of Palliative Nursing Vol 7, No 2. Twycross et al (2017) 6th Edition Palliative Care SUPPORTING Formulary and Palliative Care Formulary online, REFERENCES accessed June 2018 Twycross R., Wilcock A., (2001) Symptom Management in Advanced Cancer 3rd edition Radcliffe medical press Oxon. -
Approach to the Poisoned Patient
PED-1407 Chocolate to Crystal Methamphetamine to the Cinnamon Challenge - Emergency Approach to the Intoxicated Child BLS 08 / ALS 75 / 1.5 CEU Target Audience: All Pediatric and adolescent ingestions are common reasons for 911 dispatches and emergency department visits. With greater availability of medications and drugs, healthcare professionals need to stay sharp on current trends in medical toxicology. This lecture examines mind altering substances, initial prehospital approach to toxicology and stabilization for transport, poison control center resources, and ultimate emergency department and intensive care management. Pediatric Toxicology Dr. James Burhop Pediatric Emergency Medicine Children’s Hospital of the Kings Daughters Objectives • Epidemiology • History of Poisoning • Review initial assessment of the child with a possible ingestion • General management principles for toxic exposures • Case Based (12 common pediatric cases) • Emerging drugs of abuse • Cathinones, Synthetics, Salvia, Maxy/MCAT, 25I, Kratom Epidemiology • 55 Poison Centers serving 295 million people • 2.3 million exposures in 2011 – 39% are children younger than 3 years – 52% in children younger than 6 years • 1-800-222-1222 2011 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System Introduction • 95% decline in the number of pediatric poisoning deaths since 1960 – child resistant packaging – heightened parental awareness – more sophisticated interventions – poison control centers Epidemiology • Unintentional (1-2 -
Identification Ofa D1 Dopamine Receptor, Not Linked To
Br. J. Pharmacol. (1991), 103, 1928-1934 11--" Macmillan Press Ltd, 1991 Identification of a D1 dopamine receptor, not linked to adenylate cyclase, on lactotroph cells 'Danny F. Schoors, *Georges P. Vauquelin, *Hilde De Vos, fGerda Smets, Brigitte Velkeniers, Luc Vanhaelst & Alain G. Dupont Department of Pharmacology, Medical School, Vrije Universiteit Brussel (V.U.B.), Laarbeeklaan 103, B-1090, Brussels, Belgium; *Protein Chemistry Laboratory, Instituut voor Moleculaire Biologie, V.U.B., Paardenstraat 65, St-Genesius-Rode, Belgium and tDepartment of Experimental Pathology, Medical School, V.U.B., Laarbeeklaan 103, B-1090, Brussels, Belgium 1 We studied the lactotroph cells of the rat by both in vivo and in vitro pharmacological techniques for the presence of D1-receptors. Both approaches revealed the presence of a D2-receptor, stimulated by quinpirole (resulting in an inhibition of prolactin secretion) and blocked by domperidone. 2 Administration of fenoldopam, the most selective Dl-receptor agonist currently available, resulted in a dose-dependent decrease of prolactin secretion in vivo (after pretreatment with a-methyl-p-tyrosine) and in vitro (cultured pituitary cells). This increase was dose-dependently blocked by the selective D1-receptor antagonist, SCH 23390, and although the effect of fenoldopam was less than that obtained by D2-receptor stimulation, these data suggest that a D,-receptor also controls prolactin secretion. 3 In order to detect the location of these dopamine receptors, autoradiographic studies were performed by use of [3H]-SCH 23390 and [3H]-spiperone as markers for D1- and D2-receptors, respectively. Specific binding sites for [3H]-SCH 23390 were demonstrated. Fenoldopam dose-dependently reduced [3H]-SCH 23390 binding, but had no effect on [3H]-spiperone binding. -
Sandostatin® Injection
Sandostatin® octreotide acetate Injection Rx Only T2002-XX XXXXXXXX DESCRIPTION Sandostatin® (octreotide acetate) Injection, a cyclic octapeptide prepared as a clear sterile solution of octreotide, acetate salt, in a buffered lactic acid solution for administration by deep subcutaneous (intrafat) or intravenous injection. Octreotide acetate, known chemically as L-Cysteinamide, D-phenylalanyl-L-cysteinyl-L-phenylalanyl-D-tryptophyl-L-lysyl-L- threonyl-N-[2-hydroxy-1-(hydroxymethyl)propyl]-, cyclic (2→7)-disulfide; [R-(R*, R*)] acetate salt, is a long-acting octapeptide with pharmacologic actions mimicking those of the natural hormone somatostatin. Sandostatin® (octreotide acetate) Injection is available as: sterile 1 mL ampuls in 3 strengths, containing 50, 100, or 500 mcg octreotide (as acetate), and sterile 5 mL multi-dose vials in 2 strengths, containing 200 and 1000 mcg/mL of octreotide (as acetate). Each ampul also contains: lactic acid, USP............................................................ 3.4 mg mannitol, USP .............................................................. 45 mg sodium bicarbonate, USP.............................qs to pH 4.2 ± 0.3 water for injection, USP ........................................ qs to 1 mL Each mL of the multi-dose vials also contains: lactic acid, USP ........................................................... 3.4 mg mannitol, USP .............................................................. 45 mg phenol, USP ................................................................ 5.0 mg sodium -
Acute Poisoning: Understanding 90% of Cases in a Nutshell S L Greene, P I Dargan, a L Jones
204 REVIEW Postgrad Med J: first published as 10.1136/pgmj.2004.027813 on 5 April 2005. Downloaded from Acute poisoning: understanding 90% of cases in a nutshell S L Greene, P I Dargan, A L Jones ............................................................................................................................... Postgrad Med J 2005;81:204–216. doi: 10.1136/pgmj.2004.024794 The acutely poisoned patient remains a common problem Paracetamol remains the most common drug taken in overdose in the UK (50% of intentional facing doctors working in acute medicine in the United self poisoning presentations).19 Non-steroidal Kingdom and worldwide. This review examines the initial anti-inflammatory drugs (NSAIDs), benzodiaze- management of the acutely poisoned patient. Aspects of pines/zopiclone, aspirin, compound analgesics, drugs of misuse including opioids, tricyclic general management are reviewed including immediate antidepressants (TCAs), and selective serotonin interventions, investigations, gastrointestinal reuptake inhibitors (SSRIs) comprise most of the decontamination techniques, use of antidotes, methods to remaining 50% (box 1). Reductions in the price of drugs of misuse have led to increased cocaine, increase poison elimination, and psychological MDMA (ecstasy), and c-hydroxybutyrate (GHB) assessment. More common and serious poisonings caused toxicity related ED attendances.10 Clinicians by paracetamol, salicylates, opioids, tricyclic should also be aware that severe toxicity can result from exposure to non-licensed pharmaco- -
Title 16. Crimes and Offenses Chapter 13. Controlled Substances Article 1
TITLE 16. CRIMES AND OFFENSES CHAPTER 13. CONTROLLED SUBSTANCES ARTICLE 1. GENERAL PROVISIONS § 16-13-1. Drug related objects (a) As used in this Code section, the term: (1) "Controlled substance" shall have the same meaning as defined in Article 2 of this chapter, relating to controlled substances. For the purposes of this Code section, the term "controlled substance" shall include marijuana as defined by paragraph (16) of Code Section 16-13-21. (2) "Dangerous drug" shall have the same meaning as defined in Article 3 of this chapter, relating to dangerous drugs. (3) "Drug related object" means any machine, instrument, tool, equipment, contrivance, or device which an average person would reasonably conclude is intended to be used for one or more of the following purposes: (A) To introduce into the human body any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (B) To enhance the effect on the human body of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (C) To conceal any quantity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; or (D) To test the strength, effectiveness, or purity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state. (4) "Knowingly" means having general knowledge that a machine, instrument, tool, item of equipment, contrivance, or device is a drug related object or having reasonable grounds to believe that any such object is or may, to an average person, appear to be a drug related object. -
Pharmacological and Ionic Characterizations of the Muscarinic Receptors Modulating [3H]Acetylcholine Release from Rat Cortical Synaptosomes’
0270.6474/85/0505-1202$02.00/O The Journal of Neuroscience CopyrIght 0 Society for Neuroscrence Vol. 5, No. 5, pp. 1202-1207 Printed in U.S.A. May 1985 Pharmacological and Ionic Characterizations of the Muscarinic Receptors Modulating [3H]Acetylcholine Release from Rat Cortical Synaptosomes’ EDWIN M. MEYER* AND DEBORAH H. OTERO Department of Pharmacology and Therapeutics, University of Florida School of Medicine, Gainesville, Florida 32610 Abstract brain (Gonzales and Crews, 1984). M,-receptors, however, appear pre- and postsynaptically in brain, are regulated by an intrinsic The muscarinic receptors that modulate acetylcholine membrane protein that binds to GTP (g-protein), and may not be release from rat cortical synaptosomes were characterized coupled to changes in phosphatidylinositol turnover. with respect to sensitivity to drugs that act selectively at M, The present studies were designed to determine whether M,- or or Ma receptor subtypes, as well as to changes in ionic Mp-receptors mediate the presynaptic modulation of ACh release. strength and membrane potential. The modulatory receptors These studies involve dose-response curves for the release of appear to be of the M2 type, since they are activated by synaptosomal [3H]ACh in the presence of selected muscarinic ago- carbachol, acetylcholine, methacholine, oxotremorine, and nists and antagonists, as well as treatments that selectively alter MI- bethanechol, but not by pilocarpine, and are blocked by or M,-receptor activity. Our results indicate that the presynaptic atropine, scopolamine, and gallamine (at high concentra- modulation of [3H]ACh release is mediated by MP- but not MI- tions), but not by pirenzepine or dicyclomine. -
Protective Effects of Inhaled Ipratropium Bromide on Bronchoconstriction Induced by Adenosine and Methacholine in Asthma
Eur Aesplr J 1992, 5, 56()-665 Protective effects of inhaled ipratropium bromide on bronchoconstriction induced by adenosine and methacholine In asthma N. Crimi, F. Palermo, R. Oliveri, R. Polosa, I. Settinieri, A. Mistretta Protective effects of inhaled ipratropium bromide on bronchoconstriction induced by Istituto di Malattie dell' Apparato adenosine and methacholine in asthma. N. Crimi, F. Palermo, R. Oliveri, R. Po/osa, Respiratorio e Tisiologia, Universita' di Catania, Catania, Italy. I. Seuinier~ A. Mistretta. ABSTRACT: Although adenosine-Induced bronchoconstrictlon is mainly due to Correspondence: N. Crimi mast cell mediator release, vagal reflexes have also been Implicated in this Istituto di Malattie dell' Appara.to response. Respiratorio e Tisiologia We have Investigated the effect of a speciflc muscarlnlc-receptor antagonist, Universita' di Catania ipratroplum bromide, on methacholine- and adenosine-Induced bronchoconstriction Via Passo Gravina 187 In a randomized, placebo-controlled, double-blind study of 12 asthmatic subjects. 95125 Catania Airway response was evaluated as forced expiratory volume in one second (FEV,). Italy Inhaled lpratroplum bromide (40 Jlg), administered 20 mln prior to bronchoprovocation, Increased the provocation dose of Inhaled methacholine and Keywords: Adenosine adenosine required to reduce FEV, by 20% from baseline (PD,.) from 0.11 to 0.79 asthma ipratropium bromide mg (p<O.Ol) and from 0.57 to 1.27 mg (p<0.01), respectively. The mean baseline methacholine FEV, values after administration of lpratroplum bromide were signlfkantly higher than after placebo administration (p<O.OS). However, there was no correlation Received: May 22 1991 between the degree of bronchodllatatlon and dose-ratios for methacholine and Accepted after revision January 7 1992 adenosine.