Evidence Review E

Total Page:16

File Type:pdf, Size:1020Kb

Evidence Review E National Institute for Health and Care Excellence Draft for consultation Hypertension in pregnancy [E] Evidence review for postnatal management of hypertension NICE guideline CG107 (update) Evidence review February 2019 Draft for Consultation This evidence review was developed by the National Guideline Alliance hosted by the Royal College of Obstetricians and Gynaecologists DRAFT FOR CONSULTATION Error! No text of specified style in document. Disclaimer The recommendations in this guideline represent the view of NICE, arrived at after careful consideration of the evidence available. When exercising their judgement, professionals are expected to take this guideline fully into account, alongside the individual needs, preferences and values of their patients or service users. The recommendations in this guideline are not mandatory and the guideline does not override the responsibility of healthcare professionals to make decisions appropriate to the circumstances of the individual patient, in consultation with the patient and/or their carer or guardian. Local commissioners and/or providers have a responsibility to enable the guideline to be applied when individual health professionals and their patients or service users wish to use it. They should do so in the context of local and national priorities for funding and developing services, and in light of their duties to have due regard to the need to eliminate unlawful discrimination, to advance equality of opportunity and to reduce health inequalities. Nothing in this guideline should be interpreted in a way that would be inconsistent with compliance with those duties. NICE guidelines cover health and care in England. Decisions on how they apply in other UK countries are made by ministers in the Welsh Government, Scottish Government, and Northern Ireland Executive. All NICE guidance is subject to regular review and may be updated or withdrawn. Copyright © NICE 2019. All rights reserved. Subject to Notice of Rights ISBN: DRAFT FOR CONSULTATION Contents Review question HiP5. What is the optimal management of hypertension for women during the postnatal period? .................................................................................. 6 Introduction ........................................................................................................... 6 Summary of the protocol ....................................................................................... 6 Methods and process ............................................................................................ 7 Clinical evidence ................................................................................................... 7 Summary of clinical studies included in the evidence review ................................. 7 Quality assessment of clinical studies included in the evidence review ............... 12 Economic evidence ............................................................................................. 12 Evidence statements ........................................................................................... 13 Comparison 1. Beta blockers / mixed alpha-beta blockers versus centrally acting α2-adrenoceptor agonists .............................................................. 13 Comparison 2. Beta blockers versus beta blockers. ............................................ 13 Comparison 2.1 Atenolol versus metoprolol ........................................................ 13 Comparison 2.2 Atenolol versus propranolol ....................................................... 14 Comparison 3. Beta blockers/mixed alpha-beta blockers versus placebo ............ 14 Comparison 4. Centrally acting α2-adrenoceptor agonists versus ACE inhibitors .................................................................................................. 14 Comparison 5. Calcium channel blockers versus placebo/ low sodium diet ......... 15 Comparison 6. Calcium channel blockers versus beta blockers .......................... 15 Comparison 7. Diuretics versus placebo/no intervention ..................................... 16 Comparison 8. Vasodilators versus beta blockers / mixed alpha-beta blockers ... 16 Beta-blockers (non-comparative studies)............................................................. 16 Calcium channel blockers (non-comparative studies) .......................................... 17 Recommendations .............................................................................................. 17 Rationale and impact ........................................................................................... 18 The committee’s discussion of the evidence ........................................................ 19 References ................................................................................................................... 22 Appendices ........................................................................................................................ 24 Appendix A – Review protocol ...................................................................................... 24 Appendix B – Literature search strategies .................................................................... 32 Review question search strategies ...................................................................... 32 Databases: Medline; Medline EPub Ahead of Print; and Medline In-Process & Other Non-Indexed Citations .................................................................... 32 Database: Embase; and Embase Classic ............................................................ 34 Databases: Cochrane Central Register of Controlled Trials; Cochrane Database of Systematic Reviews; Database of Abstracts of Reviews of Effects; and Health Technology Assessment ........................................... 36 Health economics search strategies .................................................................... 38 4 DRAFT FOR CONSULTATION Databases: Medline; Medline EPub Ahead of Print; and Medline In-Process & Other Non-Indexed Citations .................................................................... 38 Databases: Embase; and Embase Classic .......................................................... 40 Databases: Cochrane Central Register of Controlled Trials; Health Technology Assessment; and NHS Economic Evaluation Database ........................... 43 Appendix C – Clinical evidence study selection ............................................................ 45 Appendex D – Clinical evidence tables ......................................................................... 46 Appendix E – Forest plots............................................................................................. 83 Appendix F – GRADE tables ........................................................................................ 84 Appendix G – Economic evidence study selection ...................................................... 104 Appendix H – Economic evidence tables .................................................................... 105 Appendix I – Health economic evidence profiles ......................................................... 106 Appendix J – Health economic analysis ...................................................................... 107 Appendix K – Excluded studies .................................................................................. 108 Clinical studies .................................................................................................. 108 Economic studies .............................................................................................. 113 Appendix L – Research recommendations ................................................................. 114 5 DRAFT FOR CONSULTATION Postnatal management 1 Review question HiP5. What is the optimal management of 2 hypertension for women during the postnatal period? 3 Introduction 4 Hypertension in the postnatal period affects several groups of women, including those with 5 chronic hypertension, gestational hypertension and pre-eclampsia. Hypertension may also 6 present for the first time in the postnatal period. Regardless of the different underlying 7 causes and clinical presentations, treatment of hypertension is broadly similar. 8 There is limited information about the use of antihypertensive drugs in the postnatal period, 9 particularly in women who choose to breastfeed, and some antihypertensive drugs are 10 contraindicated or must be used with caution by women who are breastfeeding. The choice 11 of medication should therefore be discussed with women requiring antihypertensive drugs so 12 that women can make informed choices. Encouraging and supporting breastfeeding is a key 13 priority for maternity care providers. 14 The aim of this review is to identify the efficacy and safety of different antihypertensives for 15 the management of hypertension in the postnatal period. 16 Summary of the protocol 17 See Table 1 for a summary of the population, intervention, comparison and outcome (PICO) 18 characteristics of this review. 19 Table 1: Summary of the protocol (PICO table) Population Postnatal women who require antihypertensive treatment up to 6 weeks after delivery Intervention Beta blockers / mixed alpha-beta blockers Centrally acting α2-adrenoceptor agonists Calcium channel blockers Angiotensin receptor blockers Angiotensin converting enzyme (ACE) inhibitors Diuretics Vasodilators Comparison Other antihypertensive agents Placebo No treatment Outcome Critical outcomes: Outcomes for women
Recommended publications
  • Pindolol of the Activation of Postsynaptic 5-HT1A Receptors
    Potentiation by (-)Pindolol of the Activation of Postsynaptic 5-HT1A Receptors Induced by Venlafaxine Jean-Claude Béïque, Ph.D., Pierre Blier, M.D., Ph.D., Claude de Montigny, M.D., Ph.D., and Guy Debonnel, M.D. The increase of extracellular 5-HT in brain terminal regions antagonist WAY 100635 (100 ␮g/kg, i.v.). A short-term produced by the acute administration of 5-HT reuptake treatment with VLX (20 mg/kg/day ϫ 2 days) resulted in a inhibitors (SSRI’s) is hampered by the activation of ca. 90% suppression of the firing activity of 5-HT neurons somatodendritic 5-HT1A autoreceptors in the raphe nuclei. in the dorsal raphe nucleus. This was prevented by the The present in vivo electrophysiological studies were coadministration of (-)pindolol (15 mg/kg/day ϫ 2 days). undertaken, in the rat, to assess the effects of the Taken together, these results indicate that (-)pindolol coadministration of venlafaxine, a dual 5-HT/NE reuptake potentiated the activation of postsynaptic 5-HT1A receptors inhibitor, and (-)pindolol on pre- and postsynaptic 5-HT1A resulting from 5-HT reuptake inhibition probably by receptor function. The acute administration of venlafaxine blocking the somatodendritic 5-HT1A autoreceptor, but not and of the SSRI paroxetine (5 mg/kg, i.v.) induced a its postsynaptic congener. These results support and extend suppression of the firing activity of dorsal hippocampus CA3 previous findings providing a biological substratum for the pyramidal neurons. This effect of venlafaxine was markedly efficacy of pindolol as an accelerating strategy in major potentiated by a pretreatment with (-)pindolol (15 mg/kg, depression.
    [Show full text]
  • TABLE 1 Studies of Antagonist Activity in Constitutively Active
    TABLE 1 Studies of antagonist activity in constitutively active receptors systems shown to demonstrate inverse agonism for at least one ligand Targets are natural Gs and constitutively active mutants (CAM) of GPCRs. Of 380 antagonists, 85% of the ligands demonstrate inverse agonism. Receptor Neutral Antagonist Inverse Agonist Reference Human β2-adrenergic Dichloroisoproterenol, pindolol, labetolol, timolol, Chidiac et al., 1996; Azzi et alprenolol, propranolol, ICI 118,551, cyanopindolol al., 2001 Turkey erythrocyte β-adrenergic Propranolol, pindolol Gotze et al., 1994 Human β2-adrenergic (CAM) Propranolol Betaxolol, ICI 118,551, sotalol, timolol Samama et al., 1994; Stevens and Milligan, 1998 Human/guinea pig β1-adrenergic Atenolol, propranolol Mewes et al., 1993 Human β1-adrenergic Carvedilol CGP20712A, metoprolol, bisoprolol Engelhardt et al., 2001 Rat α2D-adrenergic Rauwolscine, yohimbine, WB 4101, idazoxan, Tian et al., 1994 phentolamine, Human α2A-adrenergic Napthazoline, Rauwolscine, idazoxan, altipamezole, levomedetomidine, Jansson et al., 1998; Pauwels MPV-2088 (–)RX811059, RX 831003 et al., 2002 Human α2C-adrenergic RX821002, yohimbine Cayla et al., 1999 Human α2D-adrenergic Prazosin McCune et al., 2000 Rat α2-adrenoceptor MK912 RX821002 Murrin et al., 2000 Porcine α2A adrenoceptor (CAM- Idazoxan Rauwolscine, yohimbine, RX821002, MK912, Wade et al., 2001 T373K) phentolamine Human α2A-adrenoceptor (CAM) Dexefaroxan, (+)RX811059, (–)RX811059, RS15385, yohimbine, Pauwels et al., 2000 atipamezole fluparoxan, WB 4101 Hamster α1B-adrenergic
    [Show full text]
  • Alpha^ and Beta^Blocking Agents: Pharmacology and Properties
    CURRENT DRUG THERAPY DONALD G. VIDT, MD AND ALAN BAKST, PharmD, EDITORS Alpha^ and beta^blocking agents: pharmacology and properties PROFESSOR B.N.C. PRICHARD • Adrenergic receptors have been separated into alpha and beta groups, which have then been further subdivided. Agents have been developed that block each type of receptor with varying degrees of specificity between the sub-types, leading to differences in pharmacodynamic profile. A more recent innovation has been the development of multiple action beta-blocking drugs, ie, those not only blocking the beta receptors but also posessing a peripheral vasodilator effect that may be due to alpha blockade, beta-2 stimulation, or a vasodilator action independent of either alpha or beta receptors. • INDEX TERMS: ALPHA BLOCKERS; BETA BLOCKERS; HYPERTENSION • CLEVE CLIN ] MED 1991; 58:33 7-350 HE CONCEPT that binding of Rosenblueth suggested that a transmitter released at catecholamines to receptors leads to differ- sympathetic nerve endings produced either inhibitory ing responses was first described by Langley, or excitatory responses as a result of combination with who in 1905 noted that a cell may make sympathin I or sympathin E at the receptor.3 Tmotor or inhibitory substances or both, and that "the The current classification of alpha and beta respon- effect of a nerve impulse depends upon the proportion ses is based on the classic work of Ahlquist,4 who of the two kinds of receptive substance which is af- studied six sympathomimetic amines and found two fected by the impulse."1 In 1906, Dale reported that patterns of reactivity. One group of actions, mediated ergot blocked the excitatory but not the inhibitory ac- by what were termed "alpha receptors," were principally tions of adrenaline.2 In 1933, Cannon and excitatory.
    [Show full text]
  • The In¯Uence of Medication on Erectile Function
    International Journal of Impotence Research (1997) 9, 17±26 ß 1997 Stockton Press All rights reserved 0955-9930/97 $12.00 The in¯uence of medication on erectile function W Meinhardt1, RF Kropman2, P Vermeij3, AAB Lycklama aÁ Nijeholt4 and J Zwartendijk4 1Department of Urology, Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; 2Department of Urology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands; 3Pharmacy; and 4Department of Urology, Leiden University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands Keywords: impotence; side-effect; antipsychotic; antihypertensive; physiology; erectile function Introduction stopped their antihypertensive treatment over a ®ve year period, because of side-effects on sexual function.5 In the drug registration procedures sexual Several physiological mechanisms are involved in function is not a major issue. This means that erectile function. A negative in¯uence of prescrip- knowledge of the problem is mainly dependent on tion-drugs on these mechanisms will not always case reports and the lists from side effect registries.6±8 come to the attention of the clinician, whereas a Another way of looking at the problem is drug causing priapism will rarely escape the atten- combining available data on mechanisms of action tion. of drugs with the knowledge of the physiological When erectile function is in¯uenced in a negative mechanisms involved in erectile function. The way compensation may occur. For example, age- advantage of this approach is that remedies may related penile sensory disorders may be compen- evolve from it. sated for by extra stimulation.1 Diminished in¯ux of In this paper we will discuss the subject in the blood will lead to a slower onset of the erection, but following order: may be accepted.
    [Show full text]
  • Adrenoceptor Subtype 1Ian Marshall, Richard P
    Brifish Journal of Pharmacology (I995) 115, 781 - 786 1995 Stockton Press All rights reserved 0007-1188/95 $12.00 X Noradrenaline contractions of human prostate mediated by aClA- (cxlc) adrenoceptor subtype 1Ian Marshall, Richard P. Burt & *Christopher R. Chapple Department of Pharmacology, University College London, Gower Street, London WC1E 6BT and *Department of Urology, The Royal Hallamshire Hospital, Glossop Road, Sheffield SlO 2JF 1 The subtype of a1-adrenoceptor mediating contractions of human prostate to noradrenaline was characterized by use of a range of competitive and non-competitive antagonists. 2 Contractions of the prostate to either noradrenaline (pD2 5.5), phenylephrine (pD2 5.1) or methoxamine (pD2 4.4) were unaltered by the presence of neuronal and extraneuronal uptake blockers. Noradrenaline was about 3 and 10 times more potent than phenylephrine and methoxamine respectively. Phenylephrine and methoxamine were partial agonists. 3 Pretreatment with the alkylating agent, chlorethylclonidine (10-4 M) shifted the noradrenaline concentration-contraction curve about 3 fold to the right and depressed the maximum response by 31%. This shift is 100 fold less than that previously shown to be produced by chlorethylclonidine under the same conditions on OlB-adrenoceptor-mediated contractions. 4 Cumulative concentration-contraction curves for noradrenaline were competitively antagonized by WB 4101 (pA2 9.0), 5-methyl-urapidil (pA2 8.6), phentolamine (pA2 7.6), benoxathian (pA2 8.5), spiperone (pA2 7.3), indoramin (pA2 8.2) and BMY 7378 (pA2 6.6). These values correlated best with published pKi values for their displacement of [3H]-prazosin binding on membranes expressing cloned oczc-adrenoceptors and poorly with values from cloned lb- and cld-adrenoceptors.
    [Show full text]
  • Compositions and Methods for Selective Delivery of Oligonucleotide Molecules to Specific Neuron Types
    (19) TZZ ¥Z_T (11) EP 2 380 595 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 26.10.2011 Bulletin 2011/43 A61K 47/48 (2006.01) C12N 15/11 (2006.01) A61P 25/00 (2006.01) A61K 49/00 (2006.01) (2006.01) (21) Application number: 10382087.4 A61K 51/00 (22) Date of filing: 19.04.2010 (84) Designated Contracting States: • Alvarado Urbina, Gabriel AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Nepean Ontario K2G 4Z1 (CA) HR HU IE IS IT LI LT LU LV MC MK MT NL NO PL • Bortolozzi Biassoni, Analia Alejandra PT RO SE SI SK SM TR E-08036, Barcelona (ES) Designated Extension States: • Artigas Perez, Francesc AL BA ME RS E-08036, Barcelona (ES) • Vila Bover, Miquel (71) Applicant: Nlife Therapeutics S.L. 15006 La Coruna (ES) E-08035, Barcelona (ES) (72) Inventors: (74) Representative: ABG Patentes, S.L. • Montefeltro, Andrés Pablo Avenida de Burgos 16D E-08014, Barcelon (ES) Edificio Euromor 28036 Madrid (ES) (54) Compositions and methods for selective delivery of oligonucleotide molecules to specific neuron types (57) The invention provides a conjugate comprising nucleuc acid toi cell of interests and thus, for the treat- (i) a nucleic acid which is complementary to a target nu- ment of diseases which require a down-regulation of the cleic acid sequence and which expression prevents or protein encoded by the target nucleic acid as well as for reduces expression of the target nucleic acid and (ii) a the delivery of contrast agents to the cells for diagnostic selectivity agent which is capable of binding with high purposes.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2012/0115729 A1 Qin Et Al
    US 201201.15729A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2012/0115729 A1 Qin et al. (43) Pub. Date: May 10, 2012 (54) PROCESS FOR FORMING FILMS, FIBERS, Publication Classification AND BEADS FROM CHITNOUS BOMASS (51) Int. Cl (75) Inventors: Ying Qin, Tuscaloosa, AL (US); AOIN 25/00 (2006.01) Robin D. Rogers, Tuscaloosa, AL A6II 47/36 (2006.01) AL(US); (US) Daniel T. Daly, Tuscaloosa, tish 9.8 (2006.01)C (52) U.S. Cl. ............ 504/358:536/20: 514/777; 426/658 (73) Assignee: THE BOARD OF TRUSTEES OF THE UNIVERSITY OF 57 ABSTRACT ALABAMA, Tuscaloosa, AL (US) (57) Disclosed is a process for forming films, fibers, and beads (21) Appl. No.: 13/375,245 comprising a chitinous mass, for example, chitin, chitosan obtained from one or more biomasses. The disclosed process (22) PCT Filed: Jun. 1, 2010 can be used to prepare films, fibers, and beads comprising only polymers, i.e., chitin, obtained from a suitable biomass, (86). PCT No.: PCT/US 10/36904 or the films, fibers, and beads can comprise a mixture of polymers obtained from a suitable biomass and a naturally S3712). (4) (c)(1), Date: Jan. 26, 2012 occurring and/or synthetic polymer. Disclosed herein are the (2), (4) Date: an. AO. films, fibers, and beads obtained from the disclosed process. O O This Abstract is presented solely to aid in searching the sub Related U.S. Application Data ject matter disclosed herein and is not intended to define, (60)60) Provisional applicationpp No. 61/182,833,sy- - - s filed on Jun.
    [Show full text]
  • Modulation of Dialysate Levels of Dopamine, Noradrenaline
    Modulation of Dialysate Levels of Dopamine, Noradrenaline, and Serotonin (5-HT) in the Frontal Cortex of Freely-Moving Rats by (-)-Pindolol Alone and in Association with 5-HT Reuptake Inhibitors: Comparative Roles b of -Adrenergic, 5-HT1A, and 5-HT1B Receptors Alain Gobert, Ph.D. and Mark J. Millan, Ph.D. (-)-Pindolol, which possesses significant affinity for 5-HT1A, involved. (-)-Pindolol potentiated the increase in FCX levels b 5-HT1B, and 1/2-adrenergic receptors (AR)s, dose- of 5-HT elicited by the 5-HT reuptake inhibitors, fluoxetine dependently increased extracellular levels of dopamine and duloxetine, and also enhanced their ability to elevate (DA) and noradrenaline (NAD) versus 5-HT, in dialysates FCX levels of DA—though not of NAD. In contrast to of the frontal cortex (FCX), but not accumbens and (-)-pindolol, betaxolol and ICI118,551 did not affect the striatum, of freely-moving rats. In distinction, the actions of fluoxetine, whereas both WAY100,635 and b preferential 1-AR antagonist, betaxolol, and the SB224,289 potentiated the increase in levels of 5-HT—but b preferential 2-AR antagonist, ICI118,551, did not increase not DA or NAD levels—elicited by fluoxetine. In basal levels of DA, NAD, or 5-HT. Further, they both dose- conclusion, (-)-pindolol modulates, both alone and together dependently and markedly blunted the influence of with 5-HT reuptake inhibitors, dopaminergic, adrenergic, (-)-pindolol upon DA and NAD levels. The selective 5-HT1A and serotonergic transmission in the FCX via a complex b receptor antagonist, WAY100,635, slightly attenuated the pattern of actions at 1/2-ARs, 5-HT1A, and 5-HT1B (-)-pindolol-induced increase in DA and NAD levels, while receptors.
    [Show full text]
  • Association of Oral Anticoagulants and Proton Pump Inhibitor Cotherapy with Hospitalization for Upper Gastrointestinal Tract Bleeding
    Supplementary Online Content Ray WA, Chung CP, Murray KT, et al. Association of oral anticoagulants and proton pump inhibitor cotherapy with hospitalization for upper gastrointestinal tract bleeding. JAMA. doi:10.1001/jama.2018.17242 eAppendix. PPI Co-therapy and Anticoagulant-Related UGI Bleeds This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Appendix: PPI Co-therapy and Anticoagulant-Related UGI Bleeds Table 1A Exclusions: end-stage renal disease Diagnosis or procedure code for dialysis or end-stage renal disease outside of the hospital 28521 – anemia in ckd 5855 – Stage V , ckd 5856 – end stage renal disease V451 – Renal dialysis status V560 – Extracorporeal dialysis V561 – fitting & adjustment of extracorporeal dialysis catheter 99673 – complications due to renal dialysis CPT-4 Procedure Codes 36825 arteriovenous fistula autogenous gr 36830 creation of arteriovenous fistula; 36831 thrombectomy, arteriovenous fistula without revision, autogenous or 36832 revision of an arteriovenous fistula, with or without thrombectomy, 36833 revision, arteriovenous fistula; with thrombectomy, autogenous or nonaut 36834 plastic repair of arteriovenous aneurysm (separate procedure) 36835 insertion of thomas shunt 36838 distal revascularization & interval ligation, upper extremity 36840 insertion mandril 36845 anastomosis mandril 36860 cannula declotting; 36861 cannula declotting; 36870 thrombectomy, percutaneous, arteriovenous
    [Show full text]
  • 9719087.Pdf (3.190Mb)
    US009719087B2 a2) United States Patent (0) Patent No.: US 9,719,087 B2 Olson et al. (45) Date of Patent: *Aug. 1, 2017 (54) MICRO-RNA FAMILY THAT MODULATES A61LK 39/3955 (2013.01); AGLK 45/06 FIBROSIS AND USES THEREOF (2013.01); A6IL 31/08 (2013.01); AGIL 31/16 (2013.01); C12N 9/16 (2013.01); C12N (71) Applicant: THE BOARD OF REGENTS, THE 15/8509 (2013.01); AOIK 2207/30 (2013.01); UNIVERSITY OF TEXAS SYSTEM, AOIK 2217/052 (2013.01); AOLK 2217/075 Austin, TX (US) (2013.01); AOIK 2217/15 (2013.01); AOIK 2217/206 (2013.01); AOIK 2227/105 (72) Inventors: Erie N. Olson, Dallas, TX (US); Eva (2013.01); AOIK 2267/0375 (2013.01); AIL van Rooij, Utrecht (NL) 2300/258 (2013.01); A6IL 2300/45 (2013.01); : AOIL 2420/06 (2013.01); C12N 2310/113 (73) Assignee: THE BOARD OF REGENTS, THE (2013.01); CI2N 2310/141 (2013.01); CI2N UNIVERSITY OF TEXAS SYSTEM, 2310/315 (2013.01); C12N 2310/321 Austin, TX (US) (2013.01); C12N 2310/346 (2013.01); C12N (*) Notice: Subjectto any disclaimer, the termbe this (013.01ars orb01301CDN US.C.patent154(b)is extendedby 0 ordays.adjusted under 2320/32 (2013.01);4 . CI2N 2330/10yor(2013.01) (58) Field of Classification Search This patent is subject to a terminal dis- CPC vieceeceseeseeeeeeee C12N 15/113; C12N 2310/141 claimer. See application file for complete search history. — (21) Appl. No.: 14/592,699 (56) References Cited (22) Filed: Jan. 8, 2015 U.S. PATENT DOCUMENTS (65) Prior Publication Data 7,232,806 B2 6/2007 Tuschlet al.
    [Show full text]
  • Drugs Affectin the Autonomic Nervous System
    Fundamentals of Medical Pharmacology Paterson Public Schools Written by Néstor Collazo, Ph.D. Jonathan Hodges, M.D. Tatiana Mikhaelovsky, M.D. for Health and Related Professions (H.A.R.P.) Academy March 2007 Course Description This fourth year course is designed to give students in the Health and Related Professions (H.A.R.P.) Academy a general and coherent explanation of the science of pharmacology in terms of its basic concepts and principles. Students will learn the properties and interactions between chemical agents (drugs) and living organisms for the rational and safe use of drugs in the control, prevention, and therapy of human disease. The emphasis will be on the fundamental concepts as they apply to the actions of most prototype drugs. In order to exemplify important underlying principles, many of the agents in current use will be singled out for fuller discussion. The course will include the following topics: ¾ The History of Pharmacology ¾ Terminology Used in Pharmacology ¾ Drug Action on Living Organisms ¾ Principles of Pharmacokinetics ¾ Dose-Response Relationships ¾ Time-Response Relationships ¾ Human Variability: Factors that will modify effects of drugs on individuals ¾ Effects of Drugs Attributable to Varying Modes of Administration ¾ Drug Toxicity ¾ Pharmacologic Aspects of Drug Abuse and Drug Dependence Pre-requisites Students must have completed successfully the following courses: Biology, Chemistry, Anatomy and Physiology, Algebra I and II Credits: 5 credits Basic Principles of Drug Action Introduction to Pharmacology a. Basic Mechanisms of Drug Actions b. Dose-response relationships c. Drug absorption d. Biotransformation of Drugs e. Pharmacokinetics f. Factors Affecting Drug Distribution g. Drug Allergy and Pharmacogenetics h.
    [Show full text]
  • Drug and Medication Classification Schedule
    KENTUCKY HORSE RACING COMMISSION UNIFORM DRUG, MEDICATION, AND SUBSTANCE CLASSIFICATION SCHEDULE KHRC 8-020-1 (11/2018) Class A drugs, medications, and substances are those (1) that have the highest potential to influence performance in the equine athlete, regardless of their approval by the United States Food and Drug Administration, or (2) that lack approval by the United States Food and Drug Administration but have pharmacologic effects similar to certain Class B drugs, medications, or substances that are approved by the United States Food and Drug Administration. Acecarbromal Bolasterone Cimaterol Divalproex Fluanisone Acetophenazine Boldione Citalopram Dixyrazine Fludiazepam Adinazolam Brimondine Cllibucaine Donepezil Flunitrazepam Alcuronium Bromazepam Clobazam Dopamine Fluopromazine Alfentanil Bromfenac Clocapramine Doxacurium Fluoresone Almotriptan Bromisovalum Clomethiazole Doxapram Fluoxetine Alphaprodine Bromocriptine Clomipramine Doxazosin Flupenthixol Alpidem Bromperidol Clonazepam Doxefazepam Flupirtine Alprazolam Brotizolam Clorazepate Doxepin Flurazepam Alprenolol Bufexamac Clormecaine Droperidol Fluspirilene Althesin Bupivacaine Clostebol Duloxetine Flutoprazepam Aminorex Buprenorphine Clothiapine Eletriptan Fluvoxamine Amisulpride Buspirone Clotiazepam Enalapril Formebolone Amitriptyline Bupropion Cloxazolam Enciprazine Fosinopril Amobarbital Butabartital Clozapine Endorphins Furzabol Amoxapine Butacaine Cobratoxin Enkephalins Galantamine Amperozide Butalbital Cocaine Ephedrine Gallamine Amphetamine Butanilicaine Codeine
    [Show full text]