Psychotropic Medication Policy
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Clinical Biochemistry of Hepatotoxicity
linica f C l To o x l ic a o n r l o u g Singh, J Clinic Toxicol 2011, S:4 o y J Journal of Clinical Toxicology DOI: 10.4172/2161-0495.S4-001 ISSN: 2161-0495 ReviewResearch Article Article OpenOpen Access Access Clinical Biochemistry of Hepatotoxicity Anita Singh1, Tej K Bhat2 and Om P Sharma2* 1CSK Himachal Pradesh, Krishi Vishva Vidyalaya, Palampur (HP) 176 062, India 2Biochemistry Laboratory, Indian Veterinary Research Institute, Regional Station, Palampur (HP) 176 061, India Abstract Liver plays a central role in the metabolism and excretion of xenobiotics which makes it highly susceptible to their adverse and toxic effects. Liver injury caused by various toxic chemicals or their reactive metabolites [hepatotoxicants) is known as hepatotoxicity. The present review describes the biotransformation of hepatotoxicants and various models used to study hepatotoxicity. It provides an overview of pathological and biochemical mechanism involved during hepatotoxicity together with alteration of clinical biochemistry during liver injury. The review has been supported by a list of important hepatotoxicants as well as common hepatoprotective herbs. Keywords: Hepatotoxicity; Hepatotoxicant; In Vivo models; In Vitro production of bile thus leading to the body’s inability to flush out the models; Pathology; Alanine aminotransferase; Alkaline phosphatase; chemicals through waste. Smooth endoplasmic reticulum of the liver is Bilirubin; Hepatoprotective the principal ‘metabolic clearing house’ for both endogenous chemicals like cholesterol, steroid hormones, fatty acids and proteins, and Introduction exogenous substances like drugs and alcohol. The central role played by liver in the clearance and transformation of chemicals exposes it to Hepatotoxicity refers to liver dysfunction or liver damage that is toxic injury [4]. -
6) Hepatotoxic Drugs
ILOs § Define the role of liver in drug detoxification § Discuss the types (patterns) of hepatotoxicity § Classify hepatotoxins § Explain how a drug can inflict hepatotoxicity § State the pathological consequences of hepatic injury § Contrast the various clinical presentation of hepatotoxicity § Enlist the possible treatment PHYSIOLOGICAL has multiple functions (>5000) è can be categorized into: 1. Regulation, synthesis & secretion. èutilization of glucose, lipids & proteins + bile for digesting fats. 2. Storage. è Glucose (as glycogen), fat soluble vitamins (A, D, E & K) & minerals 3. Purification, transformation & clearance è of endogenous (steroid hormones, cholesterol, FA, & proteins..) & exogenous (drugs, toxins, herbs…etc ) chemicals. Human body identifies almost all drugs as foreign substances i.e. XENOBIOTIC Has to get rid of them "METABOLIC CLEARING HOUSE" PHARMACOLOGICAL HEPATOTOXIC DRUGS Subjects drugs to chemical transformation (METABOLISM) è to become inactive & easily excreted. Since most drugs are lipophilic è they are changed into hydrophilic water soluble products è suitable for elimination through the bile or urine Such metabolic transformation usually occur in 2 PHASES: Phase 1 reactions Yields intermediates è Oxidation, Reduction, polar, transient, usually highly reactive è Hydrolysis, Hydration far more toxic than parent substrates è Catalyzed by CYT P-450 may result in liver injury Drug-Induced Liver Injury (DILI) Phase 2 reactions Yields products of increased solubility Conjugation with a moiety If of high molecular weight è (acetate, a.a., glutathione, excreted in bile glucuronic a., sulfate ) If of low molecular weight è to blood è excreted in urine Hepatotoxicity è Is the Leading cause of ADRs Injury / damage of the liver è Caused by exposure to a drug è Inflict varying impairment in liver functions è Manifests clinically a long range è hepatitis ðfailure Inflammation ðApoptosis ð Necrosis Why the liver is the major site of ADRs ? It is the first organ to come in contact with the drug after absorption from the GIT. -
Drug and Alcohol Induced Hepatotoxicity
From The Department of Physiology and Pharmacology, Section of Pharmacogenetics Karolinska Institutet, Stockholm, Sweden DRUG AND ALCOHOL INDUCED HEPATOTOXICITY Angelica Butura Stockholm 2008 All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. © Angelica Butura, 2008 ISBN 978-91-7409-055-0 To my parents for always believing in me ABSTRACT Drug induced hepatotoxicity is the most common reason cited for withdrawal of already approved drugs from the market and accounts for more than 50 percent of cases of acute liver failure in the United States. Ethanol (EtOH) causes a further substantial amount of liver insufficiencies world wide. The current thesis was focused on the mechanisms behind hepatotoxicity caused by these agents. Using a rat in vivo model for alcoholic liver disease (ALD) it was found that cytokine and chemokine levels in blood accompanied the fluctuating levels of blood EtOH, indicating that they are directly influenced by absolute EtOH concentration. During the early phases of ALD in this model, a strong initial Th1 response was observed as revealed by increased levels of cytokine as well as transcription factor mRNAs, followed by a downregulation, whereas Th2 response was decreased by EtOH over the entire treatment period of four weeks. We found that supplementation with the antioxidant NAC to ethanol treated animals decreases severity of liver damage and somewhat decreases initial inflammatory response mediated by TNFα. NAC also diminished the ethanol-induced formation of protein adducts of lipid peroxidation products like MDA and HNE. Also, the formation of antibodies against neo-antigens formed by MDA, HNE and HER protein adducts was lowered. -
Doxepin Hydrochloride Capsule Mylan Pharmaceuticals Inc.
DOXEPIN HYDROCHLORIDE- doxepin hydrochloride capsule Mylan Pharmaceuticals Inc. ---------- Suicidality and Antidepressant Drugs Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders. Anyone considering the use of doxepin or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need. Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older. Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide. Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. Doxepin is not approved for use in pediatric patients. (See WARNINGS: Clinical Worsening and Suicide Risk, PRECAUTIONS: Information for Patients and PRECAUTIONS: Pediatric Use.) DESCRIPTION Doxepin hydrochloride is one of a class of psychotherapeutic agents known as dibenzoxepin tricyclic compounds. The molecular formula of the compound is C19H21NO • HCl having a molecular weight of 315.84. It is a white crystalline powder freely soluble in water, in ethanol (96%), and methylene chloride. It may be represented by the following structural formula: Chemically, doxepin hydrochloride is a dibenzoxepin derivative and is the first of a family of tricyclic psychotherapeutic agents. -
SINEQUAN® (Doxepin Hcl) CAPSULES ORAL CONCENTRATE
69-2135-00-1 SINEQUAN® (doxepin HCl) CAPSULES ORAL CONCENTRATE DESCRIPTION SINEQUAN® (doxepin hydrochloride) is one of a class of psychotherapeutic agents known as dibenzoxepin tricyclic compounds. The molecular formula of the compound is C19H21NO•HCl having a molecular weight of 316. It is a white crystalline solid readily soluble in water, lower alcohols and chloroform. Inert ingredients for the capsule formulations are: hard gelatin capsules (which may contain Blue 1, Red 3, Red 40, Yellow 10, and other inert ingredients); magnesium stearate; sodium lauryl sulfate; starch. Inert ingredients for the oral concentrate formulation are: glycerin; methylparaben; peppermint oil; propylparaben; water. CHEMISTRY SINEQUAN (doxepin HCl) is a dibenzoxepin derivative and is the first of a family of tricyclic psychotherapeutic agents. Specifically, it is an isomeric mixture of: 1-Propanamine, 3-dibenz[b,e]oxepin-11(6H)ylidene-N,N-dimethyl-, hydrochloride. 1 ACTIONS The mechanism of action of SINEQUAN (doxepin HCl) is not definitely known. It is not a central nervous system stimulant nor a monoamine oxidase inhibitor. The current hypothesis is that the clinical effects are due, at least in part, to influences on the adrenergic activity at the synapses so that deactivation of norepinephrine by reuptake into the nerve terminals is prevented. Animal studies suggest that doxepin HCl does not appreciably antagonize the antihypertensive action of guanethidine. In animal studies anticholinergic, antiserotonin and antihistamine effects on smooth muscle have been demonstrated. At higher than usual clinical doses, norepinephrine response was potentiated in animals. This effect was not demonstrated in humans. At clinical dosages up to 150 mg per day, SINEQUAN can be given to man concomitantly with guanethidine and related compounds without blocking the antihypertensive effect. -
The Role of Oxidative Stress in Α-Amanitin-Induced Hepatotoxicity in an Experimental Mouse Model
Turkish Journal of Medical Sciences Turk J Med Sci (2017) 47: 318-325 http://journals.tubitak.gov.tr/medical/ © TÜBİTAK Research Article doi:10.3906/sag-1503-163 The role of oxidative stress in α-amanitin-induced hepatotoxicity in an experimental mouse model 1 1, 2 1 3 1 Zerrin Defne DÜNDAR , Mehmet ERGİN *, İbrahim KILINÇ , Tamer ÇOLAK , Pembe OLTULU , Başar CANDER 1 Department of Emergency Medicine, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey 2 Department of Biochemistry, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey 3 Department of Medical Pathology, Meram Faculty of Medicine, Necmettin Erbakan University, Konya, Turkey Received: 31.03.2015 Accepted/Published Online: 11.01.2016 Final Version: 27.02.2017 Background/aim: This study aimed to evaluate oxidative stress markers of liver tissue in a mouse α-amanitin poisoning model with three different toxin levels. Materials and methods: The mice were randomly divided into Group 1 (control), Group 2 (0.2 mg/kg), Group 3 (0.6 mg/kg), and Group 4 (1.0 mg/kg). The toxin was injected intraperitoneally and 48 h of follow-up was performed before sacrifice. Results: Median superoxide dismutase activities of liver tissue in Groups 3 and 4 were significantly higher than in Group 1 (for both, P = 0.001). The catalase activity in Group 2 was significantly higher, but in Groups 3 and 4 it was significantly lower than in Group 1 (for all, P = 0.001). The glutathione peroxidase activities in Groups 2, 3, and 4 were significantly higher than in Group 1 (P = 0.006, P = 0.001, and P = 0.001, respectively). -
Handbook of Common Poisonings in Children. INSTITUTION Food and Drug Administration (DREW), Washington, D.C
O DOCUMENT BESUME ED 144 708 PS 099 577 $ ...,, / 1.- . ,TITLE - Handbook of CommOn Poisonings in Children. INSTITUTION Food and Drug Administration (DREW), Washington, D.C. " fEPORT NO , HEW-FDA-707004 pus DATE /6, ' NOTE -114p. ,.. 1 AyAILABLEFRO!! Superintendent of Documents, U.S. Government Printing ..... Office, Washington, D.C. 20402 (Stock No. 017-C12-0024074, $1.50) . EDRS PRICE NF -$0.83 HC-$6.01. Pins Postage. DESCRtPTORS Accident Prevention;*Children;Emergency'SqUad Personnel; *Governm'ent Publications; icGuidaS; Hospital Pe onnel; Pharmacists;- Physicians;_ *Reference Bo ks IDENTtFIERS, *Poisoning ABSTRACT This handbook for physicians, emergency room. personhel and pharmacists lists- the manufacturer, descriptiOn, / toxiaity, symptoms and findings, treatment, and references.for-73 . / poison substances considered by the Subcommittee on 1Ccidental 1 Poisoning of the American-Academi% of'Pediatrics to be most significant in terms of accidental poisoning of.ehildFen.' (BF) 1 *****************************f**************,************************** * .DOcuments acquirNd by ERIC inclUde many inforMal unpublished *. * materials not available from other-sources. ERIC makes every effort * * to obtain the'best copy available. Nevertheless, items of marginal * * reproducibility are often encountered and this affects the quality * *sof the 'microfiche and hardcopy reproddctions ERIC makes available * via the ERIC Document (reproduction Service (EDRS) .EDRS is not . * * responsible for the quality bf the original document. Reproductions * . *.supplied by EDRS, are the best that can beemade from the 'original. ******************41********r****************************************** U.S. DEPARTtAENT OF HEALTH, EDUCATION, AND WELFARE Public vice/Fo©d and Drug Administration 5600Fi Rockville, Maryland 20857 HEW (FDA) 16-7004 , , , Handbook of # ,. Common Poisonings in Children 1976,. 0 r FDA 4,1 . For we by the 044rorinlyndsrot el Deoumenes. -
Study Regarding Photodegradation Processes of Tricyclic Antidepressants and the Toxicity of the Degradation Products
University of Medicine and Pharmacy Faculty of Pharmacy Department of Pharmaceutical Chemistry STUDY REGARDING PHOTODEGRADATION PROCESSES OF TRICYCLIC ANTIDEPRESSANTS AND THE TOXICITY OF THE DEGRADATION PRODUCTS Author: Scientific guider: Székely Pál Prof. dr. Gyéresi Árpád Depression is classified as a mood disorder that manifests itself through a feeling of sadness, melancholy, and it is often accompanied by anxiety and irritability. This state of mind is characterized by slow thinking, lack of imagination, loss of memory and concentration capacity, the emergence of obsessive ideas (pessimistic and suicidal), as well as psychomotor disturbances, fatigue and restlessness. It requires special psychiatric and pharmaceutical treatment. There are a wide variety of pharmaceutical substances used in the therapy of depression, one of the most important being the group of tricyclic antidepressants (TCAs). TCAs have been used since the early 50s to treat depression, as they were the first group of pharmaceutical substances that were synthesized for this specific purpose. The basic structure of TCA is composed of a linear system consisting of three condensed cycles, which bind to a structure having a side chain N atom of basic character. Based on the basic structure, the classic tricyclic antidepressants can be divided into derivatives of dihydro- dibenzazepine, dibenzazepine, dibenzocycloheptadiene, dibenzoxepin, and dibenzothiophene. In cases of clinical depression, the classic tricyclic compounds have antidepressive, sedative, anxiolytic or stimulant effects. Lately their effectiveness in neuropathic pain treatment has also been recognized. TCAs and their metabolites act on a large number of receptors and their adverse effects are numerous, which is a major impediment in clinical use. In order to induce photochemical skin reactions, the ultraviolet radiation must penetrate to the peripheral capillaries, so that the UV light reaches the absorbing molecule. -
(12) United States Patent (10) Patent No.: US 9.486,437 B2 Rogowski Et Al
USOO94864-37B2 (12) United States Patent (10) Patent No.: US 9.486,437 B2 Rogowski et al. (45) Date of Patent: *Nov. 8, 2016 (54) METHODS OF USING LOW-DOSE DOXEPIN 5,858.412 A 1/1999 Staniforth et al. FOR THE IMPROVEMENT OF SLEEP 5,866,166 A 2f1999 Staniforth et al. 5.948,438 A 9, 1999 Staniforth et al. (71) Applicants: Pernix Sleep, Inc., Morristown, NJ 5,965,166 A 10, 1999 Hunter et al. (US); ProCom One, Inc., San Marcos, 6,103,219 A 8, 2000 Sherwood et al. TX (US) 6,106,865 A 8, 2000 Staniforth et al. 6,211,229 B1 4/2001 Kavey (72) Inventors: Roberta L. Rogowski, Rancho Santa 6,217,907 B1 4/2001 Hunter et al. Fe, CA (US); Susan E. Dubé, Carlsbad, 6,217.909 B1 4/2001 Sherwood et al. CA (US); Philip Jochelson, San Diego, 6,219,674 B1 4/2001 Classen CA (US); Neil B. Kavey, Chappaqua, 6,344,487 B1 2/2002 Kavey 6,358,533 B2 3/2002 Sherwood et al. NY (US) 6,391,337 B2 5, 2002 Hunter et al. (73) Assignees: Pernix Sleep, Inc., Morristown, NJ 6,395,303 B1 5, 2002 Staniforth et al. (US); ProCom One, Inc., San Marcos, 6,403,597 B1 6/2002 Wilson et al. 6,407,128 B1 6/2002 Scaife et al. TX (US) 6,471.994 B1 10/2002 Staniforth et al. 6,521,261 B2 2/2003 Sherwood et al. (*) Notice: Subject to any disclaimer, the term of this 6,584,472 B2 6/2003 Classen patent is extended or adjusted under 35 6,683,102 B2 1/2004 Scaife et al. -
Drug-Facilitated Sexual Assault in the U.S
The author(s) shown below used Federal funds provided by the U.S. Department of Justice and prepared the following final report: Document Title: Estimate of the Incidence of Drug-Facilitated Sexual Assault in the U.S. Document No.: 212000 Date Received: November 2005 Award Number: 2000-RB-CX-K003 This report has not been published by the U.S. Department of Justice. To provide better customer service, NCJRS has made this Federally- funded grant final report available electronically in addition to traditional paper copies. Opinions or points of view expressed are those of the author(s) and do not necessarily reflect the official position or policies of the U.S. Department of Justice. AWARD NUMBER 2000-RB-CX-K003 ESTIMATE OF THE INCIDENCE OF DRUG-FACILITATED SEXUAL ASSAULT IN THE U.S. FINAL REPORT Report prepared by: Adam Negrusz, Ph.D. Matthew Juhascik, Ph.D. R.E. Gaensslen, Ph.D. Draft report: March 23, 2005 Final report: June 2, 2005 Forensic Sciences Department of Biopharmaceutical Sciences (M/C 865) College of Pharmacy University of Illinois at Chicago 833 South Wood Street Chicago, IL 60612 ABSTRACT The term drug-facilitated sexual assault (DFSA) has been recently coined to describe victims who were given a drug by an assailant and subsequently sexually assaulted. Previous studies that have attempted to determine the prevalence of drugs in sexual assault complainants have had serious biases. This research was designed to better estimate the rate of DFSA and to examine the social aspects surrounding it. Four clinics were provided with sexual assault kits and asked to enroll sexual assault complainants. -
Toxicological Profile for Carbon Tetrachloride
CARBON TETRACHLORIDE 213 9. REFERENCES *Abraham P, Wilfred G, Catherine SP, et al. 1999. Oxidative damage to the lipids and proteins of the lungs, testis and kidney of rats during carbon tetrachloride intoxication. Clin Chim Acta 289(1-2):177-179. *ACGIH. 1986. Documentation of the threshold limit values and biological exposure indices. 5th edition. Cincinnati, OH: American Conference of Government Industrial Hygienists Inc., 109-110. *ACGIH. 2003. Carbon tetrachloride. Threshold limit values for chemical substances and physical agents and biological exposure indices. Cincinnati, OH: American Conference of Governmental Industrial Hygienists. *Acquavella JF, Friedlander BR, Ireland BK. 1994. Interpretation of low to moderate relative risks in environmental epidemiologic studies. Annu Rev Public Health 15:179-201. *Adams EM, Spencer HC, Rowe VK, et al. 1952. Vapor toxicity of carbon tetrachloride determined by experiments on laboratory animals. AMA Arch Ind Hyg Occup Med 6:50-66. Adamson DT, Parkin GF. 1999. Biotransformation of mixtures of chlorinated aliphatic hydrocarbons by an acetate-grown methanogenic enrichment culture. Water Res 33:1482-1494. *Adaramoye OA, Akinloye O. 2000. Possible protective effect of kolaviron on CCl4-induced erythrocyte damage in rats. Biosci Rep 20:4. *Adinolfi M. 1985. The development of the human blood-CSF-brain barrier. Dev Med Child Neurol 27:532-537. *Adlercreutz H. 1995. Phytoestrogens: Epidemiology and a possible role in cancer protection. Environ Health Perspect Suppl 103(7):103-112. ++ *Agarwal AK, Mehendale HM. 1984a. CCl4-induced alterations in Ca homeostasis in chlordecone and phenobarbital pretreated animals. Life Sci 34:141-148. *Agarwal AK, Mehendale HM. 1984b. Excessive hepatic accumulation of intracellular Ca2+ in chlordecone potentiated CCl4 toxicity. -
Medicines Issues in Liver Disease
Medicines issues in liver disease Penny North-Lewis Paediatric Liver Pharmacist Leeds General Infirmary September 2011 Aim To illustrate some of the enquiries encountered regarding the use of medicines in patients with liver dysfunction To define a strategy for finding solutions to these queries Plan for session Types of liver related MI enquiries Why it is so hard to answer them BihBasic hepa tltology Interpreting laboratory tests Pharmacokinetics and dynamics Pulling together an answer Types of liver en quir y 152 enquiries from Apr 10 to Mar 11 109 choice/dose of drug in a liver pt 20 requests for protocol information 9 for ADR/hepatotoxicity information Others incl . compatability, general background Types of liver enquiry – choice/dose Antimicrobials 34 Analgesia 11 Psychotropics 11 Antiepileptics 6 AtidAntidepressan ts 6 Chemotherapy 6 Hormones 4 Others incl. antihistamines, antiemetics Whyyp the problem? Lack of information in regular sources e.g BNF, SPC (misinformation/lack of data) Lack of research, small numbers of patients NtitNo easy equation to use Poor understanding of liver dysfunction Where to start Taking in an enquiry Liver Enquiry proforma LIVER ENQUIRIES - Patient Considerations Do you have results of any tests? Gathering the Information Ultra Sound Scan LFT Date Date Date Date Bioppysy Range ALT <40iu/L ERCP/HIDA AST <40iu/L Alk Phos 30-300iu/L Endoscopy Bil 3-15 mol/L Alb 34-48g/L GGT 0-40iu/L Is there known Portal Hypertension INR 0.9-1.2 PT 9-14.5 secs Does the patient have any other