Hyperkalemia Induced by the Calcium Channel Blocker
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Effect of Amlodipine and Indomethacin in Electrical and Picrotoxin Induced Convulsions in Mice
DOI: 10.5958/2319-5886.2014.00402.0 International Journal of Medical Research & Health Sciences www.ijmrhs.com Volume 3 Issue 3 Coden: IJMRHS Copyright @2014 ISSN: 2319-5886 Received: 9th Apr 2014 Revised: 3rd Jun 2014 Accepted: 14th Jun 2014 Research Article EFFECT OF AMLODIPINE AND INDOMETHACIN IN ELECTRICAL AND PICROTOXIN INDUCED CONVULSIONS IN MICE *Jagathi Devi N1, Prasanna V2 1Assistant Professor, 2Professor and Head, Department of Pharmacology, Osmania Medical College, Hyderabad *Corresponding author email: [email protected] ABSTRACT Background and Objectives: Antiepileptic drugs (AEDs) are the drugs used in the treatment of epilepsy. Many AEDs have been developed, but the ideal AED which can not only prevent but also abolish seizures by correcting the underlying pathophysiology is still not in sight. Calcium channel blockers (CCBs) may form such a group, as the initiation of epileptogenic activity in the neuron is connected with a phenomenon known as “intrinsic burst firing” which is activated by inward calcium current. In this study, Amlodipine, a CCB of the dihydropyridine class was evaluated for its anticonvulsant activity in mice. It was compared with Phenytoin sodium, one of the oldest anti epileptic drugs. Amlodipine was also combined with Indomethacin, a conventional NSAID, to look for any potentiating effect of this prostaglandin-synthesis inhibitor. Materials and Methods: A total of 48 adult Swiss albino mice of either sex weighing 20-30 G were used for this study; 48 were divided into 8 groups, each group containing 6 mice. Group 1-4 MES (50 m Amp for 0.1 secs) induced convulsion method, Group 5-8 evaluated by using the chemo-convulsant, picrotoxin (0.7 mg / kg). -
Case Report Carbamazepine Toxicity Following Oxybutynin And
Spinal Cord (2005) 43, 252–255 & 2005 International Spinal Cord Society All rights reserved 1362-4393/05 $30.00 www.nature.com/sc Case Report Carbamazepine toxicity following Oxybutynin and Dantrolene administration: a case report T Vander*,1, H Odi1, V Bluvstein1, J Ronen1,2 and A Catz1,2 1Department of Spinal Rehabilitation, Loewenstein Rehabilitation Hospital, Raanana, Israel; 2Tel-Aviv University, Tel-Aviv, Israel Objective: To report a case of Carbamazepine toxicity following the administration of Oxybutynin and Dantrolene. Study design: A case report. Setting: The Spinal Rehabilitation Department, Loewenstein Hospital, Raanana, Israel. Methods: A patient with C6D tetraplegia who sustained intoxication because of drug interaction is presented. She had been treated by Carbamazepine 1000 mg/day for neuropathic pain for 2 years without clinical or laboratory signs of toxicity. After administration of Oxybutynin concomitantly with an increase in the dose of Dantrolene, she presented the clinical symptoms and laboratory finding of Carbamazepine intoxication. Trying to adjust the treatment to the patient’s requirements, Carbamazepine together with Oxybutynin and Dantrolene was readministrated in lower doses. Results: The combination of these drugs, even small doses, caused toxicity. Adding Dantrolene and Oxybutynin elevated the blood level of Carbamazepine, possibly by inhibition of cytochrome P450. Conclusion: A possible pharmacokinetic interaction between Dantrolene and Oxybutynin should be borne in mind when considering Carbamazepine medication for a patient with a spinal cord lesion. Spinal Cord (2005) 43, 252–255. doi:10.1038/sj.sc.3101689; Published online 1 February 2005 Keywords: Carbamazepine; Oxybutynin; Dantrolene; drug interaction; cytochrome P450 Introduction Both Oxybutynin chloride and Dantrolene sodium are be required when patients have concomitant post- widely used in patients with spinal cord lesion (SCL). -
Neurochemical Mechanisms Underlying Alcohol Withdrawal
Neurochemical Mechanisms Underlying Alcohol Withdrawal John Littleton, MD, Ph.D. More than 50 years ago, C.K. Himmelsbach first suggested that physiological mechanisms responsible for maintaining a stable state of equilibrium (i.e., homeostasis) in the patient’s body and brain are responsible for drug tolerance and the drug withdrawal syndrome. In the latter case, he suggested that the absence of the drug leaves these same homeostatic mechanisms exposed, leading to the withdrawal syndrome. This theory provides the framework for a majority of neurochemical investigations of the adaptations that occur in alcohol dependence and how these adaptations may precipitate withdrawal. This article examines the Himmelsbach theory and its application to alcohol withdrawal; reviews the animal models being used to study withdrawal; and looks at the postulated neuroadaptations in three systems—the gamma-aminobutyric acid (GABA) neurotransmitter system, the glutamate neurotransmitter system, and the calcium channel system that regulates various processes inside neurons. The role of these neuroadaptations in withdrawal and the clinical implications of this research also are considered. KEY WORDS: AOD withdrawal syndrome; neurochemistry; biochemical mechanism; AOD tolerance; brain; homeostasis; biological AOD dependence; biological AOD use; disorder theory; biological adaptation; animal model; GABA receptors; glutamate receptors; calcium channel; proteins; detoxification; brain damage; disease severity; AODD (alcohol and other drug dependence) relapse; literature review uring the past 25 years research- science models used to study with- of the reasons why advances in basic ers have made rapid progress drawal neurochemistry as well as a research have not yet been translated Din understanding the chemi- reluctance on the part of clinicians to into therapeutic gains and suggests cal activities that occur in the nervous consider new treatments. -
Cocaine Intoxication and Hypertension
THE EMCREG-INTERNATIONAL CONSENSUS PANEL RECOMMENDATIONS Cocaine Intoxication and Hypertension Judd E. Hollander, MD From the Department of Emergency Medicine, University of Pennsylvania, Philadelphia, PA. 0196-0644/$-see front matter Copyright © 2008 by the American College of Emergency Physicians. doi:10.1016/j.annemergmed.2007.11.008 [Ann Emerg Med. 2008;51:S18-S20.] with cocaine intoxication is analogous to that of the patient with hypertension: the treatment should be geared toward the Cocaine toxicity has been reported in virtually all organ patient’s presenting complaint. systems. Many of the adverse effects of cocaine are similar to When the medical history is clear and symptoms are mild, adverse events that can result from either acute hypertensive laboratory evaluation is usually unnecessary. In contrast, if the crisis or chronic effects of hypertension. Recognizing when the patient has severe toxicity, evaluation should be geared toward specific disease requires treatment separate from cocaine toxicity the presenting complaint. Laboratory evaluation may include a is paramount to the treatment of patients with cocaine CBC count; determination of electrolyte, glucose, blood urea intoxication. nitrogen, creatine kinase, and creatinine levels; arterial blood The initial physiologic effect of cocaine on the cardiovascular gas analysis; urinalysis; and cardiac marker determinations. system is a transient bradycardia as a result of stimulation of the Increased creatine kinase level occurs with rhabdomyolysis. vagal nuclei. Tachycardia typically ensues, predominantly from Cardiac markers are increased in myocardial infarction. Cardiac increased central sympathetic stimulation. Cocaine has a troponin I is preferred to identify acute myocardial13 infarction. cardiostimulatory effect through sensitization to epinephrine A chest radiograph should be obtained in patients with and norepinephrine. -
Skeletal Muscle Relaxants Review 12/17/2008
Skeletal Muscle Relaxants Review 12/17/2008 Copyright © 2007 - 2008 by Provider Synergies, L.L.C. All rights reserved. Printed in the United States of America. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, digital scanning, or via any information storage and retrieval system without the express written consent of Provider Synergies, L.L.C. All requests for permission should be mailed to: Attention: Copyright Administrator Intellectual Property Department Provider Synergies, L.L.C. 5181 Natorp Blvd., Suite 205 Mason, Ohio 45040 The materials contained herein represent the opinions of the collective authors and editors and should not be construed to be the official representation of any professional organization or group, any state Pharmacy and Therapeutics committee, any state Medicaid Agency, or any other clinical committee. This material is not intended to be relied upon as medical advice for specific medical cases and nothing contained herein should be relied upon by any patient, medical professional or layperson seeking information about a specific course of treatment for a specific medical condition. All readers of this material are responsible for independently obtaining medical advice and guidance from their own physician and/or other medical professional in regard to the best course of treatment for their specific medical condition. This publication, inclusive of all forms contained herein, is intended to -
Drug Class Review on Skeletal Muscle Relaxants
Drug Class Review on Skeletal Muscle Relaxants Final Report Update 2 May 2005 Original Report Date: April 2003 Update 1 Report Date: January 2004 A literature scan of this topic is done periodically The purpose of this report is to make available information regarding the comparative effectiveness and safety profiles of different drugs within pharmaceutical classes. Reports are not usage guidelines, nor should they be read as an endorsement of, or recommendation for, any particular drug, use or approach. Oregon Health & Science University does not recommend or endorse any guideline or recommendation developed by users of these reports. Roger Chou, MD Kim Peterson, MS Oregon Evidence-based Practice Center Oregon Health & Science University Mark Helfand, MD, MPH, Director Copyright © 2005 by Oregon Health & Science University Portland, Oregon 97201. All rights reserved. Note: A scan of the medical literature relating to the topic is done periodically (see http://www.ohsu.edu/ohsuedu/research/policycenter/DERP/about/methods.cfm for scanning process description). Upon review of the last scan, the Drug Effectiveness Review Project governance group elected not to proceed with another full update of this report. Some portions of the report may not be up to date. Prior versions of this report can be accessed at the DERP website. Final Report Update 2 Drug Effectiveness Review Project TABLE OF CONTENTS Introduction........................................................................................................................4 Scope and -
Anaesthetic Implications of Calcium Channel Blockers
436 Anaesthetic implications of calcium channel Leonard C. Jenkins aA MD CM FRCPC blockers Peter J. Scoates a sc MD FRCPC CONTENTS The object of this review is to emphasize the anaesthetic implications of calcium channel block- Physiology - calcium/calcium channel blockers Uses of calcium channel blockers ers for the practising anaesthetist. These drugs have Traditional played an expanding role in therapeutics since their Angina pectoris introduction and thus anaesthetists can expect to see Arrhythmias increasing numbers of patients presenting for anaes- Hypertension thesia who are being treated with calcium channel Newer and investigational Cardiac blockers. Other reviews have emphasized the basic - Hypertrophic cardiomyopathy pharmacology of calcium channel blockers. 1-7 - Cold cardioplegia - Pulmonary hypertension Physiology - calcium/calcium channel blockers Actions on platelets Calcium plays an important role in many physio- Asthma Obstetrics logical processes, such as blood coagulation, en- - Premature labor zyme systems, muscle contraction, bone metabo- - Pre-eclampsia lism, synaptic transmission, and cell membrane Achalasia and oesophageal spasm excitability. Especially important is the role of Increased intraocular pressure therapy calcium in myocardial contractility and conduction Protective effect on kidney after radiocontrast Cerebral vasospasm as well as in vascular smooth muscle reactivity. 7 Induced hypotensive anaesthesia Thus, it can be anticipated that any drug interfering Drag interactions with calcium channel blockers with the action of calcium could have widespread With anaesthetic agents effects. Inhalation agents In order to understand the importance of calcium - Effect on haemodynamics - Effect on MAC in cellular excitation, it is necessary to review some Neuromuscular blockers membrane physiology. Cell membranes are pri- Effects on epinephrine-induced arrhythmias marily phospholipids arranged in a bilayer. -
Verapamil Inhibits TRESK (K2P18.1) Current in Trigeminal Ganglion Neurons Independently of the Blockade of Ca2+ Influx
International Journal of Molecular Sciences Article Verapamil Inhibits TRESK (K2P18.1) Current in Trigeminal Ganglion Neurons Independently of the Blockade of Ca2+ Influx Hyun Park 1, Eun-Jin Kim 2, Ji Hyeon Ryu 2,3, Dong Kun Lee 2,3, Seong-Geun Hong 2,3, Jaehee Han 2, Jongwoo Han 1,* and Dawon Kang 2,3,* ID 1 Department of Neurosurgery, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju 52727, South Korea; [email protected] 2 Department of Physiology and Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, South Korea; [email protected] (E.-J.K.); [email protected] (J.H.R.); [email protected] (D.K.L.); [email protected] (S.-G.H.); [email protected] (J.H.) 3 Department of Convergence Medical Science, Gyeongsang National University, Jinju 52727, South Korea * Correspondence: [email protected] (J.H.); [email protected] (D.K.); Tel.: +82-55-772-8044 (D.K.) Received: 5 June 2018; Accepted: 2 July 2018; Published: 4 July 2018 Abstract: Tandem pore domain weak inward rectifier potassium channel (TWIK)-related spinal cord + + K (TRESK; K2P18.1) channel is the only member of the two-pore domain K (K2P) channel family 2+ 2+ that is activated by an increase in intracellular Ca concentration ([Ca ]i) and linked to migraines. This study was performed to identify the effect of verapamil, which is an L-type Ca2+ channel blocker and a prophylaxis for migraines, on the TRESK channel in trigeminal ganglion (TG) neurons, as well as in a heterologous system. -
Patent Application Publication ( 10 ) Pub . No . : US 2019 / 0192440 A1
US 20190192440A1 (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2019 /0192440 A1 LI (43 ) Pub . Date : Jun . 27 , 2019 ( 54 ) ORAL DRUG DOSAGE FORM COMPRISING Publication Classification DRUG IN THE FORM OF NANOPARTICLES (51 ) Int . CI. A61K 9 / 20 (2006 .01 ) ( 71 ) Applicant: Triastek , Inc. , Nanjing ( CN ) A61K 9 /00 ( 2006 . 01) A61K 31/ 192 ( 2006 .01 ) (72 ) Inventor : Xiaoling LI , Dublin , CA (US ) A61K 9 / 24 ( 2006 .01 ) ( 52 ) U . S . CI. ( 21 ) Appl. No. : 16 /289 ,499 CPC . .. .. A61K 9 /2031 (2013 . 01 ) ; A61K 9 /0065 ( 22 ) Filed : Feb . 28 , 2019 (2013 .01 ) ; A61K 9 / 209 ( 2013 .01 ) ; A61K 9 /2027 ( 2013 .01 ) ; A61K 31/ 192 ( 2013. 01 ) ; Related U . S . Application Data A61K 9 /2072 ( 2013 .01 ) (63 ) Continuation of application No. 16 /028 ,305 , filed on Jul. 5 , 2018 , now Pat . No . 10 , 258 ,575 , which is a (57 ) ABSTRACT continuation of application No . 15 / 173 ,596 , filed on The present disclosure provides a stable solid pharmaceuti Jun . 3 , 2016 . cal dosage form for oral administration . The dosage form (60 ) Provisional application No . 62 /313 ,092 , filed on Mar. includes a substrate that forms at least one compartment and 24 , 2016 , provisional application No . 62 / 296 , 087 , a drug content loaded into the compartment. The dosage filed on Feb . 17 , 2016 , provisional application No . form is so designed that the active pharmaceutical ingredient 62 / 170, 645 , filed on Jun . 3 , 2015 . of the drug content is released in a controlled manner. Patent Application Publication Jun . 27 , 2019 Sheet 1 of 20 US 2019 /0192440 A1 FIG . -
Verapamil 40Mg, 80Mg, 120Mg and 160Mg Tablets
6 Contents of the pack and other information What Verapamil tablets contain • The active substance is verapamil hydrochloride. Package leaflet: Information for the patient Each tablet contains either 40mg, 80mg, 120mg or 160mg of verapamil hydrochloride. • The other ingredients are croscarmellose Verapamil 40mg, 80mg, 120mg sodium, magnesium stearate, maize starch, and 160mg tablets propylene glycol, sunset yellow aluminium lake (E110), quinoline yellow aluminium lake Read all of this leaflet carefully before you • manage high blood pressure (hypertension), (E104), titanium dioxide (E171), microcrystalline start taking this medicine because it contains used alone or with other drugs for high blood cellulose (E460), hydroxypropylcellulose (E463), pressure. methylhydroxypropylcellulose (E464), purified talc important information for you. • manage and prevent angina. (E553). • Keep this leaflet. You may need to read it again. • treat and prevent certain types of abnormal heartbeats. What Verapamil tablets look like and contents of • If you have any further questions, ask your the pack doctor or pharmacist. 2 What you need to know before you Verapamil 40mg tablets are yellow, circular, biconvex, • This medicine has been prescribed for you film-coated tablets, impressed “C” on one face and only. Do not pass it on to others. It may harm take Verapamil tablets Do not take Verapamil tablets if you: the identifying letters “VR” on the reverse. Tablet them, even if their signs of illness are the • are allergic to verapamil hydrochloride or any of diameter: 6.18-6.82mm. same as yours. the other ingredients of this medicine (listed in Verapamil 80mg tablets are yellow, circular, biconvex • If you get any side effects, talk to your doctor film-coated tablets, impressed “C” on one face and section 6) or pharmacist. -
Cyclobenzaprine and Back Pain: a Meta-Analysis
ORIGINAL INVESTIGATION Cyclobenzaprine and Back Pain A Meta-analysis Robert Browning, MD; Jeffrey L. Jackson, MD, MPH; Patrick G. O’Malley, MD, MPH Background: Back pain is a common problem for which 14 as were those treated with placebo. Slightly fewer than cyclobenzaprine hydrochloride is frequently pre- 3 individuals (2.7; 95% confidence interval, 2.0-4.2) scribed. needed treatment for 1 to improve. The magnitude of this improvement was modest, with an effect size of 0.38 to Objective: To perform a systematic review of cyclo- 0.58 in all 5 outcomes (local pain, muscle spasm, ten- benzaprine’s effectiveness in the treatment of back pain. derness to palpation, range of motion, and activities of daily living). Treatment efficacy for these 5 outcomes was Methods: We searched MEDLINE, PsycLIT, CINAHL, greatest early, in the first few days of treatment, declin- EMBASE, AIDSLINE, HEALTHSTAR, CANCERLIT, the ing after the first week. Patients receiving cyclobenzap- Cochrane Library, Micromedex, Federal Research in rine also experienced more adverse effects, the most com- Progress, and the references of reviewed articles, and con- mon being drowsiness. tacted Merck, Sharpe and Dohme for English-language, randomized, placebo-controlled trials of cyclobenzap- Conclusions: Cyclobenzaprine is more effective than rine in adults with back pain. Outcomes included global placebo in the management of back pain; the effect is improvement and 5 specific domains of back pain (local modest and comes at the price of greater adverse effects. pain, muscle spasm, range of motion, tenderness to pal- The effect is greatest in the first 4 days of treatment, sug- pation, and activities of daily living). -
Dental Management for the Hypertensive Patient
HYPERTENSION AND ORAL HEALTH: EPIDEMIOLOGIC AND CLINICAL PERSPECTIVES Janet H Southerland, DDS, MPH, PhD Professor, Department of Oral and Maxillofacial Surgery School of Dentistry, Meharry Medical College December 9, 2016 Provide an overview of concerns with treating patients with hypertension and GOAL provide recommendations that will be helpful in managing a broad spectrum of these patients. EVALUATION Evaluation for hypertension has three objectives: 1. to assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment. 2. to reveal identifiable causes of high BP. 3. to assess the presence or absence of target organ damage and cardiovascular disease (CVD). TARGET ORGAN DAMAGE Heart Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart Failure Brain Stroke or transient ischemic attack Chronic kidney disease Peripheral artery disease Retinopathy The relationship between BP and risk of CVD events is continuous, consistent, and independent of other risk factors. The higher the BP, the greater is the chance of heart attack, heart failure, stroke, and kidney disease. INTRODUCTION The risk of developing CVD doubles for every increment of 20 mm Hg Systolic (SBP) or 10 mm Hg of Diastolic (DBP). The risk of dying of ischemic heart disease and stroke increases progressively and linearly when blood pressure exceeds 115/75 mm Hg. The 7th and 8th Joint National Committee (JNC-7 and 8) reports provide guidelines for blood pressure management and treatment. The JNC-8 panel confirms that the >140/90 mmHg definition for hypertension from the INTRODUCTION JNC 7 report remains the standard for diagnosis for individuals who do not have additional comorbidities.