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Books on the topic 'Drugs acting on the central nervous system'

Author: Grafiati

Published: 24 April 2022

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1

Drug action in the central nervous system. New York: Oxford University Press, 1998.

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2

Zhong yao ying xiang shen jing xi tong huo xing cheng fen: Active components on nervous system in TCM. Beijing: Ke xue chu ban she, 2012.

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3

Welling, Peter G. Pharmacokinetics of cardiovascular, central nervous system, and antimicrobial drugs. London: The Royal Society of Chemistry, 1985.

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4

Miller, Richard Lawrence. The encyclopedia of addictive drugs. Westport, Conn. USA: Greenwood Press, 2002.

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5

The encyclopedia of addictive drugs. Westport, Conn: Greenwood Press, 2002.

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6

J, Whalley Lawrence, ed. ACE inhibitors: Central actions. New York: Raven Press, 1994.

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7

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 8th ed. Oxford: Oxford University Press, 2003.

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8

E, Bloom Floyd, ed. The biochemical basis of neuropharmacology. 7th ed. New York: Oxford University Press, 1996.

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9

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 5th ed. New York: Oxford University Press, 1986.

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10

E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 6th ed. New York: Oxford University Press, 1991.

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11

An introduction to drugs and the neuroscience of behavior. Australia: Wadsworth Cengage Learning, 2014.

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12

Engs, Ruth C. Alcohol and other drugs: Self-responsibility. Bloomington, Ind: Tichenor Pub., 1987.

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13

International Bioanalytical Forum (6th 1985 University of Surrey). Bioactive analytes: Including CNS drugs, peptides, and enantiomers. New York: Plenum Press, 1986.

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14

Alan, Stoudemire, ed. Psychiatric side effects of prescription and over-the-counter medications: Recognition and management. Washington, DC: American Psychiatric Press, 1998.

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15

Fever and antipyresis: The role of the nervous system. Cambridge: Cambridge University Press, 1995.

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16

Liu, Ray H. Quantitation and mass spectrometric data of drugs and isotopically labeled analogs. Boca Raton: Taylor & Francis, 2010.

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17

Liu, Ray H. Quantitation and mass spectrometric data of drugs and isotopically labeled analogs. Boca Raton: Taylor & Francis, 2010.

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18

Liu, Ray H. Quantitation and mass spectrometric data of drugs and isotopically labeled analogs. Boca Raton: CRC Press, 2010.

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19

Kier, Lemont B. The chemistry and physics of drugs used in anesthesia. Park Ridge, IL: American Association of Nurse Anesthetists, 2014.

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20

Stahl's essential psychopharmacology. 3rd ed. New York: Cambridge University Press, 2008.

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21

Sheng-Meng, Wang, and Canfield Dennis V. 1943-, eds. Quantitation and mass spectrometric data of drugs and isotopically labeled analogs. Boca Raton: Taylor & Francis, 2010.

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22

Diaz, Jaime. How drugs influence behavior: A neuro behavioral approach. Upper Saddle River, N.J: Prentice Hall, 1997.

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23

Wang, John Q. Drugs of abuse: Neurological reviews and protocols. Totowa, N.J: Humana Press, 2010.

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24

1947-, Meyer Jerrold S., and Quenzer Linda F, eds. Principles of neuropsychopharmacology. Sunderland, Mass: Sinauer Associates, 1997.

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25

Scott, Celicia. Dangerous Depressants & Sedatives. Broomall, PA: Mason Crest, 2015.

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26

Neuropeptides in neuroprotection and neuroregeneration. Boca Raton, FL: CRC Press, 2012.

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27

Perrine, Daniel M. The chemistry of mind-altering drugs: History, pharmacology, and cultural context. Washington, DC: American Chemical Society, 1996.

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28

Helmut, Fink. Künstliche Sinne, gedoptes Gehirn: Neurotechnik und Neuroethik. Paderborn: Mentis, 2010.

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29

A, Deitrich Richard, and Erwin V. Gene, eds. Pharmacological effects of ethanol on the nervous system. Boca Raton: CRC Press, 1996.

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30

C, Horwell David, ed. Drugs in central nervous system disorders. New York: Dekker, 1985.

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31

1945-, Horwell David C., ed. Drugs in central nervous system disorders. New York: Dekker, 1985.

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32

Mason, Peggy. Receiving the Synaptic Message. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0013.

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Ionotropic and metabotropic receptors differ in their speed of action, the variety of effects produced after ligand-binding, and in the number of types present in the nervous system. The participation of two ionotropic glutamate receptors in synaptic plasticity is thought to be the cellular basis of learning. The actions of acetylcholine on nicotinic acetylcholine receptors present at the neuromuscular junction are described. The pharmacological profile of the GABAA receptor, central to most neural functions, is introduced. The properties of metabotropic receptors that are coupled to G proteins, termed G protein-coupled receptors (GPCRs), are detailed. Three canonical second-messenger systems through which GPCRs act are briefly described. An introduction to clinical pharmacology focused on how drugs acting on muscarinic and adrenergic receptors produce peripheral and central psychotropic effects is provided. Finally, the role of connexins and gap junctions in myelination and hearing is introduced.

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33

Devlin, Hugh, and Rebecca Craven. Central nervous system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759782.003.0012.

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The central nervous system (CNS) in relation to dentistry is the topic of this chapter. Nerve conduction is described, then the physiology of facial and dental pain and processing of afferent pain nerve impulses in the cerebral cortex. We discuss abnormal sensations of allodynia and paraesthesia. Pain control with non-steroidal anti-inflammatory drugs or paracetamol is explained. The function of the cranial nerves and the autonomic nervous system are described. We explain the nerve pathways involved in salivation, lachrymation, and taste sensation. We propose some techniques for treating the nervous patient, e.g. modelling, systematic desensitization, and feedback. Effective local anaesthesia is essential in gaining the cooperation of nervous patients. The major types of local anaesthetics are compared. The techniques for inferior alveolar and superior alveolar nerve blocks are described as are drugs commonly used in dental sedation. There are final sections on drug problems encountered in dental practice and on dementia.

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34

Harrison, Mark. Central nervous system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0041.

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This chapter describes the pharmacology of the central nervous system as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of hypnotics and anxiolytics, antipsychotics, antimania drugs, tricyclic antidepressants, nausea and vomiting, analgesics, non-opioid analgesics, opioid analgesics, antiepileptics, and status epilepticus. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

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35

Pharmacokinetics of Cardiovascular, Central Nervous System and Antimicrobial Drugs. Royal Society of Chemistry, 1985.

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36

Analgesia Methods And Protocols. Humana Press, 2010.

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37

Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Therapy-related issues: central nervous system. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0019.

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Pain: a definition 396Assessment of pain 398Acute pain: incidence 401Acute pain 402Treating cancer pain 404Equianalgesic doses for opioids 406Compatibility of drugs in pain and palliative care 407Chronic pain 408The International Association for the Study of Pain defines pain as ‘...

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38

Gill, Steven J., and Michael H. Nathanson. Central nervous system pathologies and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0081.

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Anaesthesia induces changes in many organ systems within the body, though clearly none more so than the central nervous system. The physiology of the normal central nervous system is complex and the addition of chronic pathology and polypharmacy creates a significant challenge for the anaesthetist. This chapter demonstrates a common approach for the anaesthetist and specific considerations for a wide range of neurological conditions. Detailed preoperative assessment is essential to gain understanding of the current symptomatology and neurological deficit, including at times restrictions on movement and position. Some conditions may pose challenges relating to communication, capacity, and consent. As part of the consent process, patients may worry that an anaesthetic may aggravate or worsen their neurological disease. There is little evidence to support this understandable concern; however, the risks and benefits must be considered on an individual patient basis. The conduct of anaesthesia may involve a preference for general or regional anaesthesia and requires careful consideration of the pharmacological and physiological impact on the patient and their disease. Interactions between regular medications and anaesthetic drugs are common. Chronically denervated muscle may induce hyperkalaemia after administration of succinylcholine. Other patients may have an altered response to non-depolarizing agents, such as those suffering from myasthenia gravis. The most common neurological condition encountered is epilepsy. This requires consideration of the patient’s antiepileptic drugs, often relating to hepatic enzyme induction or less commonly inhibition and competition for protein binding, and the effect of the anaesthetic technique and drugs on the patient’s seizure risk. Postoperative care may need to take place in a high dependency unit, especially in those with limited preoperative reserve or markers of frailty, and where the gastrointestinal tract has been compromised, alternative routes of drug delivery need to be considered. Overall, patients with chronic neurological conditions require careful assessment and preparation, a considered technique with attention to detail, and often higher levels of care during their immediate postoperative period.

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39

Bloom, Floyd E., Robert H. Roth, and Jack R. Cooper. The Biochemical Basis of Neuropharmacology. 8th ed. Oxford University Press, USA, 2002.

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40

Bloom, Floyd E., Robert H. Roth, and Jack R. Cooper. The Biochemical Basis of Neuropharmacology. Oxford University Press, USA, 2002.

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41

Barbiturates and Your Central Nervous System: The Incredibly Disgusting Story (Incredibly Disgusting Drugs). Rosen Publishing Group, 2001.

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42

Nikravan, Sara, and Frederick Mihm. Pathophysiology and management of functional endocrine tumours in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0264.

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Thyroid hormones act on most tissues via nuclear T3 receptors. Thyroid hormones stimulate oxygen consumption and heat production, influence cell growth and maturation (central nervous system, bone), and modulate metabolism (carbohydrates, lipids, proteins, drugs). Treatment for presumed thyroid disease frequently has to be initiated before the results of diagnostic tests are available. Treatment of hyperthyroidism should result in the reduction of serum thyroid hormone levels and their action on peripheral tissues with concurrent treatment of the precipitating event. In severe hypothyroidism the choice of thyroid hormone (thyroxine or tri-iodothyronine), optimal dosing, and the route of administration remain controversial

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43

Reid, E. "Bioactive Analytes, Including Cns Drugs, Peptides, and Enantiomers". Springer, 2013.

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44

Porterfield, Jason. Downers: Depressant Abuse (Incredibly Disgusting Drugs). Rosen Central, 2007.

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45

Bioactive Analytes, Including CNS Drugs, Peptides, and Enantiomers (Methodological Surveys in Biochemistry & Analysis, Vol 16). Springer, 1987.

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46

Jones, Alison L. Management of opioid poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0319.

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Opioids are ‘morphine like’ substances that have actions at specific opioid receptors (especially µ receptors) in the central nervous system (CNS). Tolerance of respiratory depression develops at a slower rate than analgesic tolerance, placing patients with a long history of opioid use at particular risk for respiratory depression. If chronic users abruptly stop taking opioids, they develop an acute withdrawal syndrome. Most opioid toxicity is the result of inadvertent overdosage during recreational use or in self-harm, but it can also be due to medication misuse and drug errors. It is characterized by three main clinical features (all may not be consistently present); depressed respiratory rate (the sine qua non of opioid poisoning) and respiratory volume, and reduced arterial oxygen desaturation, CNS depression, and small or pin-point pupils. Opioid-poisoned patients require early clinical assessment, appropriate administration of intravenous naloxone (competitive opioid antagonist) and meticulous respiratory supportive care, with close observation. Because of the longer half-life of opioids than naloxone, repeated doses may be needed for long-acting opioids or large doses of shorter acting opioids. If opioid antagonists are given to regular opioid users in excess, they can precipitate acute withdrawal symptoms. The need for ITU admission usually occurs as a result of a complication of the opioid toxicity.

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47

Winter, Jerrold. Our Love Affair with Drugs: The History, the Science, the Politics. Oxford University Press, Incorporated, 2020.

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48

Stahl's Essential Psychopharmacology : Neuroscientific Basis and Practical Applications: Print and Online. University of Cambridge ESOL Examinations, 2008.

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49

Lheureux, Philippe, and Marc Van Nuffelen. Management of benzodiazepine poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0320.

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The wide use of benzodiazepines is associated with some inconveniences and are most frequently implicated in acute self-poisoning and accidental poisoning in children. Some of them are recognized as submission drugs, used to commit date rape or robbery. Prolonged use of a benzodiazepine leads to dependence, with a risk of developing a life-threatening withdrawal syndrome. Overdose has usually a good prognosis—most patients recover well with careful observation and prevention of complications, although care should be taken with elderly people, and patients with chronic obstructive pulmonary disease or liver dysfunction. Fast-acting agents and co-ingestion of other central nervous system depressants may be present greater risk. Early administration of activated charcoal in patients able to protect their airway is only needed if there are co-ingestants. Flumazenil may help confirm the diagnosis, improve alertness, and prevent the need for respiratory support in some patients, especially after accidental poisoning in children. Contraindications include patients on long-term treatment and/or dependent on benzodiazepines, or those who have simultaneously ingested proconvulsant or prodysrhythmic substances or at risk of increased intracranial pressure.

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50

Matthew, Verderame, ed. CRC Handbook of CNS agents and local anesthetics. Boca Raton, Fla: CRC Press, 1986.

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