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Books on the topic 'Anticholinergika'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Fanapour, Philip, Peggy White, and Brenda G. Fahy. Anticholinergic Overdose. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0095.

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Anticholinergic toxidrome can be a side effect of medications or herbal therapies or can result from intentional or inadvertent overdose of prescribed medications or abused substances. The diagnosis of anticholinergic toxicity involves symptomatology, including tachycardia, hyperthermia, central nervous system dysfunction including delirium, and urinary retention. The diagnosis can be challenging, as it is based on clinical symptoms with presentation mimicking other etiologies. Early diagnosis and intervention with treatment are key with the specific identification of the agent involved and other confounding substances. Discontinuation of the agent(s) involved as early as possible and providing supportive care are early interventions, with additional therapeutic options determined by the severity of the toxicity and the agent(s) involved.

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2

1946-, Barnes P. J., and Buist A. Sonia 1940-, eds. The role of anticholinergics in chronic obstructive pulmonary disease and chronic asthma. Macclesfield: Gardiner-Caldwell Communications, 1997.

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3

Parker, Philip M. The 2007-2012 World Outlook for Synthetic Antispasmodics and Anticholinergics Pharmaceutical Preparations. ICON Group International, Inc., 2006.

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4

The 2006-2011 World Outlook for Antispasmodic and Anticholinergic H2 Blocking Agents. Icon Group International, Inc., 2005.

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5

Parker, Philip M. The 2007-2012 World Outlook for Antispasmodic and Anticholinergic H2 Blocking Agents. ICON Group International, Inc., 2006.

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6

Parker, Philip M. The 2007-2012 Outlook for Synthetic Antispasmodics and Anticholinergics Pharmaceutical Preparations in India. ICON Group International, Inc., 2006.

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7

Parker, Philip M. The 2007-2012 Outlook for Synthetic Antispasmodics and Anticholinergics Pharmaceutical Preparations in Japan. ICON Group International, Inc., 2006.

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8

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic H2 Blocking Agents in Japan. ICON Group International, Inc., 2006.

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9

Parker, Philip M. The 2007-2012 Outlook for Synthetic Antispasmodics and Anticholinergics Pharmaceutical Preparations in Greater China. ICON Group International, Inc., 2006.

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10

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic H2 Blocking Agents in Greater China. ICON Group International, Inc., 2006.

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11

Anticholinergic Agents in the Upper and Lower Airways (Lung Biology in Health and Disease). Informa Healthcare, 1999.

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12

Parker, Philip M. The 2007-2012 Outlook for Synthetic Antispasmodics and Anticholinergics Pharmaceutical Preparations in the United States. ICON Group International, Inc., 2006.

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13

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic H2 Blocking Agents in the United States. ICON Group International, Inc., 2006.

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14

Harrison, Mark. Cardiovascular system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0039.

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This chapter describes the pharmacology of the cardiovascular system as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of cardiac glycosides, diuretics, antiarrhythmics, beta-adrenoceptor blockers, hypertension and heart failure, nitrates and antianginal drugs, sympathomimetics, anticholinergics, anticoagulants, antiplatelet drugs, fibrinolytics, and lipid-regulating drugs. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

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15

Parker, Philip M. The 2007-2012 World Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents. ICON Group International, Inc., 2006.

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16

The 2006-2011 World Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents. Icon Group International, Inc., 2005.

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17

Williams, Jeri Yvonne, and David G. Standaert. Dystonia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0011.

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Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions. Classification of dystonia is based on age of onset, distribution of body parts affected, and underlying etiology. A large number of different genetic forms of dystonia have been discovered in recent years. Although these syndromes are important to recognize, the majority of dystonias encountered in clinical practice are of unknown cause. Therapy of dystonia includes medications, particularly anticholinergic drugs, use of botulinum toxins, and deep brain stimulation.

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18

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents in India. ICON Group International, Inc., 2006.

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19

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents in Japan. ICON Group International, Inc., 2006.

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20

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents in Greater China. ICON Group International, Inc., 2006.

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21

Parker, Philip M. The 2007-2012 Outlook for Antispasmodic and Anticholinergic Pharmaceutical Preparations Excluding Synthetic and H2 Blocking Agents in the United States. ICON Group International, Inc., 2006.

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22

Fox, Susan H. Twists and Turns. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0020.

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Focal dystonia is the most common clinical manifestation of primary dystonia. The focal and sometimes task-specific nature of the symptoms makes daily drug therapy less attractive due to a requirement for exposure to high doses of anticholinergic agents that are typically only minimally effective. Botulinum toxin therapy can be targeted to a specific muscle group that is judged to be most active, providing relief for 3 months although not necessarily modifying the underlying disease pathophysiology, which remains uncertain. Deep-brain stimulation is currently reserved for the most resistant cases in which the disability or pain derived from the dystonia justifies consideration of neurosurgery.

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23

Alvis, Bret D., and Christopher G. Hughes. Delirium. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0061.

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Delirium in the postoperative period, characterized by inattention, disorganized thinking, disorientation, and/or altered levels of consciousness within the first few days after surgery, has been associated with significant increases in hospital stay, functional decline, prolonged cognitive dysfunction, and mortality. It is underdiagnosed without routine assessments with validated tools such as the Confusion Assessment Method (CAM), the 4AT, the Confusion Assessment Method for Intensive Care Unit (CAM-ICU), or the Intensive Care Delirium Screening Checklist (ICDSC). Prevention strategies for postoperative delirium include multimodal pain control, judicious use of medications that affect the sensorium, including benzodiazepines and anticholinergics, maintenance of appropriate volume status, and optimization of the patient’s environment. In patients who develop delirium with severe agitation, antipsychotic and alpha-2 agonist medications may be useful. Because postoperative delirium occurs commonly and is associated with worse outcomes, an understanding of its disease process, risk factors, and management is essential for an anesthesiologist.

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24

Awan, Kanwal, and Martin Steinberg. Medical Conditions That May Cause Cognitive Impairment and Depression. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199959549.003.0005.

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Ruling out medical conditions that can cause depression or cognitive impairment is essential in effectively caring for elderly patients. Case examples illustrate how these may present. Diabetes can cause confusion due to either hyper- or hypoglycemia. Congestive heart failure and chronic obstructive lung disease can cause hypoxia and resulting confusion. Sleep apnea can present with amnesia, apathy, and depression. Physiological changes make elderly patients especially susceptible to adverse drug effects, including hyponatremia and anticholinergic symptoms. Depression and cognitive changes have been associated with both hyper- and hypothyroidism, as well as with hyperparathyroidism. Elderly patients are at risk for developing subdural hematomas which can present with cognitive deficits and blunting of mood, and some patients may not have taken notice of the traumatic incident. Vitamin B12 deficiency can present with neurological symptoms including dementia, and cancer may present with fatigue and weight loss, which may be interpreted as depression.

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25

Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Cognitive dysfunction and sleep disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0014.

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Cognitive dysfunction is largely a problem in the elderly, but it can occur at any age. The two major presentations, delirium and postoperative cognitive dysfunction (POCD), are compared. Risks for delirium are explored; key points from the patient’s history and possible ways to ameliorate the onset are then reviewed. The presentation of POCD is described, and the lack of our understanding of its causes is highlighted. Known triggers such as centrally active anticholinergic drugs or pain are identified. Current thinking in the inflammatory responses within microglia and astrocytes is summarized. Sleep in the elderly is contrasted with that in younger persons, and the main stages of sleep, SWS and REM, described. The impact and importance of the effects that surgery/anaesthesia has on sleep stages is reviewed. Obstructive sleep apnoea is described, including its effect on the safety of anaesthesia and recovery. Periodic limb movement disorders and early Parkinson disease are described.

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26

Dhand, Rajiv, and Michael McCormack. Bronchodilators in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0033.

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Inhaled beta-agonists and anticholinergic agents, as well as systemically administered methylxanthines, are frequently employed to achieve bronchodilation in critically-ill patients. Inhaled agents are given by pressurized metered dose inhaler (pMDI), nebulizer, or dry powder inhaler. In ventilator-supported patients, aerosolized agents are generally only administered by pMDI or nebulizer. The ventilator circuit, artificial airway, and circuit humidity complicate the delivery of aerosolized agents, and there is a wide variability in drug delivery efficiency with various bench models of mechanical ventilation. Aerosolized drug by pMDI is affected by the use of spacer devices, synchronization of pMDI actuation and ventilator breath delivery, and appropriate priming of the pMDI device. The efficiency of aerosolized drug delivery by jet nebulization is also affected by device placement in the circuit, as well as by a number of other factors. Several investigators have demonstrated comparable efficiency of aerosol delivery with mechanically-ventilated and ambulatory patients when careful attention is given to the technique of administration. Appropriate administration of aerosolized bronchodilators in patients receiving invasive or non-invasive positive pressure ventilation produces significant therapeutic effects.

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27

Fortier, Martin. Sense of reality, metacognition, and culture in schizophrenic and drug-induced hallucinations. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789710.003.0016.

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Hallucinations possess two main components: (i) a sensory content; (ii) a sense that the sensory content is real. Influential models of schizophrenic hallucination claim that both the sensory content and the sense of reality can be explained in terms of metacognitive dysfunction. This chapter assesses whether such a claim holds for schizophrenic and drug-induced hallucinations; it further attempts to determine the actual role of metacognition in hallucination and how this role is liable to vary across cultures. It is first argued that the notion of sense of reality is heterogeneous and should therefore be divided into distinct kinds. Next, some monitoring-based models of hallucination are presented, and it is shown that they fail to explain important aspects of hallucinations. It is subsequently suggested that the main mechanisms of serotoninergic hallucinogens are not metacognitive, whereas those of anticholinergic hallucinogens importantly tap into subpersonal metacognitive processes. Finally, after specific consideration of the use of ayahuasca across different Amazonian indigenous groups, it is proposed that the metacognitive properties of hallucinogenic experiences can be variously exploited or ignored depending on cultural expectations.

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28

Chan, Kin-Sang, Doris M. W. Tse, and Michael M. K. Sham. Dyspnoea and other respiratory symptoms in palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0082.

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Dyspnoea is prevalent among palliative care patients with increased severity over time. There are two patterns of dyspnoea-breakthrough dyspnoea and constant dyspnoea-and three separate qualities of dyspnoea-air hunger, work or effort, and tightness. The measurement of dyspnoea includes three domains: sensory-perceptual experience, affective distress, and symptom impact. The management of dyspnoea includes specific disease management, non-pharmacological intervention, pharmacological treatment, and palliative non-invasive ventilation. Cough is prevalent and disturbing in patients with cancer and chronic lung diseases, and is often associated with airway hypersecretion and impaired mucociliary clearance. Management includes specific treatments for underlying non-cancer and cancer-related causes, symptomatic treatment by antitussives, mucoactive agents, and airway clearance techniques for expectoration and reduction in mucus production. Anticholinergics may be indicated for death rattles to facilitate a peaceful death. Haemoptysis occurs in 30-60% of lung cancer patients and initial management of haemoptysis includes airway protection and volume resuscitation. Localization of the site and source of bleeding may determine the choice of treatment. If a life-threatening haemoptysis occurs, sedation should be given as soon as possible. Support should be given to the family, and debriefing provided to team members.

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29

Dyer, Robert A., Michelle J. Arcache, and Eldrid Langesaeter. The aetiology and management of hypotension during spinal anaesthesia for caesarean delivery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0023.

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The management of hypotension during spinal anaesthesia for caesarean delivery remains a challenge for anaesthesiologists. Close control of maternal haemodynamics is of great importance for maternal and fetal safety, as well as maternal comfort. Haemodynamic responses to spinal anaesthesia are influenced by aortocaval compression, the baricity and dose of local anaesthetic and opioid employed, the rational use of fluids, and the goal-directed use of vasopressors. The most common response to spinal anaesthesia is hypotension and an increased heart rate, which reflects a decreased systemic vascular resistance and a partial compensatory increase in cardiac output. Phenylephrine is therefore the vasopressor of choice in this scenario. Less commonly, hypotension and bradycardia may occur, possibly due to the activation of cardiac reflexes. This requires anticholinergics and/or ephedrine. The rarest occurrences are persistent refractory hypotension, or high spinal block with respiratory failure. Special considerations include patients with severe pre-eclampsia, in whom spinal anaesthesia is associated with haemodynamic stability, and less hypotension than in the healthy patient. Careful use of neuraxial anaesthesia in specialized centres has an important role to play in the management of patients with cardiac disease, in conjunction with careful monitoring. Prevention is better than cure, but should hypotension occur, rapid intervention is essential, based upon the exact clinical scenario and individual haemodynamic response.

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30

Sampson, Brett G., and Andrew D. Bersten. Therapeutic approach to bronchospasm and asthma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0111.

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The optimal management of bronchospasm and acute asthma is reliant upon confirmation of the diagnosis of asthma, detection of life-threatening complications, recognition of β‎2 agonist toxicity, and exclusion of important asthma mimics (such as vocal cord dysfunction and left ventricular failure). β‎2 agonists, anticholinergics, and corticosteroids are the mainstay of treatment. β‎2 agonists should be preferentially administered by metered dose inhaler via a spacer, and corticosteroids by the oral route, reserving nebulized (and intravenous) salbutamol, as well as intravenous hydrocortisone, for situations when these routes are not possible. A single intravenous dose of magnesium may be of benefit in severe asthma, but repeat dosing is likely to cause serious side effects. Parenteral administration of adrenaline may prevent the need for intubation in the patient in extremis. Aminophylline has an unfavourable side effect profile and has not been shown to offer additional benefit in adults. However, it does have a role in paediatric asthma. Unproven medical therapies with potential benefit include ketamine, heliox, inhalational anaesthetics, and leukotriene antagonists. The need for ventilatory support is usually preceded by worsening dynamic hyperinflation, exhaustion, hypoxia, reduced conscious state, or a combination of these. While non-invasive ventilation may have a temporizing role to allow time for response to medical therapy, there is insufficient evidence for its use, and should not delay invasive ventilation. If invasive ventilation is indicated, a strategy of hypoventilation and permissive hypercapnoea, minimizes barotrauma and dynamic hyperinflation. Extracorporeal support may have a role as a rescue therapy.

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31

Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.

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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.

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