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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 ot
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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. 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 ca
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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 p
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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 hav
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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 summarize
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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 mechani
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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
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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 a
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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 vascu
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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, f
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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. Howe
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