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Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Tricyclic antidepressants often produce toxic side effects related to two major actions: blockade of amine metabolism and the central-peripheral cholinergic system.177 Tricyclics block the amine reuptake mechanism in the presynaptic area, and therefore the synaptic transmitter remains in a functionally active state for longer periods. These drugs show selective activity. Tricyclics with teritary amine groups block more strongly the amino pump for serotonin than for nonepinephrine.537 Acute intoxication is followed by a central nervous system anticholinergic syndrome, with confusion and delirious state, followed by sedation and central anticholinergic effects causing coma. Severe complications may also occur, particularly in aged patients.576
Fever Of Unexplained Origin — Psychiatric Aspects
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
Differential Diagnosis (a) Phenothiazine heat stroke as a result of inhibiting sweating.30(b) Idiopathic acute lethal catatonia is a very rare syndrome, with great similarity to NMS. Stopping neuroleptics helps in the differential diagnosis of these syndromes.(c) Drug interactions with monoamino-oxidase inhibitors.36(d) Central anticholinergic syndrome — peripheral signs of atropine poisoning like dry skin and mouth, dilated pupils, decreased bowel sounds, and urinary retention. The temperature is elevated and confusion appears.
Answers
Published in John D Firth, Professor Ian Gilmore, MRCP Part 2 Self-Assessment, 2018
John D Firth, Professor Ian Gilmore
Anticholinergic syndrome occurs following overdose with drugs that have prominent anticholinergic activity, including tricyclic antidepressants, antihistamines and atropine. Features include dry, warm, flushed skin, urinary retention, tachycardia, mydriasis (dilated pupils) and agitation. Although physostigmine, a reversible inhibitor of acteylcholinesterase, is effective in treating symptoms, there is a significant risk of cardiac toxicity (bradycardia, AV conduction defects and asystole). Treatment therefore consists of withdrawal of the precipitating drug and supportive care.
Mass spectrometry in emergency toxicology: Current state and future applications
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Xander M. R. Van Wijk, Robert Goodnough, Jennifer M. Colby
Comprehensive drug screening by mass spectrometry (MS) has the potential to positively impact the care of the poisoned patient, as we hope to illustrate in this work. We would like to begin by presenting a case that captures the profound impact this technique can have. This case involves an 18-year-old female who fell out of bed as a result of a witnessed seizure. She did not have a history of seizure disorders. Upon arrival of emergency medical services (EMS), she admitted smoking marijuana and disclosed that she had just started taking citalopram for anxiety. She denied any other medications. Her roommates reported to EMS that she was “emotionally unstable” and has a history of suicidal gestures. Her condition worsened on arrival in the emergency department (ED), where she became agitated and delirious, and unable to respond to questions. Her admission urine drug screen was negative for all tested drugs. The medical toxicologist who was consulted suspected a citalopram overdose may have been causing serotonin syndrome and requested comprehensive toxicology testing. The test showed that citalopram was absent from the patient’s blood, but unexpectedly, diphenhydramine was present. Based on these results, the medical toxicologist diagnosed the patient with anticholinergic syndrome due to diphenhydramine overdose and recommended treatment with physostigmine. After administration, the patient woke up immediately was alert, and oriented. This vignette illustrates the power of a comprehensive drug screen that is able to detect a variety of drugs and produce results in a clinically relevant timeframe when available locally.
Reduction of oculocardiac reflex with Tetracaine eye drop in strabismus surgery
Published in Strabismus, 2019
Mojtaba Rahimi Varposhti, Darioush Moradi Farsani, Keyvan Ghadimi, Mehrdad Asadi
Although some studies believed that pretreatment with anticholinergic compounds could reduce the incidence of OCR, there were conflicting results with this hypothesis. While Misurya et al. reported an absence of OCR incidence in pretreatment with atropine and injection of retrobulbar xylocaine 2%20; Gupta et al. study suggested a significant reduction in the incidence and severity of OCR when using peribulbar bupivacaine 0.25%, but using Atropine as an anticholinergic was associated with conflicting results, including dysrhythmia, dangerous arrhythmias, and a significant reduction in cardiac output.10 On the other hand, the probable influence of atropine on the central nervous system can also cause central anticholinergic syndrome.21
“Purple Drank” (Codeine and Promethazine Cough Syrup): A Systematic Review of a Social Phenomenon with Medical Implications
Published in Journal of Psychoactive Drugs, 2020
A. Miuli, G. Stigliano, A. Lalli, M. Coladonato, L. D’Angelo, F. Esposito, C. Cappello, M. Pettorruso, G. Martinotti, F Schifano, M. Di Giannantonio
Another key component of Purple Drank is promethazine (PM) ((RS)-N, N-dimethyl-1-(10 H-phenothiazine-10-yl) propan-2-amine hydrochloride), a phenothiazine’s derivative. It is a first-generation H1 receptor antagonist, an antihistamine and antiemetic medication that can also have strong sedative effects (Balthazar et al. 2010). Moreover, promethazine has strong anticholinergic properties, since it blocks responses to acetylcholine through the mediation of muscarinic receptors. This explains why an overdose of promethazine could lead to anticholinergic toxidrome, caused by the competitive antagonism of acetylcholine at the peripheral and central muscarinic receptors, accompanied by a wide range of signs and symptoms (Naicker et al. 2017). At a peripheral level symptoms include: dry mouth, difficulty swallowing, mydriasis with blurred vision and photophobia. Pupils are dilated and not responsive to light, the skin becomes dry and red due to cutaneous vasodilation, and gastrointestinal effects and urinary retention are common. At a cardiovascular level sinus tachycardia is also frequent. Extrasystole and blood pressure could be either low, due to peripheral vasodilation, or elevated because of agitation. Agitation causes heat production that may lead to fever; anhidrosis causes minor heat loss and a dysregulation of the hypothalamic site in controlling the body temperature, a dopamine mediated process (Rinder et al. 1988; Schwartz and Erk 2004). The central anticholinergic syndrome is characterized by agitation, hyperactive delirium, slurred speech, psychosis, visual and/or auditory hallucinations and seizures (Erickson et al. 2005; Martinotti et al. 2018; Verheijden et al. 2016). This clinical situation can be described with a doggerel: “Blind as a bat, mad as a hatter, red as a beet, hot as Hades, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone” (Stead et al. 2006).