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Other Reactions from Gloves
Published in Robert N. Phalen, Howard I. Maibach, Protective Gloves for Occupational Use, 2023
T. Bullock, A. Sood, J.S. Taylor
Cholinergic (sweat or exertion) urticaria follows an increase in body temperature. Tiny, confluent, pruritic wheals on patchy erythema develop; lesions usually occur on the upper body after physical exertion or sweating and urticarial dermographism may be present.9
Targeting the Nervous System
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Where two neurones meet at a synapse, the nerve impulse is interrupted because there is a gap between the neurones, called the synaptic cleft. In order for the signal travelling down the presynaptic neurone to be continued, it must be propagated in the postsynaptic neurone across the synapse via neurotransmitters, such as acetylcholine. Neurotransmitters are molecules that, upon activation by an action potential, are released from the presynaptic neurone into the synaptic cleft. The neurotransmitter molecules diffuse across the gap and bind to receptors on the postsynaptic neurone, causing a chain of reactions that result in the propagation of the action potential in the postsynaptic nerve and the signal can proceed to its final destination. The actions of the neurotransmitter acetylcholine are instrumental in the operation of the cholinergic nervous system.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Cholinergic receptors are divided into two subtypes: nicotinic receptors and muscarinic receptors. Most organs are innervated by sympathetic and parasympathetic fibres. The major exception is the vascular system, which is generally under sympathetic control. The systemic effects of the sympathetic and parasympathetic nervous system can be seen in Table 9.1.
Design, synthesis and biological evaluation of novel N-phosphorylated and O-phosphorylated tacrine derivatives as potential drugs against Alzheimer’s disease
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Maja Przybyłowska, Krystyna Dzierzbicka, Szymon Kowalski, Sebastian Demkowicz, Mateusz Daśko, Iwona Inkielewicz-Stepniak
Alzheimer’s disease is an age – related most common cause of dementia among elderly people. That is already the third leading cause of death after cancer and heart diseases1,2. According to an update to the estimates in the World Alzheimer Report 2015 (2020), there are over 50 million people worldwide living with dementia in 2020. This number will almost double every 20 years, reaching 152 million in 20503. The life activity of the patients depends on the stage of disease. Mostly, at the beginning they are characterised only by mild loss of the memory, whereas in the advanced stage, they are totally dependent on someone, not able to function by their own4. It should be mentioned that many other symptoms occur simultaneously with AD, like depression, psychosis or cognitive impairment5–7. The cause of this disease is still unknown, but the main therapeutic strategies are based on cholinergic hypothesis, so available drugs are cholinesterase inhibitors8,9. Regarding the hydrolysis of acetylcholine by acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) to choline and acetate, the concentration of this neurotransmitter in the central nervous system is insufficient to enable the proper work of brain10–14. Another characteristics of AD are the presence of thick extracellular β-amyloid plaques (Aβ) and intra-neuronal neurofibrillary tangles (NFTs), that lead to the death of neurons and as a result to the behavioural symptoms mentioned above15–18.
Lipid emulsion for the treatment of acute organophosphate poisoning: an Open-Label randomized trial
Published in Clinical Toxicology, 2022
Ashok Kumar Pannu, Sahil Garg, Ashish Bhalla, Deba Prasad Dhibar, Navneet Sharma
The cholinergic crisis was defined with characteristic muscarinic or/and nicotinic manifestations of typical anticholinesterase poisoning. Muscarinic features include diarrhea, urination, miosis, bronchorrhea (or bronchospasm), bradycardia, emesis, lacrimation, low blood pressure, and salivation (acronym - DUMBBELLS). Nicotinic stimulation at sympathetic ganglia and neuromuscular junction include mydriasis, tachycardia, weakness, hypertension, fasciculations, shallow breathing (diminished respiratory effort), and sweating (a memory aid using the first letter of the days’ names from Monday to Sunday) [4–6,38]. Thus, a mnemonic “DUMBBELLS - Monday to Sunday” is helpful to describe the overall cholinergic crisis [6,38]. Peradeniya OP severity scale was used to define toxidrome severity at ED admission [39]. It consists of five clinical variables - pupil size, respiratory rate, heart rate, muscle fasciculation, level of consciousness, on a scale of 0 to 2 for each of five variables, with aggregated scores of 0–3 indicating mild poisoning, 4–7 for moderate, and 8–11 for severe toxidrome.
Organophosphate induced delayed neuropathy after an acute cholinergic crisis in self-poisoning
Published in Clinical Toxicology, 2021
A. K. Pannu, A. Bhalla, R. I. Vishnu, D. P. Dhibar, N. Sharma, R. Vijayvergiya
Patients aged between 13 and 40 years presenting with a history of OP consumption and clinical features of cholinergic toxidrome of typical anticholinesterase poisoning were recruited. The cholinergic crisis comprises muscarinic effects (e.g., bradycardia, increased trachea-bronchial secretions, lacrimation, urination) and nicotinic effects (e.g., muscle weakness, fasciculations) [7–9]. Patients with doubtful history, poisoning with unknown compounds, poisoning with more than one compound, chronic exposure to OP, history of pre-existing medical comorbidities (e.g., neurological disorders, diabetes mellitus, renal failure, hypothyroidism, or chronic alcohol use disorders) were excluded. Because the prevalence of PN increases with age, we also excluded middle and older aged patients [29].