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As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).
Individuals symptoms vary in severity and type. Severe, subacute gastrointestinal dysmotility and orthostatic hypotension are the most common symptoms in two-thirds of patients. Symptoms can be severe in some cases and gradually worsen in others. [1] Sympathetic failure manifests itself as orthostatic hypotension and anhidrosis.
Standard treatment for nerve agent poisoning is a combination of an anticholinergic to manage the symptoms, and an oxime as an antidote. [12] Anticholinergics treat the symptoms by reducing the effects of acetylcholine, while oximes displaces phosphate molecules from the active site of the cholinesterase enzymes, allowing the breakdown of ...
Choline acetyltransferase was first described by David Nachmansohn and A. L. Machado in 1943. [6] A German biochemist, Nachmansohn had been studying the process of nerve impulse conduction and utilization of energy-yielding chemical reactions in cells, expanding upon the works of Nobel laureates Otto Warburg and Otto Meyerhof on fermentation, glycolysis, and muscle contraction.
Acquired myasthenia gravis is the most common neuromuscular junction disease.(reference 7) Important observations were made by Patrick and Lindstrom in 1973 when they found that antibodies attacking the acetylcholine receptors were present in around 85% of cases of myasthenia gravis.(reference renamed form 13)(reference 36) The remaining ...
Chemical structure of acetylcholine. Cholinergic blocking drugs are a group of drugs that block the action of acetylcholine (ACh), a neurotransmitter, in synapses of the cholinergic nervous system. [1] They block acetylcholine from binding to cholinergic receptors, namely the nicotinic and muscarinic receptors.
Acetylcholinesterase (HGNC symbol ACHE; EC 3.1.1.7; systematic name acetylcholine acetylhydrolase), also known as AChE, AChase or acetylhydrolase, is the primary cholinesterase in the body. It is an enzyme that catalyzes the breakdown of acetylcholine and some other choline esters that function as neurotransmitters :
The resulting decrease in acetylcholine in the brain is thought to contribute to the decline in mental function of affected patients. [ 3 ] [ 2 ] For this reason, most currently available pharmacological treatments for dementia focus on compensating for faltering function of the nucleus basalis through artificially increasing acetylcholine levels.