![]() ![]() Understanding the general function of each muscarinic receptor at each organ system is necessary to understand the anticholinergic reaction. There are at least five subtypes of muscarinic receptors (M1, M2, M3, M4, and M5) present throughout the body. Therefore the remainder of this article, "anticholinergic" is used synonymously with "antimuscarinic." Organ Systems Involved There are a limited number of medication classes with antinicotinic properties. Medications with anticholinergic activity usually affect muscarinic receptors but not nicotinic receptors. This activity can result from normal physiology, abnormal pathology, or medication. Īny process that attenuates the effects of acetylcholine at its receptors, whether by reducing its synthesis or release, increasing acetylcholinesterase activity, or inhibiting the receptor, is termed an anticholinergic effect. In general, the ACh binds to ACh receptors are nicotinic-type at the NMJ, and muscarinic-type at the CNS and ANS, although some exceptions exist.Īcetylcholinesterase is an enzyme in the synaptic cleft, functioning to degrade acetylcholine and decrease its concentration, thereby, decreasing its action on its receptors. Upon stimulation of the neuron, ACh vesicles are exocytosed, out of the neuron, and into the synaptic cleft, where it can act on receptors present on postsynaptic neurons. ![]() It is subsequently transferred to vesicles within the presynaptic neuron for storage. It is synthesized within the cytosol of the presynaptic neuron from acetyl-coenzyme A and choline by the enzyme choline acetyltransferase. Cellular LevelĪcetylcholine (ACh) is a neurotransmitter found within synaptic vesicles in presynaptic cholinergic neurons present in the central nervous system (CNS), autonomic nervous system (ANS), and neuromuscular junction (NMJ). Dry as a bone (anhidrosis/dry mouth/dry skin)Ĭlinically the most significant feature is delirium, particularly in the elderly, who are most likely to be affected by the anticholinergic reaction.The features of the anticholinergic reaction are deducible from an understanding of the normal function of muscarinic receptors at various organs, and the following mnemonic summarizes these effects: Many also contribute to the development of an anticholinergic reaction: a constellation of symptoms resulting from the antagonism of muscarinic receptors throughout the body. At least 600 drugs/medicinal products are recognized to have anticholinergic activity, and the most common of these are responsible for a significant amount of poisoning admissions. These medications should be more appropriately termed "antimuscarinics," as they usually block muscarinic but not nicotinic receptors. Processes that enhance ACh function are termed “cholinergic” while processes that inhibit the action of ACh at its receptors are termed “anticholinergic.” Anticholinergic effects are most commonly the result of medication. As a reminder, these receptors are functionally and structurally different nicotinic ACh receptors are ligand-gated ion channels, whereas muscarinic ACh receptors are G-protein coupled receptors. Generally, ACh receptors at the NMJ are nicotinic type while in the CNS and ANS they are usually muscarinic type. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.Acetylcholine (ACh) is a neurotransmitter that acts on the central nervous system (CNS), the autonomic nervous system (ANS), and at the neuromuscular junction (NMJ). ![]() Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. The symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Substances that may cause this toxidrome are opioids. Complications include bradycardia, hypotension, and hypothermia. The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness.
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