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Neuromuscular-blocking drugs, or Neuromuscular blocking agents (NMBAs), block transmission at the neuromuscular junction, [1] causing paralysis of the affected skeletal muscles. This is accomplished via their action on the post-synaptic acetylcholine (Nm) receptors.
Botulinum toxin, or botulinum neurotoxin (commonly called botox), is a neurotoxic protein produced by the bacterium Clostridium botulinum and related species. [24] It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction, thus causing flaccid paralysis. [25]
Neuromuscular drugs are chemical agents that are used to alter the transmission of nerve impulses to muscles, causing effects such as temporary paralysis of targeted skeletal muscles. Most neuromuscular drugs are available as quaternary ammonium compounds which are derived from acetylcholine (ACh). [ 1 ]
When immune cells attack the myelin sheath, this causes inflammation and interrupts the passage of nerve impulses around the body, leading to neurological symptoms which may include: Muscle ...
Damage to skeletal muscle may take various forms. Crush and other physical injuries cause damage to muscle cells directly or interfere with blood supply, while non-physical causes interfere with muscle cell metabolism. When damaged, muscle tissue rapidly fills with fluid from the bloodstream, including sodium ions.
Porphyria / p ɔːr ˈ f ɪr i ə / is a group of disorders in which substances called porphyrins build up in the body, adversely affecting the skin or nervous system. [1] The types that affect the nervous system are also known as acute porphyria, as symptoms are rapid in onset and short in duration. [1]
GLP-1’s are known to cause a delay in gastric emptying, as noted in the label of each of our GLP-1 RA medications. Symptoms of delayed gastric emptying, nausea and vomiting are listed as side ...
The effect with which injected curare poison is usually associated is muscle paralysis and resultant death. [87] Curare notably functions to inhibit nicotinic acetylcholine receptors at the neuromuscular junction. Normally, these receptor channels allow sodium ions into muscle cells to initiate an action potential that leads to muscle contraction.
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