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Related Concept Videos

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
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Depolarizing Blockers: Pharmocokinetics01:19

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Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
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Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics01:11

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics

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All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...
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Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
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Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
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Local Anesthetics: Adverse Effects01:12

Local Anesthetics: Adverse Effects

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While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
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Related Experiment Video

Updated: May 5, 2026

Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain
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Exploring the link between pholcodine exposure and neuromuscular blocking agent anaphylaxis.

Anna M Brusch1, Russell C Clarke, Peter R Platt

  • 1Department of Clinical Immunology, Fremantle Hospital, Fremantle, WA, Australia; Sir Charles Gairdner Hospital, Perth, WA, Australia.

British Journal of Clinical Pharmacology
|November 21, 2013
PubMed
Summary
This summary is machine-generated.

Neuromuscular blocking agents (NMBAs) cause anaphylaxis during anesthesia. Pholcodine, an antitussive, may increase NMBA allergy risk due to shared ammonium ions, prompting its withdrawal in some regions.

Keywords:
anaphylaxisdrug hypersensitivityneuromuscular blocking agentpholcodinesubstituted ammonium ions

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Area of Science:

  • Anesthesiology
  • Immunology
  • Pharmacology

Background:

  • Neuromuscular blocking agents (NMBAs) are a leading cause of perioperative anaphylaxis.
  • Geographical variations in NMBA anaphylaxis suggest external contributing factors.
  • Substituted ammonium ions, present in NMBAs, are implicated as the primary allergens.

Purpose of the Study:

  • To review the evidence linking pholcodine exposure to NMBA hypersensitivity.
  • To explore the potential mechanisms of pholcodine-induced sensitization.
  • To discuss implications for understanding NMBA allergy pathophysiology.

Main Methods:

  • Review of epidemiological studies and clinical observations.
  • Analysis of chemical structures and allergenic determinants (substituted ammonium ions).
  • Examination of the impact of pholcodine withdrawal on NMBA anaphylaxis rates.

Main Results:

  • Pholcodine, containing a tertiary ammonium ion, shows epidemiological parallels with NMBA anaphylaxis incidence.
  • Withdrawal of pholcodine in some countries correlated with a decrease in NMBA anaphylaxis rates.
  • Shared substituted ammonium ions are hypothesized as the link between pholcodine and NMBA hypersensitivity.

Conclusions:

  • Pholcodine exposure is a compelling potential factor in NMBA hypersensitivity.
  • Further research is needed to elucidate the exact mechanisms of sensitization.
  • Identifying other sensitizing agents is crucial for preventing NMBA-related anaphylaxis.