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Related Concept Videos

Skeletal Muscle Relaxants: Adverse Effects01:21

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Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
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Parenteral Anesthetics: Overview01:24

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Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
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Antiepileptic Drugs: Potassium Channel Activators01:20

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Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
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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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Local Anesthetics: Adverse Effects01:12

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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.
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Depolarizing Blockers: Mechanism of Action01:28

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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.
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Updated: Nov 17, 2025

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
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Magnesium-induced ketamine toxicity.

Robert McConnell1, Anne Pelham2, Felicity Dewhurst3

  • 1Saint Oswald's Hospice, Gosforth, Tyne and Wear, UK robertmcconnell@stoswaldsuk.org.

BMJ Supportive & Palliative Care
|February 17, 2021
PubMed
Summary
This summary is machine-generated.

This study highlights a potential interaction between ketamine and magnesium in managing neuropathic pain. Correcting hypomagnesaemia may trigger ketamine toxicity, even at stable doses.

Keywords:
drug administrationhospice carepainpharmacology

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Area of Science:

  • Pain Management
  • Neuropharmacology
  • Oncology

Background:

  • Neuropathic pain in metastatic duodenal cancer poses complex management challenges.
  • Ketamine is explored for its analgesic properties in refractory pain.
  • N-methyl-D-aspartate (NMDA) receptor antagonism is a key mechanism for both ketamine and magnesium.

Observation:

  • A patient receiving stable oral ketamine for abdominal pain developed ketamine toxicity after intravenous hypomagnesaemia treatment.
  • Symptoms of toxicity, described as a 'K-hole', emerged following the subsequent ketamine dose.
  • The patient was on a stable ketamine dosage prior to magnesium repletion.

Findings:

  • This case suggests a potential interaction between serum magnesium levels and ketamine's side effect profile.
  • Correction of hypomagnesaemia may unmask or potentiate ketamine toxicity.
  • The relationship between magnesium and ketamine in analgesia and toxicity is not fully understood.

Implications:

  • Clinicians should consider monitoring magnesium levels in patients on ketamine therapy.
  • Further research is warranted to elucidate the synergistic or antagonistic effects of ketamine and magnesium.
  • This finding may inform safer ketamine dosing strategies in patients with electrolyte imbalances.