PHAR20040: Neuromuscular Junction Blockade
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Questions and Answers

What type of inhibition is seen with triethylcholine?

  • Competitive inhibition (correct)
  • Non-competitive inhibition
  • Uncompetitive inhibition
  • Allosteric inhibition
  • Which ion is involved in the blockade of Ca2+-mediated exocytosis of synaptic vesicle?

  • Na+
  • Ca2+
  • Mg2+ (correct)
  • K+
  • What is the mechanism of action of botulinum toxin?

  • Inhibition of SNARE proteins (correct)
  • Activation of SNARE proteins
  • Inhibition of choline transporter
  • Hydrolysis of membrane phospholipids
  • What is the effect of β-bungarotoxin on the neuromuscular junction?

    <p>Hydrolysis of membrane phospholipids</p> Signup and view all the answers

    What is the primary use of drugs that enhance ACh transmission in the context of botulinum toxin?

    <p>Ineffective due to irreversible action</p> Signup and view all the answers

    What type of blockers are structural analogues of acetylcholine?

    <p>Postsynaptic blockers</p> Signup and view all the answers

    What is the primary function of acetylcholinesterase (AChE) in the neuromuscular junction?

    <p>To break down acetylcholine into inactive components</p> Signup and view all the answers

    How many synaptic vesicles are typically released by a single nerve impulse in the neuromuscular junction?

    <p>300</p> Signup and view all the answers

    What is the site of action for drugs that inhibit acetylcholine synthesis and release?

    <p>Motor neuron terminal</p> Signup and view all the answers

    What is the primary mechanism of pharmacological blockade of the neuromuscular junction?

    <p>Blockade of nicotinic receptors</p> Signup and view all the answers

    What is the primary function of the nicotinic receptor in the neuromuscular junction?

    <p>To bind and respond to acetylcholine released from motor neurons</p> Signup and view all the answers

    How long do acetylcholine molecules interact with nicotinic receptors in the neuromuscular junction?

    <p>2 milliseconds</p> Signup and view all the answers

    What happens to sodium in the ion channel when a depolarizing neuromuscular blocker is used?

    <p>It is blocked from entering the cell</p> Signup and view all the answers

    Why do patients with muscle denervation have an increased risk of heart dysrhythmia or arrest when using depolarizing blockers?

    <p>Due to hyperkalemia</p> Signup and view all the answers

    What is the main difference between depolarizing and non-depolarizing blockers?

    <p>Depolarizing blockers are non-competitive inhibitors, while non-depolarizing blockers are competitive</p> Signup and view all the answers

    What is the primary mechanism of action of suxamethonium?

    <p>Depolarizing the muscle fiber</p> Signup and view all the answers

    Why is suxamethonium used during anesthesia induction?

    <p>To facilitate intubation</p> Signup and view all the answers

    What is a rare but potential side effect of using suxamethonium?

    <p>Malignant hyperthermia</p> Signup and view all the answers

    Study Notes

    Pharmacological Blockade of the Neuromuscular Junction (NMJ)

    Inhibitors of ACh Synthesis and Release

    • Hemicholinium: blocks choline transporter, competitive inhibition
    • Triethylcholine: blocks ACh synthesis, competitive inhibition, transported into terminal and converted into false neurotransmitter
    • Vesamicol: inhibits ACh transport into synaptic vesicle

    Inhibitors of ACh Release

    • Mg2+: blocks Ca2+-mediated exocytosis of synaptic vesicle
    • Aminoglycoside antibiotics (streptomycin, neomycin): specific block of ACh release
    • Botulinum toxin (Botox): inactivates SNARE proteins required for exocytosis, high potency, causes botulism, used for relief of muscle spasm, eyelid spasm, and wrinkle removal
    • β-Bungarotoxin: hydrolyses membrane phospholipids

    Postsynaptic Neuromuscular Blockers

    • Act as antagonists (non-depolarizing blockers) or agonists (depolarizing blockers) at nicotinic receptors
    • Used during surgery to promote complete muscle relaxation without higher doses of anaesthetic

    Depolarizing (Non-Competitive) Neuromuscular Blockers

    • Cause continued depolarization leading to repolarization and block of sodium channel
    • Prevent further depolarization, leading to twitching becoming flaccid paralysis
    • Muscle twitching is short-lived
    • No ganglionic block, except at very high doses
    • Side effects: bradycardia, post-operative muscle pain, apnea, hyperkalemia, increased intraocular pressure, prolonged paralysis, and malignant hyperthermia

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    Description

    This quiz covers the key components of the neuromuscular junction and various drug strategies for modulating its function. Topics include neuromuscular junction blockade and its pharmacological applications. Assess your knowledge of neuropharmacology and pharmacology in this lecture-based quiz.

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