Cholinergic Transmission Quiz
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Questions and Answers

Which step in cholinergic transmission is the rate-limiting step?

  • ACh Release
  • ACh Synthesis (correct)
  • ACh Storage
  • Presynaptic autoreceptors (M2)

    • Where are the subtypes of nicotinic receptors found?

  • CNS, adrenal medulla, neuromuscular junction
  • Blood vessels, CNS, sweat glands
  • Brain, ganglia, adrenal medulla, neuromuscular junction (correct)
  • CNS, autonomic ganglia, medulla and neuromuscular junction

    • What is the general effect of muscarinic antagonists?

  • Bind to muscarinic G-protein coupled receptors
  • Activate muscarinic receptors
  • Compete with ACh for binding at muscarinic receptors (correct)
  • Increase Na+ and K+ permeability

    • Which type of cholinesterase inhibitor is irreversible and interacts only with the esteratic site?

    <p>Irreversible inhibitors</p> Signup and view all the answers

    What is the primary role of cholinesterase inhibitors in clinical applications?

    <p>Treatment of Alzheimer's disease</p> Signup and view all the answers

    Which type of cholinesterase inhibitor is a peripheral and CNS inhibitor of AChE?

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

    What is the mechanism of action of Botulinum toxin (BoTox)?

    <p>It blocks the release of acetylcholine</p> Signup and view all the answers

    Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?

    <p>Lambert-Eaton</p> Signup and view all the answers

    Which autoimmune disease is characterized by fatigable weakness of skeletal muscles?

    <p>Myasthenia Gravis</p> Signup and view all the answers

    What are the major pharmacodynamic properties of competitive NMJ blockers?

    <p>Highly polar, quaternary compounds with poor oral bioavailability</p> Signup and view all the answers

    What is the difference in pharmacokinetics between nondepolarizing and depolarizing NMJ blockers?

    <p>Nondepolarizing blockers are metabolized at the synapse, while depolarizing blockers are metabolized in the liver and/or eliminated by the kidney</p> Signup and view all the answers

    Which step in cholinergic transmission is Ca2+-dependent?

    <p>ACh release</p> Signup and view all the answers

    Where are the subtypes of muscarinic receptors found?

    <p>Parasympathetic postganglionic endings</p> Signup and view all the answers

    What is the primary role of muscarinic agonists?

    <p>Activate muscarinic receptors</p> Signup and view all the answers

    Which type of receptors are controlled by ligand gating?

    <p>Nicotinic receptors</p> Signup and view all the answers

    Which type of receptors occur in the CNS, autonomic ganglia, medulla, and neuromuscular junction?

    <p>Nicotinic receptors</p> Signup and view all the answers

    What is the rate-limiting step in cholinergic transmission?

    <p>ACh synthesis</p> Signup and view all the answers

    Which type of cholinesterase inhibitor interacts only with the esteratic site and is irreversible?

    <p>Irreversible cholinesterase inhibitor</p> Signup and view all the answers

    What is the general effect of muscarinic antagonists?

    <p>Reduce the effects of ACh</p> Signup and view all the answers

    Where are the subtypes of nicotinic receptors found?

    <p>Central nervous system</p> Signup and view all the answers

    What drives the transport of ACh into vesicles?

    <p>Exchange with H+</p> Signup and view all the answers

    Which type of cholinesterase inhibitor is a slowly reversible inhibitor of AChE?

    <p>Reversible inhibitors</p> Signup and view all the answers

    What is the primary role of cholinesterase inhibitors in clinical applications?

    <p>Reversal of paralysis from neuromuscular drugs</p> Signup and view all the answers

    What is the mechanism of action of pralidoxime in treating organophosphate toxicity?

    <p>It displaces the dialkylphosphate residue from the phosphorylated enzyme</p> Signup and view all the answers

    What is the target tissue of Botulinum toxin (BoTox)?

    <p>Both smooth and skeletal muscle synapses</p> Signup and view all the answers

    What is the effect of Botulinum toxin (BoTox) on ACh release?

    <p>It decreases ACh release</p> Signup and view all the answers

    Which autoimmune disease is associated with dysfunction at the neuromuscular junction?

    <p>Myasthenia Gravis</p> Signup and view all the answers

    What is the pharmacologic treatment for Myasthenia Gravis?

    <p>Cholinesterase inhibitors</p> Signup and view all the answers

    Which type of cholinesterase is primarily responsible for the metabolism of ACh at cholinergic synapses?

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

    Which type of cholinesterase is found in plasma, liver, and glia?

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

    Which type of cholinesterase inhibitor is irreversible and interacts only with the esteratic site?

    <p>Irreversible inhibitors</p> Signup and view all the answers

    Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?

    <p>Lambert-Eaton</p> Signup and view all the answers

    Which autoimmune disease affects the postsynaptic neuromuscular junction and is characterized by fatigable weakness of skeletal muscles?

    <p>Myasthenia Gravis</p> Signup and view all the answers

    What is the primary pharmacodynamic property of competitive NMJ blockers?

    <p>Highly polar, quaternary compounds with poor oral bioavailability</p> Signup and view all the answers

    What is the primary pharmacokinetic difference between nondepolarizing and depolarizing NMJ blockers?

    <p>Metabolism at the synapse</p> Signup and view all the answers

    What drug class is used to reverse the effects of NMJ blockers by increasing the concentration of ACh at NMJ synapses?

    <p>Acetylcholinesterase inhibitors</p> Signup and view all the answers

    How does sugammadex reverse the effects of NMJ blockers?

    <p>By sequestering NMJ antagonist in blood</p> Signup and view all the answers

    What are the consequences of genetic variation on succinylcholine metabolism?

    <p>Prolonged post-succinylcholine neuromuscular blockade</p> Signup and view all the answers

    What is the duration of action of succinylcholine?

    <p>2-6 minutes</p> Signup and view all the answers

    What is the primary mechanism of action of competitive NMJ blockers?

    <p>Blockade of ACh neurotransmission at NMJ</p> Signup and view all the answers

    What is the effect of competitive NMJ blockers on sensation?

    <p>Sensation is unaffected</p> Signup and view all the answers

    Study Notes

    Cholinergic Transmission

    • The rate-limiting step is the synthesis of acetylcholine (ACh).
    • Cholinergic transmission is calcium-dependent during the release of ACh into the synaptic cleft.

    Nicotinic Receptors

    • Subtypes are found in the CNS, autonomic ganglia, medulla, and neuromuscular junction.
    • Nicotinic receptors are ligand-gated ion channels.

    Muscarinic Receptors

    • Subtypes are located in various locations including the heart, smooth muscle, and glands.
    • Muscarinic agonists primarily promote parasympathetic actions such as decreased heart rate and increased glandular secretion.

    Muscarinic Antagonists

    • General effects include inhibition of parasympathetic responses, leading to increased heart rate and reduced secretions.

    Cholinesterase Inhibitors

    • Irreversible inhibitors interact only with the esteratic site on acetylcholinesterase (AChE).
    • The primary role in clinical applications is to enhance synaptic ACh levels, useful in conditions such as myasthenia gravis.
    • There are peripheral and CNS cholinesterase inhibitors, with different action sites across the body.
    • A slowly reversible inhibitor of AChE acts to prolong ACh effectiveness at the synapse.

    Botulinum Toxin (BoTox)

    • Mechanism of action involves blocking the release of ACh at the neuromuscular junction, leading to muscle paralysis.
    • Target tissue is primarily the neuromuscular junction, affecting skeletal muscle contraction.
    • Alters the release of ACh, resulting in decreased muscle activation.

    Autoimmune Disorders

    • Myasthenia gravis is characterized by fatigable weakness of skeletal muscles due to dysfunction at the neuromuscular junction.
    • Lambert-Eaton Myasthenic Syndrome (LEMS) involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal.

    Neuromuscular Junction (NMJ) Blockers

    • Competitive NMJ blockers primarily prevent ACh from binding to nicotinic receptors, leading to muscle paralysis.
    • Depolarizing NMJ blockers, like succinylcholine, act as agonists at the ACh receptor, causing initial muscle fasciculation followed by paralysis.
    • The key pharmacodynamic property of competitive blockers is their ability to compete with ACh.
    • Pharmacokinetics differ; nondepolarizing blockers can be reversed with agents like sugammadex while depolarizing blockers have a shorter duration.

    Cholinesterase and ACh Metabolism

    • Acetylcholinesterase (AChE) is chiefly responsible for metabolizing ACh at synapses.
    • Butyrylcholinesterase is found in plasma, liver, and glial cells, contributing to ACh metabolism at various sites.

    Treatment for Myasthenia Gravis

    • Pharmacologic treatment includes cholinesterase inhibitors to increase the availability of ACh.
    • Pralidoxime is used for treating organophosphate toxicity by reactivating AChE.

    Succinylcholine

    • Genetic variation can influence metabolism and response to succinylcholine, affecting duration of action.

    Effects on Sensation

    • Competitive NMJ blockers do not directly affect sensation but can produce muscle weakness, impacting proprioception and motor reflexes.

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    Description

    Test your knowledge of the major processes in cholinergic transmission, including ACh synthesis, storage, release, and elimination. Learn about the rate-limiting step in ACh synthesis, the concentration of ACh in vesicles, and the role of presynaptic autoreceptors.

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