Podcast
Questions and Answers
Which step in cholinergic transmission is the rate-limiting step?
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?
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?
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?
Which type of cholinesterase inhibitor is irreversible and interacts only with the esteratic site?
What is the primary role of cholinesterase inhibitors in clinical applications?
What is the primary role of cholinesterase inhibitors in clinical applications?
Which type of cholinesterase inhibitor is a peripheral and CNS inhibitor of AChE?
Which type of cholinesterase inhibitor is a peripheral and CNS inhibitor of AChE?
What is the mechanism of action of Botulinum toxin (BoTox)?
What is the mechanism of action of Botulinum toxin (BoTox)?
Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?
Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?
Which autoimmune disease is characterized by fatigable weakness of skeletal muscles?
Which autoimmune disease is characterized by fatigable weakness of skeletal muscles?
What are the major pharmacodynamic properties of competitive NMJ blockers?
What are the major pharmacodynamic properties of competitive NMJ blockers?
What is the difference in pharmacokinetics between nondepolarizing and depolarizing NMJ blockers?
What is the difference in pharmacokinetics between nondepolarizing and depolarizing NMJ blockers?
Which step in cholinergic transmission is Ca2+-dependent?
Which step in cholinergic transmission is Ca2+-dependent?
Where are the subtypes of muscarinic receptors found?
Where are the subtypes of muscarinic receptors found?
What is the primary role of muscarinic agonists?
What is the primary role of muscarinic agonists?
Which type of receptors are controlled by ligand gating?
Which type of receptors are controlled by ligand gating?
Which type of receptors occur in the CNS, autonomic ganglia, medulla, and neuromuscular junction?
Which type of receptors occur in the CNS, autonomic ganglia, medulla, and neuromuscular junction?
What is the rate-limiting step in cholinergic transmission?
What is the rate-limiting step in cholinergic transmission?
Which type of cholinesterase inhibitor interacts only with the esteratic site and is irreversible?
Which type of cholinesterase inhibitor interacts only with the esteratic site and is irreversible?
What is the general effect of muscarinic antagonists?
What is the general effect of muscarinic antagonists?
Where are the subtypes of nicotinic receptors found?
Where are the subtypes of nicotinic receptors found?
What drives the transport of ACh into vesicles?
What drives the transport of ACh into vesicles?
Which type of cholinesterase inhibitor is a slowly reversible inhibitor of AChE?
Which type of cholinesterase inhibitor is a slowly reversible inhibitor of AChE?
What is the primary role of cholinesterase inhibitors in clinical applications?
What is the primary role of cholinesterase inhibitors in clinical applications?
What is the mechanism of action of pralidoxime in treating organophosphate toxicity?
What is the mechanism of action of pralidoxime in treating organophosphate toxicity?
What is the target tissue of Botulinum toxin (BoTox)?
What is the target tissue of Botulinum toxin (BoTox)?
What is the effect of Botulinum toxin (BoTox) on ACh release?
What is the effect of Botulinum toxin (BoTox) on ACh release?
Which autoimmune disease is associated with dysfunction at the neuromuscular junction?
Which autoimmune disease is associated with dysfunction at the neuromuscular junction?
What is the pharmacologic treatment for Myasthenia Gravis?
What is the pharmacologic treatment for Myasthenia Gravis?
Which type of cholinesterase is primarily responsible for the metabolism of ACh at cholinergic synapses?
Which type of cholinesterase is primarily responsible for the metabolism of ACh at cholinergic synapses?
Which type of cholinesterase is found in plasma, liver, and glia?
Which type of cholinesterase is found in plasma, liver, and glia?
Which type of cholinesterase inhibitor is irreversible and interacts only with the esteratic site?
Which type of cholinesterase inhibitor is irreversible and interacts only with the esteratic site?
Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?
Which autoimmune disorder involves a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal?
Which autoimmune disease affects the postsynaptic neuromuscular junction and is characterized by fatigable weakness of skeletal muscles?
Which autoimmune disease affects the postsynaptic neuromuscular junction and is characterized by fatigable weakness of skeletal muscles?
What is the primary pharmacodynamic property of competitive NMJ blockers?
What is the primary pharmacodynamic property of competitive NMJ blockers?
What is the primary pharmacokinetic difference between nondepolarizing and depolarizing NMJ blockers?
What is the primary pharmacokinetic difference between nondepolarizing and depolarizing NMJ blockers?
What drug class is used to reverse the effects of NMJ blockers by increasing the concentration of ACh at NMJ synapses?
What drug class is used to reverse the effects of NMJ blockers by increasing the concentration of ACh at NMJ synapses?
How does sugammadex reverse the effects of NMJ blockers?
How does sugammadex reverse the effects of NMJ blockers?
What are the consequences of genetic variation on succinylcholine metabolism?
What are the consequences of genetic variation on succinylcholine metabolism?
What is the duration of action of succinylcholine?
What is the duration of action of succinylcholine?
What is the primary mechanism of action of competitive NMJ blockers?
What is the primary mechanism of action of competitive NMJ blockers?
What is the effect of competitive NMJ blockers on sensation?
What is the effect of competitive NMJ blockers on sensation?
Flashcards
Cholinergic Transmission
Cholinergic Transmission
The process of nerve signal transmission involving acetylcholine.
Rate-limiting step
Rate-limiting step
The slowest/most crucial step in a biochemical pathway.
Acetylcholine (ACh)
Acetylcholine (ACh)
A neurotransmitter crucial in cholinergic transmission.
Calcium-dependent release
Calcium-dependent release
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Nicotinic Receptors
Nicotinic Receptors
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Ligand-gated ion channels
Ligand-gated ion channels
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Muscarinic Receptors
Muscarinic Receptors
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Muscarinic Agonists
Muscarinic Agonists
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Muscarinic Antagonists
Muscarinic Antagonists
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Parasympathetic Actions
Parasympathetic Actions
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Cholinesterase Inhibitors
Cholinesterase Inhibitors
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Acetylcholinesterase (AChE)
Acetylcholinesterase (AChE)
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Myasthenia Gravis
Myasthenia Gravis
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Neuromuscular Junction (NMJ)
Neuromuscular Junction (NMJ)
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NMJ Blockers
NMJ Blockers
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Botulinum Toxin (BoTox)
Botulinum Toxin (BoTox)
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Competitive NMJ Blockers
Competitive NMJ Blockers
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Depolarizing NMJ Blockers
Depolarizing NMJ Blockers
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Lambert-Eaton Myasthenic Syndrome (LEMS)
Lambert-Eaton Myasthenic Syndrome (LEMS)
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Succinylcholine
Succinylcholine
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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.
