53 Questions
Which type of ion channels do anesthetics primarily target?
Sodium, potassium, HCN, and GABA-activated chloride channels
What effect do anesthetics have on nerves?
Hyperpolarization
Which receptors do volatile anesthetics, propofol, barbiturates, and neurosteroids potentiate?
Glycine receptors
What is the primary site of action for general anesthetics?
Synapse
Which rule explains the relationship between anesthetic potency and chain length?
Meyer-Overton Rule
What is the main reason for enantiomers exhibiting different anesthetic potency?
Different binding to specific lipophilic amino acids
What are the exceptions to the Meyer-Overton Rule explained by?
Anesthetic binding of specific lipophilic amino acids
Which ligand-gated ion channels are affected by anesthetics?
GABA-activated and glycine-activated channels
What is the effect of different anesthetics on subtypes of the GABA receptor?
Potentiation, direct gating, or inhibition
Which receptors are affected by etomidate and ketamine?
NMDA receptors
Where can graphic summaries on the topic be found?
Barash Clinical Anesthesia, Flood Stoelting’s Pharmacology and Physiology in Anesthetic Practice, and Evers Anesthetic Pharmacology.
Which component is not part of general anesthesia?
Long-term memory impairment
What is the primary site of action of dexmedetomidine?
Locus coeruleus
Where is immobility thought to be primarily mediated?
Spinal cord level
What is now thought to be the primary target for anesthetic action?
Protein
Which component is thought to be primarily mediated at the spinal cord level?
Immobility
What is the primary source of cholinergic input to the cerebral cortex?
Nucleus basalis of Meynert
Which nucleus is the primary site of action of dexmedetomidine?
Locus coeruleus
What is now thought to be the primary target for anesthetic action?
Protein
Which of the following components are NOT part of general anesthesia?
Euphoria
What is the primary site of action for immobility during anesthesia?
Spinal cord
Which of the following anesthetics exhibits a biphasic dose response for analgesia?
Ketamine
Which brain region stabilizes the sleep-wake switch?
Tuberomammillary nucleus (TMN)
What is the primary mechanism for preventing awareness during anesthesia monitoring?
$\gamma$-aminobutyric acid (GABA)ergic inhibition
What is the effect of general anesthesia on long-term memory?
It ablates conscious memory (explicit) and unconscious memory (implicit)
Which of the following sites are NOT considered anesthetic targets?
Endoplasmic reticulum
What do volatile anesthetics primarily target for their effect on autonomic homeostatic mechanisms?
Hypothalamus
Which nucleus likely interferes with thalamic input to the cerebral cortex during unconsciousness induced by general anesthesia?
Ventrolateral preoptic nucleus (VLPO)
What is the effect of general anesthesia on new memories?
It prevents the formation of new memories.
Which rule initially suggested a single mechanism of anesthesia but faced challenges due to the dissimilar effects of halogenated anesthetics with similar structures and octanol:water partition coefficients?
Meyer-Overton Rule
Which of the following is not a component of general anesthesia?
Hypothermia
What is the primary site of action for immobility during anesthesia?
Spinal cord
Which monitoring method is not more successful in preventing awareness during anesthesia than a protocol using MAC?
Blood pressure monitoring
What exhibits a biphasic dose response for analgesia during anesthesia?
Volatile anesthetics
Which of the following structures likely interferes with thalamic input to the cerebral cortex during unconsciousness?
$\text{VLPO}$ (ventrolateral preoptic nucleus)
What mechanism primarily mediates immobility during anesthesia?
GABAergic inhibition
Which of the following components does general anesthesia generally prevent?
Formation of new memories
Which rule initially suggested a single mechanism of anesthesia?
Meyer-Overton Rule
What primarily impairs autonomic homeostatic mechanisms during general anesthesia?
Hypothalamus
What is involved in long-term memory formation during general anesthesia?
Hippocampus and amygdala
Which receptors do volatile anesthetics potentiate?
GABA receptors
Which of the following is NOT a component of general anesthesia?
Hypothermia
What is the primary effect of general anesthesia on memory formation?
Prevents formation of new memories
Which monitoring method is NOT significantly more successful in preventing awareness during anesthesia?
Blood pressure monitoring
What is the primary mediator of immobility during anesthesia?
Spinal cord level
Which of the following is NOT a likely anesthetic target for unconsciousness?
$\beta$-amyloid plaques
Which mechanism contributes to analgesia under volatile anesthetics?
Activation of opioid receptors
What is the primary site of action for mediating autonomic homeostatic mechanisms during anesthesia?
Hypothalamus
What do volatile anesthetics exhibit in terms of dose response for analgesia?
Biphasic response
Which area activates various brain regions and stabilizes the sleep-wake switch?
Perifornical area
What is the primary effect of general anesthesia on unconscious memory (implicit)?
Erases all unconscious memories
What do anesthetics primarily affect at the spinal cord level to induce immobility?
Descending motor pathways
Which rule initially suggested a single mechanism of anesthesia but faced challenges due to dissimilar effects of halogenated anesthetics with similar structures?
Meyer-Overton rule
Study Notes
Electrophysiological Effects of Anesthetics
- Anesthetic potency increases with chain length but has a cutoff effect.
- Enantiomers exhibit different anesthetic potency despite identical octanol:water partition coefficient.
- Meyer-Overton Rule and its exceptions are explained by anesthetic binding of specific lipophilic amino acids.
- Anesthetics hyperpolarize nerves and this effect correlates with anesthetic potency.
- General anesthetics primarily act at the synapse, inhibiting glutamate release and potentiating GABA.
- Anesthetics target ion channels including Na+, K+, HCN, and GABA-activated chloride channels.
- Anesthetics also affect ligand-gated ion channels such as glutamate-activated NMDA and GABA-activated channels.
- Different anesthetics act at different subtypes of the GABA receptor, leading to potentiation, direct gating, or inhibition.
- Anesthetics affect other ligand-gated ion channels like nicotinic acetylcholine, 5-HT3, and glycine receptors.
- Volatile anesthetics, propofol, barbiturates, and neurosteroids potentiate glycine receptors but not etomidate or ketamine.
- There are graphic summaries available on the topic.
- Sources include Barash Clinical Anesthesia, Flood Stoelting’s Pharmacology and Physiology in Anesthetic Practice, and Evers Anesthetic Pharmacology.
Understanding General Anesthesia and Anesthetic Targets
- General anesthesia is a reversible depression of the CNS, causing loss of response to external stimuli and consists of components such as unconsciousness, amnesia, analgesia, immobility, and attenuation of the autonomic response.
- Unconsciousness involves impairment of connectivity and integration between cortical structures, similar to NREM sleep, and likely interferes with thalamic input to the cerebral cortex and other subcortical structures.
- The sleep/wake cycle involves the interaction between the tuberomammillary nucleus (TMN) and ventrolateral preoptic nucleus (VLPO), with orexin from the perifornical area activating various brain regions and stabilizing the sleep-wake switch.
- Likely anesthetic targets for unconsciousness include the cerebral cortex, thalamus, TMN, VLPO, perifornical area, and locus coeruleus, with GABAergic inhibition and cholinergic stimulation affecting these areas.
- Anesthesia generally prevents the formation of new memories, but leaves previous memories intact, with different mechanisms involved in short-term and long-term memory.
- Long-term memory formation involves critical steps in the hippocampus and amygdala, and the conversion of short-term to long-term memory requires anatomical changes in the synapse and takes time.
- General anesthesia ablates conscious memory (explicit) and unconscious memory (implicit), with varying incidences of awareness with recall observed in different patient groups.
- Awareness monitoring during anesthesia is based on processed EEG and BIS (Bispectral Index), but studies have shown that the BIS monitor is not more successful in preventing awareness than a protocol using MAC.
- Volatile anesthetics exhibit a biphasic dose response for analgesia, while opioids, non-opioids, α2 agonists, neostigmine, ketamine, barbiturates, nitrous oxide, xenon, and adenosine also contribute to analgesia through different mechanisms.
- Immobility during anesthesia is primarily mediated at the spinal cord level, affecting afferent pathways, efferent pathways, and reflex spinal arcs, with different anesthetics working through different mechanisms.
- Multiple anesthetics impair autonomic homeostatic mechanisms, including those related to respiratory, cardiac, and temperature regulation, mediated by the hypothalamus.
- Anesthetic targets sites include the lipid, protein, neuron, synapse, presynaptic, postsynaptic, and ion channels, with the Meyer-Overton Rule initially suggesting a single mechanism of anesthesia, but facing challenges due to the dissimilar effects of halogenated anesthetics with similar structures and octanol:water partition coefficients.
Test your knowledge about the components of general anesthesia and the mechanisms of consciousness. Learn about unconsciousness, amnesia, analgesia, immobility, and the effects of anesthetics on the sleep-wake cycle.
Make Your Own Quizzes and Flashcards
Convert your notes into interactive study material.
Get started for free
