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Questions and Answers
What is the mechanism of action of propofol?
What is the mechanism of action of propofol?
- Inhibits the function of glycine receptors
- Increases the rate of dissociation of GABA from the GABAA receptor (correct)
- Directly activates glutamate receptors
- Induces the release of lysophosphatidate signaling in the brain
How is propofol excreted from the body?
How is propofol excreted from the body?
- By metabolic breakdown in the liver
- Excreted by kidneys (correct)
- Via sweat glands
- Through bile secretion
What is the primary factor contributing to the rapid clearance of propofol?
What is the primary factor contributing to the rapid clearance of propofol?
- Rapid breakdown in the stomach
- Excretion through the skin
- Tissue uptake and elimination in the lungs (correct)
- High metabolism in the liver
Why is propofol provided in an emulsion of soybean oil and glycerol?
Why is propofol provided in an emulsion of soybean oil and glycerol?
Which component is added to propofol to prevent bacterial growth?
Which component is added to propofol to prevent bacterial growth?
What is the pH range of propofol when provided with sodium metabisulfite?
What is the pH range of propofol when provided with sodium metabisulfite?
What is the context-sensitive half-time of propofol after 8-hour infusions?
What is the context-sensitive half-time of propofol after 8-hour infusions?
How does initial termination of action for propofol occur?
How does initial termination of action for propofol occur?
What does propofol inhibit as part of its mechanism of action?
What does propofol inhibit as part of its mechanism of action?
Which model best describes the pharmacokinetics of propofol?
Which model best describes the pharmacokinetics of propofol?
What is the typical dose of propofol for induction of anesthesia in healthy adults?
What is the typical dose of propofol for induction of anesthesia in healthy adults?
What is the effect of propofol on evoked potentials in the CNS?
What is the effect of propofol on evoked potentials in the CNS?
What is the mechanism behind the attenuation of bronchoconstriction by propofol?
What is the mechanism behind the attenuation of bronchoconstriction by propofol?
How does propofol compare to midazolam in terms of memory impairment at equal sedation levels?
How does propofol compare to midazolam in terms of memory impairment at equal sedation levels?
What is the typical dose of propofol for maintenance of anesthesia?
What is the typical dose of propofol for maintenance of anesthesia?
What organ system experiences a 30-40% decrease in intraocular pressure with propofol induction?
What organ system experiences a 30-40% decrease in intraocular pressure with propofol induction?
Which group requires a 25-50% reduction in propofol dose?
Which group requires a 25-50% reduction in propofol dose?
In which system does propofol induce a direct myocardial depression?
In which system does propofol induce a direct myocardial depression?
What is the effect of propofol on systemic blood pressure?
What is the effect of propofol on systemic blood pressure?
What is the primary use of propofol in induction and maintenance of anesthesia, similar to ondansetron?
What is the primary use of propofol in induction and maintenance of anesthesia, similar to ondansetron?
What is the primary use of propofol in induction and maintenance of anesthesia, similar to ondansetron?
What is the primary use of propofol in induction and maintenance of anesthesia, similar to ondansetron?
Which of the following is true regarding the effect of barbiturates on GABAA receptors?
Which of the following is true regarding the effect of barbiturates on GABAA receptors?
Which organ system effect is induced by barbiturates in terms of cardiovascular response?
Which organ system effect is induced by barbiturates in terms of cardiovascular response?
What is not a contraindication for the use of barbiturates?
What is not a contraindication for the use of barbiturates?
Which procedure was barbiturate use previously associated with for neuroprotection?
Which procedure was barbiturate use previously associated with for neuroprotection?
What is a mechanism of the neuroprotective effect of barbiturates?
What is a mechanism of the neuroprotective effect of barbiturates?
What is a side effect associated with low blood levels of thiopental?
What is a side effect associated with low blood levels of thiopental?
What organ system effect do barbiturates cause in terms of intracerebral pressure?
What organ system effect do barbiturates cause in terms of intracerebral pressure?
Which condition is triggered by induction of heme synthesis and is a contraindication for barbiturate use?
Which condition is triggered by induction of heme synthesis and is a contraindication for barbiturate use?
What is the primary route of metabolism for barbiturates?
What is the primary route of metabolism for barbiturates?
What type of dosages is required for barbiturates in premedicated patients?
What type of dosages is required for barbiturates in premedicated patients?
What is the mechanism of action of ketamine?
What is the mechanism of action of ketamine?
What is the primary reason for ketamine being the drug of choice for electroconvulsive therapy (ECT)?
What is the primary reason for ketamine being the drug of choice for electroconvulsive therapy (ECT)?
What is the unique characteristic of S(+) ketamine compared to R(-) ketamine?
What is the unique characteristic of S(+) ketamine compared to R(-) ketamine?
What is the effect of ketamine on the voltage gated sodium channels?
What is the effect of ketamine on the voltage gated sodium channels?
How does ketamine produce its analgesic and amnesic effects?
How does ketamine produce its analgesic and amnesic effects?
What is the primary route of metabolism for ketamine?
What is the primary route of metabolism for ketamine?
What contributes to the brief duration of action of ketamine?
What contributes to the brief duration of action of ketamine?
Which receptor type does ketamine NOT antagonize?
Which receptor type does ketamine NOT antagonize?
What effect does S(+) ketamine have on cognitive function compared to the racemic mixture?
What effect does S(+) ketamine have on cognitive function compared to the racemic mixture?
What is the most accepted form of ketamine available in Europe and not in the United States?
What is the most accepted form of ketamine available in Europe and not in the United States?
Which benzodiazepine undergoes rapid absorption from the GI tract and has a high hepatic clearance?
Which benzodiazepine undergoes rapid absorption from the GI tract and has a high hepatic clearance?
Which benzodiazepine exhibits delayed elimination in the presence of drugs that inhibit cytochrome P450, and has a prolonged elimination in the elderly?
Which benzodiazepine exhibits delayed elimination in the presence of drugs that inhibit cytochrome P450, and has a prolonged elimination in the elderly?
Which benzodiazepine is insoluble in water and dissolved in organic solvents like propylene glycol and sodium benzoate?
Which benzodiazepine is insoluble in water and dissolved in organic solvents like propylene glycol and sodium benzoate?
Which benzodiazepine is metabolized via hepatic oxidative reduction of the methylene group, with principle metabolites including desmethyldiazepam and oxazepam?
Which benzodiazepine is metabolized via hepatic oxidative reduction of the methylene group, with principle metabolites including desmethyldiazepam and oxazepam?
Which benzodiazepine is relatively unaffected by inhibition of cytochrome P-450 or changes in hepatic function, and is unique for its lower lipid solubility resulting in delayed onset of effect in the CNS?
Which benzodiazepine is relatively unaffected by inhibition of cytochrome P-450 or changes in hepatic function, and is unique for its lower lipid solubility resulting in delayed onset of effect in the CNS?
Which benzodiazepine has a primary metabolite with approximately 50% activity of the parent compound and is conjugated to 1-hydroxymidazolam glucuronide for subsequent clearance by the kidneys?
Which benzodiazepine has a primary metabolite with approximately 50% activity of the parent compound and is conjugated to 1-hydroxymidazolam glucuronide for subsequent clearance by the kidneys?
Which benzodiazepine exhibits greater hemodynamic stability, delayed emergence, and reliable amnesia compared to Propofol for sedation?
Which benzodiazepine exhibits greater hemodynamic stability, delayed emergence, and reliable amnesia compared to Propofol for sedation?
Which benzodiazepine has a slower onset than thiopental or propofol but provides reliable amnesia, with dose required and time of onset affected by premedication, concurrent anesthetic agents, ASA physical status classification, and age?
Which benzodiazepine has a slower onset than thiopental or propofol but provides reliable amnesia, with dose required and time of onset affected by premedication, concurrent anesthetic agents, ASA physical status classification, and age?
Which benzodiazepine is unique for its lower lipid solubility resulting in delayed onset of effect in the CNS, despite having higher clearance and similar volume of distribution to Diazepam?
Which benzodiazepine is unique for its lower lipid solubility resulting in delayed onset of effect in the CNS, despite having higher clearance and similar volume of distribution to Diazepam?
Which benzodiazepine is metabolized via hepatic glucuronidation to inactive metabolites that are excreted by the kidneys, and is relatively unaffected by inhibition of cytochrome P-450 or changes in hepatic function?
Which benzodiazepine is metabolized via hepatic glucuronidation to inactive metabolites that are excreted by the kidneys, and is relatively unaffected by inhibition of cytochrome P-450 or changes in hepatic function?
What is the proposed mechanism behind propofol infusion syndrome?
What is the proposed mechanism behind propofol infusion syndrome?
Which side effect is NOT associated with propofol use?
Which side effect is NOT associated with propofol use?
What is the main effect of propofol on pulmonary ventilation?
What is the main effect of propofol on pulmonary ventilation?
Which factor may require a direct acting beta agonist during propofol anesthesia?
Which factor may require a direct acting beta agonist during propofol anesthesia?
What is the effect of propofol on IOP (intraocular pressure)?
What is the effect of propofol on IOP (intraocular pressure)?
Which statement is true regarding propofol's effect on coagulation?
Which statement is true regarding propofol's effect on coagulation?
What is the recommended handling for propofol in the ICU?
What is the recommended handling for propofol in the ICU?
Which clinical feature is NOT associated with propofol infusion syndrome?
Which clinical feature is NOT associated with propofol infusion syndrome?
What is the best described model for propofol's pharmacokinetics?
What is the best described model for propofol's pharmacokinetics?
Which statement about propofol's mechanism of action is accurate?
Which statement about propofol's mechanism of action is accurate?
What is the main route of clearance for propofol?
What is the main route of clearance for propofol?
What is the primary clinical use of propofol?
What is the primary clinical use of propofol?
Which of the following is a benefit of using etomidate?
Which of the following is a benefit of using etomidate?
How does etomidate affect cardiovascular function?
How does etomidate affect cardiovascular function?
What is the mechanism of action of etomidate at the γ-aminobutyric acid-A (GABA) receptor?
What is the mechanism of action of etomidate at the γ-aminobutyric acid-A (GABA) receptor?
Which property does etomidate possess in relation to seizure threshold and neuroprotection?
Which property does etomidate possess in relation to seizure threshold and neuroprotection?
What is the effect of etomidate on the respiratory system?
What is the effect of etomidate on the respiratory system?
What pharmacological property do etomidate derivatives have compared to etomidate?
What pharmacological property do etomidate derivatives have compared to etomidate?
What is a side effect associated with the administration of etomidate?
What is a side effect associated with the administration of etomidate?
In what way does flumazenil act as a benzodiazepine receptor ligand?
In what way does flumazenil act as a benzodiazepine receptor ligand?
What is one of the uses of flumazenil?
What is one of the uses of flumazenil?
What is the effect of flumazenil on benzodiazepine-induced sedation?
What is the effect of flumazenil on benzodiazepine-induced sedation?
Study Notes
- Etomidate is a sedative-hypnotic drug that can benefit patients with compromised cardiovascular status, questionable intravascular volume status, or elevated intracranial pressure (ICP).
- Etomidate improves cerebral oxygen supply-to-demand ratio and reduces cerebral blood flow by up to 35%, while reducing cerebral metabolic rate of oxygen by up to 45%.
- Etomidate maintains or improves cerebral perfusion pressure and reduces intracranial pressure due to decreased cerebral blood flow.
- Etomidate is useful in mapping seizure foci during ablative procedures and may prolong seizure duration during electroconvulsive therapy.
- Etomidate has minimal effect on cardiovascular function as it does not significantly affect the sympathetic nervous system or blood pressure.
- Etomidate has fewer respiratory depressant effects than other induction agents, with less depression of ventilation and a decreased ventilatory response to CO2.
- Etomidate inhibits cortisol and mineralocorticoid production for up to 72 hours after a single induction dose, but does not significantly inhibit steroidogenesis as a sedative-hypnotic.
- Etomidate derivatives, such as methoxycarbonyletomidate and carboetomidate, have different structures and pharmacological properties compared to etomidate.
- Etomidate can cause excitatory activity, including myoclonus and hiccups, and has a high incidence of postoperative nausea and vomiting (PONV) when given with narcotics.
- Etomidate acts as a positive allosteric modulator of the γ-aminobutyric acid-A (GABA) receptor, increasing the affinity of the receptor for GABA and resulting in increased chloride conductance and hyperpolarization of the postsynaptic cell membrane.
- Etomidate is highly protein-bound, has a similar volume of distribution to other benzodiazepines, and has a rapid clearance rate.
- Etomidate has anxiolytic, sedative, anticonvulsant, skeletal muscle relaxation, and amnesic properties, and is used for various indications including seizure activity, delirium tremens, skeletal muscle relaxation, insomnia, anxiety, and nausea/vomiting prophylaxis.
- Etomidate can increase seizure threshold to local anesthetic exposure and has neuroprotective activity, but these effects are not well-documented in humans.
- Etomidate can cause a modest decrease in blood pressure primarily due to decreased systemic vascular resistance, and produces a dose-related central respiratory depression with decreased ventilatory response to CO2 and decreased hypoxic drive to ventilation.
- Etomidate can cause apnea in large doses and has minimal musculoskeletal effects, as skeletal muscle relaxation occurs via interaction with spinal interneurons, not at the neuromuscular junction.
- Flumazenil is a benzodiazepine receptor ligand that acts as a competitive antagonist, preventing or reversing the effects of other benzodiazepines in a dose-dependent manner.
- Flumazenil has a rapid clearance rate and is used for reversing residual benzodiazepine-induced sedation and suspected benzodiazepine overdose.
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Description
Test your knowledge on the mechanism of action and pharmacokinetics of GABAA receptor modulators. Explore the effects of low and high concentrations and their impact on GABA receptors, as well as the metabolism of these medications.
