Talk:Etomidate: Difference between revisions

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{{headerpanel|{{Approval}}}}

Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation~~[4]~~ for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.

Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.

The most common side effects include venous pain on injection and skeletal muscle movements.

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|EffectClass=[[Psychoactive class::~~Stimulant]] / [[Psychoactive class::Entactogen~~]]

|EffectClass=[[Psychoactive class::Depressants]]

|ChemicalClass=[[chemical class::Cathinone]]

|OralROA=~~true~~

|OralROA=false

|OralROA_Collapsed=false

|OralROA_Caption=

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==Pharmacology==

Etomidate is an imidazole-derived, non-barbiturate, short-acting intravenous anesthetic. The etomidate distribution model conforms to the three-compartment drug distribution model, and the distribution volume is 2.2-4.5L/kg. Because of its high binding capacity to serum proteins and rapid drug metabolism, the time-dose-related half-life does not extend significantly with continuous infusion. It is not only suitable for single administration during induction, but also for intraoperative maintenance. The site of action of intravenous anesthetics is generally related to gamma-aminobutyric acid, and the important target of etomidate's molecular mechanism of action is the GABA-A receptor.

Forman found in experimental studies that different concentrations of etomidate act on GABA-A receptors in different ways. Commonly used doses of etomidate are similar to GABA-A receptor agonists, prolonging the decay time of postsynaptic inhibitory currents, lengthening the duration of inhibition, and also activating extrasynaptic GABA receptors. Excessive doses of etomidate act directly on GABA-A receptors and are similar to GABA allosteric activators. Studies have found that etomidate not only acts on GABA receptors, but also on α-2β adrenergic receptors, thereby causing vasoconstriction and maintaining hemodynamic stability.<ref>[https://www.sohu.com/a/343157114_668064#google_vignette 依托咪酯持续输注在临床中的应用], additional text.</ref>

==Subjective effects==

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You may select physical effects to add below [[Subjective effect index#Physical effects|here]].

*'''[[Effect::~~Physical effect~~]]'''

*'''[[Effect::Motor control loss]]'''<ref>[https://www.bilibili.com/video/BV1ZG411B7QW/ Abuse etomidate can be motor control loss], 禁毒宣传：滥用右美沙芬者的状态</ref>

*'''[[Effect::Physical effect2]]'''

*'''[[Effect::Physical effect3]]'''

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You may select from a list of cognitive effects to add below [[Subjective effect index#Cognitive effects|here]].

*'''[[Effect::~~Cognitive effect1~~]]'''

*'''[[Effect::Irritability]]''' Excessive use of etomidate can cause irritability

*'''[[Effect::Cognitive effect2]]'''

*'''[[Effect::Cognitive effect3]]'''

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 {{headerpanel|{{Approval}}}}
 {{SummarySheet}}
-Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation[4] for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.
+Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.
 The most common side effects include venous pain on injection and skeletal muscle movements.
@@ Line 53: / Line 53: @@
      <!-- Class Membership -->
-     |EffectClass=[[Psychoactive class::Stimulant]] / [[Psychoactive class::Entactogen]]
+     |EffectClass=[[Psychoactive class::Depressants]]
      |ChemicalClass=[[chemical class::Cathinone]]
       <!-- Dosage/Duration per ROA -->
-     |OralROA=true
+     |OralROA=false
      |OralROA_Collapsed=false
      |OralROA_Caption=
@@ Line 241: / Line 241: @@
 {{chemistry}}
 ==Pharmacology==
 {{pharmacology}}
+Etomidate is an imidazole-derived, non-barbiturate, short-acting intravenous anesthetic. The etomidate distribution model conforms to the three-compartment drug distribution model, and the distribution volume is 2.2-4.5L/kg. Because of its high binding capacity to serum proteins and rapid drug metabolism, the time-dose-related half-life does not extend significantly with continuous infusion. It is not only suitable for single administration during induction, but also for intraoperative maintenance. The site of action of intravenous anesthetics is generally related to gamma-aminobutyric acid, and the important target of etomidate's molecular mechanism of action is the GABA-A receptor.
+Forman found in experimental studies that different concentrations of etomidate act on GABA-A receptors in different ways. Commonly used doses of etomidate are similar to GABA-A receptor agonists, prolonging the decay time of postsynaptic inhibitory currents, lengthening the duration of inhibition, and also activating extrasynaptic GABA receptors. Excessive doses of etomidate act directly on GABA-A receptors and are similar to GABA allosteric activators. Studies have found that etomidate not only acts on GABA receptors, but also on α-2β adrenergic receptors, thereby causing vasoconstriction and maintaining hemodynamic stability.<ref>[https://www.sohu.com/a/343157114_668064#google_vignette 依托咪酯持续输注在临床中的应用], additional text.</ref>
 ==Subjective effects==
 {{EffectStub}}
@@ Line 253: / Line 256: @@
 You may select physical effects to add below [[Subjective effect index#Physical effects|here]].
-*'''[[Effect::Physical effect]]'''
+*'''[[Effect::Motor control loss]]'''<ref>[https://www.bilibili.com/video/BV1ZG411B7QW/ Abuse etomidate can be motor control loss], 禁毒宣传：滥用右美沙芬者的状态</ref>
 *'''[[Effect::Physical effect2]]'''
 *'''[[Effect::Physical effect3]]'''
@@ Line 283: / Line 286: @@
 You may select from a list of cognitive effects to add below [[Subjective effect index#Cognitive effects|here]].
-*'''[[Effect::Cognitive effect1]]'''
+*'''[[Effect::Irritability]]''' Excessive use of etomidate can cause irritability
 *'''[[Effect::Cognitive effect2]]'''
 *'''[[Effect::Cognitive effect3]]'''