Toxicity, Sedative Hypnotics 中山急诊姚晨玲
Toxicity, SedativeHypnotics 中山急诊 姚晨玲
Background Sedative-hypnotics are a group of drugs that cause CNs depression Benzodiazepines(bzd)the most commonly a barbiturates used agents a nonbarbiturate nonbenzodiazepine sedative hypnotics(nBnB
Background Sedative-hypnotics are a group of drugs that cause CNS depression. ◼ Benzodiazepines (BZD) ◼ barbiturates ◼ nonbarbiturate nonbenzodiazepine sedativehypnotics (NBNB) the most commonly used agents
Background acute sedative-hypnotics poisoning withdrawal syndrome
Background ◼ acute sedative-hypnotics poisoning ◼ withdrawal syndrome
Etiology Benzodiazepines(bzd) Long acting(half life >30h) chlordiazepoxide(利眠宁 diazepam(地西泮、安定) flurazepam(氟安定) Short acting(half life 6-30h) alprazolam(阿普唑仑) Ultrashort acting triazolam(三唑仑)
Etiology Benzodiazepines (BZD) • Long acting (half life >30h): chlordiazepoxide (利眠宁) diazepam（地西泮、安定） flurazepam （氟安定） • Short acting (half life 6-30h): alprazolam(阿普唑仑) • Ultrashort acting : triazolam(三唑仑)
Etiology Barbiturates Ultrashort acting Methohexital( Brevita甲己炔巴比妥) thiopental( Pentothal硫喷妥那) Short acting pentobarbital( Nembuta巴比妥) secobarbital( Seconal司可巴比妥 Intermediate acting Amobarbital( Amytal异戊巴比妥) butalbital( Fioricet, Fiorinal异丁巴比妥) ■ Long acting Phenobarbital( Lumina鲁米那)
Etiology ◼ Barbiturates ◼ Ultrashort acting ◼ Methohexital (Brevital甲己炔巴比妥) ◼ thiopental (Pentothal硫喷妥那) ◼ Short acting ◼ pentobarbital (Nembutal戊巴比妥) ◼ secobarbital (Seconal司可巴比妥) ◼ Intermediate acting ◼ Amobarbital (Amytal异戊巴比妥) ◼ butalbital (Fioricet, Fiorinal异丁巴比妥) ◼ Long acting ◼ Phenobarbital (Luminal鲁米那)
Etiology Nonbarbiturate, nonbenzodiazepine sedative-hypnotics(NBNB) Chloral hydrate(水合氯醛) Ethchlorvynol(乙氯维诺 Glutethimide(导眠能) Methyprylon(甲乙哌酮) Meprobamate(眠尔通)
Nonbarbiturate, nonbenzodiazepine sedative-hypnotics (NBNB) Chloral hydrate (水合氯醛) Ethchlorvynol (乙氯维诺) Glutethimide (导眠能) Methyprylon (甲乙哌酮) Meprobamate (眠尔通) Etiology
Pathogenesis 、 Pharmacokinetics: 1 Pharmacokinetics of the bzd Most bzd are extensively metabolized by the liver. Some are metabolized to products which are active and may have a much longer half life than the parent drug The major route of metabolism is N-demethylation in the elderly Cimetidine t
一、Pharmacokinetics ： 1、Pharmacokinetics of the BZD • Most BZD are extensively metabolized by the liver. • Some are metabolized to products which are active and may have a much longer half life than the parent drug. • The major route of metabolism is N-demethylation. in the elderly Cimetidine Pathogenesis
Pathogenesis 2 Pharmacokinetics of Barbiturates Barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys. ie phenobarbital(苯巴比妥) Barbiturates with high lipid solubility are metabolized to more polar compounds in the liver before being excreted via the kidneys. ie thiopental(硫喷妥)
Pathogenesis 2、Pharmacokinetics of Barbiturates ◼ Barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys. ie phenobarbital（苯巴比妥）. ◼ Barbiturates with high lipid solubility are metabolized to more polar compounds in the liver before being excreted via the kidneys. ie thiopental （硫喷妥）
Pathogenesis 3 Pharmacokinetics of nbnb Most NBNB are extensively metabolized by the liver
3、Pharmacokinetics of NBNB ◼ Most NBNB are extensively metabolized by the liver Pathogenesis
Pathogenesis The mechanism of action ◆BZD In the CNS benzodiazepines exert their clinical effect by enhancing the activity of the inhibitory neurotransmitter gaba he clinical effects of gaba release and GABa-gated chloride channels include sleep induction and excitement inhibition) ◆ Barbiturates in prolongation of the duration of opening of GABA-gated Chloride channels, leading to hyperpolarization of the membrane and suppression of neurotransmission ◆NBNB similar to the action of barbiturates
BZD In the CNS, benzodiazepines exert their clinical effect by enhancing the activity of the inhibitory neurotransmitter GABA. (The clinical effects of GABA release and GABA-gated chloride channels include sleep induction and excitement inhibition) Barbiturates in prolongation of the duration of opening of GABA-gated chloride channels, leading to hyperpolarization of the membrane and suppression of neurotransmission. 。 NBNB similar to the action of Barbiturates 二、 The mechanism of action Pathogenesis