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Benzodiazepine Zu Natur Und Kultur Einer Beliebten Substanzklasse

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Benzodiazepine Zu Natur Und Kultur Einer Beliebten Substanzklasse voll langweilig! Benzodiazepine zu Natur und Kultur einer beliebten Substanzklasse walter heuberger psgn klinik wil FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Inhalt Naturwissenschaft: Pharmakologie Wirkung/Indikationen/KI Benzodiazepinabhängigkeit Mehrfachabhängigkeit Benzodiazepinentzug Substitution Natur Geschichte der Benzodiazepine Was wesensgemäss von selbst da ist Leo Sternbach und der Zufall und sich selbst reproduziert. Kultur im 21. Jahrhundert Kultur Kultur und Benzodiazepine Alles, was der Mensch geschaffen hat, was also nicht naturgegeben ist. voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Pharmakologie der Benzodiazepine voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 GABA (Gammaaminobuttersäure) • Wichtigster hemmender Neurotransmitter im Hirn O NH2 HO Relative Häufigkeit von Neuronen nach Neurotransmitter Neuroscience of Clinical Psychiatry Higgins 2007 • Die Aktivierung des GABAA Rezeptors bewirkt durch Chlorideinstrom in die Nervenzelle eine Hyperpolarisation der Zellmembran. • Die Nervenzelle wird so stabilisiert und reagiert weniger schnell. voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Wirkort GABAA Rezeptor Aufbau Proteinkette gefaltet Untereiheit GABAA -Rezeptor GABAA Rezeptor Komplex elektronenmikroskopische Darstellung Nutt BJP 2001 179 Out In (a) (b) Cl – Figure 6.24 Orientation of the GABAA receptor in the membrane. voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Wirkort GABAA Rezeptor Bindungsstellen • Pro Rezeptorkomplex binden zwei Moleküle GABA, jeweils zwischen der α- und der β- Untereinheit. • Benzodiazepine wirken als allosterischer (an anderer Stel- le als GABA angreifender) Modulator des GABA, sind alleine aber nicht am Rezeptor wirksam. GABA-Bindungsstelle Benzodiazepin-Bindungsstelle Barbiturat-Bindungsstelle Steroid-Bindungsstelle Aäesthetica Picrotoxin-Bindungsstelle Cl – Convulsantien voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 188 PART V Drugs That Act in the Central Nervous System subtypes. In contrast to benzodiazepines, these drugs bind more C. Anesthesia selectively, interacting only with GABAA receptor isoforms that At high doses of most older sedative-hypnotics, loss of con- contain α1 subunits. Their CNS depressant effects can be antago- sciousness may occur, with amnesia and suppression of reflexes. nized by flumazenil. Anterograde amnesia is more likely with benzodiazepines than with other sedative-hypnotics. Anesthesia can be produced by most barbiturates (eg, thiopental) and certain benzodiazepines PHARMACODYNAMICS (eg, midazolam). The CNS effects of most sedative-hypnotics depend on dose, as D. Anticonvulsant Actions shown in Figure 22–2. These effects range from sedation and Suppression of seizure activity occurs with high doses of most of relief of anxiety (anxiolysis), through hypnosis (facilitation of the barbiturates and some of the benzodiazepines, but this is usu- sleep), to anesthesia and coma. Depressant effects are additive ally at the cost of marked sedation. Selective anticonvulsant action when 2 or more drugs are given together. The steepness of the (ie, suppression of convulsions at doses that do not cause severe dose–response curve varies among drug groups; those with flat- sedation) occurs with only a few of these drugs (eg, phenobarbital, ter curves, such as benzodiazepines and the newer hypnotics (eg, clonazepam). High doses of intravenous diazepam, lorazepam, or zolpidem), are safer for clinical use. phenobarbital are used in status epilepticus. In this condition, heavy sedation is desirable. A. Sedation E. Muscle Relaxation Sedative actions, with relief of anxiety, occur with all drugs in this class. Anxiolysis is usually accompanied by some impairment Relaxation of skeletal muscle occurs only with high doses of most of psychomotor functions, and behavioral disinhibition may also sedative-hypnotics. However, diazepam is effective at sedative occur. In animals, most conventional sedative-hypnotics release dose levels for specific spasticity states, including cerebral palsy. punishment-suppressed behavior. Meprobamate also has some selectivity as a muscle relaxant. F. Medullary Depression B. Hypnosis High doses of conventional sedative-hypnotics, especially alcohols Wirkung der Benzodiazepine Sedative-hypnotics can promote sleep onset and increase the dura- and barbiturates, can cause depression of medullary neurons, lead- tion of the sleep state. Rapid eye movement (REM) sleep duration ing to respiratory arrest, hypotension, and cardiovascular collapse. is usually decreased at high doses; a rebound increase in REM These effects are the cause of death in suicidal overdose. sleep may occur on withdrawal from chronic drug use. Effects on sleep patterns occur infrequently with newer hypnotics such as • In Anwesenheit von Benzodiazepinen führtzaleplon die and zolpidem. gleiche SKILL KEEPER: LOADING DOSE Menge GABA zu mehr Wirkung. (SEE CHAPTER 3) Three hours after ingestion of an unknown quantity of diaz- Coma epam, a patient was hospitalized and the drug concentration (Barbiturates) in the plasma was found to be 2 mg/L. Assume that in this patient the pharmacokinetic parameters for diazepam are as • Benzodiazepine sind darum so sicher, weil follows: oral bioavailability, 100%; V 80 L; CL, 38 L/day; half- d, Medullary depression life, 2 days. Estimate the dose of diazepam ingested. The Skill sie nicht selbständig am Rezeptor wirken, Keeper Answer appears at the end of the chapter. Anesthesia (Benzodiazepines) G. Tolerance and Dependence sondern die Wirkung des körpereigenen Tolerance—a decrease in responsiveness—occurs when sedative- Hypnosis hypnotics are used chronically or in high dosage. Cross-tolerance may occur among different chemical subgroups. Psychological Neurotransmitters GABA verstärken. Central nervous system effects dependence occurs frequently with most sedative-hypnotics and Possible selective Sedation, disinhibition, is manifested by the compulsive use of these drugs to reduce anticonvulsant and anxiolysis muscle-relaxing activity anxiety. Physiologic dependence constitutes an altered state Physiologische Rückkopplungs- that leads to an abstinence syndrome (withdrawal state) when the drug is discontinued. Withdrawal signs, which may include Increasing sedative-hypnotic dose anxiety, tremors, hyperreflexia, and seizures, occur more com- FIGURE 22–2 Relationships between dose of benzodiazepines monly with shorter-acting drugs. The dependence liability of mechanismen bleiben so erhalten. and barbiturates and their CNS effects. zolpidem, zaleplon, and eszopiclone may be less than that of the Katzung & Trevor’s Pharmacology 2015 S. 188 • Barbiturate sind viel toxischer, weil sie in höherer Konzentration wie GABA direkt am Rezeptor wirken. • Wahrscheinlich existiert kein «endogenes Benzodiazepin», die verschiedenen Bindungsstellen am GABAA-Rezeptor sind relativ unspezifisch. • Nomenklatur: GABAA-Rezeptor aber Benzodiazepin-Bindungsstelle voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Vielfalt der GABAA Rezeptoren • Am GABAA Rezeptor herrscht kein einfaches Ursache-Wirkungs- Verhältnis sondern komplexe, differenzierte Interaktionen. • Untereinheiten des GABAA -Rezeptors existieren in verschiedenen Isoformen: 6 alpha (α) Isoformen 3 beta (β) Isoformen 3 gamma (γ) Isoformen je 1 delta (δ), epsilon (ε), pi (π), theta (θ) Isoform 3 rho (ρ) Isoformen • Dazu kommen spezifischeModifikationen in Transkription und Translation der Genprodukte (splice variants). • Resultat: über 500 verschiedene Formen von GABAA Re- zeptoren können zusammengestellt werden. (Sieghart & Sperk, 2002) Benzodiazepine zeigen die gleiche Aktivität bei α1, α2, α3 und α5 Untereinheiten des GABAA Rezeptors. Falls am Rezeptor kein γ2, oder aber α4 oder α6 vorhanden sind, wird der GABAA- Rezeptor nicht empfindlich auf Benzodiazepine sein. voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 aus Goodman und Gilmans Table 14–2 Composition, Distribution, and Major Functions of GABAA Receptors SUBUNIT COMPOSITION LOCATION FUNCTION COMMENTS α1β2γ2 Widespread Sedation, Adult, BZ-sensitive, GABA Neurons anticonvulsant activity reduced in drug tolerance? α2β3γ2 Forebrain, spinal cord Anxiety, muscle relaxant Axon hillock in some cells, BZ-sensitive α2β1γ1 Glia α3β3γ2 Cortex Anticonvulsant activity Embryonic and adult BZ-sensitive α4β2γ2 Thalamus Insensitive to agonist BZ α4β2/3γ2 Dentate gyrus Elevated in drug withdrawal? α4β2δ Thalamus Tonic inhibition Extrasynaptic, BZ-insensitive in adults α4β2/3δ Dentate gyrus α5β3γ2 Hippocampus CA1 Tonic inhibition Extrasynaptic, BZ-insensitive Sensory Ganglia α6β2/3γ2 Cerebellar granule cells Insensitive to agonist BZ α6β2/3δ Cerebellar granule cells Tonic inhibition Extrasynaptic, BZ-insensitive, adult γ3, θ, ε Little information BZ, benzodiazepines. Goodman & Gilman’s The Pharmacological Basis of Therapeutics 12th Ed. 2011 Merke: Benzodiazepine treffen auf eine hoch individuelle, differenzierte, zeitlich variable Rezeptorlandschaft und induzieren selber Veränderungen in dieser Struktur. Ihre Wirkung ist kontextabhängig! voll langweilig! Benzodiazepine FOSUMOS Regionale Gesprächsgruppe St. Gallen März 2018 Klinische Wirkung der Benzodiazepine • anxiolytisch • sedativ • hypnotisch • muskelrelaxierend • antiepileptisch aber auch: amnestisch, enthemmend, appetitanregend,
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