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− | {{unfinished}}
| + | ==Introduction== |
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− | |maplink= Anaesthesia Content Map - WikiClinical
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− | |sublink1=Anaesthetic Drugs
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− | |subtext1=Anaesthetic Drugs
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− | |sublink2=Injectable Agents
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− | |subtext2=Injectable Agents
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− | |pagetype=Clinical
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| The drugs within this group are '''short acting''' and have been classically used agents for anaesthesia. They produce a state of hypnosis and higher doses are required to produce an anaesthetised state but they are '''poor analgesics'''. | | The drugs within this group are '''short acting''' and have been classically used agents for anaesthesia. They produce a state of hypnosis and higher doses are required to produce an anaesthetised state but they are '''poor analgesics'''. |
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| ==Mechanism of Action== | | ==Mechanism of Action== |
− | Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing there use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state. | + | Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing their use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state. |
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| ==Pharmacological Considerations== | | ==Pharmacological Considerations== |
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| ===Pentobarbital=== | | ===Pentobarbital=== |
| Pentobarbital is an oxybarbiturate which is no longer available at anaesthetic doses, but used as an euthansia agent. It causes a rapid onset of anaesthesia (40-120s) but has a longer duration of action compared with thiopental (1-2 hours). Recovery is dependent on hepatic metabolism. Its main indication of use is for the treatment of intractable seizures, long term sedation in ICU and euthansia. | | Pentobarbital is an oxybarbiturate which is no longer available at anaesthetic doses, but used as an euthansia agent. It causes a rapid onset of anaesthesia (40-120s) but has a longer duration of action compared with thiopental (1-2 hours). Recovery is dependent on hepatic metabolism. Its main indication of use is for the treatment of intractable seizures, long term sedation in ICU and euthansia. |
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| + | ===[[Primidone]]=== |
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| + | [[Category:Injectable Anaesthetic Agents]] |