Barbituric acid,

The basic structure of all barbiturates is barbituric acid.

Refers to drugs that act as a central nervous system depressant, and can therefore produce a wide spectrum of effects, from mild sedation to total anesthesia.

Are effective as anxiolytics, hypnotics, and anticonvulsants.

Barbiturates display weak analgesic effects.

May react with sedatives, precluding using barbiturates in surgery or in the presence of other analgesics.

Have addiction potential, both physical and psychological.

They have largely been replaced by benzodiazepines. particularly in the treatment of anxiety and insomnia.

Drugs lack of an antidote for overdose.

Used in general anesthesia, epilepsy, treatment of acute migraines or cluster headaches, euthanasia, capital punishment, and assisted suicide.

Thiopental is an ultra-short-acting barbiturate, sodium pentothal.

Sodium amytal, an intermediate-acting barbiturate that is used for sedation and to treat insomnia.

Sodium amytal decreases inhibitions and slow creative thinking, making subjects more likely to reveal information through emotional outbursts

Barbiturate recreational drugs are ranked 5th in dependence, 3rd in physical harm, and 4th in social harm.

People over the age of sixty-five are at higher risk of experiencing harmful effects of barbiturates, including drug dependence and accidental overdose.

During pregnancy, the drug passes through to the fetus, and after delivery the neonate may experience withdrawal symptoms and have trouble breathing.

Barbiturates may be transmitted through breast milk.

Rarely associated with Stevens-Johnson syndrome.

Tolerance to the effects of barbituates develops, with regular use.

Withdrawal produces potentially fatal effects such as seizures similar to delirium tremens.

Withdrawal more severe than that of alcohol or benzodiazepines.

One of the most dangerous withdrawals of any known addictive substance.

The longer acting barbiturates produce a less severe withdrawal syndrome than short acting and ultra short acting barbiturates.

Withdrawal symptoms are dose-dependent.

The treatment of barbiturate withdrawal often consists of converting the patient to a long acting benzodiazepine, followed by slowly tapering off the benzodiazepine.

Mental cravings for barbiturates can last for months or years.

Symptoms of an overdose typically include sluggishness, incoordination, difficulty in thinking, slowness of speech, faulty judgement, drowsiness, shallow breathing, staggering, and, in severe cases, coma or death.

The lethal dosage of barbiturates varies greatly with individual patient tolerance.

The lethal dose is highly variable among different members of the class: with very potent barbiturates such as pentobarbital being potentially fatal in considerably lower doses than the low-potency barbiturates such as butalbital.

Dangerous withdrawal symptoms can result when the drug is stopped after dependence has developed.

Because tolerance to the anxiolytic and sedative effects of barbiturates tends to develop faster than tolerance to their effects on smooth muscle, respiration, and heart rate, making them generally unsuitable for a long time psychiatric use.

A viable option for long-term epilepsy treatment.

Barbiturates in overdose with other CNS depressants have additive CNS and respiratory depressant effects.

Benzodiazepines have additive effects to barbitrates, and also increase the binding affinity of the benzodiazepine binding site, leading to exaggerated benzodiazepine effects.

The longest-acting barbiturates have half-lives of a day or more, and subsequently result in drug accumulation.

The effects of long-acting barbiturates wear off significantly faster than the drug can be eliminated, allowing the drug to reach toxic concentrations in the blood following repeated administration.

Barbiturates induce a number of hepatic CYP enzymes, CYP2C9, CYP2C19 and CYP3A4.

Inducing hepatic CYP enzymes leads to exaggerated effects from many prodrugs and decreased effects from drugs which are metabolized by these enzymes to inactive metabolites.

Inducing hepatic CYP enzymes can result in fatal overdoses from drugs such as codeine, tramadol, and carisoprodol, which become considerably more potent after being metabolized by CYP enzymes.

Phenobarbital and secobarbital are the most potent enzyme inducers and butalbital and talbutal being among the weakest enzyme inducers in the class.

Barbiturates promote feelings of relaxed contentment and euphoria, but physical and psychological dependence may develop with repeated use.

Barbiturate intoxication include: drowsiness, nystagmus, slurred speech, ataxia, decreased anxiety and loss of inhibitions.

Can be used to alleviate the adverse or withdrawal effects of illicit drug use.

The most commonly used barbituates are amobarbital (Amytal), pentobarbital (Nembutal), secobarbital (Seconal) and a combination of amobarbital and secobarbital (called Tuinal) is also highly used.

Short-acting and intermediate-acting barbiturates are usually prescribed as sedatives and sleeping pills.

Barbituates begin acting fifteen to forty minutes after they are swallowed, and their effects last from five to six hours.

Act as positive allosteric modulators, and at higher doses, as agonists of GABAA receptors.

GABA is the principal inhibitory neurotransmitter in the central nervous system (CNS).

They bind to the GABAA receptor.

Like benzodiazepines, barbiturates potentiate the effect of GABA at the receptor.

Barbiturates also block AMPA and subtypes of ionotropic glutamate receptor.

Glutamate is the principal excitatory neurotransmitter in the CNS.

Produce their effects by increasing the duration of chloride ion channel opening at the GABAA receptor increasing the efficacy of GABA.

The opening of the chloride ion channel is the reason for the increased toxicity of barbiturates compared to benzodiazepines in overdose.

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