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DOWNLOAD PDFBarbiturates can be remembered for having "barb" in their names. Common examples are phenobarbital, pentobarbital, and secobarbital, with the anesthetic thiopental being the exception, and primidone which is used for essential tremor treatment.
Barbiturates facilitate GABA-A action by increasing the duration of chloride channel opening, leading to CNS depression. Unlike benzodiazepines, which increase the frequency of chloride channel opening, barbiturates increase the duration of opening.
Barbiturates allosterically modulate GABA-A receptors, potentiating GABA’s action and increasing the duration of chloride channel opening. In contrast, benzodiazepines increase the frequency of chloride channel opening.
Barbiturates decrease neuron firing by prolonging the duration of GABA-A receptor-mediated chloride channel opening, leading to hyperpolarization of the neuronal membrane and CNS depression.
Enhance GABA-A action → ↑ Cl- influx → Hyperpolarization → ↓ Neuron firing
Ultra-short-acting barbiturates, such as thiopental, are used for anesthesia induction due to their rapid onset and short duration of action. Thiopental is administered intravenously, with an onset of action typically occurring within 30 seconds and a duration lasting a few minutes, making it ideal for quick anesthesia induction.
Thiopental is sometimes referred to as "truth serum" due to its CNS depressant effects. These effects may cause disinhibition, leading to relaxed or impaired judgment. However, this effect is not scientifically reliable for eliciting truthful statements and is not recommended for clinical use.
Barbiturates such as phenobarbital are used for seizure treatment, particularly in generalized tonic-clonic seizures and neonatal seizures. They are less commonly used for partial seizures.
For neonatal seizures, phenobarbital is the first-line choice.
Primidone is used for essential tremors but it is not the first choice (propranolol is usually the first-line drug).
Primidone is metabolized to phenobarbital (which also helps with seizures) and PEMA (phenylethylmalonamide), both contributing to its therapeutic effects.
Barbiturates, once used for treating insomnia and anxiety, are no longer commonly prescribed for these purposes due to their sedating effects and high potential for dependence. Patients often reported feeling groggy or "hungover" the next day, which led to a decline in their use for these indications. Additionally, barbiturates have a narrow therapeutic index, and their overdose potential makes them less favorable compared to other sedatives like benzodiazepines or non-benzodiazepine sleep aids.
Barbiturates can cause severe CNS depression, leading to respiratory depression and cardiovascular instability. This effect is especially dangerous in overdose situations, where patients may experience respiratory arrest and hypotension. While ethanol can also cause CNS depression, it is typically less potent in inducing fatal respiratory depression compared to barbiturates. Barbiturate overdose is associated with a higher risk of life-threatening effects, particularly respiratory arrest.
Barbiturates can cause severe CNS depression in overdose situations, and this effect is potentiated when taken concurrently with ethanol. Both substances bind to GABA-A receptors, leading to additive CNS depressant effects. Patients may exhibit symptoms such as ataxia, dizziness, impaired judgment, and, in severe cases, the condition can progress to respiratory depression and death.
Barbiturates are known to induce cytochrome P450 enzymes (particularly CYP3A4, among others), which increases the metabolism and clearance of many other drugs from the bloodstream. This enzyme induction can lead to reduced blood levels of concurrently administered medications, shortening their effects and potentially making them less effective.
Barbiturates are contraindicated in porphyria because they induce cytochrome P450 enzymes, which increase heme synthesis.
Barbiturates induce CYP450, which upregulates ALA synthase, the rate-limiting enzyme in heme synthesis. This leads to an accumulation of toxic porphyrin precursors (like ALA and PBG) in acute intermittent porphyria (AIP) and other porphyrias. The accumulation of these precursors can trigger acute attacks, leading to severe symptoms.
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