Top Gene Interactions
- Metabolism: By hepatic microsomal enzyme system. Route of Elimination: Barbiturates are metabolized primarily by the hepatic microsomal enzyme system, and the metabolic products are excreted in the urine, and less commonly, in the feces. Approximately 25 to 50 percent of a dose of aprobarbital or phenobarbital is eliminated unchanged in the urine, whereas the amount of other barbiturates excreted unchanged in the urine is negligible. Half Life: 5 to 50 hours (dose dependent)
- Uses/Sources: For the short-term treatment of insomnia.
- Health Effects: They cause slurred speech, disorientation and "drunken" behavior. They are physically and psychologically addictive. They cause slurred speech, disorientation and "drunken" behavior. They are physically and psychologically addictive.
- Symptoms: Symptoms of an overdose typically include sluggishness, incoordination, difficulty in thinking, slowness of speech, faulty judgment, drowsiness or coma, shallow breathing, staggering, and in severe cases coma and death.
- Treatment: Treatment of overdosage is mainly supportive and consists of maintaining an adequate airway, with assisted respiration and oxygen administration as necessary, monitoring of vital signs and fluid balance, and fluid therapy and other standard treatment for shock, if needed. If renal function is normal, forced diuresis may aid in the elimination of the barbiturate. Alkalinization of the urine increases renal excretion of some barbiturates, especially phenobarbital, also aprobarbital and mephobarbital (which is metabolized to phenobarbital). Although not recommended as a routine procedure, hemodialysis may be used in severe barbiturate intoxications or if the patient is anuric or in shock. The patient should be rolled from side to side every 30 minutes and antibiotics should be given if pneumonia is suspected. Appropriate nursing care to prevent hypostatic pneumonia, decubiti, aspiration, and other complications of patients with altered states of consciousness. (L1712)
- Route of Exposure: Barbiturates are absorbed in varying degrees following intravenous, oral, rectal, or parenteral administration.
Mechanism of Action
|Target Name||Mechanism of Action||References|
Potassium voltage-gated channel subfamily H member 2
Gamma-aminobutyric acid receptor subunit alpha-2
Gamma-aminobutyric acid receptor subunit alpha-3
Gamma-aminobutyric acid receptor subunit alpha-4
Gamma-aminobutyric acid receptor subunit alpha-5
Gamma-aminobutyric acid receptor subunit alpha-6
Gamma-aminobutyric acid receptor subunit beta-3
Neuronal acetylcholine receptor subunit alpha-4
Neuronal acetylcholine receptor subunit alpha-7
Glutamate receptor 2
Glutamate receptor ionotropic, kainate 2
Nuclear receptor subfamily 1 group I member 2
Histamine H1 receptor
GABA-A receptor (anion channel)
|Gamma-aminobutyric acid receptor subunit alpha-1||Pentobarbital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission.||