| Class |
Antiepileptic
|
| Chemistry |
Barbiturate (barbituric acid derivative)
|
| Routes of administration |
|
| Absorption |
Good oral bioavailability (80-100%), slowly but completely absorbed
|
| Solubility |
pKa = 7.2; moderately water-soluble, but solubility increases in alkaline solutions.
|
| Distribution |
VOD=0.5-1.0 L/kg, about 40-60% protein-bound
|
| Metabolism |
Hepatic metabolism primarily via hydroxylation by cytochrome P450 enzymes (especially CYP2C9).
|
| Elimination |
Minimal renal excretion - only about 25% of the drug is excreted unchanged in the urine
|
| Time course of action |
Extremely long half-life: 53-118 hours
|
| Target receptor |
Main target is the GABA-A receptor, where barbiturates increase the duration of chloride channel opening
|
| Mechanism of action |
Multiple anticonvulsant mechanisms, but mostly GABA-related, by increasing GABA activity.
|
| Clinical effects |
Sedation and cognitive impairment, respiratory depression, dependence, withdrawal seizures upon abrupt cessation; increased risk of osteoporosis and depression in the long term
|
| Literature reference |
|
| CICM details of understanding |
Level 3
|
| Mentioned around Deranged Physiology |
|
| Related SAQs |
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