| Class | Mood stabiliser |
|---|---|
| Chemistry |
Monovalent cation salt; dilithium carbonate to be precise (Li2CO3)
|
| Routes of administration |
Oral only |
| Absorption |
Oral bioavailability close to 100%
|
| Solubility |
pKa = 10.33; excellent water solubility.
|
| Distribution |
VOD ~0.6-0.7 L/k, roughly proportional to total body water. Therapeutic levels are 1.0 mmol/L, which means one has about 40-50 mmol of lithium on board when one is properly medicated
|
| Metabolism |
Not metabolised
|
| Elimination |
100% renally excreted, by mechanisms identical to those involved in handling sodium (which means any scenario where sodium is retained will also result in the increased reuptake and retention of lithium)
|
| Time course of action |
Onset of antimanic effects is 6-8 days; takes at least 24 hrs to cross the blood brain barrier. Half-life of 12-24 hrs, up to 36 hrs in the elderly
|
| Target receptor |
Multiple pharmacological targets, mostly enzyme systems that regulate the synthesis and activity of secondary messengers such as IP3 |
| Mechanism of action |
By interfering with the synthesis of secondary messengers and regulatory molecules, lithium exerts numerous effects, of which some are neuroprotective. The mechanism of action specifically responsible for the desirable mood effects is unknown |
| Clinical effects |
Apart from improved mood regulation: - fine tremor - downbeat nystagmus - Nausea, headache - hypothyroidism - nephrogenic DI - high cholesterol - hyperparathyroidism - hypercalcemia - psoriasis and dermatitis |
| Literature reference |
Oruch et al (2014) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |