Litcab Mechanism of Action

Pharmacology: Pharmacodynamics: Lithium is an alkali metal available for medical use as lithium carbonate or lithium citrate. The exact mechanism of action of lithium in the treatment of bipolar disorders is not known. Mode of action of lithium is still not fully understood. However, lithium modifies the production and turnover of certain neurotransmitters, particularly serotonin, and it may also block dopamine receptors. It modifies concentrations of some electrolytes, particularly calcium and magnesium and it may reduce thyroid activity.
Pharmacokinetics: Lithium ions are rapidly absorbed from the gastrointestinal tract and plasma lithium peaks are reached 2 to 4 hours after lithium administration. The distribution of lithium in the body approximates that of total body water, but its passage across the blood-brain barrier is slow and at equilibration the CSF lithium level reaches only approximately half the plasma concentration.
The elimination half-life of lithium averages 20-24 hours. Half-life in geriatric patients and patients with impaired renal function is increased, 36 and 40 to 50 hours have been reported respectively.
Lithium is excreted primarily in urine with less than 1% being eliminated with feces. Lithium is filtered by the glomeruli and 80% of the filtered lithium is reabsorbed in the tubules, probably by the same mechanism responsible for sodium reabsorption. The renal clearance of lithium is proportional to its plasma concentration. About 50% of a single dose of lithium is excreted in 24 hours. A low salt intake resulting in low tubular concentration of sodium will increase lithium reabsorption and might result in retention or intoxication.