## Lithium Pharmacokinetics: Absorption, Distribution, and Elimination ### Correct Understanding of Lithium Metabolism **Key Point:** Lithium is NOT metabolized by hepatic enzymes. It is an inorganic ion that undergoes NO hepatic metabolism and is eliminated entirely unchanged by the kidneys. ### Accurate Pharmacokinetic Profile | Parameter | Details | |-----------|----------| | **Absorption** | Rapid and complete from GI tract; peak levels 1–3 hours post-dose | | **Distribution** | Distributes to all body water compartments; crosses blood–brain barrier slowly | | **Metabolism** | NONE — lithium is not metabolized | | **Elimination** | 100% renal excretion; filtered at glomerulus, ~80% reabsorbed in proximal tubule | | **Therapeutic Range** | 0.6–1.2 mEq/L (acute mania); 0.4–0.8 mEq/L (maintenance) | | **Half-life** | 18–24 hours (longer in elderly, renal impairment) | ### Why This Matters Clinically **High-Yield:** Because lithium is not metabolized, it does NOT interact with drugs that induce or inhibit the cytochrome P450 system. However, it DOES interact with drugs that affect renal function or sodium handling (NSAIDs, ACE inhibitors, thiazide diuretics). **Clinical Pearl:** Lithium toxicity risk increases dramatically with: - Renal impairment (reduced clearance) - Dehydration (increased proximal tubule reabsorption) - Sodium depletion (lithium competes with Na^+^ for reabsorption) - Concurrent diuretics or NSAIDs ### Therapeutic Drug Monitoring **Key Point:** Serum lithium levels must be monitored regularly because: 1. Narrow therapeutic window (0.6–1.2 mEq/L) 2. Levels should be drawn 12 hours post-dose (at steady state) 3. Toxicity can occur even at therapeutic levels if renal function declines **Mnemonic: LITHIUM RENAL RISK** — **L**ow sodium, **I**ncreased reabsorption, **T**hiazides, **H**ypovolemia, **I**ncreased levels, **U**remia, **M**aintenance of renal perfusion is critical.
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