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• [Diseases also during pregnancy are to be treated!]
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ACUTE EXPOSURE INFORMATION

  1. USES: Anticonvulsant for a broad spectrum of seizure disorders. Also used as a mood stabilizer in the treatment of bipolar affective disorder, used to treat chronic pain and as prophylaxis for migraine headaches.
  1. PHARMACOLOGY: Inhibits voltage-gated sodium channels (membrane stabilizing effects). Inhibits T-type calcium channels (excessive conductance causes seizures). Competitive antagonist of N-methyl-D-aspartic acid (NMDA) {excitatory} neuroreceptor. Inhibits GABA transaminase, increasing GABA (inhibitory neurotransmitter) concentrations in the brain.
  1. TOXICOLOGY: Causes CNS depression in overdose by extension of the pharmacologic mechanisms. Valproic acid depletes hepatic carnitine stores by forming valproylcarnitine, which inhibits the carnitine transported on the plasma membrane. Fatty acids cannot be metabolized due to lack of carnitine, resulting in chronic fatty liver. Valproic acid also depletes coenzyme A (CoA) stores in the liver by trapping CoA in the mitochondria by the valproic acid beta-oxidation metabolites. Depletion of CoA affects the activation of the carbamyl phosphate synthetase I (CPS I), which is needed for incorporating ammonia into the urea cycle, leading to hyperammonemia.
  1. EPIDEMIOLOGY: Poisoning is common with moderate severity.
  1. WITH THERAPEUTIC USE
    1. ADVERSE EFFECTS: COMMON: Anorexia, nausea, alopecia, peripheral edema, rash, sedation, weight gain, and teratogenicity. IDIOSYNCRATIC: Pancreatitis, hepatotoxicity, thrombocytopenia, hyperammonemia, and encephalopathy.
  1. WITH POISONING/EXPOSURE
    1. MILD TO MODERATE TOXICITY: Primary effect is CNS depression, generally lethargy and sedation, vomiting and tachycardia.
    1. SEVERE TOXICITY: Patients typically develop more severe CNS depression, coma, miotic pupils, tachycardia, hypotension, QTc prolongation, and respiratory depression following severe poisoning. Seizures and cerebral edema are less common. Laboratory abnormalities may include hypernatremia, hypocalcemia and hyperammonemia. Bone marrow suppression may develop 3 to 5 days after massive overdose, and usually resolves spontaneously. Pancreatitis, acute hepatotoxicity, renal insufficiency, and acute lung injury are uncommon, but have been reported. Valproate-induced hyperammonemic encephalopathy can develop after overdose or therapeutic use. It is characterized by deterioration of mental status (i.e., lethargy, confusion, coma) AND an elevated ammonia concentration; it may also be associated with hepatotoxicity.
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