<unk>  (INH) used for latent and active TB treatment<unk> ’s metabolites restrict the conversion of pyridoxine to pyrodoxal-5’-phosphate and binds to pyridoxine, facilitating its excretion in the urine
Loss of pyridoxine leads to decreased GABA synthesis due to the decreased function of glutamic acid decarboxylase (GAD)
Anion gap acidosis likely results from lactic acid buildup as a consequence of persistent seizure activity
Finally come due to decreased catecholamine synthesis secondary to pyridoxine depletion
2-3g ingested can lead to symptoms, 10-15g can lead to death
Absorbed via GI tract (small intestine), peak concentrations at 1-2 hours after ingestion
Volume of Distribution: 0.6L/kg
Clearance of 46mL/min, metabolized by acetylation.
T1/2 for fast acetylators = 70 minutes
T1/2 for slow acetylators = 3 hours
T1/2 for fast acetylators = 70 minutes
T1/2 for slow acetylators = 3 hours
Via kidneys with levels successfully measured in urine
Isoniazid toxicity
Theophylline toxicity
Arsenic toxicity
Ipecac toxicity
Mold toxicity
Xylazine toxicity
Aluminum toxicity
Paraquat toxicity