Study Set Content:
Formaldehyde →
aldehyde dehydrogenase
(aldehyde dehydrogenase) →
Formic acid
Acute methanol poisoning in humans is characterized by an asymptomatic period of ()()h followed by()()()()
12 to 24 , formic acidemia, ocular toxicity, coma, and in extreme cases death.
First few hours:()(); noticeable elevation in () gap. •
inebriation and gastritis, osmol
After latent period: severe () gap metabolic acidosis (formic acidemia), ocular toxicity (18-48h; “like standing in a snowfield”), (), coma, AFR with (), death.
anion, myoglobinuria, seizures
The target of methanol within the eye is the (), specifically the optic disk and optic nerve
retina
are altered functionally and structurally, because cytochrome c oxidase activity in mitochondria is inhibited, resulting in a reduction in ATP.
Müller cells, rod, and cone cells
; within 30- 60 mins can aspirate gastric contents; Hemodialysis
Fomepizole/Ethanol; Leucovorin/Folic Acid
1,2-dihydroxyethane is a major constituent of antifreeze, deicers, hydraulic fluids, drying agents, and inks, and is used to make plastics and polyester fibers
ETHYLENE GLYCOL
mportant routes of exposure are dermal and accidental or intentional ingestion. EG is rapidly () in environmental media.
degraded
Three clinical stages of acute poisoning entail:
o A period of (), the duration and degree depending on dose
o The () 12 to 24 h after exposure, characterized by tachycardia and tachypnea, which may progress to cardiac failure and pulmonary edema
o The () 24 to 72 h postexposure. Metabolic acidosis can progress in severity during stages 2 and 3
inebriation, cardiopulmonary stage, renal toxicity stage
EG is metabolized by NAD+ -dependent ADH to ()and on to ().
glycolaldehyde , glycolic acid
Glycolic acid is oxidized to ()acid by () and ()
Glyoxilic, glycolic acid oxidase and lactic dehydrogenase
may be converted to formate and CO2, or oxidized by glyoxylic acid oxidase to oxalic acid.
Glyoxylic acid
in humans appears to be due to accumulation of glycolic acid.
Metabolic acidosis
can result from calcium chelation by oxalic acid to form calcium oxalate crystals.
Hypocalcemia
and direct cytotoxicity by other metabolites may act as damaging agents to the kidney in EG exposure.
Hippuric acid crystals
Treatment: ETHYLENE GLYCOL
Emergency and supportive measures • Fomepizole/ethanol; Pyridoxine, Folate, and Thiamine • Lavage if recent • Hemodialysis
Used as an intermediate in the synthesis of polyester fibers and resins, as a component of automotive antifreeze/coolants, and as a deicing fluid for aircraft. • “Generally recognized as safe” by the FDA, it is a constituent of many cosmetics and processed foods.
PROPYLENE GLYCOL
The most important routes of exposure are ingesting and dermal contact
PROPYLENE GLYCOL
