Ethylene glycol & Boric acid poisoning

Ethanol acts by competing with ethylene glycol for alcohol dehydrogenase, the first enzyme in the degradation pathway.

Because ethanol has a much higher affinity for alcohol dehydrogenase, about a 100-times greater affinity, it successfully blocks the breakdown of ethylene glycol into glycoaldehyde, which prevents the further degradation.

Ref: Lehninger Principles of Biochemistry, 4th Edition, Page 336; Updates in Emergency Medicine By John Cahill, 2002, Page 115

Ans. is ‘C’ i.e., Fomepizole

• I.V. fomepizole or ethanol is given in ethylene glycol poisoning.
• Fomepizole (an alcohol dehydrogenase inhibitor) is the DOC.

Ans. B

Competitive inhibitor of alcohol dehydrogenase [Ref Lehninger Principles of Biochemistry 4^th/e p. 336]

• Ethylene glycol poisoning should be suspected in an intoxicated patient with anion gap acidosis, hypocalcemia, urinary crystals, and nontoxic blood alcohol concentration. 
• Oxidative reactions convert ethylene glycol to glycoaldehyde, and then to glycolic acid, which is the major cause of metabolic acidosis.
• The conversion of glycolic acid to glyoxylic acid proceeds slowly, further increasing the serum concentration of glycolic acid.
• Glyoxylic acid is eventually converted to oxalic acid and glycine. Oxalic acid does not contribute to the metabolic acidosis, but it is deposited as calcium oxalate crystals in many tissues.

The clinical syndrome of ethylene glycol intoxication has traditionally been divided into three stages:

• progressive involvement of the CNS, the cardiopulmonary systems, and the kidneys. However, presentation is highly variable and dependent on the amount ingested, the combined ingestion with ethanol, and the timing of medical intervention.

Ans. Oxalates

When broken down by the body it results in glycolic acid and oxalic acid which cause most of the toxicity. 

The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increased osmol gap is present in the blood.

Diagnosis may be confirmed by measuring ethylene glycol levels in the blood.

Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze.^[9] During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetence may be seen.^[9] Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure.

Ethylene Glycol

• It is used as an antifreeze.

• It is not absorbed through the skin.

• It is metabolised to glyceraldehyde, glycolic acid and oxalic acid.

• It inhibits oxidative phosphorylation

• Symptoms: vomiting, lethargy, ataxia, convulsions & coma

• In 12-24hrs, tachycardia, tachypnea, electrolyte impedance metabolic acidosis.

• In 1-3 days, hypocalcemia, oliguria, tubular necrosis & renal failure occurs due to formation of calcium oxalate crystal.

Treatment- gastric lavage, activated charcoal, ethanol, hemodialysis