Ethanol poisoning

Ethanol poisoning

Q. 1 MacEwen’s sign is seen in:

 A Lead poisoning

 B

Arsenic poisoning

 C

Ethanol poisoning

 D

Copper poisoning

Q. 1

MacEwen’s sign is seen in:

 A

Lead poisoning

 B

Arsenic poisoning

 C

Ethanol poisoning

 D

Copper poisoning

Ans. C

Explanation:

MacEwen signs (MacEwen pupil) The pupil of a patient comatose from alcohol intoxication dilates briefly when the patient is stimulated but not awakened, while that of a patient comatose from structural disease does not  get dilated for mild stimulation.

Ref: Principles of forensic medicine, Apurva nandy, 3rd Edition,Page 847.


Q. 2

Fatal level of ethanol in blood:  

NIMHAS 13

 A

100-200 mg/dl

 B

200-300 mg/dl

 C

300-400 mg/dl

 D

> 500 mg/dl

Ans. C

Explanation:

Ans. 300-400 mg/dl


Q. 3

Ethanol is used for ethylene glycol poisoning because it is a: 

JIPMER 13

 A

Competitive inhibitor of NADpH oxidase

 B

Competitive inhibitor of alcohol dehydrogenase

 C

Competitive inhibitor of aldehyde dehydrogenase

 D

Non-competitive inhibitor of aldehyde dehydrogenase

Ans. B

Explanation:

Ans. B

Competitive inhibitor of alcohol dehydrogenase [Ref Lehninger Principles of Biochemistry 4th/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.


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