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Review Question - QID 100083

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QID 100083 (Type "100083" in App Search)
An 18-year-old college student presents to the ED straight from chemistry lab where he ingested an unknown compound. He complains of a headache, and is flushed, tachypneic and tachycardic. Suspecting cyanide poisoning, you administer amyl nitrite which causes which of the following?

Oxidation of ferrous iron in hemoglobin to ferric iron

59%

197/335

A decrease in serum methemoglobin levels

8%

26/335

Formation of thiocyanate

17%

56/335

Chelation of the residue

7%

23/335

Increase in intracellular NADH/NAD+ ratio

7%

25/335

Select Answer to see Preferred Response

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In cyanide poisoning, amyl nitrite is given to oxidize hemoglobin ferrous iron and increase circulating methemoglobin.

Cyanide poisoning may be due to nitroprusside overdose, toxic ingestion or burning of furniture/mattresses. Cyanide inhibits the electron transport chain, specifically cytochrome a/a3, causing a decrease in proton gradient, ATP synthesis, and O2 consumption and increasing NADH/NAD in the cell as well as possible seizures and lactic acidosis. Amyl nitrite is given in cyanide poisoning because it oxidizes the iron in hemoglobin (ferrous (Fe2+)->ferric (Fe3+)), changing the molecule to methemoglobin. Cyanide binds preferentially to methemoglobin and when bound, is safely sequestered in the extracellular space and unable to interfere with the electron transport chain.

Gracia and Shepherd indicate that amyl nitrite is part of what is known as the cyanide antidote kit. Additional components include sodium nitrite. It is administered intravenously and acts to increase methemoglobin levels by 8-20%. The last medication is sodium thiosulfate. This compound combines with cyanide extracellularly to form thiocyanate and may also enhance mitochondrial sulfurtransferase reactions.

Hamel indicates that cyanide poisoning can also be treated with the antidote hydroxocobalamin. Hydroxocobalamin binds cyanide to form a nontoxic compound cyanocobalamin which can be excreted renally. Additionally, cyanocoblamain can release cyanide at an appropriate rate for the liver enzyme rhodanase to detoxify cyanide.

Illustration A demonstrates the production of methemoglobin following administration of amyl nitrate and the preferential binding of cyanide to methemoglobin to form cyanomethemoglobin.

Incorrect Answers:
Answer 2: Administration of amyl nitrate directing increases serum methemoglobin. It does not decrease serum concentration.
Answer 3: Thiocyante is a metabolite of the breakdown of cyanomethemoglobin. It is formed following the addition of sodium thiosulfate, is less toxic and excreted by the kidneys.
Answer 4: Chelation is a technique used to remove dangerous metal compounds such as lead, from the body. Cyanide is not a heavy metal.
Answer 5: An increase in the intracellular NADH/NAD+ ratio is a result of cyanide poisoning, not an effect of amyl nitrate.

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