I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?
The curiosity lead to this post.
In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .
Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.
Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.
Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).
Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.
Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.
Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.
Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside
Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)
That's all!
-IkaN
Fell in love with this post!
ReplyDeleteSo beautifully explained.
Thanks Ikan for such wonderful posts
You're most welcome love :)
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