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    Subjects/Pharmacology/Drug Poisoning and Antidotes
    Drug Poisoning and Antidotes
    medium
    pill Pharmacology

    A 35-year-old woman is admitted after deliberate ingestion of cyanide-containing pesticide. She is unconscious with severe metabolic acidosis and elevated venous oxygen saturation. Regarding the management of acute cyanide poisoning, all of the following are true EXCEPT:

    A. Activated charcoal is the primary antidote and should be given orally as soon as possible to prevent further cyanide absorption
    B. Hydroxocobalamin directly binds cyanide to form cyanocobalamin, which is then excreted in urine
    C. Sodium thiosulfate enhances the conversion of cyanide to thiocyanate by the enzyme rhodanese
    D. Sodium nitrite should be administered first to induce methemoglobinemia, which binds cyanide with higher affinity than cytochrome c oxidase

    Explanation

    ## Acute Cyanide Poisoning Management **Key Point:** Cyanide inhibits cytochrome c oxidase in the electron transport chain, causing histotoxic hypoxia (cells cannot use oxygen despite normal oxygen saturation). The antidotes work by binding cyanide or converting it to non-toxic forms — NOT by adsorption. ### Antidotes in Cyanide Poisoning | Antidote | Mechanism | Timing | Notes | | --- | --- | --- | --- | | **Sodium nitrite** | Induces methemoglobinemia; cyanide binds Hb-Fe³⁺ with higher affinity than cytochrome c oxidase | First (if available) | Risk: hypotension, methemoglobinemia toxicity | | **Sodium thiosulfate** | Substrate for rhodanese enzyme; converts CN⁻ → SCN⁻ (thiocyanate), which is renally excreted | Second; can be repeated | Slower acting; safe; enhances nitrite effect | | **Hydroxocobalamin** | Direct binding of CN⁻ → cyanocobalamin; excreted in urine | Preferred in modern protocols | Faster, safer; no methemoglobinemia risk; now first-line in many countries | | **Activated charcoal** | Adsorbs cyanide in GI tract | Oral/gastric only | **NOT a systemic antidote**; only useful if ingestion is recent and patient is conscious | **High-Yield:** The classic triad of cyanide antidotes is **"SNS"** — **S**odium nitrite, **N**a-thiosulfate, and **S**odium hydroxocobalamin (modern). Activated charcoal is NOT a systemic antidote — it works only in the GI tract and is irrelevant once cyanide is absorbed. **Clinical Pearl:** The "pink" appearance of cyanide poisoning (flushed skin, pink lips) is due to high venous oxygen saturation (cells cannot extract oxygen), not hypoxemia. This is histotoxic hypoxia, not hypoxic hypoxia. **Warning:** Activated charcoal does NOT reverse systemic cyanide toxicity. In an unconscious patient with cyanide poisoning, activated charcoal is contraindicated (aspiration risk) and ineffective (cyanide is already absorbed). The focus is on IV antidotes: hydroxocobalamin (preferred) or sodium nitrite + thiosulfate.

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