Sodium nitroprusside (SNP) toxicity manifests as lactic acidosis because:

• A SNP directly inhibits Complex IV (cytochrome c oxidase) of the mitochondrial electron transport chain
• B SNP causes excessive vasodilation and reduced tissue oxygen delivery
• C Thiocyanate accumulation inhibits thyroperoxidase causing hypothyroidism and metabolic slowing
• D Cyanide released from SNP metabolism inhibits Complex IV, impairing aerobic respiration ✓

Explanation

Each SNP molecule releases 5 cyanide (CN−) ions in tissues. Cyanide binds irreversibly to ferric iron of cytochrome c oxidase (Complex IV), blocking the terminal step of the mitochondrial electron transport chain and forcing anaerobic glycolysis, producing lactic acidosis. Treatment involves thiosulfate (provides sulfur donor for rhodanese to convert CN− to thiocyanate) and hydroxocobalamin (binds CN−). Thiocyanate toxicity causes hypothyroidism but is distinct from cyanide toxicity.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.