Tumour lysis syndrome pathophysiology and risk
Core concept
- Lysis dumps intracellular contents faster than the kidney can clear them
- inc K, inc PO4, inc urate -> dec Ca (the hypocalcaemia is secondary, from calcium-phosphate complexing)
- K -> arrhythmia; the earliest killer
- Nucleic acid -> hypoxanthine -> xanthine -> urate -> crystallises in the acidic distal tubule
- PO4 binds Ca -> CaPO4 deposits in tubules -> AKI, and hypocalcaemia -> tetany, seizures, long QT
- AKI is self-amplifying: urate crystals + CaPO4 deposition + urate-driven vasoconstriction -> dec clearance -> worse everything
3 more sections, plus exam facts
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