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Questions and Answers
What is a common CNS symptom of severe iron overdose?
What is a common CNS symptom of severe iron overdose?
What blood iron level indicates a potential toxicity?
What blood iron level indicates a potential toxicity?
Which treatment method is considered the most effective for decontamination in iron overdose?
Which treatment method is considered the most effective for decontamination in iron overdose?
What metabolic complication is commonly observed in severe iron overdose cases?
What metabolic complication is commonly observed in severe iron overdose cases?
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In the context of iron overdose, what does a blood iron level greater than 90 μmol/L indicate?
In the context of iron overdose, what does a blood iron level greater than 90 μmol/L indicate?
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Which of the following is a potential late complication of severe iron poisoning?
Which of the following is a potential late complication of severe iron poisoning?
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What blood iron level corresponds to a potentially toxic dose of elemental iron?
What blood iron level corresponds to a potentially toxic dose of elemental iron?
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What is the recommended action for symptomatic patients with confirmed iron levels above 60 μmol/L?
What is the recommended action for symptomatic patients with confirmed iron levels above 60 μmol/L?
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Which phase of iron poisoning is characterized by severe hemorrhagic gastroenteritis?
Which phase of iron poisoning is characterized by severe hemorrhagic gastroenteritis?
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What leads to the development of iron toxicity in the bloodstream?
What leads to the development of iron toxicity in the bloodstream?
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What is the primary mechanism through which free circulating iron causes damage to organs?
What is the primary mechanism through which free circulating iron causes damage to organs?
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In which phase do gastrointestinal symptoms typically improve after an iron overdose?
In which phase do gastrointestinal symptoms typically improve after an iron overdose?
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What is NOT a common source of iron exposure leading to toxicity?
What is NOT a common source of iron exposure leading to toxicity?
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What is the primary route of elimination for excess iron in the body?
What is the primary route of elimination for excess iron in the body?
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Which symptom is NOT typically associated with the gastrointestinal phase of iron toxicity?
Which symptom is NOT typically associated with the gastrointestinal phase of iron toxicity?
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What crucial role does transferrin play in the context of iron toxicity?
What crucial role does transferrin play in the context of iron toxicity?
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Study Notes
Acute Iron Toxicity
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Common Sources & Exposure: Often occurs in children; ingestion of 3-5 tablets can cause significant toxicity depending on elemental iron content.
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Toxic Action: Toxicity arises when serum iron exceeds transferrin’s binding capacity, leading to free circulating iron. This damages organs via cellular toxicity, vascular effects, and vasodilator release.
Toxicokinetics
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Absorption: Poorly absorbed in therapeutic doses (duodenum/jejunum); absorption increases with gastrointestinal toxicity in overdose, resulting in later peak concentrations and higher bioavailability.
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Distribution: Transported by transferrin; unbound iron (when transferrin is saturated) reacts with blood vessels and platelets.
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Elimination: No significant natural elimination route except gastrointestinal/blood loss.
Clinical Picture: Four Phases
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Gastrointestinal Phase: Hemorrhagic gastroenteritis (vomiting, colic, diarrhea) within hours; potential hypotension and acidosis due to fluid loss.
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Window Phase: (4-12 hours post-ingestion) Gastrointestinal symptoms improve.
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Multi-Organ Failure Phase: Systemic toxicity affecting GIT (severe gastroenteritis, perforation), CNS (lethargy, coma, convulsions), CVS (hypotension, pulmonary edema), Renal (acute tubular necrosis, renal failure), Hepatic (severe necrosis, hypoglycemia), Metabolic (lactic acidosis), and Coagulation (early & late coagulopathy).
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Late Complications Phase: Gastric/pyloric scarring and obstruction.
Investigations
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Blood Iron Level: Crucial for treatment decisions; measured before desferrioxamine therapy; Normal: 10-30 μmol/L; Significant toxicity unlikely: 30-60 μmol/L; Possible toxicity (desferrioxamine indicated in symptomatic patients): 60-90 μmol/L; Frank toxicity (desferrioxamine indicated regardless of symptoms): >90 μmol/L.
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Abdominal X-ray: Identifies radiopaque tablets (absence doesn't rule out overdose).
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Other Tests: Electrolytes, arterial blood gases, blood glucose, full blood count, renal/liver function tests, coagulation studies.
Severity Determination
- Clinical evaluation.
- Blood iron level.
- Ingested elemental iron dose: <10-20 mg/kg (non-toxic); 20-60 mg/kg (potentially toxic); 60-120 mg/kg (toxic, unlikely fatal); >120 mg/kg (potentially fatal).
Treatment
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Emergency & Supportive Care: Close monitoring (ABCs, CVP line, electrolytes, blood gases, blood sugar); volume replacement (blood, fresh frozen plasma, crystalloids); acidosis correction.
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Decontamination: Activated charcoal ineffective; gastric lavage has limited value; whole bowel irrigation is the preferred method (especially for ingestions >60 mg/kg confirmed on X-ray, undissolved tablets on X-ray, or sustained/enteric-coated tablets).
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Description
This quiz covers the critical aspects of acute iron toxicity, including common sources of exposure, toxic mechanisms, and toxicokinetics. Understand the clinical phases and the implications of iron overload for patient care. Test your knowledge on the effects of iron on the body and its management.
