last authored: Jan 2009, David LaPierre
Organic, is iron bound to heme. Inorganic refers to free iron.
Ferrous (Fe 2+) is soluble, while ferric (Fe 3+) is insoluble.
Iron measures of the blood can be use to estimate total iron.
Pregnancy increases iron requirments by 1g elemental iron per fetus. This is broken down into 500mg for fetal and placental growth, 500mg for increased maternal RBCs, and 200mg for losses. Most iron is transferred after 26 weeks.
All pregnant women should receive 150mg ferrous sulfate, 300 ferrous gluconate, or 30mg ferrous iron daily during secind and 3rd trimester. If anemic, pregnant mothers should take 1 g ferrous sulfate, or 180mg elemental iron.
Premature infants have lower stores of iron and increased external losses. Their rapid growth necessitates greater need - perhaps 2 mg/kg/day
Term infants have total iron supplies of 75 mg/kg, making iron deficiency rare before 4 months
Infants 4-12 months have a very large iron need as their birth weight doubles by 5 months and triples by 12 months. They need 1 mg/kg/day.
Children 1-4 years have the highest prevalence of iron deficiency, often due to "milk baby syndrome", where babies drink loads of milk and little else. Toddlers need 10 mg/day.
School-aged children rarely have iron deficiency due to nutritional status, making detailed investigations necessary.
Adolescents are increased risk of iron deficiency due to increased growth, the onset of menstration in girls, and often poor diets.
Men need x, but they normally ingest 15-20 mg of iron daily.
Women need x, but they normally take in 10-15 mg iron daily.
Dietary iron is the primary source of iron. Meats have much more bioavailable iron than vegetables, which also contain absorption-inhibiting phosphates and phytates. Sources include:
An adult male takes in 15-20 mg/day, while females take in 10-15 mg daily.
Red blood cell turnover releases 25-30 mg of iron each day into the marrow and spleen, with transport back to sites of new red blood cell production.
Normal men have a total body iron content close to 4000 mg, with 500-1000 mg in storage. Women usually have less than 200 mg iron storage levels.
Iron is most absorbed in the proximal small intestine.
Organic (heme) iron binds to mucosal cell receptors and passes into the cytoplasm, where the porphyrin ring is cleaved and the iron released.
Inorganic iron is converted to ferrous iron and bound to transferrin. Its absorption is increased by the presence of heme iron and decreased by the presence of phytates and phosphates.
Intracellular iron is transported to the liver via the portal circulation for metabolism. The plasma protein transferrin is reponsible for this. At any one time, about 3 mg of iron is found in the blood.
Transferrin secretion by the liver is inversely proportional to hepatic iron stores.
Excess iron in the gut combines with apoferritin on mucosal cells, where it is bound and lost through sloughing off. Levels of apoferritin are proportional to levels of iron stores.
Iron's key role is as a component of heme, the component of hemoglobin which binds oxygen for transport around the body. It is distributed across the body in the following locales:
co-factor for some neurotransmitters
Iron toxicity can cause nutritional hemosiderinosis and organ damage.
Iron is a direct GI irritant: damage
gets into blood: anion gap
coagulopathy
CV collapse
encephalopathy
amount of elemental iron determines toxicity.
intracellular iron is the worst
GI toxicity: 50-90 SI
moderate systemic toxicity:
TIBC is not useful; can be falsely elevated
abdo
Five stages of toxicity, but in practice
stage 1: abdominal pain, diarrhea, vomiting; absence of these in 1st 6 hours effectivey excludes dx
stage 2: 6-24 hours: not always seen. GI symptoms improve
stage 3: systemic toxicity: coagulopathym hepatica, renal, cardiac
stage 4: hepatic stage 2-5 days
stage 5: delayed 4-6 weeks: gastric obstruction