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6 Cards in this Set
- Front
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Explain the distribution of iron in the body.
Which state reversibly binds to O2? Why is iron usually chelated in the body? |
70% in Hgb, ~5% in myoglobin, ~1% in Fe-requiring proteins (cytochromes, e- carriers in mitochondria)
~25% stored in ferritin (hemosiderin) Ferrous (2+) binds to O2 free iron causes ROS - H2O2, O2-; also limits availability to bacteria |
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RDA of iron for men/women?
Absorption enhanced by: Absorption diminished by: What are some good dietary sources of iron? |
Men - 10 mg/d; Women - 18 mg/d
enhanced - ascorbic acid, animal proteins diminished - phytates, oxalates, phosphates, coffee, tea, soda, ASA Diet - spinach, seafood, bran flakes |
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Explain the binding capacity/function of ferritin and transferrin.
Fe is transported in what state? Which organs store excess? How much is absorbed per day? |
Ferritin - high capacity - 1000's of Fe molecules (hemosiderin granules)
Transferrin - low binding capacity - 1-2 Fe at a time; about 70% is unbound transported as Fe2+ liver, pancreas, lungs; 1-2 mg/d absorbed |
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Iron starvation/deficiency:
What happens to transferrin and ferritin? What modulates transcription of transferrin receptors and blocks ferritin? Iron excess - what happens? |
Starvation - cytosolic aconitase blocks ferritin, promotes transferrin receptors
Excess - Iron binds to aconitase, promotes ferritin, blocks transferrin |
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Serum lab values:
What does TIBC measure? How to calculate transferrin saturation: Some causes of iron overload? What is hemosiderosis? Hemochromatosis? |
TIBC = transferrin levels
saturation - serum [Fe]/TIBC Overload - transfusions, excess absorption Hemosiderosis - elevated total body iron, no cell injury Hemochromatosis - elevated total body iron, + cell injury |
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Three major complications of hemochromatosis?
Lab values for serum [Fe], serum ferritin, TIBC, transferrin saturation in hemochromatosis: |
liver damage, diabetes, heart failure
[Fe] - usually normal [ferritin] - elevated (>200 ug/L) TIBC - elevated saturation - elevated (>62%) |
