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14 Cards in this Set
- Front
- Back
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FUNCTION OF IRON
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Oxygen storage and transport via Hb/Mb Erythropoiesis Energy production molecules eg cytochromes Liver detox molecule CYP450 Host defence molecule NADPH oxidase |
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IRON DISTRIBUTION
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35-45mg/kg 50% RBC 30% stored (ferritin) in liver, BM and RES cells 7% Mb 5% proteins 0.1% free in serum |
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IRON HOMEOSTASIS
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Excretion unregulated but normally 1-2mg/d from GI tract Absorption is strictly regulated as excess Fe is toxic and promotes bacteria growth |
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IRON CYCLE - RAUS
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Recycling: RES m'phages clear senescent RBC and release Fe from haem Absorption: Duodenal enterocytes; increases if low Fe stores, hypoxia, anaemia; decreases with inflammation Utilisation: transferrin-bound then used by marrow erythroid precursors for haem Storage: ferritin in RES m'phages and hepatocytes |
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IRON SCAVENGING
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Ways to conserve Fe in pathological states 1) Free Hb binds to haptoglobins and go to liver 2) Free haem binds to haemopexin and goes to liver 3) Haem is filtered through kidneys and reab |
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FERRITIN
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Stores Fe for controlled release; 4500 atoms per molecule Apoferritin cell with Fe-PO4-OH core Increases in overload, acute phase response, tissue release ie in hepatitis, leukaemia Decreases in Fe deficiency (but normal does not exclude) |
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IRON IN BLOOD
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Non exchangeable as Hb in RBC Transferrin-bound so changing locations |
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TRANSFERRIN
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Made in liver 2 Fe:1 transferrin Normally 30% saturated Decreases in overload and increases in deficiency |
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HEPCIDIN - WHAT
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Main Fe regulatory hormone secreted in liver Blocks Fe release from enterocytes and RES m'phages by degrading ferroportin |
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HEPCIDIN- REGULATION
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Inc erythropoiesis = dec hepcidin Dec pO2 = dec hepcidin (FURIN/TMPRS6) Inc Fe in body = inc hepcidin (ferrotransferrin signal) Infection/inflame = inc hepcidin (1l-6 and LPS) |
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IRON TESTS
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Serum Iron: 0.1% body Fe Limited use unless grossly abnormal Transferrin saturation: Increases sensitivity in combo In overload, increased iron and decreased transferring = increased saturation (80%) |
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HEPCIDIN DEFICIENCY
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Hereditary hemochromatosis: excess Fe absorption due to altered set point Ineffective erythropoiesis: increased destruction of eythroid precursors and increased Fe absorption |
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HEPCIDIN EXCESS
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Anaemia of chronic disease: Infection/inflammation = Fe sequestration in m'phages and decreased Fe absorption
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GENETIC HAEMACHROMATOSIS |
Defective HFE gene Less HFE = less hepcidin so overactivity of ferroportin and increased Fe absorption
Can be due to DMT1 transporter so hepcidin-independent
Limited penetrance
Vulnerable tissues = pancreas, liver, articular surfaces, heart muscle, pituitary gonadotrophs |
