Flashcards in Iron in Health and Disease Deck (30):
Major site of iron storage
vast majority of iron is present in
hemoglobins in RBCs
divalent metal transporter that transports Fe2+ into enterocytes
stores protein within cells
oxidzes Fe2+ to Fe3+ when leaving the enterocyte to prep it for for binding to transferrin
receptors that take in Fe2+ from transferrin
HFE (High Fe)
interacts with TFN receptors (TFN1)
____ levels in serum usually reflect body Fe stores
An important exporter cell
transferrin receptors --all cells have this for import
Hepcidin is produced almost exclusively by _____
Master hormone regulating iron export and role
Hepcidin: acts as a brake by binding and degrading ferroportin. Blocks cellular Fe export
Factors that regulate serum hepcidin levels and order of priority
inflamation/infection > anemia/hypoxia > iron levels
How does intracellular iron levels regulate serum hepcidin?
-high intracellular Fe increases hepcidin production
How does anemia/hypoxia affect hepcidin levels?
Low hemoglobin decreases hepcidin production. Need to maintain oxygen carrying capacity
How does inflammation/infection affect hepcidin levels?
Increase hepcidin production and decreases serum iron levels
(want to deprive infection from iron--evolution)
True or false: The factors regulating serum hepcidin levels can coexist and do not exert equal control
Decreased hepcidin levels increase _____
Iron deficiency anemia results in (increased/decreased) hepcidin levels
condition response to iron supplementation
In anemia of chronic inflammation, what would you expect these levels from lab to be?
-Fe binding capacity
-low serum Fe
-low Fe serum binding capacity
-normal serum Ferritin
-normal or small sized RBCs
In anemia of chronic inflammation, what happens to hepcidin levels?
Is Fe supplementation effective?
inflammation overrides anemia stimulus
-you get increased hepcidin to inhibit ferroportin and thus export of Fe from enterocytes and macrophages.
-in anemia, you would want decreased hepcidin to get more Fe out to RBCs.
-supplement not effective-primary problem is Fe incorporation into RBCs
In anemia with ineffective erythropoeisis, what would you expect the levels to be of lab results?
-Fe binding capacity
-high, highly saturated (transfusions increases Fe load and RBCs cant take up as much)
-high serum ferritin
In ineffective erythropoeisis, what happens to hepcidin?
Anemia overrides Iron levels. So you will get decreased hepcidin and increased ferroportin. Gut, macrophages, liver increase Fe export to bone marrow. Transfusions add Fe. = Fe OVERLOAD!
What is used to assess iron binding capacity?
Uncontrolled Fe uptake from gut, iron overload
What is the most frequent defect in genetic hemochromatosis?
HFE mutation! One of the components of the TFR1 receptor
Lab results with someone with genetic hemochromatosis:
-high serum Fe (since defective transferrin receptor into cells)
-very high ferritin levels
Effect of hepcidin with genetic hemochromatosis
consumer cells with TfR2 (non mutated) have to take up more iron, so decrease hepcidin to increase ferroportin. Enterocytes, macrophages, hepatocytes, increase Fe export.
HFE mutations effect which organ first