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Flashcards in Iron in Health and Disease Deck (30):
1

Major site of iron storage

liver

2

vast majority of iron is present in

hemoglobins in RBCs

3

DMT1

divalent metal transporter that transports Fe2+ into enterocytes

4

Ferritin

stores protein within cells

5

Hephaestin

oxidzes Fe2+ to Fe3+ when leaving the enterocyte to prep it for for binding to transferrin

6

TFR

receptors that take in Fe2+ from transferrin

7

HFE (High Fe)

interacts with TFN receptors (TFN1)

8

____ levels in serum usually reflect body Fe stores

Ferritin levels

9

An important exporter cell

enterocyte

10

TFR

transferrin receptors --all cells have this for import

11

Hepcidin is produced almost exclusively by _____

hepatocytes

12

Master hormone regulating iron export and role

Hepcidin: acts as a brake by binding and degrading ferroportin. Blocks cellular Fe export

13

Factors that regulate serum hepcidin levels and order of priority

inflamation/infection > anemia/hypoxia > iron levels

14

How does intracellular iron levels regulate serum hepcidin?

-feedback mechanism
-high intracellular Fe increases hepcidin production

15

How does anemia/hypoxia affect hepcidin levels?

Low hemoglobin decreases hepcidin production. Need to maintain oxygen carrying capacity

16

How does inflammation/infection affect hepcidin levels?

Increase hepcidin production and decreases serum iron levels

(want to deprive infection from iron--evolution)

17

True or false: The factors regulating serum hepcidin levels can coexist and do not exert equal control

True.

18

Decreased hepcidin levels increase _____

ferroportin levels

19

Iron deficiency anemia results in (increased/decreased) hepcidin levels

decreased

condition response to iron supplementation

20

In anemia of chronic inflammation, what would you expect these levels from lab to be?
-Hgb
-Hct
-serum Fe
-Fe binding capacity
-serum ferritin
-RBC size

-low Hgb
-low Hct
-low serum Fe
-low Fe serum binding capacity
-normal serum Ferritin
-normal or small sized RBCs

21

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

22

In anemia with ineffective erythropoeisis, what would you expect the levels to be of lab results?
-Hgb
-Hct
-Serum Fe
-Fe binding capacity
-serum ferritin
-RBCs

-low Hgb
-low Hct
-high, highly saturated (transfusions increases Fe load and RBCs cant take up as much)
-high serum ferritin
-small, microcytosis

23

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!

24

What is used to assess iron binding capacity?

transferrin

25

Genetic Hemochromatosis

Uncontrolled Fe uptake from gut, iron overload

26

What is the most frequent defect in genetic hemochromatosis?

HFE mutation! One of the components of the TFR1 receptor

27

Lab results with someone with genetic hemochromatosis:
-Hgb
-Hct
-Serum Fe
-Ferritin

-normal Hgb
-normal Hct
-high serum Fe (since defective transferrin receptor into cells)
-very high ferritin levels

28

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.

29

HFE mutations effect which organ first

liver

30

treatment for hereditary hemochromatosis

phlebotomy/chelation.