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Year 1 > Iron in Health and Disease > Flashcards

Iron in Health and Disease Flashcards

1
Q

Major site of iron storage

A

liver

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2
Q

vast majority of iron is present in

A

hemoglobins in RBCs

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3
Q

DMT1

A

divalent metal transporter that transports Fe2+ into enterocytes

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4
Q

Ferritin

A

stores protein within cells

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5
Q

Hephaestin

A

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

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6
Q

TFR

A

receptors that take in Fe2+ from transferrin

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7
Q

HFE (High Fe)

A

interacts with TFN receptors (TFN1)

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8
Q

____ levels in serum usually reflect body Fe stores

A

Ferritin levels

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9
Q

An important exporter cell

A

enterocyte

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10
Q

TFR

A

transferrin receptors –all cells have this for import

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11
Q

Hepcidin is produced almost exclusively by _____

A

hepatocytes

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12
Q

Master hormone regulating iron export and role

A

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

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13
Q

Factors that regulate serum hepcidin levels and order of priority

A

inflamation/infection > anemia/hypoxia > iron levels

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14
Q

How does intracellular iron levels regulate serum hepcidin?

A
  • feedback mechanism

- high intracellular Fe increases hepcidin production

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15
Q

How does anemia/hypoxia affect hepcidin levels?

A

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

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16
Q

How does inflammation/infection affect hepcidin levels?

A

Increase hepcidin production and decreases serum iron levels

want to deprive infection from iron–evolution

17
Q

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

A

True.

18
Q

Decreased hepcidin levels increase _____

A

ferroportin levels

19
Q

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

A

decreased

condition response to iron supplementation

20
Q

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
A
  • low Hgb
  • low Hct
  • low serum Fe
  • low Fe serum binding capacity
  • normal serum Ferritin
  • normal or small sized RBCs
21
Q

In anemia of chronic inflammation, what happens to hepcidin levels?

Is Fe supplementation effective?

A

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
Q

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
A
  • low Hgb
  • low Hct
  • high, highly saturated (transfusions increases Fe load and RBCs cant take up as much)
  • high serum ferritin
  • small, microcytosis
23
Q

In ineffective erythropoeisis, what happens to hepcidin?

A

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
Q

What is used to assess iron binding capacity?

A

transferrin

25
Q

Genetic Hemochromatosis

A

Uncontrolled Fe uptake from gut, iron overload

26
Q

What is the most frequent defect in genetic hemochromatosis?

A

HFE mutation! One of the components of the TFR1 receptor

27
Q

Lab results with someone with genetic hemochromatosis:

  • Hgb
  • Hct
  • Serum Fe
  • Ferritin
A
  • normal Hgb
  • normal Hct
  • high serum Fe (since defective transferrin receptor into cells)
  • very high ferritin levels
28
Q

Effect of hepcidin with genetic hemochromatosis

A

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
Q

HFE mutations effect which organ first

A

liver

30
Q

treatment for hereditary hemochromatosis

A

phlebotomy/chelation.

Year 1 (48 decks)

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