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Erik's IHO Week 4 > 5-14 GOUELI Iron Metabolism > Flashcards

5-14 GOUELI Iron Metabolism Flashcards

1
Q

What’s the advantage of decreasing iron utilization during inflammation?

A

Bacteria use iron, so it helps them live. You don’t want that.

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2
Q

What is absorbed better by the body: heme iron or Fe3+ iron?

A

Heme iron

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3
Q

How is iron eliminated from the body?

A

Obligatory loss due to sloughing of cells (GI, GU, and skin)

There is no physiological mech to get rid of EXCESSSSSSS iron

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4
Q

What is the physiologic pathway for excreting EXCESS iron?

A

Trick question! THERE IS NONE

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5
Q

In what form is most of the iron in your body?

A

Most of the iron in your body is in the for of hemoglobin (Hb)

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6
Q

What is the significance of Ferroportin 1?

A

It is the only known mechanism to transport iron OUT of cells!

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7
Q

What is the significance of the low pH of the GI tract?

A

It helps the Fe3+  Fe2+ rxn

Thus, people on proton-pump inhibitors could become iron deficient!

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8
Q

How is iron eliminated from the body?

A

These epithelial cells of the intestine are constantly being sluffed off and excreted in feces. If a lot of iron is present in them, it gets excreted too

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9
Q

How many iron atoms can each Transferrin (Tf) hold?

A

2 Fe3+ atoms

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10
Q

What is Total Iron Binding Capacity (TIBC)?

A

It is a lab test you will be ordering someday
Measures the amount of Tf in circulation.
↑Tf  ↑TIBC
TIBC = Tf x 2 (b/c each Tf can hold 2 Fe3+)

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11
Q

How does iron get from transferrin back INTO the cells?

A

Tf binds TfR1 (transferrin receptor 1) molecule on cell surface
Tf-TfR1 complex is endocytosed.
Vesicle is acidified to facilitate Tf release of Fe3+
Fe3+ reduced via STEAP3 enzyme
Fe2+ moves OUT of vesicle INTO cell via DMT1 transporter

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12
Q

What cells express the TfR1 protein?

A

Any cell that needs iron. So virtually all (iron is a cofactor for many enzymes)
Most iron goes to Erythroid Progenitor cells to make RBCs

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13
Q

What happens to iron in the Erythroid progenitors?

A

Combined w/ PPIX (protoporphyrin) to form heme

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14
Q

What is the role of the macrophage WR2 iron?

A

Macrophage recycles iron
Old RBCs are phagocytized by phage (in spleen or wherever)
ALSO, RBCs lysed in circulation have floating Hb. That’s taken up by
phage
Iron REMOVED from heme in macrophage
Iron is exported via Ferroportin and reduced via Ceruloplasmin to Fe3+ for transport on Tf

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15
Q

Where is hepcidin produced?

A

In the hepatocyte

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16
Q

What does hepcidin do?

A

Master regulator of iron
Signaling molecule:
Causes ferroportin to be internalized and degraded in lysosomes
-> decreased Fe release from cells!

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17
Q

What does excess hepcidin cause?

A

Low iron utilization (iron is trapped in cells)

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18
Q

What does deficient hepcidin cause?

A

Iron overload

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19
Q

What gene produces hepcidin?

A

HAMP gene

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20
Q

What cytokine causes production of hepcidin?

A

IL-6 -> ↑expression of HAMP gene

21
Q

How does amount of iron in the body regulate expression of HAMP gene?

A

Lots of iron in body -> high Tf saturation  activation of TRF2-HFE complex  ↑HAMP signaling

22
Q

What is the most common mutation found in ppl w/ hereditary hemachromatosis (HH)?

A

HFE mutation  ↓hepcidin

23
Q

What is the 2nd most common mutation in HH?

A

Hemojuvelin (another regulation pthwy of Hepcidin)

24
Q

What are IC ferritin, serum ferritin, and hemosiderin?

A

Ferritin – iron storage molecule
IC ferritin – intracellular ferritin (where most ferritin is)
Serum ferritin – ferritin in blood (↑IC ferritin  ↑serum ferritin)
Hemosiderin – many ferritin molecules combine into hemosiderin

25
Q

What form of iron is stored in Ferritin?

A

It enters as Fe2+ but is quickly oxidized to prevent Fenton rxns
Fenton rxns would mess shit up in Ferritin

26
Q

How is iron released from ferritin?

A

Proteolysis

27
Q

CLINICAL CORRELATE: What will a classic iron deficient patient’s ferritin levels look like?

A

LOW. If < 10, BOOM, you know it’s iron deficiency

This makes sense! If low iron, patient won’t make STORAGE for iron!

28
Q

How are the post-transcriptional regulation of ferritin and transferrin related?

A

The same protein regulates them.
IRE (iron response element) is bound by IBP (IRE binding protein)
IBP binds iron, causing it to not bind IRE region of mRNA
For ferritin mRNA this allows translation
For transferrin mRNA, this allows mRNA degredation

29
Q

Why does this make sense?

A

IBP binds intracellular iron
If IC Fe is high, we want MORE ferritin to store it
If IC Fe is high, we want LESS Tf to bring it in (recall Tf binds TFR
allowing iron to enter cell!)
If IC Fe is low, the reverse is true.

30
Q

What lab values do we use to determine a patient’s Fe status?

A

Serum [Fe]
Serum Ferritin
Tf saturation (Fe/TIBC x 100)
TIBC (total iron binding capacity = 2 x Transferrin)

31
Q

If we want more than just lab values, what can we do?

A

Look directly at the disuse to see iron deposits (liver biopsy, bone marrow biopsy, MRI, etc)

32
Q

Define anemia

A

Deficiency of RBCs or hemoglobin in the blood

33
Q

What does iron deficiency anemia look like with labs and RBCs?

A 
Microcytic anemia
	↓Fe  ↓IC Fe  ↓ferritin & ↑transferrin
		↓Serum Fe
		↓Serum ferritin
		↓Tf sat (b/c ↓Fe / ↑transferrin = ↓Tf saturation)
		↑TIBC (b/c ↑transferrin)
34
Q

What can cause iron deficiency anemia?

A

Blood loss
↑physiologic need (pregnancy, growth spurts)
Reduced iron absorption (eg celiac disease)

35
Q

What are clinical manifestations?

A

Fatigue (duh, it’s anemia….)
Koilonychia (spoon nails)
Glossitis (smoothing of tongue)
Angular stomatitis

36
Q

If you see an elevated platelet count, what might that indicate?

A

Nothing. It’s VERY normal for iron deficient patients

37
Q

If you have a patient over 50 (male or post-menopausal female) and they have Fe deficiency anemia, what do you have to do next?

A

LOOK FOR CANCER (that’s boards shit), GI or GU malignancy
This is b/c blood loss could be secondary to tumor, and these patients are
high risk for that

38
Q

What is Anemia of Chronic Disease?

A

Anemia secondary to chronic disease such as inflammation or malignancy
Microcytic OR normocytic anemia

39
Q

What’s the pathogenesis?

A

Infl/malig  ↑IL-6  ↑Hepcidin  ↓Ferroportin ↑IC Fe & ↓EC Fe
↑IC Fe  ↑ferritin and ↓transferrin

Labs:
	↓serum Fe
	↑ferritin
	??? Tf sat (decreased to normal, probably b/c less serum Fe)
	↓TIBC (b/c ↓transferrin)
40
Q

What is the key to differentiating iron deficiency anemia from AOCD?

A

The ferritin! It’s low in IDA

41
Q

How do we treat anemia?

A

Treat the underlying condition (blood loss, malignancy, inflammation, iron deficiency, etc)

42
Q

What is it? What is the pathogenesis?

A

Group of diseases (most are autosomal recessive)
Iron overload due to genetic mutation in activation of Hepcidin
↓Hepcidin  ↑Ferroportin  ↑IC and EC Fe
↑IC Fe  ↑ferritin and ↓Transferrin

	Labs:
	↑serum Fe
	↑serum Ferritin
	↑Tf sat (=↑serum Fe / ↓TIBC)
	↓TIBC
43
Q

What is Type 1 HH?

A

Classic mutation of HFE gene  ↓Hepcidin

44
Q

What is the mutation in HFE gene?

A

C282Y (cysteine to tyrosine substitution at AA 282)

45
Q

Does the HFE defect demonstrate complete or incomplete penetrance?

A

Incomplete. Some homozygous patients do worse than others

46
Q

What is Type 2 HH?

A

Aka Juvenile hemochromatosis

Due to mutation in hemojuvelin (HJV) gene

47
Q

What’s the only one that is inherited in an autosomal dominant manner?

A

Type 4 (mutation in ferroportin)

48
Q

What is the classic triad of HH symptoms (hint due to iron loading)?

A

Diabetes Mellitis
Hepatomegaly
Hyperpigmentation

49
Q

What is treatment for HH?

A

Phlebotomy (removal of blood, decreases iron)

Erik's IHO Week 4 (4 decks)

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