Iron Flashcards

1
Q

When RBCs are broken down, what stores the iron?

A

macrophages

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2
Q

Where does iron absorption mainly occur?

A

duodenum

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3
Q

What enhances iron absorption?

A

haem in meat
asorbic acid - reduces iron to Fe 2+ form
alcohol

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4
Q

What inhibits iron absorption?

A

tannins - tea
phylates - cereals, bran, nuts, seeds
calcium - dairy products

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5
Q

What is the role of duodenal cytochrome B?

A

reduces ferric iron Fe3+ to Fe2+

found on the luminal surface

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6
Q

What is the role of DMT?

A

transport ferrous iron into the duodenal enterocyte

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7
Q

What is the role of ferroportin?

A

facilitates iron export from the enterocyte and passes it to transferrin

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8
Q

What regulates iron absorption?

A

Hepcidin

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9
Q

What is the role of Hepcidin?

A

binds to ferroportin and degrades it meaning iron is trapped in the duodenal cells

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10
Q

When is Hepcidin upregulated?

A

more iron - more hepcidin produced
malignancy
infection

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11
Q

Where is Hepcidin produced?

A

liver

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12
Q

What are the two transferrin binding sites?

A

apo-transferrin - empty

holo-transferrin - full

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13
Q

Where in the body are there lots of transferrin receptors?

A

erythroid bone marrow

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14
Q

If there is iron deficiency, which transferrin binding site will be more abundant?

A

apo-transferrin

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15
Q

What is your maximum dietry iron absorption per day?

A

4-5mg

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16
Q

How does anaemia of chronic disease come about?

A

inflammatory cytokines cause increased synthesis of ferritin mRNA (increases storage)
increased hepcidin will degrade ferroportin mediated release of iron
this results in an impaired iron supply to marrow erythroblasts and eventually hypochromatic red cells
basically to starve bacteria of iron

17
Q

What are the two types of iron overload?

A

primary - hereditary haemochromatosis

secondary - transfusional and iron loading anaemias

18
Q

What is the problem with iron overload?

A

it ends up in tissues which causes oxidative harm

19
Q

What is hereditary haemochromatosis?

A

HFE gene mutation - incomplete penetrance

decreased Hepcidin synthesis causing increased iron absorption

20
Q

How does hereditary haemochromatosis present?

A

usually middle aged or later
iron overload >5g
non specific symptoms: weakness, fatigue, joint pains, impotence
long term: arthritis, cirrhosis, diabetes, cardiomyopathy

21
Q

What are the diagnostic features of hereditary haemochromatosis?

A

transferrin saturation >50%

serum ferritin >300g/l in men or >200g/l in women

22
Q

What is the treatment of hereditary haemochromatosis?

A

weekly venesection - want ferritin <20

screen first degree relatives

23
Q

What causes secondary iron overload?

A

massive ineffective eryhropoeisis - B thala major, sideroblastic anaemia
refractory hypoplastic anaemias - bone marrow doesnt work - myelodysplasia and red cell aphasia

24
Q

How is secondary iron overload treated?

A

iron chelating agents - desferrioxamine