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Tp2. Metabolism, Endocrinology and Haemology > Iron Metabolism And Microcytic Anaemia > Flashcards

Iron Metabolism And Microcytic Anaemia Flashcards

1
Q

What are the forms of Microcytic anaemia

A

T : thalassemia
A : anaemia of chronic disease (sometimes)
I : iron deficiency
L : lead poisoning
S : sideroblastic anaemia

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2
Q

What is important about the body’s response to iron

A

The body has no way of extracting or excreting iron

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3
Q

What form does Iron need to be in for it to be absorbed

A

The ferrous form
Fe2+

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4
Q

What is the ferrous and the ferric form of iron

A

Ferric = Fe3+
Ferrous = Fe2+

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5
Q

Where does iron absorption occur

A

In the duodenum and the upper Jejunum (the early small intestine)

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6
Q

What are the forms of iron in food and which would be more readily absorbed

A

Non-haem and haem sources of iron
Haem = liver, kidney, beef
Non-haem = fortified cereals, raisins, beans

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7
Q

What form does iron need to exists in the body

A

Cannot be in the free form
Needs to be chelated (bound to a complex)

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8
Q

What factors could increase the dietary requirements of irons

A

Menstrual losses
Endurance running
Haemorrhage
Inflammatory bowel disease (as iron would be absorbed here)

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9
Q

What are the iron daily requirements

A

Men : 8.7mg
Women : 14.8mg

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10
Q

What are the three regulators of iron

A

Diet
Store
Bone marrow

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11
Q

What do the duodenal crypt cells do

A

Sense the status of iron through transferrin and the gene complex

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12
Q

How would iron be absorbed in the apical cells

A

Fe3+ reduced to fe2+ (so can be absorbed)
Enters through the DMT1
Transferred to ferritin
Ferritin can go to ferroportin
Ferroportin can be inhibited by hepcidin
Hephaestin oxidises fe2+ back to fe3+
Transported as transferrin

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13
Q

How would iron be taken up in the cells

A

From dietary uptake
Transferrin (containing the fe3+) attaches to the transferrin receptor
Moves in (Endocytosis)
To the endosome
Released by the acidic micro environment
Goes out the DMT1 and reduced to fe2+ (in the cytosol)
Goes to ferritin, the ferroportin or the mitochondria

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14
Q

What is iron used for in the mitochondria

A

Cytochrome enzymes

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15
Q

What is ferritin

A

Store of iron in the cells

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16
Q

What is ferroportin

A

Transports iron out the cell

17
Q

What is transferrin

A

Binds to iron and allows it to be transported in the blood

18
Q

What is haemosiderin

A

What excess iron is stored in
Clumps of ferritin, denatured protein and lipids
Stored in macrophages in the liver and spleen mainly

19
Q

What is the difference between ferritin and haemosiderin

A

Ferritin = soluble
Haemosiderin = insoluble clumps of ferritin, denatured protein and lipids
Builds in the macrophages in the liver and spleen

20
Q

What factors have a negative impact on the absorption of non-haem iron

A

Tannins (from tea)
Antacids (gaviscon)
Phytates (chapattis, pulses)
Fibre

ALL CAN BIND TO THE NON-HAEM IRON IN THE SMALL INTESTINE AND WOUOD REDUCE ITS ABSORPTION

21
Q

What factors have the positive influence of the non-haem iron absorption

A

Vitamin c
Citrate

Reduces to ferrous form
Stops formation of the insoluble iron compounds

22
Q

What cells take up the iron for it to be recycled

A

Macrophages
Mainly splenic and Kupffer cells

23
Q

What happens to the iron when the red blood cells have been broken down by the macrophages

A

Iron released and exported in the blood as transferrin
Or
Taken up by the ferritin stores in the cell

24
Q

What other protein interacts with the transferrin receptor (so that iron can be taken up by the cells)

A

High iron protein (HFE)

25
Q

Where is hepcidin produced

A

The liver

26
Q

What does hepcidin do

A

Internalisation and degradation of the ferroportin
So would have less iron released to blood

27
Q

What circumstances causes the levels of hepcidin to increase

A

The increase in the erythropoiesis activity
So increase in the red blood cell production

28
Q

Why might hepcidin increase with inflammation

A

Stops release of iron which can be used by the bacteria

29
Q

Which of the following facilitates iron absorption
A) iron being bound to a haem molecule
B) iron being in the ferric form
C) presence of fibre in the diet
D) presence of the ascorbic acid in diet
E) copper, zinc and magnesium in the diet

A

A) iron being bound in a haem molecule
D) presence of the ascorbic acid in diet (would have a positive impact on the intake of the non-haem iron sources)

30
Q

What are the signs of the iron deficiency

A

Spoon nails
Angular glossitus or cheilitis
Glossy tongue

31
Q

How would you test for an iron deficiency

A

Ferritin (can have an increase in the ACD)
CHr (reticulocyte haemoglobin content) showing the amount of mature red blood cells

32
Q

What is the issue with using the CHr (reticulocyte haemoglobin content) for testing iron deficiency

A

Postitive is when is low (would be low in the inflammatory response)
BUT WOULD ALSO BE LOW IN THALASSEMIA

33
Q

Why is excess iron bad

A

Can lead to oxidative stress
Fenton’s reaction
Fe2+ and h2o2 ———— OH radical (hydroxyl)
Fe3+ and h2o2 ———— OOH radical (hydroperoxyl)

Why the bacteria want the iron

34
Q

What is transfusion associated haemosiderosis

A

Excess iron from too many transfusions
400ml of blood = 200mg of iron
Can use the chelating agents (e.g. desferrioxamine)

35
Q

What can the build up of iron cause

A

Liver cirrhosis
Increased skin pigmentation
Diabetes
Hypogonadism
Cardiomyopathy

36
Q

What is hereditary haemochromatosis

A

Autosommal recessive
Mutation in the HFE gene (chr 6)
Normally would reduce the transferrin receptors affinity for iron
Mutation would not be able to regulate
So would have high uptake
Iron would then build in the organs
Would lead to the organ damage

37
Q

How do you treat hereditary haemochromatsis

A

Venesection
Draining some of the blood in the body

38
Q

Why is there only one way to manage hereditary haemochromatosis

A

Because the body would no be able to excrete iron
So would only be able to remove through the draining of blood

Tp2. Metabolism, Endocrinology and Haemology (16 decks)

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