Minerals (iron) Flashcards

1
Q

Trace minerals?

A

Less required minerals, but still very important

We require

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2
Q

Major minerals

A

Those present in amount larger then 5g (teaspoon)
Calcium and phosphate in amounts larger then a pound.
Calcium is the most

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3
Q

In NZ we have DEFICIENCY issues with which main three minerals

A

Selenium (brazil nuts)
Iodine
Iron

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4
Q

Functions of Iron

A
  • Binds haemoglobin for O2 transport
  • involved in energy + FA metabolism
  • DNA + collagen synthesis
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5
Q

Why is iron a trace mineral, ie: why is it we only require a small amount on a daily basis?

A

Due to our ability to recycle iron, a process that is very tightly controlled and

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6
Q

How can we lose iron?

A

Blood loss: Menstruation or bleeding

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7
Q

What do we look at when someone has anaemia?

A

1) diet

2) potential causes of bleeding (colon cancer)

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8
Q

What is the daily loss and daily intake of iron?

A

Both 1-2mg

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9
Q

Storage of Iron

A

RBC: 2500mg
Plasma: 4mg
Myoglobin and resp enzymes: 300mg
Body Stores: 1000mg

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10
Q

How is iron lost?

A

Through gut enterocytes. The body stores the iron they don’t want in the enterocytes get “sloughed off”, and are excreted by the GI tract via stools.
Excess iron loss: sweat, skin and urine

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11
Q

Iron dismantling in done by

A

Liver and spleen

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12
Q

Iron recycling cycle

A

Iron-containing hemogloblin in RBC carries oxygen (some losses if bleeding occurs) > Liver (and spleen) dismantle RBC, packages iron into transferrin, and stores excess iron in ferritin (and hemosiderin) > (some excess losses) Transferrin carries iron in blood > (some iron delivered to myoglobin of muscle cells) Bone marrow incorperates iron into haemoglobin of RBCs and stores excess iron in ferritin

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13
Q

What is transferrins role?

A

Transports iron around the body, to bone marrow and muscle, as iron cannot travel freely in the blood

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14
Q

Where does ferritin store iron?

A

Liver, spleen, skeletal muscle (myoglobin), bone marrow (haemoglobin of blood cells)

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15
Q

Steps of iron absorption ?

A

1) iron in food
2) absorbed in the duodenum
3) Mucosal cells in intestine 4)store excess iron in mucosal ferritin

IF NOT NEEDED> excreted in shed intestinal cells

IF NEEDED> ferritin releases iron to mucosal transferrin > transferrin that travels through the blood to rest of body

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16
Q

You find haem iron in? How bio-available is it? Fe2+ or Fe3+? Amount of Daily iron intake?

A

Only Meat
Relatively bioavailable, ~25-30%
Fe2+
~10%

17
Q

Absorbtion path of ‘Haem iron’

A

Haem oxygenase removes the oygen, Fe2+ enter the ‘labile iron pool’ of the cell.
If required by body: released through membrane via Ireg1
If not required: stored as ferritin, ‘Fe3+’ (electron removed)

18
Q

Why is the absorption of non-haem iron more difficult?

A

Because it needs to be reduced (Fe3+ > Fe2+) before it can be absorbed but the gut enterocyte

  • HCl
  • DRAs
19
Q

Non-haem iron is found where? Bioavailability? Fe3+ or Fe2+? Amount of daily iron intake?

A

in non-meat sources (AND meat) like legume/dried fruit
BA= 0-20%
Fe3+
17%

20
Q

DRAs?

A

things we eat that can reduce and solubilise the non-haem iron so it can be absorbed by the enterocyte

21
Q

Once on transferrin, how does iron get into cells?

How does this work in hepatocytes (storage)

A

TfR1 ‘ transferrin receptor proteins’ that allow uptake of iron into cells

Liver: transferrin and TfR1 attach and get endocytosed into cell, iron released, TfR1 back into membrane, transferrin leaves cell.
When the RBCs life is over, it’s dismantled, macrophages remove iron and its released through ferriportin/Ireg1

22
Q

What the master regulator of iron absorption and release??

A

Hepcidin: a hormone produced by the liver

23
Q

How can Hepcidin be affected??

A

Haemocromtosis: genetic condition affected hepcidin and take up way too much iron with no regulation. Which is stored in the liver.
Excessive iron > liver cirrhosis > Liver cancer

Treatment: bleed them every 6 weeks to 3 months

24
Q

Why are vegans and vegetarians at risk?

A

because we absorb heme iron far more effectively.

The only iron they get in the diet is non-haem iron, so they have to eat lots more of it

25
Q

Enhancers of non-haem iron sources

A

Very Stupid Med-students Can Lick acidic HCl

  • Vitamin C (plateus as saturation occurs @ 500mg)
  • MFP factor (meat)
  • Sugars
  • Citric acid
  • Lactic Acid
  • HCl
26
Q

Inhibitors of non-heme iron absorption

A

PHYte or Flight Can Only Protect True Predators

  • Phytates and Fibres (whole grains, beans legumes)
  • Calcium
  • Oxalates (spinach)
  • Phosphorus
  • Tanins (tea stains)
  • Polyphenols
27
Q

How is so little absorbed from spinach, even though it is no high in non-heme iron?

A

Because in spinach you also find oxalates, which inhibit

28
Q

Where else can we get iron not from meat/food

A

1) Contamination iron (good for developing countries)

2) Iron supplements (often with VitC) in high amounts can cause GI symptoms so people stop using them

29
Q

When do we need more iron? Who needs more?

A

In stages of GROWTH

  • bottle-fed babies
  • adolescents
  • pregnant women
  • vegans/vegetarians
  • endurance sportspeople
30
Q

Babies iron needs?

A

babies are born with large aounts of iron, which lasts till ~6 months, then needs increase
Breastfed babies: need less, as breast milk iron is extremely well absorbed (heme)
Bottle-fed babies: need more, as infant formula (static fluid) only contains non-heme

31
Q

How to diagnose stage 1& 2 iron deficiency? Symptoms of all stages?

A

The HB would be normal (stage 3), so you need a FULL BLOOD COUNT to see that transferrin and ferritin were low
Symptoms: shorter in breath, dizzy when standing (so hard to really know as this is only really noticeable in stage 3

32
Q

What do iron deficiency anaemic RBC look like?

A

‘Microcitic anaemia’: Pale, small RBC

33
Q

Prevelance of ID

A

1/3 of the world
of this (1/3 due to diet)
common in young women and children (developing countries)

34
Q

Iron is vital for growth and

A
  • myelination
  • neuronal growth & differentiation
  • neurotransmitter regulation
35
Q

Iron in pregnancy

A

During pregnancy women’s blood volume significantly increases, they need more iron to make more RBC and ensure babies development
RDI: 27mg/d
lots of women get put onto iron during pregnancy (but can be detered by GI symptoms)

36
Q

Stage 1 of ID

A

1)Depleted Storage iron (levels start to get low)

Low serum ferritin of less the 15mcg per l

37
Q

Stage 2 of ID

A

2) Iron restricted erythropoiesis (not enough iron to put on transferrin)
low serum transferrin saturation of less then 16%

38
Q

Stage 3 of ID

A

3) Iron Deficiency Anaemia (not able to make enough RBC)

less then 120g per L