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Semester 1 - Metabolism > Iron Metabolism > Flashcards

Flashcards in Iron Metabolism Deck (31)
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1
Q

What is iron used for in the body?

A

– Transports and stores oxygen
– Integral part of many enzymes
including energy metabolism, neurotransmitter production, collagen formation and immune system function

2
Q

Why is iron content in the body carefully controlled?

A

Have no mechanism for excreting iron – must maintain a fine balance between absorption and loss

3
Q

Name the sites containing active iron in the body

A
��-- Haemoglobin
�-- Myoglobin: oxygen
reserve in muscles
��--Tissue Iron:
 enzyme systems, cytochromes
��-- Transported iron-’serum iron’
4
Q

Give two inactive stores of iron

A

�Ferritin – soluble

��Haemosiderin – Macrophage iron, Insoluble

5
Q

Where do you find the majority of iron in the body?

A

Most in haemoglobin
Stores of iron (liver)
Less in myoglobin

6
Q

Where is haem iron and non-heam iron found in the diet?

A

Haem iron – meat

Non-haem iron – cereal and vegetables

7
Q

What are the two form of iron and which is the correct form to be absorbed by the body?

A

Fe2+ – ferrous form in meat, easier to absorb

Fe3+ – ferric form in veg and cereals must be reduced by stomach acid to be absorbed

8
Q

Where does the majority of iron absorption take place?

What facilitates this in the apical surface?

A

Duodenum and upper jejunum by enterocytes (epithelial cells in jejunum and duodenum)

Transferrin brings two Fe molecules in per transferrin

9
Q

What protein exports iron out of the blood?

A

ferrroportin

10
Q

Describe the process of iron absorption into enterocytes

A

Stomach acid reduces Fe3+ to Fe2+
Transferrin transports two Fe2+ into enterocytes by endocytosis. Can be stored in RBC as ferritin.
Then enters blood by ferroportin, where it is transported to the liver for storage or used by Hb

11
Q

What affect does vitamin C have on iron absorption?

A

Enhances iron absorption

12
Q

How is iron taken into red blood cells?

A

by binding of Iron-transferrin complex to transferrin receptor (TfR)
Erythroid cells contain the highest number of TfRs

13
Q

What can be used as a good level of functional iron levels?

A

soluble TfR (sTfR) is a good indicator of functional iron levels

14
Q

What does the regulation of iron absorption depend on?

A

dietary factors, body iron stores and erythropoiesis

15
Q

What are the major mechanisms for the control of iron absorption?

A

Transporter regulation (can be up or down regulated)
Receptor expression
Crosstalk between epithelial cells and macrophages (other cells)
Hepcidin – tissue derived factor

16
Q

What does hepcidin do?

A

– negative regulator of iron absorption
by degrading ferroportin, a protein involved in moving iron out of cells
This prevents iron absorption from gut ane iron release from macrophages

17
Q

Describe hepcidin synthesis

A

– Secreted by the liver and excreted by the kidneys
�– Synthesis increased in iron overload
��– Transgenic mice constructed to over-express hepcidin died shortly after birth with iron deficiency (negative regulator)
��– Hepcidin production is decreased by high erythropoietic activity

18
Q

Where dose the majority of the iron in the body come from?

A

Recycling of iron in body (RBC) accounts for about 80%

19
Q

How do macrophages acquire iron?

A

Macrophages ‘eat’ old senescent RBCs

20
Q

Why are iron deficiencies important to recognise?

A
Most common nutritional disorder worldwide
Is a symptom of:
1. Insufficient intake/poor absorption 
2. Increased use
-- physiological eg pregnancy 
-- pathological eg bleeding
21
Q

What are some physiological affects of anaemia?

A
tiredness
reduced oxygen carrying capacity (pallour, reduced exercise tolerance)
CCF
shortness of breath
palpitations
22
Q

How can you confirm iron deficiency?

A

– Low Hb
– Small RBC and low MCV (mean cell volume)
��– Pencil cells, hypchromia, microcytosis, target cells
��– Low serum ferritin, serum iron (transferrin bound iron) and %transferrin saturation, raised TIBC (total iron binding capacity, measures transferrin levels)

23
Q

Why is serum ferritin important to look at?

A

Correlates with stores of iron in the body

24
Q

What is the most important thing to measure in iron deficiency?

A

Ferritin is the single most important measure of iron status
Reduced levels –> iron deficiency
High/normal levels –> don’t rule out iron deficiency

25
Q

When can ferritin levels be increased?

A

ferritin increased with acute or chronic
inflammation, malignancy, liver disease, and
alcoholism

26
Q

What are the main methods of iron replacement?

A

– Oral, Diet
– Supplements……
Iron replacement
����– Intravenous – anaphylaxis
����– Intramuscular

27
Q

Describe the pathology of iron excess

A

Exceeds binding capacity of transferrin
– increased free iron in the blood which is dangerous as it can produce free radical which damage lipid, protein, DNA etc

28
Q

Define haemachromotosis

A

– Disorder of iron excess resulting in end organ damage
Causes c��irrhosis, diabetes mellitus, hypogonadism, cardiomyopathy, and arthropathy and skin pigmentation
��– Normal body iron 2-3g; damage when reaches 10-15g

29
Q

Describe hereditary haemochromotosis

A

Autosomal recessive
Four genes can cause it while three interact normally
Treat with venesection (remove blood to remove iron then retransfuse in)

30
Q

What is transfusion associated aemosiderosis?

A

Transfusion dependent anaemias such as
thalassaemia, myelodysplasia
There is a gradual accumulation of iron
Treat with iron chelating agents eg desferrioxamine which delay but don’t stop inevitable effects of iron overload

31
Q

Give some tests which can confirm iron overload

A

– Raised serumferritin
��– Increased % transferrin saturation
����– Genetic testing for mutations of HFE gene
��– Evidence parenchymal iron overload on liver biopsy
��– Amount of iron removed by venesection