Iron Absorption, Overload & Malnutrition (AOCD) Flashcards

1
Q

Name the two states of iron

A

Ferric (Fe3+ ) and ferrous forms ( Fe2+ )

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2
Q

Name 3 molecules that require iron

A
  • Haemoglobin (most common)
  • Myoglobin
  • Enzymes eg cytochromes
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3
Q

Why is iron dangerous

A

Can cause oxidative damage & free radical production

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4
Q

How is iron excreted

A

No specific mechanism for excretion.
Passive excretion only e.g. RBC destruction

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5
Q

How does iron absorption compare to iron loss in a healthy person

A

Iron absorption = Iron loss

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6
Q

Where is most iron found in the body

A

RBC Hb

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7
Q

Name 3 dietary factors that can enhance iron absorption

A
  • Meat (HEAM iron - has own transporter)
  • Ascorbic acid/ Vit C (reduces iron to Fe2+)
  • Alcohol
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8
Q

Name 3 dietary factors that can inhibit iron absorption

A
  • Tannins e.g. tea
  • Phytates e.g. cereals, bran, nuts & seeds
  • Calcium e.g. dairy products
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9
Q

Where does iron absorption occur

A

Mainly absorbed into cells of duodenal mucosa

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10
Q

How is iron absorbed

A

Duodenal cytochrome B
- Found in luminal surface
- Reduces ferric iron (Fe3+) to ferrous form (Fe2+)

DMT (divalent metal transporter) -1
- Transports ferrous iron into the duodenal enterocyte

Ferroportin
- Facilitates iron export from the enterocyte

Transferrin
- ferrous form (Fe2+) is oxidised to ferric iron (Fe3+)
- Fe3+ is passed on to transferrin for transport elsewhere

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11
Q

What molecule regulates iron absorption, when is this molecule produced and how does it work

A

Hepcidin (decreases Iron absorption)

  • Produced by liver in response to increased iron load & inflammation
  • Binds to ferroportin and causes its degradation
  • Iron is then trapped in duodenal cells & macrophages
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12
Q

Name 3 measurements used to assess iron status

A
  • Hb concentration (functional iron)
  • Transferrin iron saturation (transport iron/ iron supply)
  • Serum ferritin (storage iron)
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13
Q

How many iron binding sites do transferrin have

A

2

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14
Q

Where do transferrin molecules bind to

A

Tissues expressing transferrin receptors.
Particularly erythroid marrow.
Also macrophages and hepatocytes etc

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15
Q

What is holotransferrin vs apotransferrin

A

Holotransferrin - iron-bound transferrin
Apotransferrin - unbound transferrin

ratio allows transferrin saturation to be calculated

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16
Q

What is the use of ferritin in assessing iron status and why can it be unreliable

A

Tiny amount of serum ferritin reflects intracellular ferritin synthesis – indirect measure of storage iron

Serum ferritin also acts as an acute phase protein so goes up with infection, malignancy etc

17
Q

What are three main iron metabolism disorders

A
  • iron deficiency
  • iron malutilisation (anaemia of chronic disease)
  • iron overload
18
Q

Iron deficiency pathophysiology

A

1) exhaustion of iron stores =>
2) Iron deficient erythropoiesis =>
3) microcytic anaemia =>
4) anaemia symptoms & epithelial changes (severe deficiency )

19
Q

What is anaemia of chronic disease and how would you differentiate it from iron deficiency anaemia

A

AOCD
- Chronic infection/ malignancy/ autoimmune disease
- leading to inflammatory cytokines
- that increase hepcidin and ferritin synthesis
- and decrease erythropoiesis & ferroportin-mediated iron release
- leading to normocytic and then hypochromic, microcytic anaemia

AOCD - normal/ high ferritin, Iron deficiency - low ferritin

20
Q

Anaemia of chronic disease consequences/ pathophysiology

A
  • increases synthesis of ferritin & increased iron storage
  • increases hepcidin & so inhibits ferroportin-mediated iron release
  • inhibits erythropoietin release & erythroid proliferation

=> limited iron availability & so eventually hypochromic, microcytic cells & reduced RBC survival

21
Q

Why is ferritin an acute phase protein

A

It is a protective mechanism to reduce supply of iron to pathogens

22
Q

Anaemia of chronic disease investigations & findings

A
  • Increased inflammatory markers (inflammation)
  • Anaemia (low Hb)
  • Reduced transferrin saturation and serum iron (low iron availability)
  • Normal or increased serum ferritin (iron ‘stuck’)
  • Reduced reticulocytes & erythropoietin (decreased erythropoiesis)
  • Normal or reduced MCV (normocytic or microcytic)
23
Q

Anaemia of chronic disease treatment

A

Treat the cause of inflammation!

24
Q

Iron overload aetiology

A

Primary - hereditary haemochromatosis
Secondary - transfusional, iron overload anaemias

25
Hereditary haemochromatosis aetiology & pathophysiology
- usually due to mutation in HFE gene - decreases synthesis of hepcidin - increases iron absorption - gradual iron accumulation - end-organ damage
26
Hereditary haemochromatosis clinical presentation
- iron overload > 5g @ middle age - Weakness & fatigue - Joint pains & arthritis (joints) - Impotence (pituitary gland -> low sex hormones) - Cirrhosis (liver) - Diabetes (pancreas) - cardiomyopathy (heart)
27
Hereditary haemochromatosis investigations
- genetic testing - blood iron status (high transferrin & ferritin) - fibroscan or liver biopsy to assess for cirrhosis
28
Hereditary haemochromatosis management
Weekly venesection
29
What types of anaemia can cause iron overload
- Massive ineffective erythropoiesis - thalassaemia, sideroblastic anaemias - Refractory hypoplastic anaemias - red cell aplasia, myelodysplasia (MDS)
30
Secondary iron overload treatment
Iron chelating drugs e.g. desferrioxamine
31
Iron overload can be classified into parenchymal overload and macrophage overload. Which is HH (primary) and which is transfusional/anaemia related (secondary)
HH (primary) - parenchymal Transfusional/anaemia related (secondary) - macrophage