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Haematology > Iron deficiency and anaemia > Flashcards

Iron deficiency and anaemia Flashcards

1
Q

Give examples of proteins in the body that require iron

A
  • Hb
  • myoglobin
  • ribonucleotide reductase
  • cyclooxygenase
  • succinate dehydrogenase
  • catalase
  • cytochrome a,b,c
  • cytochrome p450
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2
Q

Where is most of the iron ion in the body stored?

A

Hb

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3
Q

What is the role of iron in Hb?

A

It holds on to the oxygen

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4
Q

What happens if a person has low iron?

A

They have low haemolgobin and become anaemic and develop symptoms and signs.

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5
Q

What is haemoglobin made of and describe the structure?

A

Composite protein - made of globin chains and a haem group (which contains iron)
Each haem group is associated with a single globin chain. In the final Hb molecule, the haem is near the surface.

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6
Q

Describe the structure of heam

A

A ring of carbon, hydrogen and nitrogen atoms and in its centre is an iron atom in the ferrous (Fe2+) state.

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7
Q

How much iron is needed to remake red blood cells every day?

A

20mg, but there is no way we would be able to absorb this quantity daily. Fortunately iron is recycled when red cells are broken down.

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8
Q

Where is iron lost from?

A

From cells of the skin and gut (desquamated cells). Iron is also lost in bleeding (particularly menstruation, but also pathological bleeding)

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9
Q

How much iron do men and women need daily?

A

men - 1mg

women - 2mg

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10
Q

Which foods contain iron?

A

meat, fish, vegetables, whole grain cereal and chocolate

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11
Q

What is the difficulty in getting iron from food?

A

It is hard to absorb iron, most of the iron eaten isn’t absorbed. Iron can only be absorbed in the Fe2+ state not Fe3+.

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12
Q

How can absorption of iron be improved?

A

orange juice helps to increase Fe2+ but tea increases Fe3+

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13
Q

Why are meats and fish good sources of iron?

A

Iron has already been incorporated in the haem group

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14
Q

What are the factors affecting the absorption of iron?

A

Diet: increase haem iron in the diet and ferrous iron

Intestine: acid in the duodenum, the ligand (meat)

Systemic factors: iron deficiency, anaemia/hypoxia and pregnancy (more is absorbed for compensation)

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15
Q

How does the gut cell alter iron absorption?

A

STEP 1: iron is absorbed from the gut lumen into cells.

STEP 2: Iron needs to be transported by ferroportin – levels of transport are regulated by hepcidin.

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16
Q

If iron levels are high, what happens to hepcidin levels?

A

Also increases to block the ferroportin and stop iron absorption.

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17
Q

Where is ferroportin found?

A
  1. Enterocytes of the duodenum
  2. Macrophages of the spleen, which extract iron from old or damaged cells
  3. Hepatocytes
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18
Q

What is hepcidin?

A

The master controller of iron homeostasis. High hepcidin leads to a decrease in iron entering the blood from the duodenum, macrophages and from hepatocytes.

19
Q

What is ferroportin and hepcidin and their interaction?

A

Ferroportin – this is the iron transporter protein. This is controlled by a peptide hormone: hepcidin (25 amino acids).
Hepcidin binds to and induces degradation of ferroportin. When this happens iron is stuck in the enterocytes and when it is shed the iron is effectively lost from the body.

20
Q

What happens to Fe once it enter the blood?

A
  • It binds to transferrin protein
  • Generally, transferrin is not fully saturated with iron (only 20-40% saturated with iron)
  • In hospitals, we record the transferrin, the total iron binding capacity, and the transferrin saturation
  • It cannot transport iron inside the cells where it is needed
  • Transferrin-iron interacts with the transferrin receptor and the whole transferrin complex is internalised
  • As the pH drops iron is released and transferrin receptors are recycled
21
Q

What is the risk of having too much iron?

A

Iron is potentially toxic and insoluble.

Iron binding proteins and transport systems maintain iron in a soluble and non-toxic form.

22
Q

Where is erythropoietin made?

A

Kidney (mainly) and liver

23
Q

What happens in anaemia to erythropoietin?

A

Tissue hypoxia -> increased erythropoietin -> acts on red cell precursors

24
Q

What is anaemia of chronic disease?

A
  • Anaemia in patients who are unwell
  • It does not result from bleeding, marrow infiltration of disease or iron/B12/folate deficiency
  • No obvious cause other than that the patients are unwell
25
Q

What are the laboratory signs of being ill?

A
  • C-reactive protein increases during illness
  • Erythrocyte sedimentation rate – increased ESR due to increased inflammatory proteins
  • Acute phase response increases in: ferritin, Factor VIII, fibrinogen and immunoglobulins
26
Q

What are the associated conditions of ACD?

A
  • Chronic infections (TB/HIV)
  • Chronic inflammatory disorders (rheumatoid arthritis, systemic lupus erythematosus)
  • Underlying malignancy
  • Miscellaneous things (e.g. someone with cardiac failure may get ACD)
27
Q

What causes ACD?

A
  • ACD is underpinned by cytokine release that occurs in patients that are unwell
  • Cytokines prevent the usual flow of iron from the duodenum to the red cells -> block iron utilisation
  • Cytokines include TNF alpha and interleukins

Cytokines do several things:

  • Stop erythropoietin increasing
  • Stop iron flowing out of cells
  • Increase production of ferritin
  • Increase death of red cells

Therefore, you make less red cells, and more red cells die, so there is less availability of iron (it is stuck in the cells or with ferritin).

28
Q

What is the commonest cause of anaemia?

A

iron deficiency

29
Q

Why does ACD anaemia differ to normal anaemia and how? (why is it persistent in ACD?)

A

In normal anaemia, erythropoietin increases in order to boost red cell production. In ACD however, this increase in erythropoietin is blunted – this is one of the things that contributes to a persisting anaemia

30
Q

What are the causes of iron deficiency?

A
  1. Bleeding (most common) – e.g. menstrual blood loss, GI bleeding and pregnancy-associated blood loss
  2. Increased use – e.g. rapid growth (e.g. in adolescence), pregnancy (the baby takes iron preferentially)
  3. Dietary deficiency – e.g. in vegetarianism
  4. Malabsorption of iron– e.g. in coeliac disease
31
Q

In which patients should tests not be done for iron deficiency? (to find cause)

A

n a menstruating woman over 40, or someone with heavy periods or multiple pregnancies who has no GI symptom

32
Q

When is a full GI investigation done for iron deficiency?

A
  • The patient is male
  • The patient is a woman over 40, or a post-menopausal woman
  • The patient is a woman with scanty menstrual loss
33
Q

What is part of the full GI investigation?

A
  • Upper GI endoscopy (oesophagus, stomach and duodenum)
  • Take a duodenal biopsy
  • Colonoscopy
34
Q

What happens if there are no GI abnormalities and no antibodies for coeliac disease?

A

You can look at the small bowel. It is unusual to bleed in the small bowel. Give patient a small bowel meal (drink a radio-opaque substance) and follow through.

35
Q

What are some laboratory parameters that can be used?

A
  • Mean cell volume (MCV)
  • Serum iron
  • Ferritin
  • Transferrin (= total iron binding capacity, TIBC)
  • Transferrin saturation
36
Q

If a person has a low Hb and low MCV, do they have iron deficiency?

A

no as there are many causes of low MCV

37
Q

What are the causes of low MCV?

A
  1. Iron deficiency
  2. Thalassaemia trait (heterozygous)
  3. Anaemia of chronic disease (low or normal MCV)
38
Q

In classic iron deficiency which parameters would be affected and how?

A
  • Hb, MCV, serum iron and ferritin would be low.

- Transferrin would be high, and therefore transferrin saturation would be low.

39
Q

In classic anaemia of chronic disease which parameters would be affected and how?

A
  • Hb and serum iron would be low
  • MCV would be normal or low
  • Ferritin would be normal or high
  • Transferrin would be normal or low, and transferrin saturation would be normal.
40
Q

In classic thalassaemia trait which parameters would be affected and how?

A
  • Hb and MCV would be low
  • However, serum iron, ferritin, transferrin and transferrin saturation would all be normal
  • This can be confirmed using haemoglobin electrophoresi
41
Q

In rheumatoid arthritis with a bleeding ulcer which parameters would be affected and how?

A
  • Hb, MCV, serum iron and transferrin saturation are low

- The ferritin is normal

42
Q

Why may a blood film be used in iron deficiency investigations?

A

Additional tests include looking at the blood film (small, pale, strand shapes including pencil cells) and bone marrow.

43
Q

What would a blood film in iron deficiency look like?

A
  • Cells are very pale – they are not easy to see because they don’t have much haemoglobin
  • Red cells are normally round – pencil cells can be seen (long and thin)
  • If pencil cells are seen, the patient has iron deficiency

Haematology (11 decks)

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