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Y2 - HAEM > Iron deficiency > Flashcards

Iron deficiency Flashcards

1
Q

Which proteins in the body require iron?

A
  • Haemoglobin
  • Myoglobin
  • Cytochrome a,b,c
  • Cytochrome P450
  • Cyclooxygenase
  • Ribonucleotide reductase
  • Succinate dehydrogenase
  • Catalase
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2
Q

What is the lifespan of red cells?

A

120 days

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3
Q

1) How much iron do you need daily to synthesise red cells?
2) But how much do men and women actually need, and why is it lower than the first number?
3) How much iron is provided in a normal diet?

A

1) 20mg a day

2)

  • Men: 1mg a day
  • Women: 2mg a day
  • Iron is recycled when red cells are destroyed

3)

  • 12-15mg a day
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4
Q

1) Which form of iron can you and can’t you absorb?
2) What drink helps and hinder the absorption of iron (the correct one identified from above answer)

A

1)

  • Can absorb Fe2+ ferrous
  • Can’t absorb Fe3+ ferric

2)

  • Orange juice helps
  • Tea hinders
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5
Q

Why is there good iron absorption from eating meat and fish?

A
  • Because you eat it in the haem form
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6
Q

Give the 3 categories of factors affecting iron absorption

A
  1. DIET
  • Increase haem iron in the diet
  • Increase ferrous iron (Fe2+) in the diet
  1. INTESTINE
  • Acid in the duodenum
  • Ligand (meat)
  1. SYSTEMIC
  • Iron deficiency - compensatory increase in absorption
  • Anaemia / hypoxia - compensatory increase in absorption
  • Pregnancy - compensatory increase in absorption
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7
Q

How does iron absorption occur from the gut lumen to the enterocyte to the blood and how do enterocytes alter iron absorption?

A
  • Step 1: Iron absorbed from gut lumen into gut cells
  • Step 2: Iron transferred from gut cells into the bloodstream using ferroportin
  • Hepcidin inhibits ferroportin thereby inhibiting iron absorption
  • Hepcidin is upregulated by iron levels, in a negative feedback mechanism
  • High levels of iron → high hepcidin → inhibits ferroportin → little iron absorption
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8
Q

Where is ferroportin found (3 places)?

A
  1. Enterocytes of the duodenum
  2. Macrophages
  3. Hepatocytes
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9
Q

What is the function of hepcidin?

A
  • Inhibits ferroportin
  • Therefore inhibits iron transport from duodenal enterocytes into blood, with macrophages and from hepatocytes
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10
Q

Once iron has entered the blood from the duodenum, what transports it around the blood?

A

Transferrin

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11
Q

How is iron absorbed into the cells where it is needed from the blood?

A
  • Transferrin-iron complex binds transferrin receptors
  • Then is internalised
  • When pH drops, iron is released and the transferrin receptors are recycled
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12
Q

3 things we measure in hospitals to indicate the circulating iron?

A
  1. Transferrin
  2. Transferrin saturation
  3. Total iron binding capacity
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13
Q

How is an increase in RBC synthesis stimulated by anaemia?

A

Anaemia → Tissue hypoxia → Increase in EPO → Red cell precursors survive, grow and proliferate

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14
Q

What is anaemia of chronic disease caused by?

A
  • In patients who are unwell
  • No known cause
  • Not due to bleeding, marrow infiltration or iron / B12 / folate deficiency
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15
Q

Give 3 laboratory signs of being ill, with one of them having 4 examples

A
  1. CRP (C-reactive protein) increases
  2. ESR (erythrocyte sedimentation rate) increases
  3. Acute phase proteins increase, including:
  • FERRITIN
  • FVIII
  • Fibrinogen
  • Immunoglobulins
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16
Q

Give 4 types of conditions associated with anaemia of chronic disease, giving examples where necessary (don’t worry about accuracy of getting all or even any examples)

A
  1. Chronic infections e.g. TB / HIV
  2. Chronic inflammation e.g. Rheumatoid arthritis / Systemic Lupus Erythematosus
  3. Malignancy
  4. Miscellaneous - e.g. cardiac failure etc
17
Q

What is the pathophysiological cause of ACD (anaemia of chronic disease)?

A
  • Cytokine release such as TNF-alpha or interleukins
  • These do the following things:
  1. Decrease EPO production and thus RBC production
  2. Increase rate of RBC destruction
  3. Increase ferritin (traps it in ferritin)
  4. Inhibit release of iron from cells (traps it in cells)
18
Q

4 causes of iron deficiency with examples?

A
  1. Bleeding - e.g. menstrual blood loss, GI bleeding., pregnancy associated blood
  2. Increased use - in adolescency (fast growth), in pregnancy to provide for foetus
  3. Dietary deficiency - e.g. vegetarianism
  4. Iron malabsorption - e.g. coeliac’s disease
19
Q

When would you really only need to do a full GI investigation to check if this is causing the anaemia?

A
  • If patient is male
  • If woman over 40 / post-menopausal
  • If scanty menstruation
20
Q

What does a full GI investigation to check if it is the cause of anaemia involve?

What investigation is there to see if the cause of the iron deficiency is malabsorption?

A

1)

  • Upper GI endoscopy (of oesophagus, stomach, duodenum)
  • Colonoscopy
  • Duodenal biopsy
  • Check faecal samples

2)

  • Anti-coeliac antibodies to test to see if coeliac’s is the cause
  • And… if coeliac test negative, small bowel meal (give radio-opaque substance)
21
Q

Give 5 laboratory parameters in relation to iron absorption

A
  1. MCV
  2. Serum iron
  3. Ferritin
  4. Transferrin / total iron binding capacity
  5. Transferrin saturation
22
Q

3 causes of low MCV?

A
  1. Iron deficiency
  2. Thalassaemia trait (heterozygous)
  3. Anaemia of chronic disease (low or normal MCV)
23
Q

You find a patient has low Hb and low MCV upon a blood test. How can you determine if this is due to iron deficiency or otherwise? Outline the step-wise process of the other parameters you would look out for and the other possible causes (2 of them) of this you can rule out or like what they would show in each of these

A
  • Serum iron - but low value does not necessarily indicate iron deficiency anaemia, it could still be low in anaemia of chronic disease (but in thalassaemia trait it’s normal)
  • Hb electrophoresis - to confirm thalassaemia trait - shows additional Hb types
  • Ferritin - LOW in iron deficiency and HIGH in ACD. However, it can be unreliable because in cases where people may have both iron deficiency anaemia and chronic diseases, ferritin will appear normal. E.g. bleeding ulcer and rheumatoid arthritis. Rheumatoid arthritis increases ferritin while iron deficiency anaemia lowers it so it appears normal
  • In ACD, CRP and ESR may be raised, however if normal it could still be iron deficient
  • Transferrin - in iron deficiency, transferrin increases. However, low transferrin saturation In chronic disease as you struggle to make proteins therefore transferrin is low / normal - this is the key differentiating marker between iron deficiency and ACD
24
Q

Outline all the results for the parameters you can use to investigate what the cause of the microcytic anaemia may be - with what the results would show for each parameter in each of the 3 possible causes and 1 like mixed one below:

1) Classic iron deficiency
2) Classic anaemia of chronic disease
3) Classic thalassaemia trait
4) Rheumatoid arthritis with a bleeding ulcer

A

1) CLASSIC IRON DEFICIENCY

The haemoglobin, MCV, serum iron and ferritin would be low. Transferrin would be high, and therefore transferrin saturation would be low.

2) CLASSIC ANAEMIA OF CHRONIC DISEASE

The haemoglobin, MCV and serum iron would be low. The ferritin would be high. Transferrin would be normal or low, and transferrin saturation would be normal.

3) CLASSIC THALASSAEMIA TRAIT

The haemoglobin and MCV would be low. However, serum iron, ferritin, transferrin and transferrin saturation would all be normal. Thalassaemia can be confirmed using haemoglobin electrophoresis.

4) RHEUMATOID ARTHRITIS WITH A BLEEDING ULCER

The haemoglobin, MCV, serum iron and transferrin saturation are low. The ferritin is normal because of opposing effects of high due to acute phase protein in RhA but low because of iron deficiency due to bleeding ulcer

25
Q

How do the blood films appear in iron deficiency anaemia?

A
  • Cells appear pale due to little haemoglobin
  • Pencil cells may be present - i.e. long and thin (looks like a pencil) - this is a clear sign of iron deficiency anaemia

Y2 - HAEM (11 decks)

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