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MEH > 5. Heamopoiesis & Iron > Flashcards

5. Heamopoiesis & Iron Flashcards

1
Q

What are the main sites of haemopoiesis in adult marrow?

A

Pelvis, sternum, ribs, vertebrae, skull

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2
Q

What is the precursor for all of the blood cells?

A

Haematopoietic stem cell

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3
Q

Which cytokines trigger development of lymphocytes?

A

Interleukins

TNF

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4
Q

Which protein triggers myeloid cell development?

A

GM-CSF

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5
Q

Which hormones trigger erythrocyte and platelet development?

A

EPO - erythrocyte

Thrombopoietin (TPO) - platelet

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6
Q

In addition to GM-CSF, what other protein drives differentiation of myeloblasts?

A

G-CSF

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7
Q

What cells make up the RES?

A

Phagocytic cells - types of macrophages and neutrophils

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8
Q

What are the main organs of the RES?

A

Liver and spleen

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9
Q

What are the functions of the RES?

A
  • remove senescent or damaged blood cells from circulation

- inflammatory and immune responses

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10
Q

What is the structure of an erythrocyte?

A

Biconcave, flexible disk with important membrane proteins in its bilayer. No nucleus.

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11
Q

What is the significant of the structure of RBC’s, what happens if this is altered?

A

Allows squezing through tiny microvasculature.

If membrane is damaged, the cells become weak and vulnerable to breaking down.

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12
Q

Why are the protein components of the erythrocyte membrane so important?

A

If they are altered, it will change the shape of the RBC and alter function.

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13
Q

What is the structure of haemoglobin?

A

Tetramer - 2 alpha chains and 2 beta chains

4 haem molecules

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14
Q

When does the switch from foetal to human haemoglobin occur, how does this alter the structure?

A

3-6 months

Fetal Hb has 2 gamma chains which are swapped for beta chains in adult Hb.

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15
Q

What is the average lifespan of a RBC?

A

120 days

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16
Q

What type of stem cell are haemoatopoietic stem cells?

A

Multipotent

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17
Q

Which cells are granulocytes?

A

Basophils, neutrophils and eosinophils

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18
Q

Where is EPO produced? What is it stimulated by?

A

Interstitial peritubular cells in the kidney in response to hypoxia.

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19
Q

What is the name of immature red blood cells which are released into the circulation?

A

Reticulocytes - 1/2 days to become mature

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20
Q

What does a reticulocyte count provide useful information about?

A

Estimate of the amount of erythropoiesis occurring in a patents bone marrow.

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21
Q

Which 2 enzyme deficiencies are particularly important in eryrthrocytes, why?

A
  1. Pyruvate kinase - no mitochondria so rely on glycolysis
  2. G6PDH - pentose phosphate pathway to generate NADPH
    Genetic abnormality affecting these pathways means the membrane cannot be maintained and the cells are broken down, ANAEMIA.
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22
Q

How is haemoglobin metabolised?

A

Globin - degraded into amino acids

Haem - metabolised to bilirubin, which is removed in the liver, conjugated and secreted in bile.

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23
Q

How do bacteria in the colon affect bilirubin excretion?

A

Metablism bilirubin into urobilinogen which is oxidised into urobilin and stercobilin.

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24
Q

Which bilirubin metabolite can be reabsorbed, what is its fate?

A

Urobilinogen is reabsorbed and processed by the kidneys, giving urine its yellow colour.

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25
Q

What clinical sign results from excess erythrocyte breakdown, what metabolite is responsible?

A

Jaundice - excess bilirubin

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26
Q

How can kidney failure lead to anaemia?

A

Decreased EPO production

27
Q

Which 4 proteins in the erythrocyte bilayer are important in maintaining struture? What is their function?

A 
Spectrin
Ankyrin
Band 3
Protein 4.2
“vertical interactions” between the cytoskeleton and the lipid bilayer of the plasma membrane
28
Q

What condition results from mutation in these membrane proteins, what structural change takes place?

A

Hereditary spherocytosis - lose biconcave shape and flexibility.

29
Q

What form is iron present in within haem?

A

Ferrous state (Fe2+)

30
Q

Why must iron uptake and absorption be carefully regulated?

A

There is no mechanism for excretion iron
Free iron exceeds transferrin capacity and reduced free Fe2+ catalyses the production of free radicals (fenton reaction).

31
Q

What is iron essential for within the body?

A
  • Haemoglobin and Oxygen transport

- Enzymes - energy metabolism, collagen formation, NT production, immune system

32
Q

Which 2 forms is iron stored as?

A

Ferritin (soluble)

Haemosiderin (insoluble)

33
Q

Where are the highest concentrations of stored iron found?

A

Liver, spleen and bone marrow

34
Q

Which cells can store iron?

A

All cells have the ability to sequester iron either as ferritin or haemosiderin.

35
Q

Why is most of the bodies iron requirement met by?

A

80% come from recycling from old RBC’s

Only small amount from the diet

36
Q

Where does iron absorption occur in the GI tract?

A

Duodenum and upper jejunum

37
Q

Why is meat a better source of dietary iron on that pulses and nuts?

A

Haem iron is already in the ferrous form (Fe2+), whereas non-haem iron is ferric (Fe3+) and must be reduced before absorption can happen.

38
Q

What transport protein is iron bound to in the blood?

A

Transferrin

39
Q

Once Fe2+ is taken up into enterocytes, what its fate?

A

Storage as ferritin or release into circulation via ferroportin protein.

40
Q

Once in the blood, what happens to most of the Fe2+?

A

Transported to bone marrow for erythropoiesis

Taken up by macrophages as a storage pool.

41
Q

Which receptor is needed for iron uptake into cells, which cells are the present on in large numbers?

A

Transferrin receptor

Erythroid cells

42
Q

How does Vitamin C affect iron absorption in GI tract?

A

Ascorbic acid, low pH promotes iron absorption.

43
Q

How do chapatis, tea and antacids affect iron absorption in GI tract?

A

Chelating agents, inhibit absorption.

Antacids increase pH.

44
Q

Which peptide negatively regulates iron absorption, where is it produced?

A

Hepcidin, produced in the liver.

45
Q

How does hepcidin affect iron levels?

A

Binds to ferroportin,causing degradation.
- Inhibits gut absorption
- Inhibits macrophages release of recycled iron.
Increased non-functional iron (cannot be used).

46
Q

What conditions would hepcidin synthesis be increased?

A

Iron overload

47
Q

What conditions would hepcidin synthesis be decreased?

A

High erythropoetic activity

48
Q

What symptoms are associated with iron deficiency?

A

Tiredness, pallor, decreased exercise tolerance, palpitations

49
Q

What signs are associated with iron deficiency?

A

Pallor, tachycardia, increased RR

50
Q

What physiological and pathological reason might explain iron deficiency?

A

Physiological - pregnancy

Pathological - bleeding

51
Q

What is the most commonly used measure of iron status?

A

Serum ferritin

52
Q

Why might serum ferritin be inaccurate?

A

Acute phase protein, so increased with inflammation, malignancy, liver disease and alcoholism.
Increased levels do not rule out iron deficiency, but low levels suggest an iron deficit.

53
Q

What other parameter is recommended by NICE to identify iron deficiency, how does it differ to ferritin?

A

CHR - remains low during inflammatory response.

54
Q

Which patients would it be inappropriate to measure CHR?

A

Patients with thalassaemia - CHR is lowered in this setting.

55
Q

What are 2 causes of haemochromatosis?

A
  1. Hereditary haemochromatosis

2. Transfusion associated heamochromocytosis

56
Q

Why is haemochromatosis a cause for concern?

A

Iron accumulates in tissues and organs, disrupting function.

57
Q

Which gene is mutated in hereditary haemochromatosis, what is it’s inheritance pattern?

A

HFE gene

Autosomal recessive

58
Q

How does a mutation in HFE gene cause iron excess?

A

HFE protein usually competes with transferrin for binding to TFR. Mutated HFE can no longer bind, so transferrin has no competition and iron uptake increases.

59
Q

How is hereditary haemochromatosis treated?

A

Venesection (phlebotomy)

60
Q

Which patients are likely to be at risk of transfusion dependent haemochromatosis, why?

A

Patients with thalassaemia and myelodysplasia as they are transfusion-dependent anaemias.

61
Q

What do patients with hereditary haemochromatosis present with and why?

A

Liver cirrhosis, adrenal insufficiency, heart failure, arthritis or diabetes.
The organs most susceptible to iron overload and damage are the liver, adrenal glands, heart, joints and pancreas.

62
Q

Which transporter facilitates uptake of ferrous iron (Fe2+) from the intestinal lumen into enterocytes?

A

DMT1

63
Q

Which abnormality in white blood cells would you expect to observe in a patient suffering from asthma attack?

A

Eosinophilia

64
Q

Which drugs would be most likely to precipitate haemolysis in a patient with glucose-6-phosphate dehydrogenase deficiency?

A

Anti-malarials

MEH (19 decks)

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