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Metabolism > Haemopoiesis, Iron > Flashcards

Haemopoiesis, Iron Flashcards

1
Q

Where does haemopoiesis occur ?

A

Bone marrow
Throughout skeleton in infant
Centrally located in adult (perlvis,sternum,skull,ribs…)

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2
Q

Where do we take trephine biopsy from ?

A

Left posterior iliac crest

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3
Q

What is the origin of haematopoietic cells ?

A

Multipotent haematopoietic stem cell

aka Haemocytoblast

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4
Q

What are the precursors of the haemopoietic cell lines ? which cells do they give ?

A
  • Common myeloid progenitor , gives Erythrocyte, Megakaryocyte,Myeloblast (Granulocytes)
  • Common lymphoid progenitor , gives LB and LT
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5
Q

Which hormone stimulate the production of RBC; Platelets,granulocytes and lymphocytes ?

A
  • RBC : EPO
  • Platelets : Thrombopoietin
  • Granulocytes : GM-CSF
  • Lymphocytes : IL , TNFs
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6
Q

What is the RES ? function ?

A

Reticuloendothelial system
A network in blood and tissues which is part of the immune system containing phagocytic cells
Role is to control and remove damaged/old blood cells

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7
Q

What are the main organs of the RES ?

A

Spleen , liver

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8
Q

Which cells are part of the RES ?

A

Scavenger cells :

macrophage/monocyte/Kupffer cells / histiocytes/Microglial cells in CNS

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9
Q

Normal range of haemoglobin ?

A

130-180 g/L

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10
Q

Normal RBC count ?

A

4.5-6.5 x10^12 /L

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11
Q

Normal Mean Cell Volume ?

A

80-100 fL

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12
Q

Normal WBC count ?

A

4-11 x10^9 /L

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13
Q

Platelet count ?

A

150-400 x 10^9 / L

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14
Q

When does the switch from foetal to adult haemoglobin occur ?

A

3-6 months old

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15
Q

In which state is the iron kept by the Haemoglobin ?

A

Ferrous (reduced)

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16
Q

What happens to the RBC components when broken down by RES ?

A
  • Iron recycled
  • Globin broken down in aa
  • Heme converted Biliverdin >Bilirubin>Liver bind to sugar >Bile>Stercobilin in faeces or Urobilinogen in urine
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17
Q

Describe the control of erythropoiesis in case of low pO2

A

Reduced pO2 detected in Peritubular cells in kidney > Increase EPO production > Stimulation of maturation and release of RBC from marrow > Haemoglobin rises > pO2 rises > EPO falls

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18
Q

What are the 2 main metabolic pathways occuring in the RBC ?

A

Glycolysis : main source of energy

Pentose phosphate pathway / generates NADPH

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19
Q

True or false : We can control how we absorb and excrete iron

A

Wrong , only how we absorb

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20
Q

What are the 4 forms of Available iron ?

A
  • Haemoglobin (2g)
  • Myoglobin
  • Tissue iron (cytochrome mitochondrion)
  • Transported : Serum iron (3mg)
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21
Q

What are the 2 forms of stored iron ?

A

Ferritin: soluble
Haemosiderin: Insoluble , in Macrophages (brown)

22
Q

Approximatively how much iron is lost during a day ?

A

1-2 mg

23
Q

Which iron is better ? why ?

A

Haem iron, because Ferrous form and can enter enterocyte as is

24
Q

How is the non-haem ferric iron is transformed to ferrous ?

A

Converted by gastric acid

25
Q

How is iron absobed and where ?

A
  • Binds to TRANSFERRIN

- Through apical surface in Duodenum and upper Jejunum

26
Q

Which transporter is involved in iron absorption in intestins ?

A

DMT1 : divalent metal transporter

27
Q

How is the iron exported from the enterocyte to blood ?

A

Ferroportin

28
Q

Which transporter help absorb iron from milk ?

A

Lactoferrin

29
Q

How is the iron taken up in cells from blood ?

A

Transferrin receptor (TfR) binds the Iron-transferrin complex

30
Q

Which cell has the highest nbr of TfR ?

A

Erythroid cells

31
Q

What food increases and reduces iron absorption ?

A
  • Increases : Vit C , ascorbic acidic : orange juice

- Decreases: Tea, Chapatis,Antacids

32
Q

How are the dietary iron levels sensed ?

A

By enterocytes’ villi

33
Q

What are the absorption control mechanisms ?

A
  • Regulation of transporters
  • Expression of receptors (HFE, TfR)
  • Hepcidin and cytokines
  • Crosstalk between epithelial cells and macrophages …
34
Q

What is the function of Hepcidin ?

A

Negative regulator of iron absoprtion and release (macrophages)

35
Q

When and where is hepcidin produced ?

A

Made in liver
Excreted by the kidney
When iron overload

36
Q

How does hepcidin work ?

A

Binds to Ferroportin on Enterocyte and Macrophages and induce internalisation and degradation of ferroportin preventing absorption and release of iron in blood

37
Q

what stimulate the rpoduction of hepcidin ?

A

HFE
TfR
Cytokines

38
Q

What are the causes of iron deficiency ?

A
  • Insuficcient intake/absorption

- Increased use : physio(pregnancy) or patho(bleeding)

39
Q

What are the symptoms of iron deficiency ?

A
  • tiredness
  • reduced oxygen carrying : Palor, cant exercise
  • Cardiac symptoms : angina,palpitations…
40
Q

What are the signs of iron deficiency ?

A 
Pallor
Tachycardia
Increased resp rate
Epithelial changes (shiny tongue, around mouth)
Koilonychia (concave nails)
41
Q

What are the blood film features and blood parameters in iron deficiency ?

A

Hypochromic : low haemoglobin content
Microcytic : small RBC and low MCV
Anisopoikilocytosis : change in size and shape
Pencils and target cells
Low serum ferritin ,serum iron and transeferrin saturation
Low reticulocyte haemoglobin content

42
Q

Which test would you do to determine iron deficiency ?

A 
Ferritin levels (reduced levels indicate iron deficiency)
CHR only for functioning iron deficiency but not in thalassaemia
43
Q

Why does raised or normal Ferritin levels do not exclude iron deficiency ?

A

Because it s an acute phase protein so raised if inflammation (acute or chronic), malignancy , liver disease and alcoholism

44
Q

What is the treatment for iron deficiency ?

A
  • Dietary advice
  • Iron tablet
  • Intramuscular injections
  • intravenous iron
  • transfusion only if sever anaemia
45
Q

Why can free iron be dangerous ?

A

Can exceed Transferrin binding capacity
Reduced iron (ferrous) can produce highly reactive HYDROXYL and LIPID RADICALS > Damage lipid membranes,nucleic acid,proteins
Deposit in tissue

46
Q

What is haemochromatosis ?

A

Disorder of iron excess resulting in end organ damage due to iron deposition

47
Q

What are the consequences of haemochromatosis ?

A
  • Liver cirrhosis
  • Diabetes mellitus
  • Hypogonadism
  • Cardiomyopathy
  • Arthropathy
  • Skin pigmentation
48
Q

What is hereditary haemochromatosis due to and treatment ? and inheritance pattern ?

A

Mutation in HFE gene
Autosomal recessive
Too much iron enters cell

Treat : venesection

49
Q

What is the role of HFE protein ?

A

Binds to TfR and compete with Transferrin preventing uptake of Transferrin-Iron complex

50
Q

State a haemochromatosis disease other than Hereditary H

A

Transfusion associated haemosiderosis
in transfusion dependent patient (thalassaemia)
Gradual accumulation

51
Q

State an iron chelating agent

A

Desferriorxamine

Metabolism (6 decks)

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