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Metabolism, Endocrinology & Haematology > Haematapoesis, Erythropoiesis & Iron > Flashcards

Haematapoesis, Erythropoiesis & Iron Flashcards

1
Q

Where are RBCs platelets and most WBCs produced?

A

Bone marrow

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2
Q

Which areas of bone are responsible for haematapoesis in adults and in children?

A 
Adults: 
Pelvis 
Sternum 
Skull 
Ribs 
Vertebrae

Children:
Everywhere

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3
Q

Haematapoesis is under what kind of control?

What is this known as as from where is it released?

A

Hormonal

Erythropoeitin released from the kidneys

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4
Q

What is the Reticuloendothelial System (RES)?

A

A network of blood and tissues which is part of the immune system and responsible for the control and removal of RBCs

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5
Q

What cells make up the RES and where are they found?

What do these cells have in common?

A 
Monocytes - macrophage precursor 
Peritoneal macrophages - peritoneal cavity 
Red Pulp macrophage- Spleen 
Langerhans cells- skin and mucosa 
Kupffer cells - Liver 
Tissue histiocytes - connective tissue 
Microglial cells - CNS

They are phagocytes

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6
Q

What are the main organs containing cells of the RES?

A

Spleen and the liver

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7
Q

RE cells in the spleen are important for what vital role?

A

Disposing of old or damaged RBCs and foreign objects or organisms

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8
Q

What are the functions of RBCs?

A 
Deliver oxygen to tissues 
Carry haemoglobin 
Maintain haemoglobin in its reduced (ferrous) state 
Generate ATP 
Maintain osmotic equilibrium
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9
Q

Name 4 proteins that are found in the RBC membrane

A

Spectrum
Ankyrin
Band 3
Protein 4.2

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10
Q

What function do these membrane proteins provide for the RBC?

A

Facilitate vertical interactions with the cytoskeleton of the cell which are essential for maintaining the RBCs biconcave shape and deformability

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11
Q

What can cause diseases that result in the RBCs losing their biconcave shape?
Give an example of such a disease?

A

Gene mutations for cell membrane proteins

Spherocytosis

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12
Q

What is the inheritance pattern of heriditary spherocytosis?

A

Autosomal dominant

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13
Q

Why might a RBC with a spherocyte shape function less efficiently than normally shaped RBCs?

A

They are no longer flexible to fit through capillaries

They have a decreased surface to volume ratio

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14
Q

Why does spherocytosis cause splenomegaly?

A

The spleen has to work harder to destroy defective RBCs which leads to hypertrophy

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15
Q

What are reticulocytes?

A

Precursor cells to erthytrocytes

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16
Q

Why might the reticulocytes cell count be above the normal range in a patient with spherocytosis?

A

As the bone marrow is releasing cells early in their development pathway in order to try and make up for the low RBC count

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17
Q

Given that spherocytes are smaller than normal RBCs, why isn’t the mean cell volume below the lower limit of normal in patients with spherocytosis?

A

The abnormal spherocytes are destroyed and replaced with excess reticulocytes which are large, therefore balancing out MCV

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18
Q

Why might the platelet count of a patient with hereditary spherocytosis be low despite the disease not effecting these cells directly?

A

The common myeloid progenitor cells will be producing less platelets and more reticulocytes to try and keep up with the demand of RBCs due to their destruction

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19
Q

What are the 4 main complications that can occur in patients with HS?

A

Gallstones
Jaundice
Anaemia
Tender spleen (abdominal pain)

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20
Q

Describe the structure of haemoglobin

A

A tetramer of 2 pairs of globin chains watch with a haem group

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21
Q

What lies at the centre of the porphyrin ring of each of haemoglobins 4 subunits?

A

Ferrous iron (Fe2+)

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22
Q

When shifting between the oxygen unbound and bound states, haemoglobin does what?

A

Undergoes a conformational change which enhances the binding affinity of subsequent oxygen molecules

23
Q

What happens to haemoglobins affinity for oxygen in the presence of 2,3 BPG?
What does this do to the oxygen dissociation curve?

A

Affinity of Hb for oxygen is decreased

Rightwards shift on the oxygen dissociation curve

24
Q

What are the important roles of the globin chains?

A
  • Protect haem molecule from oxidation
  • Confer solubility
  • Permits variation in oxygen affinity (shape)
25
Q

Explain what happens to the products produced by breakdown of haemoglobin?

A

Globin chain is broken down into amino acids to be recycled

Haem: the iron removed to be recycled in the body and the heme is excreted as bilirubin

26
Q

What is the main organ responsible for detection and production of erythropoeitin?

A

The kidneys

27
Q

When partial pressure of oxygen is low, what happens to the production of erythropoeitin?

A

In increases to allow more RBCs to mature and be released from BM

28
Q

What are the two main metabolic pathways in RBCs?

A

Glycolysis (Glucose into lactate)

Pentose Phosphate Pathway (G6P into NADPH)

29
Q

True or False: The body has a very rigorous mechanism for iron excretion?

A

FALSE! It does NOT have a mechanism for iron excretion

It is lost everyday as a result

30
Q

Where would you find “available iron” in the body?

A

Haemoglobin
Myoglobin
Tissue Iron
Serum Iron

31
Q

Where would you find “stored iron” in the body?

A

95% as Ferritin in Liver hepatocytes

5% as Haemosiderin in Kupffer cells of liver

32
Q

What is the difference between iron stored as FERRITIN and iron stored as HAEMOSIDERIN?

A 
Ferritin= soluble 
Haemosiderin= insoluble
33
Q

Which is the better source of iron out of haem iron and non-haem iron?

A

Haem Iron

34
Q

How much haem iron is needed a day?

A

10-15mg

35
Q

What foods is haem iron present in?
Is this iron in ferrous or ferric form?
What does this mean?

A

Meat
Ferrous
Fe2+, doesn’t need converting before it can be used

36
Q

When Fe2+ is stored as ferritin what transporter aids its release into the blood stream and what

A

b

37
Q

Where does absorption of iron occur?

A

In the duodenum and upper jejunum

38
Q

Which transporter protein is responsible for the transport of haem ferrous iron from the intestinal lumen?

A

DMT1

Divalent metal transporter 1

39
Q

How is ferric iron converted to ferrous iron before it can be taken up by DMT1?

A

Converted by Duodenal cytochrome B reductase (DcytB)

40
Q

Once in the enterocyte of the intestinal lumen, what happens to haem?

A

It is degraded to release ferric iron and stored as ferritin or transported via ferroportin

41
Q

The absorption of iron is primarily regulated by which small peptide?

A

Hepcidin

42
Q

Where is hepcidin expressed?

A

In the liver

43
Q

How does hepcidin control iron absorption?

A

Binds to ferroportin and degrades it- prevents absorption
Inhibits transcription of DMT1 gene (down regulates iron uptake)
Prevents iron release from macrophages

44
Q

True or false: Iron deficiency is a symptom, not a diagnosis

A

True

45
Q

What are the symptoms of iron deficiency?

A

Tiredness
Decreased oxygen carrying capacity
Cardiac symptoms

46
Q

What are the signs of iron deficiency?

A

Palor
High respiratory rate
Spooning of the nails
Tachycardia

47
Q

What are the features of blood in someone with iron deficiency?

A

Low haemoglobin counts
Microcytic
Low serum ferritin

48
Q

How can we test for iron deficiency?

What are the problems with this?

A

Serum ferritin levels
It is also an acute phase protein and so will be raised during inflammatory responses
Low= deficient
High or normal does not= not deficient

49
Q

What does NICE recommend to be used to identify functional iron deficiency?
In what setting can this not be used?

A

CHR (reticulocyte haemoglobin content)

Cannot be used in patients with thalasaemia

50
Q

Why is excess iron damaging?

A

Free iron can produce highly reactive hydroxyl and lipid radicals

51
Q

What is haemochromatosis and what does it cause?

A

Disorder of iron excess resulting in end organ damage

It causes liver cirrhosis, diabetes mellitus, hypogonadism, cardiomyopathy etc.

52
Q

What are the two types of haemochromatosis depending on how it is acquired?

A 
Hereditary Haemochromatosis (HH) 
Tranfusion associated haemochromatosis
53
Q

What is the inheritance pattern of HH?

What is the pathogenesis of HH?

A

Autosomal recessive

Mutated HFE which cannot bind to transferrin to compete with it and therefore too much iron enters the cell

54
Q

How is HH treated?

A

Venesection (taking blood)

Metabolism, Endocrinology & Haematology (13 decks)

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