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Metabolism - Alex's Cards (ESA2) > Session 5 Lecture Notes - Haemotology > Flashcards

Session 5 Lecture Notes - Haemotology Flashcards

1
Q

Where are the 5 main places bone marrow is found in adulthood?

A 
Sternum
Ribs
Skull
Pelvis 
Vertebrae
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2
Q

What is the stem cell that can differentiate into myeloid progenitor cells or lymphoid progenitor cells?

A

Multipotent haemopoeitic stem cells

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3
Q

When undertaking a bone marrow examination what are the 2 types of tests called?

A

Bone marrow biopsy

Aspiration

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4
Q

What are the two main organs involved in the reticularendothelial system?

A

The liver and spleen

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5
Q

What is the function of the reticularendothelial system?

A
  1. Immune response

2. To remove damaged or senescent blood cells

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6
Q

Give some examples of cells that might be found in the reticularendothelial system

A
  1. Macrophages
  2. Monocytes
  3. Tissue histiocytes
  4. Kupffer Cells
  5. Microglial cells
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7
Q

What is the normal haemoglobin levels for a male and female?

A

Male: 130-180g/L
Female: 115-165g/L

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8
Q

What is the normal RBC level for male and females? (measurement is 10 to the power of 12/L)

A

Male: 4.5-6.5
Female: 3.9-5.6

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9
Q

In which state should iron be in haemoglobin?

A

Ferrous state (NOT ferric)

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10
Q

RBCs have proteins that make it very flexible in order to fit though capillaries.
What is the size of RBCs and what about the minimum size of the vessels?

A 
RBCs = 8 micromolar diameter 
Vessels = 3.5 micromolar diameter
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11
Q

On which chromosomes is the globin gene found?

A

11 and 16

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12
Q

How many haem groups does a haemoglobin tetramer have? Each one binds an oxygen molecule

A

4 haem groups - 1 on each globin chain

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13
Q

What globin chains do newborns have and what do adults have?

When does the change happen?

A

Newborns = pair of alpha chains and pair of gamma chains
Adult = pair of alpha chains and pair of beta chains
Change around 6 months (gamma gene is a switched off and beta on)

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14
Q

Why might a patient be jaundiced?

A

Too much haemoglobin catabolism and liver can’t process it all so it accumulates as bilirubin

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15
Q

What is bilirubin broken down into when excreted as faeces and in urine?

A 
Faeces = stercobilin 
Urine = urobilogen
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16
Q

What hormone is secreted by the kidney to increase maturation and release of RBCs from kidney?

A

Erthyropoietin

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17
Q

When is erythropoietin released from kidney?

What cells detect this?

A

It is released when PO2 levels are low

The interstitial peritubular cells detect this

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18
Q

Which 2 pathways do RBCs use to generate energy and maintain its membrane?

A
  1. Glycolysis

2. Pentose Phosphate Pathway

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19
Q

Can we excrete iron?

A

No!

The only way we lose iron is via hair loss, skin loss or bleeding

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20
Q

What are the 2 stores of iron known as?

A
  1. Ferritin

2. Haemosiderin (a macrophage iron)

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21
Q

Where is iron used functionally in the body?

A
  1. Haemoglobin
  2. Myoglobin
  3. Tissue iron eg for enzymes
  4. Transported iron ie serum iron
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22
Q

When in our lives might we require more iron?

A

If we bleed more

If we are pregnant or a child (growing more)

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23
Q

What % of iron is stored as ferritin and where is it found?

What % as haemosiderin and where is it found?

A

95% as ferritin (only 5% as haemosiderin)
Ferritin = in hepatocytes (liver cells)
Haemosiderin = in Kupffer cells (phagocytic cell in the liver sinusoid)

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24
Q

What is the difference between haem and non-haem iron and where in the diet are they found?

A 
Haem = a better source of iron as the iron released from it is already in ferrous form -found in meat
Non-haem = iron in this exists in ferric form and has to be converted to ferrous form before it can be used - found in other iron sources such as nuts and grains
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25
Q

What binds to ferrous iron when it is transported across the apical surface of small intestines?

A

Transportin

26
Q

What transports ferrous iron out of the cell?

A

Ferroportin

27
Q

If iron in the blood serum is to be taken up by cells - what receptor is present?

A

Tranferrin receptor (which binds to the iron-transferrin complex)

28
Q

Which cells have the highest number of transferrin receptors?

A

Erythrocytes

29
Q

Name some things that enhance non-haem iron absorption and some things that inhibit it

A 
Enhance = things that contain Vit C (ascorbic acid) like orange juice
Inhibit = tea, chapatis
30
Q

What is the function of hepcidin? Where is it produced and excreted ?

A

It blocks absorption of iron in enterocytes and release of iron from macrophages by degrading ferroportin (responsible for transporting iron out of the cells)
Levels are high when iron levels are too high
Levels decrease when RBC production is high
Produced by liver
Excreted by kidney

31
Q

Suggest 3 reasons a person might be deficient in iron

A
  1. Not enough iron in diet (eg a vegan)
  2. Pathological reasons (eg bleeding)
  3. Physiological reasons (eg pregnant)
32
Q

Name some symptoms of anemia

A
  1. Reduced exercise tolerance (not enough oxygen carrying capacity)
  2. Tiredness
  3. Cardiac symptoms
33
Q

Iron deficient patients will have blood cells that are hypochromic and microcytic. what does this mean?

A 
Hypochromic = low haemoglobin content
Microcytic = small RBCs (low mean cell volume)
34
Q

What is commonly used as a measure of iron status?

What is perhaps a better measure of iron status?

A 
Ferritin levels (95% of iron is stored as ferritin in hepatocytes)
A better measure may be CHR which remains low during inflammation (however can be raised if a person has thalasaemia)
35
Q

Why does a normal/high ferritin level NOT mean they are not iron deficient?

A

Ferritin levels can increase following inflammation as ferritin is an acute phase protein
Iron levels may be low but the normal ferritin levels due to inflammation disguise this

36
Q

Why is iron excess dangerous?

A

There is not enough transferrin to bind to the overload of iron
Reduced free iron (Fe2+) can produce highly reactive hydroxyl and lipid radicals
Excess iron is deposited in tissues and can cause damage

37
Q

What is the term used to describe iron overload?

A

Haemochromatosis

It results in iron being deposited in tissue

38
Q

What is hereditary haemochromatosis and how can you treat this?

A

Mutation on HFE gene (autosomal recessive)
HFE competes with transferrin to bind to the transferrin receptor (TfR)
Without HFE you get overload of iron absorption into the cells
Treat by venesection (bleeding)

39
Q

What is transfusion associated haemosiderosis? How do you treat this?

A

Patients who have to receive regular blood transfusions may become iron overloaded
You can’t stop the accumulation of iron but you can delay it but giving the patient iron chelating agents (such as desferrioxamine)

40
Q

Name 3 things that could lead to reduced erythropoiesis

A
  1. Kidney disease - it stops making erythropoietin
  2. Empty bone marrow eg following chemotherapy so it doesn’t response to signals from erythropoietin
  3. Infiltrated bone marrow by cancer cells means normal haemopoeitic cells are reduced
41
Q

What is the most common cause of dyserythropoiesis?

A

Anaemia of chronic disease (ACD)

42
Q

What is dyserythropoiesis?

A

Production of faulty RBCs

43
Q

What are the clinical clues that someone has anaemia of chronic disease?

A

The inflammatory markers (acute phase proteins) will be raised = CRP and ferritin

44
Q

What condition (apart from anaemia of chronic disease) results in dyserythropoiesis?

A

Myelodysplastic syndrome - a group of cancers which results in bone marrow blood cells not maturing into functional blood cells
RBC, WBC and platelet counts are all low

45
Q

What are the 3 ways in which haemoglobin abnormalities can arise?

A
  1. Lack of iron
  2. Deficiency in building blocks for DNA synthesis
  3. Mutation in genes that code for globin proteins
46
Q

What is megaloblastic anaemia?

A

Anaemia of macrocytic classification which results from impaired DNA synthesis during RBC production
This means cells are unable to divide (go through mitosis) but they continue to grow in the G2 stage = large RBCs and reduction in number

47
Q

Name the 4 steps by which B12 gets into the bone marrow

A
  1. B12 comes from our diet (from foods of animal origin)
  2. B12 is combined with intrinsic factor (IF) in the stomach (produced by parietal cells)
  3. The IF-B12 complex binds in the ileum - IF is destroyed and B12 absorbed
  4. B12 travels through the hepatic portal vein into the liver where it is bound to transcobalamin and transported to the bone marrow (and other tissues)
48
Q

What is trancobalamin?

A

A plasma protein that carries B12 from the liver to tissues and bone marrow

49
Q

What is intrinsic factor?

A

A glycoprotein that is produced by parietal cells in the stomach
It binds to B12 in the ileum of the small intestines before being degraded

50
Q

Name 4 things that can lead to B12 deficiency (each 1 is a step in the movement of B12 to the bone marrow)

A
  1. Lack of B12 in the diet eg vegan
  2. Lack of intrinsic factor eg if antibodies are produced against parietal cells which synthesise IF
  3. The IF and B12 not binding in the ileum eg from disease of the ileum such as Crohn’s disease
  4. Lack of transcobalamin which is needed to transport B12 from liver to bone marrow
51
Q

Why does it take a long time to become B12 deficient?

A

Because we normally consume an excess of B12 in the diet and it can be stored for a very long time in the body

52
Q

Name the steps in which folate reaches the cells for DNA synthesis

A
  1. Folate is most in most foods that we eat
  2. It is absorbed in the duodenum and jejenum in the small intestines
  3. Folate is converted to methylTHF
  4. MethylTHF circulates in plasma and is used for DNA synthesis throughout the body
53
Q

Name 3 ways in which a person may have folate deficiency

A
  1. Lack of folate (either through lack of folate in the diet or increased use of it eg pregnancy)
  2. proximal small bowel disease eg crohn’s of coeliac (folate not being absorbed in duodenum or jejunum)
  3. Lack of methylTHF - the enzyme that converts folate to methylTHF not working
54
Q

Lack of B12 or folate leads to neurological disorders?

A

Lack of B12

55
Q

Name 2 conditions that lead to abnormal globin chains

A
  1. Thalassemia (reduction in number of alpha or beta globin)

2. Sickle cell disease (abnormal haemoglobin)

56
Q

What is haemolytic anaemia?

What organ is largely responsible for removal of damaged RBCs?

A

Increased RBC destruction

The spleen is largely responsible

57
Q

What is autoimmune haemolytic anaemia?

A

Autoantibodies are produced by L lymphocytes which bind to red blood cell membranes and targeting them for removal

58
Q

What is a myeloproliferative disorder?

A

An overproduction of cells due to disregulation of multipotent haemopoeitic stem cells

59
Q

What is the mutation that causes myeloproliferative disorders?

A

Specific point mutation in one copy of the Janus Kinase 2 gene (JAK2) on chromosome 9

60
Q

What is the name for too many RBCs?

How do you diagnose it?

A 
Polycythaemia Vera (PV)
Diagnose by high haemotocrit or raised RC mass

Metabolism - Alex's Cards (ESA2) (8 decks)

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