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POM 2 G: HAEMATOLOGY > 2.1 Red Blood Cells > Flashcards

2.1 Red Blood Cells Flashcards

1
Q

Where do all blood cells originate

A

Bone marrow

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2
Q

What are blood cells derived from

A

Pluripotent haemopoietic stem cells

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3
Q

What do HSC’s give rise to

A

Common myeloid and lymphoid progenitors (stem cells)

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4
Q

Haemopoiesis

A

Formation and development of blood cells

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5
Q

Erythrocyte function

A

Oxygen transport

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6
Q

Erythrocyte life span

A

120 days

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7
Q

Platelet function

A

Haemostasis

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8
Q

Platelet life span

A

10 days

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9
Q

Monocyte function

A

Defence against infection by phagocytosis and killing of microorganisms

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10
Q

Monocyte life span

A

Several days

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11
Q

Neutrophil function

A

Defence against infection by phagocytosis and killing of microorganisms

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12
Q

Neutrophil life span

A

7-10 hours

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13
Q

Eosinophil function

A

Defence against parasitic infection

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14
Q

Eosinophil life span

A

Little less than 7 hours

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15
Q

Lymphocyte function

A

Humoral and cellular immunity

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16
Q

Lymphocyte life span

A

Very variable

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17
Q

HSC characteristics

A
  1. Self renew
  2. Differentiate to mature progeny
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18
Q

What do common myeloid progenitors give rise to

A

Megarakaryocyte (-> platelet)
Erythrocyte
Mast cell
Myeloblast (-> granulocytes and monocytes)

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19
Q

Granulocytes

A

Basophil

Neutrophil

Eosinophil

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20
Q

What do common lymphoid progenitors give rise to

A

NK cells

Small lymphocyte (-> T and B lymphocytes,, b-> plasma cell)

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21
Q

Sites of haemopoiesis

A
  1. Yolk sac (3 wks gestation) : generation of HSC
  2. Liver (6-8wks gestation) : maintenance and expansion of HSC
  3. Bone marrow (10 wks gestation)
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22
Q

Bone marrow as a site of haemopoiesis

A

Starts developing haemopoietic activity around 10 wks gestation

Occurs in all bones in children

In adults mainly pelvis, vertebrae and sternum

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23
Q

HSC distribution

A

Ordered fashion within bone marrow amongst mesenchymal cells, endothelial cells and the vasculature which HSCs interact with

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24
Q

What is haemopoiesis regulated by

A

Number of genes, transcription factors, growth factors and the micro environment

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25
Q

Disruption to balance of haemopoiesis

A

Disturb proliferation vs differentiation leading to leukaemia or bone marrow failure

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26
Q

What are haemopoietic growth factors

A

Glycoprotein hormones which bind to cell surface receptors and regulate proliferation and differentiation of HSC and function of mature blood cells

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27
Q

Examples of haemopoietic growth factors

A

Erythropoietin (EPO) - erythropoiesis

Thrombopoietin (TPO) - megakaryocytopoiesis and platelet production

G-CSF, G-M CSF and cytokines - granulocyte and monocyte production

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28
Q

Erythropoiesis

A

Development of red blood cells

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29
Q

As differentiation progresses

A

Self renewal and lineage plasticity decreass

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30
Q

Lineage of RBC changes

A

Lose nucleus

Change from polychromatic

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31
Q

What is required for erythropoiesis

A

Iron

B12

Folic acid

Erythropoietin

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32
Q

Microcytic anaemia

A

Small RBC

due to iron deficiency or low availability

33
Q

Causes of iron deficiencies

A

Increased blood loss

Reduced intake

Increased requirement (pregnancy)

34
Q

Causes of decreased iron availability

A

Anaemia of chronic disease / inflammation

35
Q

Macrocytic anaemia

A

Large RBC

B12/ folate deficiency (megaloblastic anaemia)

36
Q

EPO synthesised in response to

A

Hypoxia

37
Q

Demand supply feedback loop of EPO

A

Hypoxia -> liver inc EPO synthesis -> inc bone marrow activity <- inc red blood cell production

38
Q

Iron functions

A

Oxygen transport in haemoglobin

Mitochondrial proteins ( ytochromes abc)

39
Q

Signs of low iron

A

Hyopchromic (pale), microcytic RBC

Gloss it is (inflamed tongue)

Spoon shaped nails

Pale conjunctiva

40
Q

Where is iron absorbed

A

Duodenum

41
Q

Best absorbed iron

A

Haem iron - ferrous (2)

Animal derived

42
Q

Non haem iron

A

Ferric (3)

Requires action of a reducing substance for absorption

Sources of it reduce absorption such as soya beans which contain phytates

43
Q

Excess iron

A

Potentially toxic to organs especially the heart and liver

44
Q

How much iron per day is absorbed form diet

A

1-2 mg

45
Q

How is iron transferred

A

As transferrin in plasma (3mg)

46
Q

How much iron is in bone marrow

A

300mg

47
Q

How much iron in RBC

A

2500mg

48
Q

How much iron in reticuloendothelial system

A

500mg

49
Q

Iron loss from system

A

1-2mg a day

Via muscles and enzymes (myoglobin and enzymes)

50
Q

How much iron in myoglobin and enzymes

A

300 and 150mg

51
Q

How much iron in liver

A

250mg stored as ferritin

52
Q

How much iron is absorbed in pregnancy

A

6mg

53
Q

How is iron absorption regulated

A

Hepcidin

54
Q

What is hepcidin secreted by

A

Liver (in response to high storage iron)

55
Q

How does Hepcidin work

A

Blocks absorption of iron from the gut and release of storage iron

56
Q

Anaemia of chronic disease/ inflammation

A

Decrease in EPO production causing a decrease in iron production and availability

Pro inflammatory cytokines decrease EPO and inc Hepcidin

57
Q

What is b12 required for

A

DNA synthesis

Integrity of nervous system

58
Q

What is folic acid required for

A

DNA synthesis

Homocysteine metabolism

59
Q

DNA synthesis with b12 and folate deficiency

A

Needed for dttp synthesis for thymidine

Deficiency affect all rapidly dividing cells inc bone marrow. -cells can grow but are unable to divide giving megaloblastic anaemia (macrocytic)

60
Q

Absorption of b12

A

Stomach (cleaved with hcl then) combined with intrinsic factor made by parietal cells

Small intestine it binds to receptors in the ileum

61
Q

Causes of b12 deficiency

A

Inadequate intake

Inadequate secretion of IF (pernicious anaemia)

Malabsorption (coeliac disease, surgery)

Achlorhydria - lack of acid in stomach

62
Q

Red cell destruction

A

Heme excreted as bilirubin in bile, iron from haem transferred as transferrin in plasma and returns to bone marrow where it is recycled

Happens in spleen by macrophages

63
Q

Haemolytic anaemias

A

Can be jaundiced due to inc bilirubin levels when actively haemolysing

64
Q

What does erythrocyte function depend on

A

Integrity of membrane
Haemoglobin structure and function
Cellular metabolism

Defect in any of these leads to shortened survival (haemolysis)

65
Q

Central pallor size

A

No greater than 1/3 its diameter otherwise hypochromic

66
Q

What’s RBC membrane made up of

A

Lipid bilayer supported by a protein skeleton

Contains transmembranous proteins

67
Q

Disruption to vertical linkages in RBC membrane

A

Causes hereditary spherocytosis

(Autosomal dominant)

68
Q

Spherocytes

A

Spherical shape

Lack central pallor

Loss of membrane without equivalent cytoplasm loss

Less flexible and are removed prematurely - haemolytic anaemia

69
Q

Disruption of horizontal linkages in RBC membrane

A

Produces hereditary elliptocytosis

70
Q

Red cell metabolism includes

A

Generation of atp

Maintenance Hb function, membrane integrity, RBC volume

71
Q

PPP

A

Glucose 6 phosphate completely oxidised to CO2

Producing NADPH

72
Q

NADPH

A

Provides reducing power for maintaining reduced glutathione- viral antioxidant in RBC

73
Q

G6PD

A

Glucose 6 phosphate dehydrogenase maintains reducing power of NADPH

Deficiency causes vulnerability of RBC to oxidant damage

74
Q

G6PD Deficiency

A

Manifests in males (X linked inheritance)

Causes intravascular haemolysis (see bite cells)

75
Q

Bite cells

A

Irregular outline

Smaller and have lost central pallor

Result from oxidant damage to cell membrane and Hb

Hb is denatured and forms round inclusions called Heinz bodies (on 1 Side of cell) can be detected by specific tests

76
Q

Polycythaemia

A

Too many red cells in the circulation

Hb, RBC and hct all increased

77
Q

Pseudo polycythaemia

A

Reduced plasma volume due to dehydration etc.

78
Q

True polycythaemia

A

Inc in total volume of red cells in circulation

Blood doping, EPO increase

79
Q

Polycythaemia Vera

A

Intrinsic bone marrow disorder where an increase in erythropoiesis is independent of EPO

Myeloproliferatuve disorder

Can lead to hyperviscocity (thick blood) which can cause thrombosis

Blood can be removed to reduce viscosity and drugs to reduce by production

POM 2 G: HAEMATOLOGY (8 decks)

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