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Haematology > Physiology > Flashcards

Physiology Flashcards

1
Q

Name the different types of blood cells

A
  • white
  • red
  • platelets
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2
Q

What is haematopoiesis

A
  • production of blood from bone marrow

- derived from pluripotent stem cells

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3
Q

What is red cells dervived from?

A
  • pluripotent stem cells
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4
Q

Where does haematopoiesis occur in the embryo? and then when at birth?

A
  • embryo = yolk sac, then liver, then bone marrow

- adult = bone marrow, liver, spleen

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5
Q

Which bone marrow is responsible for the production of red blood cells?

A
  • the axial skeleton
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6
Q

Explain the formation of blood cells from the stem cells?

A
  • proliferation
  • differentiaion
  • haematopoietic trees
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7
Q

What are the 2 main routes in the haematopoietic tree and their final product

A
  • cmp (myeloid) -> granulocytes, erythrocytes, platelets, macrophages
  • CLP (lymphoid) -> B cells, T cells and NK cells
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8
Q

What state do most stem cells lie in?

A
  • quiescent state
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9
Q

Term given to red cell production, different from blood cell production

A
  • erythropoiesis
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10
Q

What is the primary cell called of erythropoiesis?

A
  • pronormoblast
  • early normoblast
  • intermediate normoblast
  • late normoblast
  • reticulocyte
  • erythrocyte
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11
Q

What is the difference between a reticulocyte and a erythrocyte?

A
  • a reticulocyte is more immature and contains a nucleus and is found in bone marrow
  • erythrocyte has no nucleus and has entered blood streem
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12
Q

Explain platelet formation

A
  • nucleus replicated but no cell division
  • forms a megakaryocyte
  • budding off -> platelets released
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13
Q

3 main granulocytes?

A
  • eosinophils
  • basophills
  • neutrophils
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14
Q

Describe neutrophils

A
  • most numerous white cell
  • fine granules
  • lobbed nucleus
  • short lived
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15
Q

What may cause an increase in neutrophils?

A
  • infection
  • trauma
  • infarction
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16
Q

Describe the appearance of eosinophils

A
  • bi-lobbed
  • bright red granules
  • involved in hypersensitivity
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17
Q

Describe appearance of basophils?

A
  • large purple granules
  • basic staining
  • release histamine
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18
Q

Monocytes vs macrophages

A
  • monocytes = in the blood stream

- macrophages = in the tissue

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19
Q

Describe the appearance of lymphocytes

A
  • big nucleus
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20
Q

3 ways of sampling blood in haematology?

A
  • immunophenotyping
  • bio-assay
  • bone marrow samples
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21
Q

Explain immunophenotyping

A
  • looking at surface proteins of cells

- much quicker method

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22
Q

Structure of RBC

A
  • 2 alpha
  • 2 beta
  • 4 porphyrin rings with Fe2+
  • biconcave
  • no nucleus
  • no mitochondria
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23
Q

Why are RBC limited to 120days?

A
  • they have no nucleus or mitochondria

- unable to repair proteins

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24
Q

What is present on the cell membrane of a RBC

A
  • Sodium potassium ATP pump
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25
Q

What is the disadvantage of Fe3+

A
  • unable for O2 to bind
  • must be in Fe2+ form

NADH generated in glycolysis helps protect Fe2+

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26
Q

Role of haemoglobin

A
  • delivers oxygen to tissue
  • acts as a buffer for H+ ions
  • Co2 transport
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27
Q

Explain the stem cell process

A
  • multipoint haematopoetic cell
  • common myeloid progenitor cell (CMP)
  • common lymphoid progenitor celll (CLP)
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28
Q

What do CMP cells become

A
  • erythrocytes
  • platelets
  • macrophages
  • basophils
  • eosinophils
  • neutrophils
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29
Q

What do CLP cells become

A
  • NK cells
  • b cells
  • t cells
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30
Q

B cells further differentiate into what?

A
  • plasma cells
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31
Q

What happens to red blood cells as they mature?

A
  • they become smaller in size
32
Q

Where is hypoxia sensed and what is the consequence

A
  • sensed in the kidney
  • erythropoietin hormone secreted
  • stimulation of RBC formation
33
Q

Where does normal RBC breakdown occur

A
  • the spleen or liver
34
Q

Explain RBC breakdown

A
  • haemoglobin - heme and globin
  • globin - amino acids
  • heme - porphyrin (bilirubin) and iron
35
Q

What is heme broken down to

A
  • porphyrin (bilirubin)

- iron

36
Q

Glycolysis role in the formation of RBC

A
  • Generates ATP
  • generated NADH (Prevents Fe2+ oxidising to Fe3+)
  • free radical formation
37
Q

Free radical formation may cause what?

A
  • dangerous
  • can cause Fe2+ to become Fe3+
  • can damage cell membrane
  • NADH acts as an electron donor to prevent Fe oxidation
38
Q

Name a reactive oxygen species

A
  • hydrogen peroxide
39
Q

What is the risk associated with hydrogen peroxide

A
  • damage to proteins
40
Q

What is vital for protection of hydrogen peroxide (reactive oxygen species)

A
  • glutathione (GSH)

- Forms water and an oxidised GSH (GSSG)

41
Q

How is oxidised glutathione regenerated to glutathione

A
  • NADPH
42
Q

What is the rate limiting step in the hexose monophosphate shunt

A
  • G-6-PD

- Glucose 6 phosphate dehydrogenase

43
Q

Role of NADPH in GSSG

A
  • Recycles to for GSH
44
Q

How is carbon dioxide transported

A
  • dissolved
  • carbamino compound in Hb
  • bicarbonate
45
Q

What enters the RBC when CO2 leaves in order to preserve the potential

A
  • Cl-
46
Q

Explain the oxygen dissociation curve

A
  • sigmoid
  • allosteric cooperative binding
  • a drop in Po2 at a lower level results in a greater % saturation drop than a higher
47
Q

What can cause the oxygen dissociation curve to shift to the right and what will that cause

A
  • increase in temp
  • decrease pH
  • Increase 2,3-BPG
  • causes oxygen to be released at a tissue level
  • lesser % saturation bound
48
Q

What can cause the oxygen dissociation curve to shift to the left and what are its consequences

A
  • decrease temp
  • increaser ph
  • decreased 2,3-BPG
  • Less o2 released at same PO2
  • Greater % saturation bound
49
Q

Describe fetal Hb compared to adult

A
  • 2 alpha and 2 gamma

- greater o2 saturation in haemoglobin at the same o2

50
Q

Explain the affect of 2,3-BPG on the oxygen dissociation curve

A
  • increased 2,3BPG = Shift to the right
  • more released
  • less bound
  • decreased 2,3-BPG = shift to the left
  • less released
  • more bound
51
Q

What affect on 2,3-BPG will occur in chronic anaemia?

A
  • up regulation
52
Q

What is termed the machinery of RBC

A
  • The erythron
53
Q

Raw materials of RBC production

A
  • iron
  • b12
  • folate
54
Q

What is released from the kidneys due to low oxygen levels

A
  • erythropoietin
55
Q

Which stem cell has the higher self-renewing ability and why is that useful

A
  • the long term stem cells

- good for transplant patients

56
Q

Pathway of RBC production from pronormoblasts

A
  • pronoromblast
  • early normoblast
  • intermediate normoblast
  • late normoblast
  • reticulocyte
  • erythrocyte
57
Q

Why is iron essential?

A
  • oxygen transport
  • electron transport
  • present in haemoglobin, myoglobin, enzymes
58
Q

Iron dangerous?

A
  • oxidative stress

- free radical formation

59
Q

Where does iron absorption take place?

A
  • in the duodenum

- uptake into cells of duodenal mucosa

60
Q

What enhances iron uptake?

A
  • haem irons
  • ascorbic acid
  • alcohol
61
Q

What reduces iron uptake?

A
  • tannins
  • phylate
  • caclcium
62
Q

What reduces Fe3+ to Fe2+

A
  • duodenal cytochrome B
63
Q

What transports Fe2+ from the lumen of duodenum into duodenal cells?

A
  • Divalent metal transport 1
64
Q

What transports iron from the duodenal cell into the body?

A
  • ferroprotein
65
Q

What regulates iron

A
  • hepcidin
  • negative regulator
  • levels decrease in anaemia = increase iron absorption
66
Q

How can iron status be analysed?

A
  • functional iron (hb concentration)
  • transport iron (transferrin saturation)
  • storage iron (ferritin)
67
Q

When might ferritin be increased?

A
  • inflammation or malignany

- increased in anaemia of chronic disease

68
Q

Microcytic anaemias are deficiencies in _____ synthesis

A
  • haemoglobin
69
Q

What is sideroblastic anaemia?

A
  • excess iron build up in the mitochondria and not incorporated into haemoglobin
70
Q

How is iron deficiency anaemia defined?

A
  • anaemia + low iron
71
Q

Explain pathophysiology of anaemia of chronic disease?

A
  • increased ferritin
  • increased plasma hepcidin
  • decreased iron release from macrophages
72
Q

Causes of primary iron overload

A
  • hereditary haemochromatosis
73
Q

Explain hereditary haemochromatosis?

A
  • HFE gene
  • increased Hepcidin
  • increased iron absorption
74
Q

Treatment of primary haemochromatosis?

A
  • venesection
75
Q

Treatment of iron overload?

A
  • iron chelating agents

e. g. desferrioxamine

Haematology (14 decks)

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