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MEH > Session 3 - Haemopoiesis > Flashcards

Session 3 - Haemopoiesis Flashcards

1
Q

Where are the haemopoietic stem cells?

Which two progenitor cells do they divide into?

A

Bone marrow

Common Lymphoid progenitor cell
Common Myeloid progenitor cell

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2
Q

Where does haemopoiesis begin in the embryo?

A
  • Vaculature of the yolk sac

- shifts to embryonic liver by weeks 5-8 in development

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3
Q

Thrombopoiesis creates which cell?

Are these cells nucleated and how many sets of chromosomes do they have?

A

Platelets

No nucleus
Several sets of chromosomes- polypoid cells

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4
Q

Platelets are polypoid cells. What does this mean?

A

They have more than 2 sets of chromosomes

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5
Q

Platelets bud off from which cell?

What drives formation of this cell and from what?

A

megakaryocytes

(TPO) thrombopoietin
drives megakaryocyte formation from the common myeloid progenitor cell

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6
Q

Granulopoiesis forms which cells?

Which are the precursor cells?

A

basophil eosinophil neutrophil
(‘fill’ with granules)

  • Common myeloid progenitor cell
  • Myeloblast
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7
Q

When do you see eosinophils in the blood?

Can they phagocytose?

A

Parasite infection or inappropriately with athsma/ allergy

Yes

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8
Q

How do macrophages protect tissues from pathogens?

Which cells do they derive from?

A
  • phagocytosis
  • secrete cytokines
  • antigen presentation

Monocytes
(circulate in blood for >3 days)

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9
Q

B and T cells are formed by which process?

How does a B cell mature fully?

Where do the lymphocytes form?

A

Lymphopoiesis

Exposure to antigen in the lymphocytes which stimulates differentiation into a plasma or memory B cell.

Foetal liver and bone marrow/ thymus

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10
Q

How are the lymphocytes able to recognise so many different antigens?

A

Rearrangement of the receptor genes

- generates many different receptors each complementary to different antigens

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11
Q

How are common myeloid progenitor cells committed to the erythroid linkage?

What drives development into RBC’s once committed?

A

expression of transcription factors

  • GATA1
  • FOG1
  • PU.1

EPO, erythropoietin

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12
Q

What stimulates more erythropoietin production?

What type of hormone is it?

What does EPO do?

A

hypoxia in the blood

glycoprotein hormone

  • Protects erythroid cell line from apoptosis (inhibits)
    by activating the EPO receptor
  • Drives RBC formation
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13
Q

How do erythroblasts become mature red blood cells?

A
  • (nucleated) extrude the nucleus and most organelles to form reticulocytes
  • Reticulocytes enter circulation
  • Extrude remaining organelles, mitochondria and ribosomes
  • Become mature RBC’s over 1-2 days
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14
Q

What is measured in the blood to estimate the amount of erythropoiesis occurring?
Explain

A

Reticulocyte count

Reticulocytes are immature RBC’s and mature quickly (1-2 days). So a low count would indicate no new erythropoiesis is occurring

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15
Q

Why are red blood cells particularly susceptible to oxidative damage?

A

They have no nucleus so can’t repair damaged proteins

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16
Q

Which cells are affected in pyruvate kinase deficiency?

Explain

A

Red blood cells

Pyruvate kinase is the last enzyme in glycolysis; it forms pyruvate. All products after the enzyme are reduced (ATP, pyruvate)

The red blood cell has no mitochondria so is reliant on glycolysis as the sole source of ATP.

17
Q

Why are RBC’s biconcave?

A
  • Optimises the laminar flow properties of blood in large vessels
  • deformability through small capillaries
18
Q

What do RBC’s do?

A

Exchange gases at the alveoli (O2 & CO2)

19
Q

What causes hereditary spherocytosis?

Which defect is most common?

A

Mutations in the genes coding for membrane proteins (ankyrin, spectrin, band 3 protein and protein 4.2) which interact with the cytoskeleton to maintain the biconcave shape of RBC’s

Spectrin mutation

20
Q

What happens in hereditary spherocytosis?

How can you treat it?

A
  • The RBC’s are sphere shaped instead of biconcave.
  • They are prone to lyse because they can’t deform in capillaries- causing haemolytic anaemia.
  • They are cleared by the spleen

Splenectomy to reduce the anaemia

21
Q

Adult haemoglobin has which subunits?

Each subunit is associated with what?

A

Hameoglobin A - tetramer
alpha2 beta2

A haem group which has Fe2+ at the centre of the porphyrin ring

22
Q

Hameoglobin takes up how much of the RBC volume?

A

95%

23
Q

What is the Bohr effect?

A

The binding affinity of haemoglobin (for oxygen) is inversely related to CO2 and pH

24
Q

2, 3 Bisphosphoglycerate
(2, 3 BPG) has what effect on oxygen binding to haemoglobin?

Why?

A

Reduces affinity for oxygen

BPG is an intermediate of glycolysis so its presence indicates a respiring tissue which needs oxygen

25
Q

How does the oxygen dissociation curve shift if haemoglobin’s affinity for oxygen is reduced?

What shape is the curve?

A

Shifts right
- the haemoglobin is less saturated at the same partial pressures

sigmoidal (s shaped)

26
Q

What does the red and white pulp of the spleen do?

A

Red pulp - removes RBC’s and metabolises haemoglobin

White pulp- synthesises antibodies, removes antibody-coated bacteria and blood cells

27
Q

Which cells pass through the red and white pulp preferentially?

What is each pulp made up of?

A

red- erythrocytes
white- WBC’s and plasma

Red - sinuses lined with endothelial macrophages and cords
White- structure similar to lymphoid follicles

(sinuses= collecting ducts which lead to internal veins)

28
Q

The spleen can pool blood, what is the advantage?

A

Platelets and red cells can be rapidly mobilised from here during bleeding

29
Q

What can cause splenomegaly?

A
  • Increased workload- haemolytic anaemia
  • Congestion (can’t empty) due to portal hypertension
    Note; portal vein drains blood from intestines and spleen to the liver)
  • Infiltration by leukaemia and lymphomas
  • expansion due to accumulation of waste products of metabolism. E.g. Gaucher’s disease
  • infectious disease; HIV, glandular fever, malaria, schistosomiasis
30
Q

What is Gaucher’s disease?

What does it present like?

A
  • Accumulation of glucocerebroside (component of red and white blood cell membranes) in fibrils
  • Due to a defect in the beta-glucosidase enzyme

splenomegaly

31
Q

Which infectious disease can cause splenomegaly?

A

HIV
Malaria
Glandular fever
Schistosomiasis

32
Q

What is hyposplenism?

What is it caused by and what are the risks?

A

Reduced splenic function

  • Trauma causing splenic rupture
  • Damaged tissue in disease; coeliac, sickle cell
  • Splenectomy

Risk of sepsis

33
Q

What is present in the blood film of a patient with hyposplenism?
Explain

A

Howell-Jolly Bodies in RBC’s

They’re nuclear remnants which are normally expelled from maturing RBC’s. The spleen would usually remove them so it indicates reduced function

34
Q

Which cells make up the reticuloendothelial system?

A

macrophages and monocytes

35
Q

Where are these cells found?

  • Kupffer cell
  • Tissue histiocyte
  • Microglia
  • Langerhans cell

They are all types of ___?

A

liver
connective tissue
CNS
skin & mucosa

Macrophage

36
Q

What is haemoglobin metabolised to?

A

(in spleen)
globin > amino acids
haem > bilirubin

37
Q

Urobilinogen
Urobilin & stercobilin
What do they do?

Where do they come from?

A
  • Give urine its colour *
  • Give stool its colour
  • Bilirubin is excreted in bile into the duodenum
  • Colon bacteria oxidise it to urobilinogen
  • Further oxidised to urobilin and stercobilin

MEH (9 decks)

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