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Block 5 > 1.1 Haematopoiesis and its regulation > Flashcards

1.1 Haematopoiesis and its regulation Flashcards

1
Q

What are the characteristics of haematopoietic stem cells?

A 
Perpetual 
Extensive proliferation 
Self renewal 
Pluripotency 
Quiescence
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2
Q

What are the characteristics of progenitor cells?

A 
Non perpetual 
Limited proliferative capacity 
Diminished or no self renewal 
Lineage commitment 
Mor actively cycling
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3
Q

What will you see for Haematopoietic Stem Cells on flow cytometery?

A

CD34+ CD45 RA -/low

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4
Q

Where does haemopoiesis occur at different stages of gestation?

A

Aorta Gonad Mesonephros (4-5 weeks)

Yolk sac (4-6 weeks)

Fetal liver (6-22 weeks)

Bone marrow (16 weeks onwards)

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5
Q

In what adult bones does haempoiesis occur?

A

pelvis, ribs, spine, skull and proximal parts of arm/leg bones

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6
Q

What types of blood cells arise from the CLP?

A

B, T and NK cells

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7
Q

What types of blood cells arise from the CMP?

A

platelets, RBC, mast cells, basophils, neutrophiles, eosinophils, monocytes

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8
Q

Describe the process of erythropoiesis

A

The kidneys detect low levels of circulating oxygen and this stimulates the production of EPO. EPO will travel to the bone marrow and stimulate precursors to make RBCs and increase the oxygen carrying capacity of the blood. This will feedback to the kidneys to stop further production of EPO

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9
Q

Describe the mechanism of the JAK/STAT pathway

A

A cytokine will bind to the cytokine receptor and activate the JAK protein. This causes phosphroylation of the STAT transcription factors. This results in their dimerization and translocation to teh cell nucleus. Here the STAT dimers activate transcription of specific genes

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10
Q

Describe the mechanism of the JAK/STAT pathway

A

A cytokine will bind to the cytokine receptor and activate the JAK protein. This causes phosphroylation of the STAT transcription factors. This results in their dimerization and translocation to teh cell nucleus. Here the STAT dimers activate transcription of specific genes

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11
Q

What regulates erythropoiesis?

A

Erythropoietin.

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12
Q

What is the role of erythroferrone?

A

Erythroferrone is released in response to increased EPO levels. This will supress the hepcidin production by the liver allowing an increased availability of iron to be used for oxygen transport

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13
Q

Describe the breakdown of RBCs

A

Macrophages in the bone marrow and spleen break down the RBCs into heme and then bilirubin. The bilirubin travels linked to albumin to the liver. Here the bilirubin is conjugated and secreted in the bile. In the small intestine the conjugated bilirubin is converted back into bilirubin and into urobilinogen. If it remains in the colon it is converted into stercobilin and excreted in teh feces, if it enters the plasma and is filtered by the kidney it is converted to urobilin and excreted in the urine.

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14
Q

What is the structure of the red cell membrane?

A

Phosopholipid bilayer with membrane proteins and a membrane skeleton

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15
Q

What forms the red cell membrane skeleton?

A

alpha and beta spectrin, ankyrin, protein 4.1 and actin

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16
Q

What are the two pathways for RBC energy production?

A

Glycolysis and antioxidant production

17
Q

What is the pathway of granulocyte production called and what are the blood cells formed?

A

Granulopoiesis - neutrophils, eosinophils, monocytes, macrophages, basophils/mast cells

18
Q

What is the role of GCSF?

A

stimulate the production of neutrophils - can be given therapeutically

19
Q

What is the role of IL-6 in grabulopoiesis?

A

Stimulates emergency white cell production. The production of IL6 indicates an infection which will sitmulate macrophages into making an enzyme ADAM which will go to teh surface of immature immune cells and macrophages cleaving off teh IL6 receptor. This receptor wil form a complex which will travel to the bone marrow to stimulate emergency granulopoiesis

20
Q

Describe the production of platelet formation and what is this process called?

A

Thrombopoiesis

TPO will go to the bone marrow causing stimulation of megakaryocytes to make platelets

21
Q

Describe the production of platelet formation and what is this process called?

A

Thrombopoiesis

TPO will go to the bone marrow causing stimulation of megakaryocytes to make platelets

22
Q

What are the processes involved in platelets forming clots?

A

Adhesion, activation, aggregation and formation of a haemostatic plug

23
Q

Describe adhesions of platelets

A

Glycoproten Ib binds to von willebrand factor leading to the adhesion to teh subendothelium

24
Q

Describe activation of plateleys

A

Adhesion triggers glycoprotein IIb/IIa activation causing irreversible binding

25
Q

Describe aggregation of platelets

A

Activated GP IIb/IIa mediates aggregation of fibrinogen and VW factor

26
Q

What do you need for stem cells to survive?

A

the haemopoietic microenvironment including glial cells, neurons, MSC, endothelial cells, CEMP cells and adipocytes

27
Q

What are the disorders of too much, too little and poor quality RBCs?

A

too much: polycythaemia

Too little: anaemia

Poor quality: haemaglobinopathy, RC enzymopathy, RC membrane defects

28
Q

What are the disorders of too much, too little and poor quality white cells?

A

Too much: leucocytosis, leukaemia, lymphoma

Too little: leucopenia, lymphopenia

Poor quality: chronic granuloma disease

29
Q

What are the disorders of too much, too little and poor quality platelets?

A

Too much: thrombocytosis/cythaemia

Too little: thrombocytopaenia

Poor quality: functional platelet disease, storage pool disease

30
Q

What are the primary and secondary causes of polycythaemia?

A

Primary: bone marrow diseases

secondary: EPO mediated (bone marrow told to make too much)

31
Q

What are the causes of true polycythaemia?

A 
Sensitization of EPO receptor 
JAK-2/CAL-R mutation in stem cell progenitor cells 
Defective EPO receptor 
Reduced O2 carrying capacity  
Polycystic kidney disease 
post transplant erythrocytosis 
any hypoxic conditions
32
Q

What are the causes of anaemia?

A 
Defective EPO receptor 
congenital conditions 
B12/folate deficiency 
Marrow damage (drugs, radiation) 
Anaemia of chronic disease 
Blood loss 
premature mechanical or immune destruction of RBC 
chronic kidney disease 
Immune deficiency of EPO
33
Q

What are the causes of anaemia?

A 
Defective EPO receptor 
congenital conditions 
B12/folate deficiency 
Marrow damage (drugs, radiation) 
Anaemia of chronic disease 
Blood loss 
premature mechanical or immune destruction of RBC 
chronic kidney disease 
Immune deficiency of EPO
34
Q

What is leukaemia?

A

disruption of the normal processes that regulate differentiation and development characterised by the accumulation of malignant haemopoietic precursors

35
Q

What are the causes of reduced granulopoiesis?

A 
Acquired mutations 
stromal cell damage 
increased destruction (immune, splenic) 
Immunosuppressive drugs 
Increased magrination 
B12/folate deficiency  
Infection 
Drugs 
Immune insult 
Defective GCSF receptor 
Genetic abnormalities (Downs)
36
Q

What causes increased thrombopoiesis?

A

Infection and inflammation

Acquired mutations in JAK2, CALR, bcr-abl and TPOR

37
Q

What causes reduced thrombopoiesis?

A 
Liver diease
B12/folate deficiency 
Acsuired muattions in MDS 
Congenital syndromes: TARS 
Immune insult 
Drugs 
Marrow insults (radiation) 
Increased destruction (immune, mechanical, spleen)
38
Q

What causes reduced thrombopoiesis?

A 
Liver disease
B12/folate deficiency 
Acquired mutations in MDS 
Congenital syndromes: TARS 
Immune insult 
Drugs 
Marrow insults (radiation) 
Increased destruction (immune, mechanical, spleen)

Block 5 (35 decks)

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