7. Stem Cells and Blood Flashcards

1
Q

Name the 8 cells produced from Haematopoietic stem cells.

A

Eosinophils, RBCs, Megakaryocytes, Basophils, Neutrophils, Macrophages, Thymocytes and B Cells

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2
Q

Name the two components of the immune system.

A

Humoral Immunity and Cellular Immunity.

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3
Q

Name the two types of immune response.

A

Innate (natural) and Adaptive (acquired)

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4
Q

What is the role of Cytokines?

A

Low molecular weight, secreted protein that stimulates or inhibits cell differentiation and proliferation

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5
Q

What are antibodies?

A

Multi-chain glycoproteins that are produced by B-lymphocytes and which contain a very variable antigen-binding site and a functional (or constant) region.

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6
Q

Name the 3 types of Lymphocytes

A

T cells, B Cells and NK Cells (latter dont need to learn)

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7
Q

Name the 3 types of phagocyte

A

Monocytes, Macrophages and Neutrophils

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8
Q

Name the 3 types of Granulocytes

A

Eosinophils, Basophils and Mast Cells

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9
Q

Which cells produced by haematopoietic stem cells, are not considered to be part of the immune system?

A

RBCs and Platelets

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10
Q

Which cells are produced from myeloid stem cells?

A

Eosinphils, RBCs,Megakaryocytes, Basophils, Neutrophils and Macrophages

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11
Q

Which cells are produced from lymphoid stem cells?

A

Thymocytes and B Cells

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12
Q

What creates the specificity of the immune responses?

A

Lymphocytes, Small nucleated leukocytes

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13
Q

Where do T cells mature?

A

Thymus

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14
Q

List the four reasons why T cells are important.

A

Enhancing B cell responses, Enhancing phagocyte killing of intracellular bacteria, Killing virally infected cells and Regulating adaptive immunity.

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15
Q

Name a disease that can be caused due to lack of T cells.

A

DiGeorge Syndrome - Thymus doesn’t develop, immunoglobulin levels disturbed Leads to Candidaiasis, Pneumonia and diarrhea

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16
Q

Which cells produce antibodies (immunoglobulin)?

A

Plasma B cells

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17
Q

Where are B cells produced and mature?

A

Bone Marrow

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18
Q

What is the function of B cells?

A

They and their products are central to attacking extracellular pathogens (bacteria)

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19
Q

Name a disease that can be caused due to lack of B cells.

A

X-linked infantile hypogammaglobulinaemia - inability to produce any immunoglobulin - recurrent bacteria infection.

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20
Q

What is the difference between innate and adaptive immunity?

A

Adaptive Immunity: Shows learning, memory, specific antigen receptors (property of T and B Cells)
Innate Immunity: No learning or memory, Pattern Recognition receptors (Property of NK cells, Macrophages, Neutrophils and Complement)

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21
Q

What is the function of the protein complement?

A

Soluble proteins that complement the action of the antibodies, can also kill pathogen directly and mainly produced by liver

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22
Q

Describe the structure of Neutrophils.

A

Have a single, multi-lobed nucleus. Fine blue granules contain proteases and anti-microbial effector molecules such as defensins

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23
Q

Which molecule shows chemotaxis and what does it mean?

A

Neutrophils show chemotaxis and they are attracted to bacterial chemical products like the peptide fMLP

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24
Q

What is the function of eosinophils?

A

Mainly responsible for killing parasites that cannot be digested and they bind to antibody coated parasites, degranulate and dissolve the cell surface.

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25
Q

What is the function of basophils and mast cells?

A

They are involved in the acute inflammatory response and important in allergy and hypersensitivity.

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26
Q

What is the main difference between basophils and mast cells?

A

Basophils are circulatory and mast cells inhabit the mucosa and connective tissue.

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27
Q

Name the 5 Haematopoietic progenitors that you need to learn.

A

Haematopoietic stem cells (HSC), Multi-potent Progentor (MPP), Common Lymphoid progenitor (CLP), Granulocyte/monocyte progenitor (GMP) and Megakaryocyte/Erythroid Progenitor (MkEP)

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28
Q

Describe Early Erythropoietic Differentiation.

A

Pluripotential Stem Cells to Multipotential Stem Cells to BFU-E to CFU-E to Proerythroblasts which give rise to 16 erythrocytes

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29
Q

What does “-blast” at the end of a word indicate?

A

Indicates nucleus is still present.

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30
Q

What does “normo-“ at the start of a word equal to?

A

“Erythro-“ at the start

31
Q

How many cell divisions do proerythroblasts normally undergo?

A

4

32
Q

List the late erythropoietic changes

A

Cell volume gets smaller, nucleus gets more smaller and more dense, ejected in progression to reticulocyte and more and more haemoglobin present.

33
Q

Describe the structure of Proerythroblast.

A

Large (12-14 micrometres), Prominent nucleus and one or more nucleoli.

34
Q

Describe the structure of Basophilic Erythroblasts.

A

High Affinity for methylene blue, Similar in size or slightly smaller, nucleus still relatively large and no nucleoli

35
Q

Describe the structure of Polychromic Erythroblast.

A

Size is about 10 micrometres, nucelus much reduced and cytoplasm much paler and pink hues.

36
Q

Describe the structure of Orthochromic Erthroblast.

A

Nucleus even smaller, denser staining, and spherical. Cytoplasm even more pink.

37
Q

Describe the structure of Reticulocyte.

A

No nucleus, methylene blue stains a network of strands in cytoplasm (RNA), Lightly larger than erythrocyte.

38
Q

Name the molecules involved in control of erythropoiesis.

A

Cytokines, SCF, IL3, Thrombopoietin and Erythropoietin (epo)

39
Q

What causes increased Epo production?

A

Anaemia - leads to more mRNA in kidney and liver.

40
Q

When are Epo expressed?

A

Low levels of expression at BFU-E and high level expression at CFU-E and Epo is very sensitive to proerythroblast

41
Q

What is the role of Epo in erythropoiesis?

A

Promotes differentiation of megakaryocytes

42
Q

What happens during primary haemostasis?

A

Reduction of blood flow, Formation of a temporary plug in wall of damaged blood vessel. This is due to interaction of platelets and blood vessels

43
Q

What happens during secondary haemostasis?

A

Conversion of soluble fibrinogen to insoluble fibrin, strengthens initial haemostatic plug and this is due to soluble plasma proteins

44
Q

What happens during Fibrinolysis?

A

Degradation of fibrin plug after repair of wound.

45
Q

What are platelets?

A

Small membrane bound packets of granular cytoplasm with no nucleus.

46
Q

How are platelets produced?

A

They are during Thrombopoiesis in which they are formed by the pinching off and shedding of megakaryocytes

47
Q

What is the importance of Thrombopoietin?

A

Stimulation of megakaryocyte differentiation and proliferation. they are produced by kidney and liver.

48
Q

What are the 3 distinct processes occurring in thrombopoiesis?

A

Proliferation, Maturation and Circulation

49
Q

How long is the process of Thrombopoiesis

A

4-15 days

50
Q

What does endomitosis mean?

A

Nuclei undergo multiple mitotic divisions but no cytoplasmic division - formation of connected lobes.

51
Q

What happens during Proliferation?

A

Megakaryocytic cells undergo endomitosis. Process takes about 4 days in total. Produces very large cytoplasmic volume from which platelets bud.

52
Q

What happens during Maturation?

A

Formation of Secretory granules and demarcation membrane system which produces large surface area of membrane required for platelet shedding. Takes place between days 3-5.

53
Q

What happens during circulation?

A

Release of proplatelet packages, large cytoplasmic fragments undergo further fragmentation to form individual platelets. End with phagocytosis of nuclei and remaining cytoplasm. Occurs over day 4-15

54
Q

What is maturation and platelet release regulated by?

A

Thrombopoietin.

55
Q

How many platelets per day are produced by a single megakaryocyte?

A

40-60 platelets (about 1.6 x 10^11 platelets produced per day)

56
Q

How many days can platelets survive in circulation?

A

9-12 days

57
Q

How are old damaged and effete platelets removed?

A

Removed by sequestration in the spleen, followed by phagocytosis.

58
Q

What is the role of Canallcull in the structure of Platelets?

A

Channels deep into interior which radically increases surface area.

59
Q

What is the role of Glycocalyx - Surface Coat?

A

Contains glycoproteins that have a role in adhesion and aggregation and receptors for coagulation factors which enhance coagulation.

60
Q

What can you find on the plasma membrane of a platelet?

A

ADP receptor and platelet factor VIII

61
Q

What do the platelet granules contain and what are their roles?

A

Calcium, magnesium, ADP/ATP (for platelet aggregation), Serotonin and Thromoxane (for vasoconstriction) and PDGF (Platelet derived growth factor)

62
Q

What are the two phases of primary haemostasis?

A

Vascular and Platelet Phase

63
Q

Why does blood vasoconstriction occurs?

A

Restricts blood flow to area after injury. Neurogenic Response.

64
Q

What do the platelet adhere to?

A

Collagen exposed after injury breaks endothelial lining.

65
Q

What further exposes the basement membrane and collagen?

A

Contraction - Further platelet recruitment

66
Q

What causes release of vasoconstrictors (thromboxane and 5-HT)

A

Activation of Platelets

67
Q

What does prostacyclin do?

A

Inhibits platelet aggregation and causes vasodilation when theres no injury.

68
Q

What does the production of vWF cause?

A

Synthesis of basement membrane (damage repair)

69
Q

Describe the role of Thromboxane and Prostacyclin.

A

Thromboxane: Supresses cAMP sythesis which elevates Ca2+ levels.
Prostacyclin: Activates cAMPsynthesis which reduces Ca2+ levels.

70
Q

What does nitric oxide cause?

A

It inhibits platelet activation and promotes vasodilation by raising cGMP levels

71
Q

What molecules act as a bridge between the platelet and membrane resulting in platelet adhesion?

A

vWF and Factor VIII

72
Q

What effect does adhesion of platelets have on the platelets themselves.

A

Changes from discoid to irregular shape with pseudopod like projections which adhere to other platelets

73
Q

What causes granule release from platelets?

A

Activation of receptors for ADp, thromboxane and thrombin.

74
Q

What is the role of ADP and thromboxane?

A

Act as platelet chemoattractants