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Clinical Immunology and Haematology > Malignant Haematology > Flashcards

Malignant Haematology Flashcards

1
Q

What two categories are white blood cells broken down into?

A

Split into myeloid cells and lymphoid cells

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2
Q

Name some myeloid cells and are these granulocytes?

A

Neutrophils, eosinophils, basophils are all granulocytes
Monocytes are tissue macrophages and are not granulocytes

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3
Q

Name some lymphoid cells?

A

Natural killer cells
B lymphocytes
T lymphocytes

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4
Q

How many lobes do neutrophils normally have and are they common in adult blood?

A

Majority of mature myeloid cells in the body with three or 4 lobes.

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5
Q

How many lobes do hypersegmented neutrophils have?

A

Hypersegmented neutrophils are neutrophils with 5+ lobes.

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6
Q

Where are neutrophil precursors from?

A

Their precursors are normally only in bone marrow

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7
Q

What diseases are neutrophils important in?

A

Bacterial and fungal infections

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8
Q

What do chemotaxins do to neutrophils?

A

They direct them to the site of infection

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9
Q

What are some examples of chemotaxins?

A

Complements, leucocyte adhesion molecules

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10
Q

Neutrophils - What is phagocytosis?

A

The ability for neutrophils to ingest invading pathogens once they have been opsonized by complement.

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11
Q

How do neutrophils kill pathogens after creating the phagosome?

A

Reactive oxygen species and hydrolytic enzymes

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12
Q

What can neutrophils release that has antimicrobial properties?

A

Granules

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13
Q

What are NETS and what are they made of?

A

Neutrophil extracellular traps made of DNA

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14
Q

What does seeing myeloblasts make you concerned about and why?

A

These are really early neutrophil precursors and so you would worry about issues in the bone marrow not letting them form properly.

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15
Q

What do we mean by saying a blood film is left shifted?

A

You are seeing more immature cells

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16
Q

What do eosinophils have a special role in?

A

Allergic responses and parasitic defence

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17
Q

What do basophils contain?

A

Heparin (blood clotter) and histamine (inflammatory response)

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18
Q

What type of receptors do basophils have?

A

IgE

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19
Q

What do monocytes do?

A

Migrate to tissues and transforms into macrophages and dendritic cells

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20
Q

What do monocytes do during infection?

A

Phagocytose, antigen presentation and cytokine production

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21
Q

Where do monocytes reside?

A

Spleen

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22
Q

What is neutrophilia and what causes this?

A

Too many neutrophils and can be caused by pregnancy, inflammation, steroids, chemotherapy etc.

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23
Q

Benign Disorders - neutropenia - does this have ethnic variations?

A

Yes

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24
Q

Symptoms of neutropenia?

A

Recurrant infections, opportunistic and unusual infections

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25
Q

Can you get neutropenia where you have the correct number of neutrophils but they are non-functional?

A

Yes

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26
Q

lymphocytes - what part of the immune system are they in and what do they do?

A

innate immunity who identify known self antigens during antigen presentation

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27
Q

Where are lymphocytes produced?

A

Bone marrow

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28
Q

Where do t cells mature?

A

thymus

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29
Q

what are the secondary lymphoid organs lymphocytes circle round?

A

Lymph nodes and spleen

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30
Q

Do lymphocytes create memory cells?

A

yes

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31
Q

Plasma cells - what do these secrete?

A

Antibodies

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32
Q

What causes multiple myeloma?

A

Clonal proliferation of plasma cells

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33
Q

B lymphocytes - what receptors for antigen do they have?

A

Immunoglobin - IgM, IgG, IgA, IgE, IgD

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34
Q

What part of the B lymphocytes are variable for antigen specificity?

A

Fab region

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35
Q

Can B lymphocytes make memory B cells?

A

Yes

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36
Q

How do you identify a multiple myelonoma?

A

Detecting a monoclunal immunoglobulin fragment made by malignant plasma cells called a paraprotein

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37
Q

What can you find out about T cells from their receptor?

A

T-cell and you can work out if these all come from the one clone or several and adjuct reaction as needed.

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38
Q

What does the thymus do in T-lymphocytes?

A

Delete self reactive T cells
Select for T-cells with host HLA specificity

39
Q

What are some types of markers T-cells express?

A

CD8 +ve cytotoxic cells
CD4 +ve helper cells

40
Q

What do CD8 +ve cytotoxic cells do?

A

Bind to virus infected or damaged cells. They release cytotoxins to kill these cells by lysis or apoptosis?

41
Q

What do CD4 +ve helper cells do?

A

Produce cytokines that activate macrophages B cells and NK cells

42
Q

Do NK cells have receptors?

A

No but they express CD8

43
Q

What part of the immune system is NK cells apart of?

A

Innate immune system

44
Q

What types of cells do NK cells destroy through cytotoxic ways?

A

Viral infections and tumours

45
Q

Immunodeficiency - what are some signs of this?

A

Clinically recurrant or unusual infections

46
Q

Primary immunodeficiency can be what diseases?

A

These are inherited disorders such as X-linked agammaglobulinaemia, SCID or CVID

47
Q

Secondary immunodeficiency diseases?

A

These are acquired disorders such as HIV, lymphoproliferative disorders, nephrotic syndrome, drug-induced lymphopenia

48
Q

What would an acute disease refer to?

A

Overproliferation of immature cells
This happens more rapidly/ aggressive

49
Q

What would chronic disease refer to?

A

Overproliferation of mature cells
There is a long history or indolent disease

50
Q

Lymphoid disorders are about what?

A

Solid organs (lymphoma)

51
Q

What are myeloid diseases concerning?

A

Blood/bone marrow (leukemia)

52
Q

How would you investigate and classify haematological malignancies?

A
  • Morphology
  • Immunophenotyping
  • Cytogenetics.
53
Q

In myeloid can you only have acute or chronic leukemia?

A

Yes

54
Q

In lymphoid can you only have acute or chronic lymphoma?

A

No you can also have acute and chronic leukemia too

55
Q

What are some differences between high Grade and Low grade lymphoid diseases?

A

High grade is quick overproliferation and needs treatment whereas low grade is slower over proliferation/ indolent disease and in some cases needs no treatment.

56
Q

Morphological changes to blood film - leukaemic blasts?

A

Large cells which more nucleus compared to cytoplasm

57
Q

Morphological changes to blood film - myeoblasts?

A

Tend to have more granules

58
Q

Can you tell lymphoid vs myeloid from a blood film?

A

No

59
Q

Immunophenotyping - what are some cell marker expressions?

A

CD45 - common leucocyte antigen
CD34, TdT - immature progenitors
Myeloid - CD13, CD33
B lineage - CD19, CD22, CD10, Ig
T lineage - CD7 and CD3

60
Q

What can CD antigens on cell surface tell you?

A

The lineage of the cell and how mature the cells are

61
Q

Genetics of haematological malignancies - what happens in stable cells?

A

There is a balance between proto-oncogenes and tumour supression genes leading to regulated proliferation and apoptosis

62
Q

Genetics of Haematological malignancies - what happens in a malignant cell?

A

Chemicals, radiation, drugs, virus, translocations, deletion etc can cause the tumour supressor gene to turn off and the oncogene increases its signal - this causes excessive proliferation and failure to apoptose

63
Q

What is cytogenetics?

A

Karyotyping cells in metaphase to look for translocations, deletions and monosomies

64
Q

What type of molecular studies can you use to genetically investigate malignancies?

A

PCR and FISH

65
Q

Why use genetics?

A

Helps diagnose disease
Helps understand prognosis and treatment choice
Helps monitor responses to treatment (tailor therapy, minimal residual disease)

66
Q

What causes acute leukemia?

A

Overproliferation of immature blast cells

67
Q

What are symptoms of acute leukemia?

A

Variable cytopenias, leucocytosis or leucopenia. This is dependant on the stage of the disease, as the malignant cells overproliferate in the bone marrow they push the leucocytes into the blood, however once the bone marrow is full of malignant cells they can no longer make leucocytes.

68
Q

When would you diagnose acute leukaemia?

A

More than 20% blasts in the bone marrow or through genetic testing

69
Q

Where could acute leukemia infiltrate to?

A

Skin, gums, lymph nodes, liver, spleen, CNS

70
Q

Who is most likely to get acute myeloid leukaemia (AML)?

A

All ages although does increase with age

71
Q

AML - does this develop from primary mechanism or treatment related?

A

Both

72
Q

What is the prognosis of AML?

A

It is variable and dependant on age and cytogenic/molecular findings.
It is poor in adults over 60 but is improving and more than 50% of children and young adults

73
Q

What is meylodysplasia?

A

Progressive bone marrow failure due to abnormalities in any or all of the myeloid cell lines.

74
Q

What age group is more likely to get myeodysplasia?

A

Older age group

75
Q

Can myelodysplasia turn into AML?

A

Yes

76
Q

What can cause myelodysplasia?

A

Radiotherapy or chemotherapy

77
Q

Chronic myeloid leukemia (CML) - what causes this?

A

Clonal proliferation of mature bone marrow stem cells caused by the philadelphia chromosome which is a BCR-ABL fusion gene encoding tyrosine kinase signalling molecules.

78
Q

CML - what are the symptoms of this?

A

High WCC but asymptomatic before this

79
Q

What are the clinical features of CML?

A

Cytopenias, splenomegaly, constiruitional symptoms

80
Q

Treatment and prognosis of CML?

A

Targeted treatment with tyrosine kinase inhibitors - good prognosis

81
Q

Acute lymphoblastic leukaemia (ALL) - what age group is this most common in?

A

Children but has a second rise after 40

82
Q

What are the clinical features of ALL?

A

Cytopenias, infilatration of marrow or other organs, constitutional.

83
Q

What is the prognosis of ALL and what is this dependant on?

A

Dependant on age, minimal residual disease, WCC

Prognosis is good 80 - 90% cure in children

84
Q

Chronic lymphocytic leukaemia (CLL) - what are the signs of this?

A

B cell lymphocytosis in peripheral blood and small mature lymphocytes.
Cytopenias either from marrow infiltration or autoimmune

85
Q

CLL - what are some symptoms of this?

A

Lymphadenopathy and splenomegaly but usually asymptomatic and picked up on routine blood tests

Also, increased frequency/severity of infections - low immunoglobin level common

86
Q

What age gets CLL?

A

Normally older ages

87
Q

What is the prognosis of CLL?

A

Its usually indolent but can change into high grade and therefore not good then.

88
Q

How would you investigate CLL?

A

Flow cytometry

Genetics - chromosomal abnormalities, p53 deletions = treatment resistance

89
Q

What is a lymphoma?

A

Accumulation of malignant lymohocytes in lymphoid tissues and can infiltrate non-lymphoid tissues.

90
Q

What are symptoms of lymphoma?

A

Fever, weight loss, night sweats

91
Q

What are haematological findings of a lymphoma?

A

Cytopenias with advanced marrow disease

92
Q

Can you get low grade or high grade lymphomas involving the B cells or T cells?

A

Yes

93
Q

What would see on a lymphoma blood film?

A

So many of the same cell - lymphocytes

Clinical Immunology and Haematology (25 decks)

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