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Kat's Pathology > Lymphoma: Multidisciplinary > Flashcards

Lymphoma: Multidisciplinary Flashcards

1
Q

What systems are part of the lymphoreticular system (3)

A

Generative LR tissue
Reactive LR tissue
Acquired LR tissue

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2
Q

What forms the generative lymphoreticular system (2)

A

Bone marrow and thymus

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3
Q

Function of generative LR tissue

A

Generation/maturation of lymphoid cells

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4
Q

Components of reactive LR tissue (2)

A

Lymph node

spleen

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5
Q

Function reactive LR tissue

A

Development of immune reaction

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6
Q

Components acquired LR tissue

A

Extranodal lymphoid tissue (skin, stomach, lung)

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7
Q

Function LR tissue

A

Development of local immune reaction

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8
Q

Cells of LR system (2)

A

Lymphocytes

Accessory cells

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9
Q

How are lymphocytes classified

A

B lymphocytes

T lymphocytes

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10
Q

Characteristics of B lymphocytes (2)

A

Express surface immunoglobulin

Antibody production

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11
Q

Characteristics of T lymphocytes (3)

A

Express surface T cell receptor
Regulation of B cell and macrophge function
Cytotoxic function

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12
Q

Some accessory cells (3)

A

Antigen presenting cells
Macrophages
Connective tissue cells

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13
Q

What comprises the B cell area in the lymph node (2)

A 
Paracortical T cell zone 
Lymphoid follicle (mantle zone, germinal centre)
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14
Q

What are the components of the lymphoid follicle (2)

A

Mantle zone - naive unstimulated B cells

Germinal centre - B cells, antigen presenting cells

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15
Q

What is significant about the germinal centre

A

This is where B cells which bind antigen epitopes are selected and activated

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16
Q

What is significant about the T cell area

A

This is where T cells which bind antigen epitopes are selected and activated

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17
Q

Components of the T cell area (3)

A

T cells
Antigen presenting cells
High endothelial vessels

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18
Q

How are lymphocyte subtypes identified

A

Identify lymphocyte subtypes and different stages of development by the different types of cell surface receptors expressed by the cells (CD markers)

Detected in tissue sampling by immunohistochemistry

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19
Q

Definition of lymphoma

A

Neoplastic proliferation of lymphoid cells forming discrete tissue masses

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20
Q

Where do lymphomas arise

A

Arise in and involve lymphoid tissues (including acquired lymphoid tissue - extranodal lymphomas)

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21
Q

Classification of lymphomas (2)

A

Hodgkin lymphoma

Non-Hodgkin lymphoma (B cell type most common, T cell type)

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22
Q

What predisposes to lymphoma

A

Immunosuppression predisposes to development of lymphoma (infection, loss of surveillance)

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23
Q

What is the pathogenesis of lymphoma (2)

A

Neoplastic proliferation of lymphoid cells - clonal

Mutation in genes to allow uncontrolled cell growth

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24
Q

Causes of mutations leading to lymphoma (5)

A

Normal lymphocytes undergo controlled genomic “instability” of lymphoid cells - mistakes in this process produce neoplastic mutations
Inherited disorders – inherited disorder resulting in increased/abnormal genomic instability
Viral agents – EBV, HTLV-1
Environmental agents – mutagens, chronic immune stimulation (e.g H pylori)
Iatrogenic causes – radiotherapy, chemotherapy

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25
Q

WHO classification of lymphoma

A

Hodgkin: Classical, lymphocyte predominant

Non-Hodgkin lymphoma: B cell (precursor B cell, peripheral B cell), T cell (precursor T cell, peripheral T cell)

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26
Q

Most common form of lymphoma

A

B cell Non-Hodgkin lymphomas (80-85%)

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27
Q

When do lymphomas arise

A

Can arise at different stages of lymphocyte development and activation
Therefore in certain lymphomas the neoplastic lymphoid cell resembles a normal counterpoint both in morphology and in the pattern of CD markers expressed

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28
Q

Where are the neoplastic lymphoid cells present

A

Circulate in the blood

Hence often disseminated at presentation - exception is Hodgkin lymphoma and some very early NHL

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29
Q

What effect do lymphomas have on the immune system

A

They may disrupt normal immune system - therefore patients may develop immunodeficiencies

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30
Q

Lymphomas arising from germinal centre (4)

A

Follicular lymphoma
Burkitt lymphoma
Diffuse large B cell lymphoma
Hodgkin lymphoma

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31
Q

Lymphomas arising from post germinal centre (4)

A

Diffuse large B cell lymphoma
marginal zone lymphoma
Small lymphocytic lymphoma
Chronic lymphocytic leukaemia

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32
Q

What are the diagnostic tools for lymphoma (2)

A

Cytology: look at single cells aspirated from a lump
Histology: look at tissue sections

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33
Q

What do you look at histologically in lymphoma (2)

A

Architecture (nodular, diffuse)

Cells (small round, small cleaved, large (centroblastic, immunoblastic, plasmoblastic))

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34
Q

What is immunohistochemistry used for

A

Used to identify proteins on/in cells in tissue sections

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35
Q

How does immunohistochemistry work

A

Use labelled antibody to cell surface receptor

Dye label is visible under light microscope in tissue sections

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36
Q

What can you determine with immunopheontyping (5)

A

Cell type (T = CD3, CD5, B = CD20)
Cell distribution
Loss of normal surface proteins (e.g. neoplastic T cells)
Abnormal expression of proteins (often secondary to specific chromosomal/gene abnormalities e.g. cyclin D1)
Clonality of B cells - light chain expression

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37
Q

What molecular tools are available for lymphoma analysis (2)

A

FISH - identify chromosome translocations

PCR - identify chromosome translocations and clonal T cell receptor or immunoglobulin gene rearrangement

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38
Q

How can PCR be used in lymphoma (2)

A

Diagnostic - e.g. 11;14 mantle cell lymphoma

Prognostic - e.g. 2;5 Anaplastic large cell lymphoma

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39
Q

Low grade Non-Hodgkin lymphomas (4)

A

Follicular lymphoma
Small lymphocytic lymphoma/chronic lymphocytic leukaemia
Marginal zone lymphoma
Mantle zone lymphoma

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40
Q

High grade Non-Hodgkin lymphoma

A

Diffuse large B cell lymphoma

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41
Q

Intermediate grade Non-Hodgkin lymphoma

A

Burkitt’s lymphoma

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42
Q

Clinical presentation of follicular lymphoma (2)

A

Lymphadenopathy

MA/elderly

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43
Q

Histopathology follicular lymphoma (2)

A

Follicular pattern

Germinal centre cell origin CD10, bcl-6+

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44
Q

Molecular pattern follicular lymphoma

A

14;18 translocation involving bcl-2 gene

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45
Q

Typical grade of follicular lymphoma

A

Indolent but can transform to high grade lymphoma

46
Q

Immunohistochemistry in follicular lymophoma

A

Detection of bcl-2 expression by neopalstic B cells in follicles

47
Q

Clinical presentation small lymphocytic lymphoma/CLL (2)

A

MA/elderly

Nodes or blood

48
Q

Histopathology small lymphocytic lymphoma/CLL

A

Small lymphocytes
Naive or post-germinal centre memory B cell
CD5, CD23

49
Q

Molecular pattern small lymphocytic lymphoma/CLL

A

Multiple genetic abnormalities

50
Q

Typical grade for small lymphocytic lymphoma/CLL

A

Indolent, but can transform to high grade lymphoma (richter transformation)

51
Q

Cause of marginal zone lymphoma/MALT

A

Thought to arise in response to chronic antigen stimulation (e.g. by Helicobacter in stomach)

52
Q

Site of origin for marginal zone lymphoma/MALT

A

Arise mainly at extranodal sites (many sites e.g. gut, lung, spleen)
Post germinal centre memory B cell

53
Q

Typical grade marginal zone lymphoma/MALT

A

Indolent but can transform to high grade lymphoma

54
Q

Treatment of low grade marginal zone lymphoma/MALT

A

Can treat low grade disease with non-chemotherapeutic modalities - i.e. remove antigen

55
Q

Clinical features mantle cell lymphoma (3)

A

MA male predominence
Lymph nodes, GI tract
Disseminated disease at presentation

56
Q

What is the histopathology of mantle cell lymphoma (3)

A

Located in mantle zone
Pre-germinal centre cell
Aberrant CD5, cyclin D1 expression

57
Q

What are the molecular features of mantle cell lymphoma (2)

A

11;14 translocation

Cyclin D1 over expression

58
Q

What is the median survival rate for mantle cell lymphoma

A

3-5 years

59
Q

Clinical features of Burkitt’s lymphoma (3)

A

Jaw or abdominal mass in children and young adults (endemic, sporadic, immunodeficiency)
EBV associated
Aggressive disease

60
Q

Histopathology of burkitt’s lymphoma (2)

A

Germinal centre cell origin

Starry sky appearance

61
Q

Molecular features of burkitt’s lymphoma

A

c-myc translocation (8;14, 2;8, 8;22)

62
Q

Clinical features of diffuse large B cell lymphoma (2)

A

MA/elderly

Lymphadenopathy

63
Q

Histopathology of diffuse large B cell lymphoma (4)

A

Germinal center or post-germinal center B cell
Sheets of large lymphoid cells
Germinal center phenotype = good prognosis
p53 positive, high proliferation fraction = poor prognosis

64
Q

Features of T cell lymphoma (5)

A 
MA/elderly
Lymphadenopathy and extranodal sites
Large T lymphocytes
Often with associated reactive cell population, esp eosinophils
Aggressive
65
Q

Special forms of T cell lymphoma (4)

A

Adult T cell leukaemia/lymphoma
Enteropathy associated T cell lymphoma
Cutaneous T cell lymphoma
Anaplastic large cell lymphoma

66
Q

What are the associations with adult T cell leukaemia/lymphoma (2)

A

Caribbean and Japan

HTLV1 infection

67
Q

What is associated with enteropathy associated T cell lymphoma

A

Some patients with long standing coeliac disease

68
Q

Clinical features of anaplastic large cell lymphoma (3)

A

Children/young adults
Lymphadenopathy
Agressive

69
Q

Histopathology anaplastic large cell lymphoma (2)

A

Large epithelioid lymphocytes

T cell or null phenotype

70
Q

Molecular features of anaplastic large cell lymphopma (2)

A

2;5 translocation

Alk-1 protein expression - better prognosis

71
Q

Features of Hodgkin lymphoma (5)

A

More often localised to a single nodal site
Spreads contiguously to adjacent lymph nodes
Classical, with several subtypes
Lymphocyte predominent
Moderately agressive

72
Q

Features of Non-Hodgkin lymphoma (2)

A

More often involves multiple lymph node sites

Spreads discontinuously

73
Q

Subtypes of classical Hodgkin’s lymphoma (3)

A

Nodular sclerosing
Mixed cellularity
Lymphocyte rich and lymphocyte depleted

74
Q

Clinical features of classical HL (2)

A

Young and MA

Often involves just a single lymph node group

75
Q

Origin of classical HL

A

Germinal centre/post-germinal centre B cell origin

76
Q

Associations of classical HL

A

EBV

77
Q

Histopathology of classical HL

A

Sclerosis, mixed cell population in which scattered Reed-Sternberg and Hodgkin cells with eosinophils

78
Q

Clinical features of nodular HL (4)

A

Isolated LN
Lymphadenopathy
Indolent
Can transform to high grade B cell lymphoma

79
Q

Origin of nodular HL

A

Germinal centre B cell (positive for some germinal centre B cell markers)

80
Q

Nodular HL associations

A

No associations, not associated with EBV

81
Q

Histopathology of nodular HL

A

B cell rich nodules with scattered L&H cells

82
Q

What is involved in haemato-oncological diagnosis (4)

A

Morphology
Immunophenotyping
Cytogenetics
Molecular genetics

83
Q

What is meant by morphology of a tumour (3)

A

Architecture of the tumour
Cytology
Cytochemistry

84
Q

What is involved in immunopheonotype (2)

A

Flow cytometry

Immunohistochemistry

85
Q

What is involved in cytogenetics (2)

A

Conventional karyotyping

FISH

86
Q

What is involved in molecular genetics (4)

A

Mutation detection
PCR analysis
Gene expression profile
Whole genome sequencing

87
Q

What is lymphoma

A

It is a neoplasm of lymphoid cells

88
Q

Where do lymphomas occur (4)

A

Lymph nodes, bone marrow and/or blood (lymphatics)
Lymphoid organs (spleen, GALT)
Skin (often T cell disease)
Rarely, anywhere (CNS, occular, testes, brest, etc…)

89
Q

What is the incidence of lymphoma

A

10,000 new cases/year in the UK
NHL - 80%
HL - 20%

90
Q

Why are cancers of the immune system so dangerous (3)

A

Rapid proliferation - increases risk of DNA replication error.
Normal cells are dependent on apoptosis - apoptosis is switched off in the geminal centre, acquired DNA mutation in pro apoptotic genes
Great potential for recombination errors and new point mutations

91
Q

What immunoglobulin gene recombinations are involved in lymphoma (2)

A

VDJ recombination. Occurs in bone marrow, Key enzymes RAG1+2, TdT

Class switch recombination. Somatic hypermutation. Key enzymes: adenosine induced deaminase.

92
Q

What chromosomal translocations are involved in lymphoma

A

t(8;14)

Lymphoma/recombination associated translocations involve the Ig locus. Ig promoter is highly active in B cells, bring intact oncogenes close to the Ig promoter. Oncogenes may be anti-apoptotic, proliferative (bcl2, bcl6, Myc, cyclinD1)

93
Q

Risk factors for lymphoma (4)

A

Majority of cases no identifiable risk factor.
Constant antigenic stimulation
Infection (direct viral infection of lymphocytes)
Loss of T cell function

94
Q

Give examples of antigenic stimulation that may lead to lymphoma (3)

A

H.Pylori : Gastric MALT (mucosa associated lymphoid tissue) Marginal Zone NHL of stomach
Sjogren syndrome : Marginal Zone NHL of Parotid lymphoma
Coeliac disease: small bowel T cell lymphoma EATL (enteropathy associated T-Cell Non Hodgkin lymphoma)

95
Q

What infections are associated with lymphoma (2)

A

HTLV1 infection of T cells

Immunosuppression and EBV infection (e.g. HIV, PTLD - post transplant lymphoproliferative disorder)

96
Q

Reed Sternberg cells

A

Classical Hodgkin Lymphoma

97
Q

B cell lymphomas (2)

A

Precursor B lymphoblastic leukaemia or lymphoma

Mature B cell neoplasm: DLBCL, Follicular, NHL, CLL

98
Q

T/NK cell lymphoma (2)

A

Precursor T lymphoblastic leukaemia or lymphoma

Mature T and NK neoplasm: PTCL, anaplastic, cutaneous

99
Q

Features of HL

A

HL is more common in males than females.
Bimodal age incidence: Most common age 20-29, young women NS subtype; Second smaller peak affecting elderly >60 years old

Painless enlargement of lymph node/nodes.
May cause obstructive symptoms/signs
Constitutional symptoms; fever, night sweats weight loss (the B symptoms) and pruritis may be present. Rarely alcohol induced pain present.

100
Q

Classical HL subtypes (4)

A

Nodular sclerosing 80%- Good prognosis (causes the peak incidence in young women)
Mixed cellularity 17% - Good prognosis
Lymphocyte rich (rare)- Good prognosis
Lymphocyte depleted (rare)- Poor Prognosis

101
Q

How are HL staged

A

FDG-PET/CT scan

Consider biopsy of other site if possibly infiltrated e.g. liver

102
Q

Staging in lymphoma

A

Stage 1 - one group of nodes
Stage 2 - >1 group of nodes on same side f diaphragm
Stage 3 - nodes above and below the diaphragm
Stage 4 - extra nodal spread

Suffix A if none of below, B if any of below:
Fever
Unexplained weight loss >10% in 6 months
Night sweats

103
Q

How does chemotherapy work for lymphoma

A

Given as a combination of drugs which affect the malignant cells in different way s

104
Q

How does radiotherapy work in lymphoma

A

HL is highly responsive to radiotherapy, can be given at end of chemo as an Involved field a small area only targeting diseased nodes (less toxicity to normal tissue)

105
Q

Chemotherapy for HL (4)

A 
ABVD - given at 4 weekly intervals (2-6 cycles)
Adriamycin 
Bleomycin
Vinbalstine 
DTIC

Effective treatment
Preserves fertility
Can cause pulmonary fibrosis and cardiomyopathy (long term)

106
Q

What are the risks of radiotherapy for lymphoma treatment (3)

A

Ca breast (risk 1:4 after 25 years)
Leukaemia/mds (3%@10years)
Lung or skin cancer

107
Q

How is radiotherapy given for lymphoma

A

Modern practice involved field only

108
Q

What is the risk of combined chemotherapy and radiotherapy treatment for lymphoma

A

Greatest risk of secondary malignancy

109
Q

Treatment of lymphoma

A

Chemotherapy for all cases (ABVD 2-6 cycles)
+/- Radiotherapy
PET CT scanning

Relapse - high dose salvage chemotherapy, autologous PB stem cell transplant as salvage.

110
Q

HL prognosis

A

Older patients generally do less well as do those with lymphocyte depleted histology

Prognosis depends on stage
Cure rates range from 50-90% (over 80% of patients with stage 1 or 2 disease are cured, only 50% of stage 4 patients are cured)

111
Q

Arguments for and against reduced therapy

A

Reduced therapy - chemotherapy only, reduce risk of secondary malignancy, increased HL relapse

Intensify therapy - chemo +/- radiotherapy. Decrease HL relapse, increase secondary malignancy after 10 years.

Kat's Pathology (105 decks)

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