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IMED2002 > Lymphoma > Flashcards

Lymphoma Flashcards

1
Q

Which sites have the capacity to undergo lymphoid malignancy

A

Primary and secondary lymphoid organs are all potential sites of lymphoid malignancy

All regions of the lymph node (primary, secondary follicles, germinal centres, mantle zone, interfollicular zone) can undergo malignant transformation –> lymphoma

T cells reside in the interfollicular zone
B cells reside in the primary, secondary follicles & the germinal centres & the mantle area

Lymphomas are malignancies of lymphoid cells, in solid tissue sites –> then the malignancies can spread to the BM and blood circulation

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2
Q

Outline the key difference between leukaemia and lymphoma

A

Leukaemias commence in the bone marrow and then they spread to the blood

Whilst lymphomas are malignancies of solid tissue sites, and will not appear in the bloodstream

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3
Q

2 types of lymphomas

A

Non-Hodgkin lymphoma

Hodgkin lymphoma

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4
Q

What is characteristic of lymphoma

A

The replacement of normal lymphoid tissue with abnormal cells

Formation of neoplasms which are an abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should. Neoplasms may be benign (not cancer) or malignant (cancer).

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5
Q

Which lymphoma type is easiest to diagnose?

A

Hodgkin lymphoma with the characteristic Reed Sternberg cell

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6
Q

What are the 2 grades of non-Hodgkin lymphoma?

A

Low or High

Low: slow-growing, indolent, generally incurable

High: fast-growing, aggressive, potentially curable

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7
Q

What determines the prognosis of non-Hodgkin lymphoma?

A

The type: B or T cell origin
The grade: Low or High
The stage: extent (amount) of disease

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7
Q

What determines the prognosis of non-Hodgkin lymphoma?

A

The type: B or T cell origin
The grade: Low or High
The stage: extent (amount) of disease

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8
Q

Explain the aetiology of non-Hodgkin lymphoma

A

1) Immune suppression due to organ transplant, AIDS
2) Viral causes like EBV (Burkitt lymphoma), HTLV-I (Adult T cell lymphoma)

3) Geography - Burkitt = tropical Africa
Adult T cell lymphoma = Japan & Caribbean

4) Chronic inflammation/antigenic stimulation with helicobacter pylori (MALT lymphoma of the stomach)
5) Age: Low grade is rare in young, incidence increases with age

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9
Q

What are the clinical features of non-Hodgkin lymphoma?

A

Lymphadenopathy (swelling of lymph nodes)
Hepatosplenomegaly

Fever, night sweats, weight loss

Interference with normal organ function:
Solid-organ infiltration (kidneys, liver, other)
Skin, brain

As we have lymphoid tissue throughout the body, the lymphoma can be anywhere in the body and can cause localised symptoms/interfere with that organ system

Lymphoma can infiltrate and evolve and grow in the bone marrow
Bone marrow failure –> pancytopenia

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10
Q

How is non-Hodgkin lymphoma diagnosed?

A

Biopsy (obtain tissue of the involved region), then determine based on pathology

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11
Q

Which pathological features do you look out for in a biopsy, when trying to diagnose non-hodgkin lymphoma?

A

The pattern: whether nodular or diffuse
Cell size: small or large
Cell differentiation: well or poorly differentiated

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12
Q

What other tests may be useful to diagnose non-hodgkin’s lymphoma?

A

cell phenotype/ lineage (B or T)

Genetics on extracted cells, FISH analysis on specific chromosomal regions
Molecular genetics for mutations in particular genes

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13
Q

Which of the following is used to determine the clinical stage of non-hodgkin lymphoma?

(a) blood film phenotyping
(b) tissue biopsy phenotyping
(c) genetical testing using FISH
(d) radiologic examination
(e) molecular genetics and flow cytometry

A

d - physical, radiologic examination determines the extent of disease and the stage (CT scanning)

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13
Q

Stage I lymphoma involves

A

a single lymph node region or single extra lymphatic site

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14
Q

Stage II lymphoma involves

A

two or more sites, on the same side of the diaphragm

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15
Q

Stage IIIs lymphoma involves

A

Both sides of the diaphragm, or spleen (s)

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16
Q

Stage IV lymphoma involves

A

Diffuse involvement of extra lymphatic sites eg. the bone marrow

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17
Q

Bone marrow failure as a feature of lymphoma is characteristic of which stage?

(a) Stage I
(b) Stage II
(c) Stage IIIs
(d) Stage IV

A

Stage IV

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18
Q

There are 2 grades of lymphoma (high and low), classify the types of non-Hodgkin lymphoma within these 2 grades

A

Low grade: Follicular lymphoma

High grade: Burkitt lymphoma
Diffuse large B cell lymphoma

19
Q

Order the 3 non-Hodgkin lymphomas based on how common they are

A

Diffuse large B cell lymphoma = most common

Follicular lymphoma

Burkitt lymphoma

20
Q

What stage is follicular lymphoma at when diagnosed?

A

Stage IV = widely disseminated, including in the BM

as it is low grade, it grows slowly, indolent

21
Q

Follicular lymphoma

A

Affects adults over 40 years old

It is a B cell type lymphoma

There is a 5 -year survival upon diagnosis
Rarely curable

Some patients can progress from the chronic, indolent phase to a much more aggressive tumour (after 7 years from initial diagnosis)

The aggressive phase can be rapidly fatal unless treated

can only teat in the aggressive state, hig-grade state, not before

this has to do with the turnover rate of the malignant cells, can kill them with cytotoxic chemotherapy when they are active in the cell cycle

22
Q

What is the growth pattern of follicular lymphoma?

A

Follicular growth pattern

23
Q

What causes follicular lymphoma?

A

The development of most FL tumours in adults depends on the overexpression of B cell leukaemia/lymphoma 2 (BCL-2) located on chromosome 18. BCL-2 is an oncogene that blocks programmed cell death (apoptosis). As such, overexpression results in increased cell survival.

The t(14; 18) chromosomal translocation of human follicular lymphoma recombines the BCL-2 gene from chromosome 18 with the immunoglobulin heavy chain joining region.

The immunoglobulin heavy chain is heavily transcribed, and now along with it, the antiapoptotic protein Bcl-2 is also upregulated in expression.

This results in inhibition of programmed cell death, and generation of abnormal follicles

24
Q

Why watch and wait?

A

Watch & wait if indolent
If not impacting other organs
Unlikely to cure the patient, can promote resistance to the drugs then aggressive lymphoma won’t be cured

25
Q

Indications to treat are

A

Constitutional symptoms, painful lymph nodes
Anatomic obstruction, organ dysfunction
Marrow failure

26
Q

Treatment options

A

Radiotherapy
Chemotherapy
Antibody-based therapy (Rituximab, anti-CD20 which is a B cell antigen, is expressed by the tumour) remember this is a B cell type cancer
Combination therapy with antibody and chemotherapy
Bone marrow transplant

27
Q

Where is Burkitt lymphoma located in the lymph node

A

in the germinal centre

28
Q

Aetiology of Burkitt lymphoma

A

Endemic, sporadic, immuno-deficiency related

The African variety causes jaw tumours, abdominal mass, orbital tumours
and is EBV driven or sometimes HIV
Most common childhood tumour in sub-Saharan Africa

29
Q

Which age group does Burkitt lymphoma affect?

A

Child or adult

30
Q

Grade low or high? Burkitt

A

Rapidly growing high grade lymphoma

31
Q

Genetics of burkitt lymphoma

A

Translocation t(8;14)

Translocation of c-MYC (proto-oncogene) from chromosome 8 to IgH gene on chromosome 14 (this coming together causes the tumour)

MYC is a cancer causing gene (oncogene), it is upregulated when in close proximity to the IgH (which is highly upregulated)

32
Q

Burkitt lymphoma biopsy

A

Again, B cell type lymphoma derived from the germinal centre B cells

Shows a monotonous B cell infiltrate
Very large nucleus of the B cells, with basophilic cytoplasm and distinct vacuoles
Starry sky nucleus - high mitotic rate

33
Q

Treatment and cure chances

A

Treatment with aggressive chemotherapy

Potentially curable

34
Q

Diffuse Large B cell Lymphoma (presentation, pathology, histology)

A 
Most common (30%) 
Disease of adults mean age = 65 years

Presentation: rapidly enlarging masses

Pathology is not follicular, it is diffuse infiltration by large cells (usually B)

Diverse histology, poorly differentiated, bizarre morphology, high proliferation rate

High grade lymphoma

35
Q

Treatment

A

Combination chemotherapy with monoclonal antibody therapy
complete remission rates = 60 - 70%
Approximately 30% curable
Stem cell transplant in younger patients
CAR T cells

potentially curable due to the high turnover rates

36
Q

DLBCL clinical features

A

enlarged lymph nodes

Spleen is involved by the lymphoma

There are poorly differentiated, large cells

37
Q

Which factors are important in determining prognosis for DLBCL

A

Age (whether over 60, or under 60)
Performance status (capable or bedridden)
LDH enzyme (less than 1 or more than 1)
Disease stage 1, 2, 3, 4
Extranodal involvement (less than 1 or more than 1)

Treatment depends upon the sites, stage, age

38
Q

Hodgkin lymphoma is characterised by

A

the Reed-Sternberg cell

which makes up a very small amount of the tumour, but causes a big inflammatory reaction

39
Q

Hodgkin lymphoma age:

A

Hodgkin lymphoma peaks in young adults (20-30 years), and then the incidence increases over 50 years of age

40
Q

What does the Reed Sternburg cell look like?

A

It is a large cell, with 2 big nuclei that are positively stained

41
Q

Hodgkin lymphoma clinical features:

A

large, painless, non-tender, rubbery lymph nodes
cervical 60-70%
axillary 10-15%

shortness of breath, mediastinal involvement

Splenomegaly is rare at presentation

Then the constitutional symptoms like
fever, itch, weight loss

42
Q

What are other features of Hodgkin lymphoma

A

Reactive blood count & film features:
Normochromic, normocytic anaemia
Leucocytosis, mild eosinophilia, neutrophilia (increase in WBC count)

Reactive granulocytic hyperplasia (as if responding to an infection)

Bone marrow has reactive changes, that are rarely involved at presentation
Noticed as staging procedure

Reduced cell immunity with the loss of immunologically competent T cells

Cell immunity is compromised and patients are susceptible to viral infections

43
Q

How is a hodgkin lymphoma diagnosed?

A

Histology of lymph tissue/node
Noticing the reed sternberg cell (large, bi or multi nucleate, prominent nucleoli cell)

Inflammatory cells like lymphocytes, plasma cells, eosinophils

Variable fibrosis

44
Q

Immunophenotyping of hodgkin lymphoma

A

Reed sternberg cells express CD15 and CD30

antigens and are CD45 negative

45
Q

Treatment of hodgkin lymphoma

A

Potentially curable, early stage is favourable (1 or 2)

short duration chemotherapy, combined with drugs

field radiotherapy

in advanced disease: stage 3 and 4
more intensive combined chemotherapy needed

46
Q

Late effects of therapy

A

Second malignancies,
10% chance at 10 years
25% chance at 30 years

Lung cancer from radiotherapy is the most common

AML from the cumulative dose of alkylating agents –> damage to HSC at large doses of chemotherapy

Breast cancer, because of radiotherapy to mediastinum / axilla
dose-response relation exists

Skin cancers

Aim is to cure, and 80 - 90% will be

47
Q

Prognosis of Hodkin lymphoma

A

It is a curable maliganancy
80% will be cured
Prognosis is based on the stage of disease
Infections mean reduced cell mediated immunity

Relapsed disease is difficult to treat
need BM transplant
second malignancies can occur 5%

IMED2002 (12 decks)

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