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HaemPath > Lymphoma 2 > Flashcards

Lymphoma 2 Flashcards

1
Q
  1. What are the stages of lymphoma?
A

1 = 1 group of nodes
2 = > 1 group of nodes on the same side of the diaphragm
3 = > 1 group of nodes above and below the diaphragm
4 = extranodal spread
Suffix ‘B’ if B symptoms are present

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2
Q
  1. Which type of scan is often used to stage lymphoma?
A

FDG-PET/CT

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3
Q
  1. Which treatment modalities are used in Hodgkin lymphoma?
A

All patients receive chemotherapy
Radiotherapy is often used because Hodgkin lymphoma is very responsive
Referred to as ‘combined modality’ if both are used

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4
Q
  1. Which chemotherapy regimen is usually used for Hodgkin lymphoma?
A

ABVD: Adriamycin, Bleomycin, Vincristine, Dacarbazine
NOTE: this is usually given at 4-weekly intervals for 2-6 cycles

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5
Q
  1. What are some possible long-term consequences of chemotherapy for Hodgkin lymphoma?
A

Pulmonary fibrosis

Cardiomyopathy

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6
Q
  1. What is a risk of radiotherapy for Hodgkin lymphoma?
A

Collateral damage to surrounding tissues

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7
Q
  1. How might a relapse of Hodgkin lymphoma be treated?
A

High-dose chemotherapy
Autologous stem cell transplant
NOTE: intensifying chemotherapy will lead to an increased cure rate but it will also lead to an increase in secondary cancers

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8
Q
  1. Describe the curability of Hodgkin lymphoma.
A

Stage I and II: > 80%

Stage IV: 50%

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9
Q
  1. What are some important tests to perform in non-Hodgkin lymphoma and why are they important?
A

LDH – marker of cell turnover
HIV serology – HIV can predispose to NHL (HTLV1 serology may also be important)
Hepatitis B serology – NHL treatment may deplete B cells resulting in fulminant liver failure due to reactivation of hepatitis B in chronic carriers

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10
Q
  1. Broadly speaking, what are the treatment approaches to non-Hodgkin lymphoma?
A

Monitor only (in indolent lymphoma)
Urgent chemotherapy
Non-chemotherapy treatment (e.g. antibiotics to eradicate H. pylori)

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11
Q
  1. What are the two most common types of non-Hodgkin lymphoma?
A

Diffuse large B cell lymphoma (DLBCL)

Follicular lymphoma

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12
Q
  1. Which types of lymphoma are associated with other pre-existing diseases?
A

Gastric MALToma (H. pylori)
Enteropathy-associated T cell lymphoma (coeliac disease)
HIV-associated

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13
Q
  1. What is the correlation between how aggressive a lymphoma is and how curable it is?
A

The more aggressive it is, the more curable

Indolent lymphoma is more likely to recur

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14
Q
  1. What proportion of NHL are diffuse large B cell lymphoma?
A

30-40%

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15
Q
  1. Which factors are taken into account by the international prognostic index (IPI) for lymphoma?
A 
Age > 60 
High LDH 
Performance status 2-4 
Stage III or IV 
More than one extranodal site
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16
Q
  1. Which chemotherapy treatment is usually used for diffuse large B cell lymphoma?
A 
R-CHOP
Rituximab
Cyclophosphamide
Doxorubicin
Vincristine
Prednisolone 
NOTE: usually 6-8 cycles 
NOTE: achieves a 50% cure rate
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17
Q
  1. What treatment option may be considered for patients with diffuse large B cell lymphoma who relapse?
A

Autologous stem cell transplantation

18
Q
  1. What proportion of NHL is follicular lymphoma?
A

35%

19
Q
  1. Which genetic abnormality is associated with follicular lymphoma?
A

T(14;18) – resulting in over-expression of Bcl2 (which is an anti-apoptosis gene)
NOTE: follicular lymphoma is incurable but is indolent

20
Q
  1. What is the usual first-line treatment approach to follicular lymphoma?
A

Watch and wait

Only treat it clinically indicated (e.g. compression symptoms, massive nodes, recurrent infection)

21
Q
  1. Which chemotherapy regimen may be used in the treatment of follicular lymphoma?
A 
R-CVP
Rituximab
Cyclophosphamide 
Vincristine 
Prednisolone
22
Q
  1. Which lymphoid tissue tends to be affected by marginal zone lymphoma?
A

Extranodal lymphoid tissue (e.g. MALT)

23
Q
  1. List some diseases that can lead to marginal zone lymphoma.
A

H. pylori infection – gastric MALToma
Sjogren’s syndrome – parotid lymphoma
Hashimoto’s thyroiditis – thyroid lymphoma
Psittaci infection – lacrimal gland

24
Q
  1. Outline the process of MALT lymphomagenesis.
A

Lymphocytes will respond to H. pylori infection and proliferate
At some point, they will over-proliferate and develop cancer-like features but they will still be dependent on antigenic stimulation by H. pylori
At this point, treating H. pylori will treat the lymphoma

25
Q
  1. How might gastric MALToma stage I-II disease be treated?
A

Triple therapy to eradicate H. pylori (2 antibiotics + 1 PPI)
Repeat breath test at 2 months
Repeat endoscopy every 6 months for 1-2 years then annually
NOTE: failure may require chemotherapy

26
Q
  1. What are the main features of enteropathy-associated T cell lymphoma?
A

Mature T cells
Involves small intestines
Aggressive
Caused by chronic antigenic stimulation by gliadin/gluten

27
Q
  1. What is the most common leukaemia in the Western world?
A

Chronic lymphocytic leukaemia

28
Q
  1. What are the typical laboratory findings in a patient with CLL?
A

Lymphocytosis
Smear cells
Normocytic normochromic anaemia
Thrombocytopaenia
Bone marrow lymphocytic replacement of normal marrow elements
NOTE: it is indolent so is often only picked up on routine blood tests

29
Q
  1. What distinctive antigen phenotype (presence and absence) is suggestive of:
    a. Mature B cells
    b. Mature T cells
A 
a.	Mature B cells	
CD19 positive 
CD5 negative
b.	Mature T cells
CD19 negative 
CD5 positive 
CD3 positive 
CD4 or CD8 positive
30
Q
  1. Which antigen phenotype is suggestive of CLL?
A

CD5+ B cells (i.e. CD19+ and CD5+)

NOTE: this could potentially also be mantle cell lymphoma

31
Q
  1. Which staging system is used for CLL?
A

Rai and Binet

Binet: stages A-C depending on number of lymphoid areas (< or > 3, Hb and platelets)

32
Q
  1. Which laboratory tests are used in CLL to help gauge prognosis?
A

CD38 expression (associated with poor prognosis)
Cytogenetics (FISH)
Immunoglobulin gene mutation status (IgH mutated or unmutated)

33
Q
  1. What are VH genes?
A

The genes that encode the ‘variable heavy’ chain and undergoes somatic hypermutation by VDJ recombination

34
Q
  1. What is the difference between the VH genes of pre- and post-germinal centre B cells?
A

Pre-germinal centre: VDJ section is unmutated and looks identical to germline
Post-germinal centre: undergone somatic hypermutation so VDJ is mutated and looks different to germline

35
Q
  1. How does VH gene mutations affect prognosis?
A 
Unmutated = poor prognosis 
Mutated = better prognosis
36
Q
  1. What is an important chromosomal abnormality in CLL that is tested for using FISH?
A

Deletion of 17p (Tp53)
This is part of the p53 tumour suppressor gene
This deletion is associated with a poor prognosis

37
Q

Describe the immunoglobulin levels you would expect to see in CLL?

A

Hypogammaglobulinaemia

Because the malignant B cells are suppressing antibody production by other B cells

38
Q
  1. What are some supportive measures used in the treatment of CLL?
A

Vaccination (flu, pneumococcus)

Infection prophylaxis and treatment (may include aciclovir, PCP prophylaxis, IVIG)

39
Q
  1. What are some indications for treatment of CLL?
A

Progressive lymphocytosis (more than doubling in < 6 months)
Progressive bone marrow failure
Massive or progressive lymphadenopathy/splenomegaly
Systemic symptoms (B symptoms)
Autoimmune cytopaenias

40
Q
  1. What is the first line treatment for TP53 intact CLL?
A

BCR inhibitor – Ibrutinib (also affective in TP53 mutated cases)
BCL2 inhibitor – Venetoclax – allows apoptosis of CLL cells – main SE is tumour lysis syndrome

41
Q
  1. Describe how CAR-T therapy for CLL works.
A

CAR-T are autologous T cells that are modified to contain chimeric antigen receptors
The internal part of the receptor is responsible for cell signalling
The external part is designed to target CD19 (on B cells) thereby enabling B cell depletion

HaemPath (8 decks)

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