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YEAR 5: Haematology > Haem: Lymphoma 2, CLL and Lymphoproliferative disorder > Flashcards

Haem: Lymphoma 2, CLL and Lymphoproliferative disorder Flashcards

1
Q

What are the two main subtypes of Hodgkin lymphoma?

A
  • Classical Hodgkin Lymphoma
  • Nodular lymphocyte predominant Hodgkin lymphoma
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2
Q

What is the fastest growing/aggresive human cancer?

A

Burkitt’s lymphoma

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3
Q

Describe the typical presentation of Non-Hodgkin’s lymphoma.

A

Painless lymphadenopathy

Compression symptoms

B symptoms

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4
Q

Which investigations may be used to stage lymphoma?

A
  • PET scan
  • CT scan
  • Bone marrow biopsy
  • Lumbar puncture (if CNS involvement)
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5
Q

What are some important tests to perform in non-Hodgkin lymphomae 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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6
Q

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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7
Q

What are the two most common types of non-Hodgkin lymphoma?

A

Diffuse large B cell lymphoma (DLBCL)

Follicular lymphoma

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8
Q

List some types of non-Hodgkin lymphoma that are:

  1. Very agressive
  2. Aggresive
  3. Indolent
A
  1. Very agressive
    • Burkitt’s lymphoma
    • T or B cell lymphoblastic lymphoma/leukaemia
  2. Aggressive
    • Diffuse large B cell lymphoma
    • Mantle cell lymphoma
  3. Indolent
    • Follicular lymphoma
    • Small lymphocytic lymphoma (CLL)
    • MALToma
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9
Q

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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10
Q

What proportion of NHL are diffuse large B cell lymphoa

A

30-40%

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11
Q

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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12
Q

Which chemotherapy treatment is usually used for diffuse large B cell lymphoma?

A
  • R-CHOP
    • Rituximab
    • Cyclophosphamide
    • Doxorubucin
    • Vincristine
    • Prednisolone

NOTE: usually 6-8 cycles

NOTE: achieves a 50% cure rate

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13
Q

What treatment option may be considered for patients with diffuse large B cell lymphoma who relapse?

A

Autologous stem cell transplantation

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14
Q

What proportion of NHL is follicular lymphoma?

A

35%

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15
Q

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

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16
Q

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)

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17
Q

Which chemotherapy regimen may be used in the treatment of follicular lymphoma?

A
  • R-CVP
    • Rituximab
    • Cyclophosphamide
    • Vincristine
    • Prednisolone
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18
Q

Which lymphoid tissue tends to be affected by marginal zone lymphoma?

A

Extranodal lymphoid tissue (e.g. MALT)

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19
Q

What is the cause of marginal zone lymphoma?

A
  • H. pylori infection - gastric MALToma
  • Sjogren’s syndrome - parotid lymphoma
  • Hashimoto’s thyroiditis - thyroid lymphoma
  • Psittaci infection - lacrimal gland
20
Q

Where is marginal zone lymphoma most commonly seen and how does it tend to present?

A
  • Usually in the stomach
  • Presenting with dyspepsia or epigastric pain
  • Usually Stage 1{E} (E=extranodal)
  • B symptoms are uncommon
21
Q

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
22
Q

How might gastrict MALToma stage I-II disease be treated?

A
  • Tripy 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

23
Q

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
24
Q

Describe the typical presenting features of enteropathy-associated T cell lymphoma.

A
  • Abdominal pain/ obstruction/ bleeding/ perforation
  • Malabsorption
  • Systemic symptoms
25
Why is it important to prevent EATL by following a strict gluten-free diet?
EATL responds poorly to chemotherapy and is usually fatal
26
What is the most common leukaemia in the Western world?
Chronic lymphocytic leukaemia
27
What are the typical laboratory findings in a patient with CLL?
1. Lymphocytosis 2. Smear cells 3. Normocytic normochromic anaemia 4. Thrombocytopaenia 5. Bone marrow lymphocytic replacement of normal marrow elements NOTE: it is indolent so is often only picked up on routine blood tests
28
What distinctive antigen phenotype (presence and absence) is suggestive of: * Mature B cells * Mature T cells
1. Mature B cells: * CD19 positive * CD5 negative 2. Mature T cells: * CD19 negative * CD5 positive * CD3 positive * CD4 or CD8 positive
29
Which antigen phenotype is suggestive of CLL?
CD5+ B cells (i.e. CD19+ and CD5+) NOTE: this could potentially also be mantle cell lymphoma
30
Which staging system is used for CLL?
Rai and Binet Binet: stages A-C depending on number of lymphoid areas (\< or \> 3, Hb and platelets)
31
Which laboratory tests are used in CLL to help gauge prognosis?
CD38 expression (associated with poor prognosis) Cytogenetics (FISH) Immunoglobulin gene mutation status (IgH mutated or unmutated)
32
What are VH genes?
The genes that encode the 'variable heavy' chain and undergoes somatic hypermutation by VDJ recombination.
33
What is the difference between the VH genes of pre- and post-germinal centre B cells?
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
34
How does VH gene mutations affect prognosis?
Unmutated = poor prognosis Mutated = better prognosis
35
What is an important chromosomal abnormality in CLL that is tested for using FISH?
* Deletion of 17p (Tp53) * This is part of the p53 tumours suppressor gene * This deletion is associated with a poor prognosis
36
Describe the immunoglobulin levels you would expect to see in CLL.
Hypogammaglobulinaemia Because the malignant B cells are suppressing antibody production by other B cells
37
What is the term used to describe CLL changing into a high grade lymphoma?
Richter transformation - 1% risk per year
38
What are some supportive measures used in the treatment of CLL?
* Vaccination (flu, pneumococcus) * Infection prophylaxis and treatment (may includ aciclovir, PCP prophylaxis, IVIG)
39
How would autoimmune cytopaenias caused by CLL be treated?
Steroids NOTE: 2nd line is rituximab
40
How would a Richter transformation be treated?
R-CHOP
41
What is leukaemia-directed therapy?
* Tailored to the patient * Usually involves watching and waiting because it is incurable by chemotherapy * Aim to establish remission NOTE: young people may be cured with allogeneic stem cell transplantation
42
What are some indications for treatment of CLL?
* Progressive lymphocytosis (more than doubling in \<6 months) * Progressive bone marrow failure * Massive or progressive lymphadenopathy/splenomegaly * Systemic symptoms (B symptoms) * Autoimmune cytopaenias
43
What is the first line treatment for TP53 intact CLL?
FCR - Fludarabine, Cyclophosphamide, Rituximab NOTE: less intensive options may include, rituximab and bendamustine or obinutuzumab (anti-CD20) and chlorambucil (alkylating agent)
44
Under what conditions might CLL be considered high risk?
Patients with TP53/17p deletion Refractory disease or early relapse (\<24 months)
45
What are some newer treatment options for high risk CLL?
Bruton Tyrosine Kinase Inhibitors - ibrutinib, idelalisib Bcl2 Inhibitors - venetoclax CAR-T therapy
46
Describe how CAR-T therapy for CLL works.
* 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

YEAR 5: Haematology (18 decks)

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