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YR5 Haematology > Lymphoma > Flashcards

Lymphoma Flashcards

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1
Q

What is lymphoma?

A

Neoplastic proliferation of lymphoid cells forming discrete tissue masses.

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2
Q

Where are lymphomas usually found?

A

LN +/- blood (Lymphatic system)
Lymphoid organs: spleen or gut associated lymphoid tissue
Skin (Often T cell disease)

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3
Q

Where can lymphomas rarely occur? (5)

A

CNS
Eyes
Testes
Breast
Kidney

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4
Q

What are the 2 classes of lymphoma and their prevalence?

A

Non-Hodgkin’s 80%
Hodgkin’s 20%

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5
Q

Describe the aetiology of lymphoma

A

Mostly sporadic with no known RFs
Some a/w specific infections/ immune disorders

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6
Q

How does immunoglobulin configuration occur? What are the benefits and risks?

A

Ig + TCR genes cut + recombined, then subjected to deliberate DNA mutagenesis

Generates diversity + Ig class switching

Potential for recombination errors + harmful point mutations

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7
Q

What are the benefits and risks of rapid cell proliferation in the germinal centre?

A

Allows rapid response to infection

Rapid multiple cell divisions = increase chance of DNA replication errors

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8
Q

What are the benefits and risks of immune response dependancy on apoptosis?

A

Eliminates self-reactive clones or ineffective Ig clones

Apoptosis is “switched off” in germinal centre
Consequences of mutations in apoptosis regulating genes

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9
Q

What are the 3 mechanisms of risk factors for certain non Hodgkin’s lymphoma subtypes?

A
  1. Constant antigenic stimulation
  2. Viral infection (direct viral integration of lymphocytes)
  3. EBV infection in a scenario of loss of T cell function
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10
Q

Give 3 examples of chronic/ AI antigenic stimulation causing B cell Non Hodgkin Lymphoma marginal zone subtype?

A

H. Pylori: Gastric MALT- mucosa associated lymphoid tissue. MZL of stomach

Sjogren syndrome: MZL of parotid gland

Hashimoto’s Thyroiditis: MZL of thyroid

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11
Q

What chronic antigenic stimulation causes enteropathy associated T-cell non Hodgkin’s lymphoma (EATL)?

A

Poorly controlled coeliac disease:
Small intestine EATL

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12
Q

How does H. pylori cause gastric MALT?

A

Chronic bacterial infection stimulates + irritates gut mucosa
Leads to lymphocytic infiltration
In chronic polyclonal reactive response, may lead to clones being produced
Increasingly malignant
Leads to MZL

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13
Q

Give an example of a direct viral integration causing non Hodgkin lymphoma.
In which populations is this more common?

A

HTLV1 retrovirus infects T cells by vertical transmission
Caribbean, Japanese endemic
Risk of adult T cell leukaemia lymphoma is 2.5% at 70y (ATLL)

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14
Q

How does EBV and loss of T cell function result in B non-hodgkins lymphoma?

A
  1. EBV infects B lymphocytes. Healthy carrier state post glandular fever. EBV driven proliferation a/w surface EBV antigens- targeted by EBV specific cytotoxic T cell response
  2. Loss of T cell function e.g. HIV, transplant immunosuppression
  3. Failure to eliminate EBV driven proliferation of B cells due to absence of cytotoxic T cells
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15
Q

What are almost all lymphomas due to?

A

immunoglobulin mutations (often heavy chain rearrangement)
BCL2
BCL6
Myc
Cyclin D1

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16
Q

Give 3 features of lymphoma presentation

A

Painless progressive lymphadenopathy
Recurrent infections
Constitutional Sx

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17
Q

How can lymphomas cause presentation with other system involvement?

A

Extrinsic compression of any “tube”: ureter, bile duct, large blood vessel, bowel, trachea, oesophagus

Infiltrate/ impair any organ system

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18
Q

Give examples of symptoms caused by lymphoma infiltration in the brain, eyes and skin

A

Brain: Stroke, memory problems
Eyes: blindness in 1 eye
Skin: Rash, inflammation, plaques, nodules

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19
Q

In which type of Lymphoma are Reed Sternberg cells seen?

A

Hodgkin’s Lymphoma

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20
Q

What are the subtypes of B cell non-hodgkins lymphoma?

A

Precursor: B lymphoblastic leukaemia or lymphoma
Mature: B cell neoplasm, DLBCL, Follicular NHL, CLL

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21
Q

What are the subtypes of T or NK cell lymphoma?

A

Precursor: T lymphoblastic leukaemia or lymphoma
Mature: T + NK neoplasm, PTCL, Anaplastic, Cutaneous

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22
Q

Give 3 epidemiological facts about Hodgkin’s lymphoma

A

1% of all cancer
M > F
Bimodal:
Most common 20-29
2nd smaller peak >60s

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23
Q

List the 3 classic B symptoms seen in Hodgkins lymphoma and 2 other less common symptoms

A

B: Fever, Night sweats, Weight loss
Pruritis
Alcohol induced pain in nodes

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24
Q

Which subtype of Hodgkins lymphoma has a peak of incidence in young women more than men?

A

Nodular sclerosing

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25
What are the 4 types of classic Hodgkin's lymphoma? What is the prevalence of each? What is the prognosis in each?
Nodular sclerosing 80%: good Mixed cellularity 17%: good Lymphocyte rich (rare): good Lymphocyte depleted (rare): poor
26
What investigations are used to stage Hodgkin's lymphoma?
FDG-PET/ CT scan Biopsy of other sites if infiltrated e.g. liver
27
How do non Hodgkin's and Hodgkins lymphoma differ in the way they spread?
H: Spreads through lymphatic system NHL: Spreads through circulation
28
What is the staging system and what are the stages of Hodgkin's lymphoma?
Ann-Arbor I: 1 group of nodes (can inc. spleen) II: >1 group of nodes SAME side of diaphragm III: nodes above + below diaphragm IV: extra-nodal spread Suffix A if none of below, B if any of below: Fever, unexplained weight loss >10% in 6m, night sweats
29
How may nodular sclerosing Hodgkin's lymphoma present?
Neck nodes + mediastinal mass (may be massive + compress SVC or trachea)
30
What is the chemotherapy regime for Hodgkins lymphoma?
ABVD Adriamycin Bleomycin Vinblastine DTIC
31
Give 2 benefits of ABVD
Effective- curative Preserves fertility (unlike original MOPP regime)
32
Give 2 potential complications of ABVD in the long term
Pulmonary fibrosis Cardiomyopathy
33
Describe the chemotherapy regime for Hodgkins lymphoma
4w intervals, 2-6 cycles PET CT after 2 cycles, response assessment + at end of tx +/- radiotherapy
34
Describe salvage chemotherapy in cases of relapsed Hodgkin's lymphoma
High dose chemo Autologous PB stem cell transplant
35
Why is radiotherapy not used in all Hodgkin's lymphoma patients?
ABVD alone can be curative Radiotherapy increases risk of secondary cancer, so in young try to avoid (secondary: Breast, Leukaemia, Lung, Skin)
36
What is the prognosis in Hodgkins lymphoma?
80% cured 10% die from relapse of HL in 10y 10% die from tx related complications after 10y
37
Which patients generally do less well despite treatment in Hodgkin's lymphoma?
Elderly Lymphocyte depleted
38
What investigations are used for staging non Hodgkins lymphoma?
CT PET scan (in aggressive lymphomas) +/- BM biopsy LP (if CNS involvement)
39
List 4 prognostic markers/ important tests to perform in non Hodgkins lymphoma
LDH (rapid cell turnover) Performance status HIV serology Hep B serology (risk of reactivation if B cell depleting therapy given)
40
Which subtypes of non Hodgkin lymphoma are considered very aggressive? What is the median survival without tx and response to chemo?
Burkitt's lymphoma T or B cell lymphoblastic leukaemia/ lymphoma 2-5w survival if no Tx Curable
41
Which subtypes of non Hodgkin lymphoma are considered aggressive? What is the median survival without tx and response to chemo?
Diffuse Large B cell 30-40% of NHL Mantle cell 3-12m survival without Tx Moderately curable
42
Which subtypes of non Hodgkin lymphoma are considered indolent? What is the median survival without tx and response to chemo?
Follicular Small lymphocytic/ CLL Mucosa associated (MALT) 10-15y survival without Tx Incurable (long remission)
43
How are very aggressive non Hodgkins lymphoma treated?
Treated like acute leukaemias
44
What is prognosis and treatment determined by in diffuse large B cell NHL?
IPI (International Prognostic Index): Age Stage (Ann Arbor) LDH Extra-nodal disease sites ECOG performance status
45
What is the chemotherapy regime for diffuse large B cell NHL?
6-8 cycles of R-CHOP Rituximab: anti-CD20 monoclonal antibody Cyclophosphamide Adriamycin Vincristine Prednisolone
46
Give 4 features of the course of follicular NHL
Indolent 35% of NHL Incurable, median survival 12-15y May require 2-3 different chemotherapy schedules over the 12-15y
47
What translocation is follicular NHL associated with?
t(14:18) which results in over expression of bcl2 an anti-apoptosis protein
48
What is the initial treatment for follicular NHL?
Watch + wait Treat only if clinically indicated e.g. nodal extrinsic compression, massive painful nodes or recurrent infections
49
What combination immunotherapy regime can be used in follicular NHL?
R-COP or R-CHOP Tx not curative
50
Give 5 features of extra nodal marginal zone lymphomas
Involve extra-nodal lymphoid tissue e.g. gastric mucosa, parotids 8% of NHL Chronic antigen stimulation Median age 55-60y H. pylori eradication may cure 75%
51
What is the most common presentation of marginal zone lymphoma?
Epigastric pain Ulceration Bleeding into the gut Usually present at Stage I B Sx uncommon
52
What is enteropathy associated T cell lymphoma?
T cell NHL in patients with coeliac due to chronic antigen stimulation (gluten) Mature T cells Involves jejunum + ileum Aggressive
53
Give 6 ways in which enteropathy associated T cell lymphoma may present
Abdo pain Obstruction Perforation GI bleeding Malabsorption Systemic Sx
54
What is the prognosis in enteropathy associated T cell lymphoma?
Generally fatal Responds poorly to chemo Aim to prevent with strict GF diet
55
What is chronic lymphocytic leukaemia? Give 3 epidemiological facts
Proliferation of mature B lymphocytes, predominantly involves BM + blood Commonest leukaemia in western world RF: Caucasian, FH Median age 72 (10% <55)
56
Give 5 laboratory findings in CLL
Lymphocytosis 5-300 x10^9 Normocytic normochromic anaemia Thrombocytopenia BM lymphocytic replacement of normal marrow elements Smear cells
57
What technique is used to diagnose CLL?
Immunophenotype by flow cytometry of peripheral blood CD5 +ve B cells in peripheral blood (should only be transiently expressed in immature)
58
What is the common clinical course of CLL?
5-10y good health until progression to 2-3y rapid phase to death
59
Do all CLL patients progress?
1/3 never progress 1/3 progress, respond to tx, die from unrelated disorder 1/3 progress, require multiple lines of Rx, refractory disease, die from CLL
60
Give 3 cell based prognostic factors in CLL
IgHV mutation status CLL FISH cytogenetic panel TP53 mutation status (Chr17p deletion +/- TP53 point mutation)
61
Describe the normal development of B cells
Start with germline immunoglobulin gene configuration Pass into germinal center Undergo recombination, generating antibody diversity
62
How does immunoglobulin heavy chain status affect prognosis in CLL?
If IGHV are mutated (post GC) = better prognosis as cells have undergone somatic hypermutation, thus differ from germline
63
What staging systems are used for CLL?
Binet or Rai
64
What are the clinical issues in CLL? What are these caused by?
Increased infection risk (population of malignant non functional mature B cells + hypogammaglobinaemia) BM failure (proliferation in BM) Lymphadenopathy +/- splenomegaly, lymphocytosis (circulates to nodes, spleen, blood) AI complications e.g. AIHA (disease of immune cells)
65
How can acquiring further mutations complicate CLL?
Transform to high grade lymphoma (Richter transformation)
66
What supportive care is given to prevent Sino-pulmonary infections in CLL?
Early tx with abx Pneumocystis prophylaxis +/- zoster prophylaxis Recurrent infection + IgG< 5g/l give IVIG replacement therapy
67
What vaccines are given to CLL patients?
Pneumococcal SARS COV 2 Seasonal flu (AVOID live vaccines)
68
In which 5 circumstances do you not watch and wait in CLL?
Progressive lymphocytosis Progressive marrow failure Massive/ progressive lymphadenopathy/ splenomegaly Systemic Sx (B Sx) AI cytopenias (treat with immunosuppression not chemo)
69
Give 3 options for therapy in CLL
Combination immune-chemotherapy Targeted: BTK inhibitor or BCL2 inhibitor Cellular: Allogenic SCT, CAR-T therapy
70
Give an example of a BCR kinase and BCL2 inhibitor
BCR: Ibrutinib PO BCL2: Venetoclax PO
71
What do the targeted therapies for CLL affect?
Constant signalling through B cell receptor to promote survival (we maintain memory B cells for protective immunity) BCR signalling requires BCR + downstream signalling proteins e.g. BTK Prevent cells dying by increasing presence of anti-apoptotic proteins e.g. BCL2
72
What is the main risk of Venetoclax?
Tumour lysis syndrome

YR5 Haematology (20 decks)

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