Lymphoma Flashcards

1
Q

What are the different tissue types in the lymphoreticular system?

A

i) Generative LR tissue
-> Bone Marrow
-> Thymus
involved in the generation/maturation of lymphoid cells

ii) Reactive LR tissue
-> Lymph Nodes
-> Spleen
involved in the development of an immune reaction

iii) Acquired LR tissue i.e. Extranodal Lymphoid Tissue
-> Skin/Stomach/Lung
involved in the development of local immune reactions

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2
Q

What are the different cell types found in the lymphoreticular system?

A

i) Lymphocytes
-> B Lymphocytes
express surface Ig, responsible for antibody production
-> T Lymphocytes
express surface T cell Receptors, responsible for B Cell/Macrophage Regulation and Cytotoxic functions

ii) Accessory Cells
- > Antigen Presenting Cells
- > Macrophages
- > Connective Tissue Cells

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3
Q

Where are B cells found in the lymph nodes?

A

the Mantle Zone and Germinal Centres

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4
Q

Where are T cells found in the lymph nodes?

A

Inbetween the follicles in the “interfollicular areas”

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5
Q

What is a lymphoma?

A

Lymphoma’s are the neoplastic proliferation of lymphoid cells forming discrete tissue masses. They arise in and involve lymphoid tisssues.

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6
Q

Why are lymphocytes physiologically susceptible to oncogenesis? (3)

A

i) Recombination
DNA molecules are cut and recombined -> undergo deliberate point mutation

ii) Rapid cell proliferation in the germinal centre
- > More cell division means more risk of DNA replication error

iii) Dependent on apoptosis
If you have rapid turnover and you acquire a mutation that blocks apoptosis, it can lead to malignancy

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7
Q

What are 3 broad risk factors for lymphoma?

A

i) Chronic Antigen Stimulation
- > H. Pylori => Marginal Zone Lymphoma of Stomach
- > Sjogren’s Syndrome => Marginal Zone Lymphoma of Parotid
- > Hashimoto’s => Marginal Zone Lymphoma of Thyroid

ii) Direct Viral Integration
i. e. HTLV1 retrovirus. Human T Cell Lymphotropic Virus Type 1.

iii) Loss of T Cell Function
This is particularly important in EBV

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8
Q

What percentage of lymphomas are hodgkins and Non-hodgkins?

A
Hodgkin = 15% REED-STERNBERG
NHL = 85%
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9
Q

What is the epidemiology of HL?

A

Bimodal Age Incidence

i) Most common age is 20-29, Young Women
ii) Second peak affecting those >60 years of age.

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10
Q

What is the most common subtype of HL?

A

Nodular Sclerosing 80% (good prognosis)

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11
Q

What are the clinical features of a patient with HL?

A

-> Painless enlargement of lymph node/nodes
this may cause secondary effects from obstructing on local areas i.e. bowel, ureter, biliary tract
-> Constitutional Symptoms i.e. B SYMPTOMS - Fever, Night sweats and Weight loss.

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12
Q

What is the staging of HL?

A

Stage 1 - One Group of Nodes
Stage 2 - >1 group of nodes on the same side of the diaphragm
Stage 3 - Nodes above and below the diaphragm
Stage 4 - Extranodal spread
A/B -> B if the patient has the constitutional B symptoms i.e. Fever, Unexplained Weight Loss over 10%), Night Sweats

*If a Lymphoma has developed extranodal spread it is immediately described as a Stage 4 Lymphoma.

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13
Q

What is the management of HL?

A
  1. Chemotherapy (all patients with HL need chemo)
    ABVD - number of cycles depends on staging
  2. Radiotherapy
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14
Q

What is the radiotherapy dilemma for HL?

A

Radiotherapy PRO
-> Reduces the risk of HL recurrence to low/negligible

Radiotherapy CON
-> Higher risk of secondary cancers as there are two mechanisms of DNA damage i.e. Chemo+Radio

Therefore intensifying treatment may reduce the risk of relapsing but will increase the risk of treatment complications.

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15
Q

What is NHL?

A

Neoplastic proliferation of lymphoid cells

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16
Q

How is NHL staged?

A

same as HL

17
Q

What are two of the most common types of HL?

A
  1. Diffuse large B-cell lymphoma

2. Follicular lymphoma

18
Q

What predicts the clinical course of NHL?

A

Histology:

Different types of NHL are more aggressive than others (Burkitt v aggressive, follicular is indolent)

19
Q

How aggressive is Diffuse large B cell lymphoma?

A

Not as aggressive as Burkitt, but more than follicular

20
Q

What is the prognosis and treatment for diffuse large B-cell lymphoma determined by?

A

i) Age>60
ii) Serum LDH>Normal
iii) Performance status 2-4
iv) Stage III/IV
v) More than one extranodal site

21
Q

What is the treatment for diffuse large B-cell lymphoma?

A

Treated with 6-8 cycles of R-CHOP (chemo and immunotherapy)

22
Q

What is follicular lymphoma?

A

It is an indolent type of lymphoma

It is incurable and has a median survival of 12-15 years

23
Q

How do you treat follicular NHL?

A
  1. At presentation = watch and wait unless
    - nodal extrinsic compression
    - massive painful nodes
  2. Treatment = chemo (not curative)
24
Q

What is extra nodal marginal zone lymphoma (MZL)?

A
  1. It is a NHL involving extra nodal lymphoid tissue (e.g. gastric mucosa or parotids)
  2. Rare
  3. Due to chronic antigen stimulation
25
75% of xtra nodal marginal zone lymphoma (MZL) patients can be cured by...
H.pylori eradication
26
How do MZL patients present?
1. Epigastric pain, ulceration or bleeding (most commonly arise in stomach) 2. Usually in stage 1
27
What is Enteropathy associated T cell lymphoma (EATL)?
1. It is aT cell NHL in patients with Coeliac disease (due to chronic antigen stimulation) 2. Involves Jejunum and Ileum 3. It is aggressive
28
How do patients with Enteropathy associated T cell lymphoma (EATL) present?
1. Abdo pain. obstruction, bleeding 2. Malabsorption 3. Systemic symptoms
29
What is Chronic Lymphocytic Leukaemia?
1. Proliferation of mature B lymphocytes 2. Involves bone marrow, blood and nodes 3. Commonest Leukaemia in western world 4. Median age 72
30
What are the laboratory findings of CLL?
1. Lymphocytosis (5-300) 2. Smear cells 3. Anaemia 4. Thrombocytopenia 5. Immunotyping
31
What are smear cells?
Found in CLL | Mature fragile B lymphocytes that break during slide presentation
32
What are the clinical issues of CLL?
1. Increased risk of infection (non functional B cells) 2. Bone marrow failure 3. Lymphadenopathy.splenomegaly 4. Richter transformation (acquire further mutations) 5. Autoimmune complications
33
What is Richter's transformation?
Low Grade CLL converts into Diffuse Large B Cell Lymphoma due to acquired mutations
34
What is the supportive care for CLL?
1. Sino-pulmonary infections - Prophylaxyis for pneumocystis - IVIG - Early Antibiotics 2. Vaccinations - seasoal flu - pneumococcal - avoid live vaccines
35
What is the treatment for CLL?
1. Watch and wait unless - Bone marrow failure - massive lymphadenopathy - progressive lymphocytosis 2. CLL therapy - Combination immuno-chemotherapy
36
What are targetted therapies for CLL?
1. BCR Kinase inhibitors 2. BCL2 inhibitors 3. Experimental cell based therapies
37
What is the immunophenotype of: 1. a normal peripheral blood B-cell 2. A malignant peripheral B-cell
1. CD19+ve | 2. CD5+ve and CD19+ve