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Haematology Path Year 5 > Lymphoma > Flashcards

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
Q

75% of xtra nodal marginal zone lymphoma (MZL) patients can be cured by…

A

H.pylori eradication

26
Q

How do MZL patients present?

A
  1. Epigastric pain, ulceration or bleeding (most commonly arise in stomach)
  2. Usually in stage 1
27
Q

What is Enteropathy associated T cell lymphoma (EATL)?

A
  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
Q

How do patients with Enteropathy associated T cell lymphoma (EATL) present?

A
  1. Abdo pain. obstruction, bleeding
  2. Malabsorption
  3. Systemic symptoms
29
Q

What is Chronic Lymphocytic Leukaemia?

A
  1. Proliferation of mature B lymphocytes
  2. Involves bone marrow, blood and nodes
  3. Commonest Leukaemia in western world
  4. Median age 72
30
Q

What are the laboratory findings of CLL?

A
  1. Lymphocytosis (5-300)
  2. Smear cells
  3. Anaemia
  4. Thrombocytopenia
  5. Immunotyping
31
Q

What are smear cells?

A

Found in CLL

Mature fragile B lymphocytes that break during slide presentation

32
Q

What are the clinical issues of CLL?

A
  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
Q

What is Richter’s transformation?

A

Low Grade CLL converts into Diffuse Large B Cell Lymphoma due to acquired mutations

34
Q

What is the supportive care for CLL?

A
  1. Sino-pulmonary infections
    - Prophylaxyis for pneumocystis
    - IVIG
    - Early Antibiotics
  2. Vaccinations
    - seasoal flu
    - pneumococcal
    - avoid live vaccines
35
Q

What is the treatment for CLL?

A
  1. Watch and wait unless
    - Bone marrow failure
    - massive lymphadenopathy
    - progressive lymphocytosis
  2. CLL therapy
    - Combination immuno-chemotherapy
36
Q

What are targetted therapies for CLL?

A
  1. BCR Kinase inhibitors
  2. BCL2 inhibitors
  3. Experimental cell based therapies
37
Q

What is the immunophenotype of:

  1. a normal peripheral blood B-cell
  2. A malignant peripheral B-cell
A
  1. CD19+ve

2. CD5+ve and CD19+ve

Haematology Path Year 5 (5 decks)

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