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Lymphoid malignancies Flashcards

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1
Q

What are primary lymph organs the site of?

A

Primary lymph organs is the site where stem cells can divide and become immunocompetent

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2
Q

What are the secondary lymph organs the site of?

A

• Secondary lymph organs is the site where most of the immune responses occur

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3
Q

What happens to T cells at the thymus?

A

T cells mature in thymus

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4
Q

Where do B cells mature?

A

B cells mature in blood

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5
Q

Example of lymphoid organs

A
  1. Lymph nodes
  2. Spleen
  3. Peyer’s patches
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6
Q

What is the presentation of ALL(Acute lymphoblastic leukemia)?

A

○ Usually non-specific symptoms of bone marrow suppression

○ Symptoms of organ infiltration more often in advanced disease

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7
Q

What is the most commonest leukemia in children?

A

Acute lymphoblastic leukemia

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8
Q

What are the ways to investigate and diagnose acute lymphoblastic leukemia?

A 
○ Bone marrow morphology
○ Immunophenotyping
○ B-cell surface markers
○ Light chain restriction
○ TdT positive
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9
Q

Bone marrow morphology in acute lymphoblastic leukemia?

A

Infiltration by undifferentiated blast cells

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10
Q

Light chain restriction in acute lymphoblastic leukaemia?

A

§ Just one type of light chain produced
instead of different types of

§ light chain, there is just one – due to a mutation

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11
Q

TdT positive in acute lymphoblastic leukaemia?

A

§ At the join some nucleotides randomly removed by exonuclease
§ Some nucleotides randomly added by terminal deoxynucleotidyl transferase (TdT)
§ Cytogenetics

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12
Q

What is the treatment of acute lymphoblastic leukaemia?

A 
○ Chemotherapy
○ Induction
○ Intensification
○ CNS directed chemotherapy
○ Maintenance
○ (Radiotherapy to CNS)
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13
Q

Prognosis in acute lymphoblastic leukaemia of children?

A

> 90% cure

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14
Q

Why do adult have a low survival rate in acute lymphoblastic leukaemia?

A

○ Different cell of origin to children
○ Different oncogene mutations
○ Older patients do not tolerate intensive treatment

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15
Q

What is the presentation of Hodgkin’s lymphoma?

A

Enlarged lymph nodes

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16
Q

What is the possible associated of hodgkin’s leukaemia with?

A

Possible association with epstein barr virus (EBV)

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17
Q

What is EBC known as and due to what?

A

§ EBV known as kissing virus due to saliva transfer

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18
Q

What happens to reed-sternberg cells in Hodgkin’s leukaemia and how’s it spread?

A

○ Reed-sternberg cells typically have bi-lobed nucleus

-Spread in a systemic wa

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19
Q

What is the treatment for Hodgkin’s leukaemia?

A

○ Chemotherapy +/-radiotherapy

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20
Q

What is the prognosis of Hodgkin’s leukaemia?

A

○ 5 year survival ~50-90% depending on age, stage and histology
§ Especially good results in young adults

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21
Q

What are the different grades in non-hodgkins lymphoma?

A

• Different grades
○ Low grade
○ High grade

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22
Q

What cell lymphoma is non-hodgkins lymphoma?

A

T-cell lymphoma

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23
Q

What happens if you get EBV with a non-hodgkins lymphoma?

A

○ If you get EBV, you get glandular fever

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24
Q

What happens to immunosuppressed patients with EBV?

A

• EBV in immunosuppressed patients = bigger problem as immune system cannot fight EBV

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25
What do many lymphomas carry and involving what?
• Many lymphomas carry chromosome translocations involving the Ig heavy chain or light chain loci
26
What are Ig genes highly expressed in?
• Ig genes are highly expressed in B-cells
27
What does each Ig gene have near the constant segment?
• Each Ig gene has a powerful tissue specific enhancer near to the constant (C) segment
28
What is the enhancer supposed to produce in order to have an effective immune system?
Enhancer is supposed to produce many types of B cells to have an effective immune system
29
What is the normal role of the enhancer?
Normal role: activating the promoter of the rearranged V segment 
30
Why is it important to have many different types of enhancers?
○ The more different types we have, the more likely it is that a foreign antigen will be picked and antibodies against it can be produced 
31
What translocations do most cases of follicular lymphoma have?
Most cases of follicular lymphoma carry t(14;18)(q32;q31) (READ THIS AS: translocation has happened on Chr14, translocated part has come from Chr18, 32 and 31 have been rearranged)
32
What does the translocation that occurs in follicular lymphoma do and cause?
○ This juxtaposes the BCL-2 gene on chromosome 18 with the IgH locus on chromosome 14 ○ Causes overexpression of BCL-2 protein
33
What is BCL-2?
BCL-2 is an apoptosis inhibitor
34
What does the expression of BCL-2 do and cause?
§ Stops any abnormal cells apoptosing  | § These abnormal cells will accumulate and form a lymphoma 
35
What is the MYC gene?
• Powerful oncogene
36
What is the translocation in some cases of high grade lymphoma?
Some cases of high grade lymphoma carry t(18;14)(q24;q32)
37
What does this translocation that is in high grade lymphoma do ? t(18;14)(q24;q32)
This juxtaposes the MYC gene on chrom 18 with the IgH locus on chrom 14
38
What other translocations do we get other than t(18;14)(q24;q32)?
○ Can also get MYC or BCL-2 translocations to one of the Ig light chain loci
39
What will the MYC gene drive forward?
○ MYC will drive forward any cancer/malignant cells that we may have 
40
What is the presentation of low grade NHL?
○ Enlarged lymph nodes | ○ May have night sweats/fever
41
What is the histology of low grade NHL?
○ Normal tissue architecture partially preserved ○ Normal cell of origin recognisable ○ Used to name lymphoma- follicular lymphoma, mantle cell lymphoma etc. 
42
What can we use for the diagnosis of low grade NHL?
``` ○ Histology ○ Immunocytochemistry ○ Cytogenetics ○ Light chain restriction ○ Light chain restriction ○ PCR ```
43
What is the treatment for low grade NHL?
``` ○ Chemotherapy ○ Glucocorticoids (e.g. prednisolone) ○ Radiotherapy ○ Monoclonal Ab therapy ○ Rituximab (anti-CD20) ```
44
What is the prognosis for low grade NHL?
○ Relatively indolent (slow-growing) ○ Respond well to therapy ○ But hard to cure
45
What is the presentation of high grade NHL?
○ Enlarged lymphnodes
46
What is the histology of high grade NHL?
○ Loss of normal tissue architecture | ○ Normal cell of origin hard to determine
47
What can we use for the diagnosis for high grade NHL?
``` ○ Histology ○ Immunocytochemistry ○ Cytogenetics ○ Light chain restriction ○ PCR § For clonal Ig gene rearrangement § For chromosome translocations ```
48
What is the treatment used for high grade NHL?
``` ○ Chemotherapy ○ Glucocorticoids ○ Radiotherapy ○ Monoclonal Ab therapy § Rituximab- anti CD20 ```
49
What is the prognosis of high grade NHL?
○ Variable depending on type, stage and other factors § Stages depend on how far it has spread ○ Overall long term survival ~65%
50
What is acute T cell leukaemia/lymphoma associated with?
• Associated with retrovirus HTLV-1 (human T-cell leukaemia/lymphoma virus 1) infection
51
What is the presentation of acute T cell leukaemia/lymphoma?
``` ○ Skin infiltration  § Sezary syndrome § Mycosis fungoides  § Named like this as it looks like fungus growing on the skin  ○ Usually CD4 cells  ```
52
What does EBV transform in culture and due to what?
• EBV or Human Herpes Virus 4 (HHV4) directly transforms B-lymphocytes in culture -Due to viral oncogene LMP-1
53
What happens with immunosuppressed individuals with EBV and what develops?
○ T cells no longer suppress EBV  ○ Endogenous latent EBV may transform B-cells  ○ No longer eliminated by cytotoxic T-cells ○ Develop high grade lymphoma
54
What happens to EBV driven lymphoma in transplant patients on the withdrawal of immunosuppression?
Lymphoma usually regresses on withdrawal of immunosuppression
55
What happens to lymphoma in on successful HAART in EBV driven immunosuppression?
Lymphoma may regress on successful HAART
56
What is the presentation of CLL?
○ Most often as incidental finding on fbc ○ Persistent infection(s)  § Due to immunosuppression § Low IgG, suppression of normal B cells ○ Lymph node enlargement ○ Symptoms of bone marrow suppression
57
What is used to diagnose CLL?
``` ○ FBC: Lymphocytosis ○ Immunophenotyping § Cell surface markers § Light chain restriction ○ Cytogenetics ```
58
What are the 3 aspects of myeloma that give rise to different clinical features?
1. Suppression of normal bone marrow, blood cell and immune cell function 2. Bone resorption and release of calcium 3. pathological effects of the paraprotein?
59
What does suppression of normal bone marrow, blood cell and immune cell function do to the patient?
○ May become anaemic  ○ May have recurrent infections  ○ Tendency to bleed 
60
What does bone resorption and release of calcium do to the patient?
○ Myeloma cells produce cytokines (esp. IL-6) ○ Which stimulate bone marrow stromal cells to release the cytokine RANKL ○ Which activates osteoclasts § Lytic lesions of bone § Bone pain § Fractures ○ Calcium released from bone causes hypercalcaemia § Multiple symptoms including mental disturbance
61
What are paraproteins?
single monoclonal Ig in the serum
62
What do high levels of paraprotein indicate?
High levels indicate malignancy
63
What are the effects of paraprotein?
§ Precipitates in kidney tubules cause renal failure | § Deposited as amyloid in many tissues
64
What do 2% of high paraprotein cases develop into and what does this lead to?
○ 2% of cases develop hyperviscosity syndrome § Increased viscosity of blood leading to § Stroke  § Heart failure
65
What is used to diagnose myeloma?
○ Serum electrophoresis for paraprotein ○ Urine electrophoresis § Bence-Jones protein represents free monoclonal light chains ○ Increased plasma cells in bone marrow  ○ ESR (very high due to rouleaux formation) ○ Radiological investigation of skeleton for lytic lesions § X-ray
66
What is the treatment for myeloma?
``` ○ Chemotherapy (not curative) § Cytotoxic drugs § Glucocorticoids § Thalidomide analogues § Bortezomib ○ Allogeneic bone marrow transplant § Only available for a small number of younger patients (<45yo, not too ill) § Need to find an HLA (MHC) matched donor § But potentially curative ```

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