Lymphoma Flashcards
Lymphoma risk factors
Constant antigenic stimulation (e.g. Coeliac disease in EATL)
Infection (e.g. EBV in Burkitts, HTLV1 in ATLL)
Loss of T cell function (normally controls B cell proliferation - e.g. in HIV)
Is Hodgkin’s or non-Hodgkin’s more common?
Non-Hodgkin’s (80%)
Hodgkin’s (20%)
Hodgkin’s vs. non-Hodgkin’s
Single site vs. multiple sites
Pain after alcohol vs. no pain after alcohol
Reed-Sternberg cells, Pal Ebstein fever (Hodgkin’s)
B cells vs. B and T cells
Contiguous spread between nodes vs. random spread between nodes
Classical / non-classical vs. B cell / T cell
Hodgkin’s sub-types
Classical: Nodular sclerosing (80%), mixed cellularity, lymphocyte rich, lymphocyte depleted
Non-classical: Nodular lymphocyte predominant
Most common Hodgkin’s
Nodular sclerosing
Pain in nodes after alcohol
Hodgkin’s
Owl eyed cells
CD15 and CD30 positive
Reed Sternberg cells
Cyclical fever lasting 1-2w
Hodgkin’s lymphoma
Pal Ebstein fever
Hodgkin’s bad prognosis
Lymphocyte depleted
Single site painless lymphadenopathy Pain after alcohol Contiguous spread between LN Reed-Sternberg cells Pal Ebstein fever B cells only
Hodgkin’s
Multiple sites painless lymphadenopathy
Random spread between LNs
B and T cells
Non-Hodgkin’s
B symptoms
Fever >38
Night sweats
Weight loss >10% in 6m
EBV in lymphoma
Hodgkins lymphoma
Non-Hodgkins Burkitts
Ann Arbor lymphoma staging
1 = 1 LN region 2 = 2 LN regions same side of diaphragm 3 = 2 LN regions opposite sides of diaphragm 4 = Extranodal spread (e.g. Liver, BM)
A = No B symptoms B = B symptoms
Causes of death lymphoma
<5y
>5y
<5y relapse
>5y secondary malignancy
Hodgkins lymphoma treatment
- Combination chemo ABVD given to all
- Radio if small targetable area but radiation can = secondary malignancy
- Intensive chemo, autologous SCT if resistant
Balance risk of relapse (give chemo and radio) vs risk of secondary malignancy (give chemo only)
ABVD
Hodgkin’s chemo
Adriamycin, bleomycin, vinblastine, dacarbazine
Are B cell or T cell non-Hodgkin’s lymphomas more common?
B cell
Non-Hodgkins lymphoma sub-types
B / T cell
B cell then divided into: Very aggressive, aggressive, indolent
Very aggressive NHL
Burkitt’s
2-5w survival without treatment
Curable
Aggressive NHL
DLBC, mantle cell
3-12m survival without treatment
Less curable
Indolent NHL
Follicular, CLL/SLL, MALTs
10-15y survival
Mostly incurable
5 main B cell NHL
Burkitts, DLBC, Mantle, Follicular, MALTs
What happens to curability and survival without Tx as aggression decreases?
Curability decreases
Survival increases
t(8;14)
Over-expression of c-myc on chromosome 8
Starry sky appearance
EBV
Burkitt’s
t(11;14)
Cyclin D1 over-expression
Middle aged man with GI involvement
Angular nuclei
Mantle cell
Lymphoma incidence
Bimodal peak
Most common 20-29yo
Second smaller peak >60
t(14;18)
BCL2 over-expression
Follicular (four)
Sjogren’s (parotid), Hashimoto’s (thyroid), H pylori (gastric)
MALT ‘marginal zone’
5 main T cell NHL
Anaplastic large cell, peripheral, ATLL, EATL, CTCL
Mycosis fungoides
Cutaneous T cells
CTCL
Coeliac disease
EATL
Cloverleaf / flower appearance
Japanese
HTLV1
Hypercalcaemia
ATLL
Large epithelioid T lymphocytes
Anaplastic large cell
Key transformations in lymphoma
CLL to DLBC (Richters)
Follicular to DLBC
t(14;18)
Large B cells
Elderly men
DLBC
Tartrate resistant acid phosphatase (TRAP)
Hairy cell leukaemia (type of NHL)
CLL patient with recurrent pneumonia + haemoptysis
Found to have endobronchial mass
Richter’s transformation
CLL -> DLBC
HL - fibrous bands separate nodules
Nodular sclerosis
HL - atypical popcorn cells
Lymphocytic + histiocytic variant
Nodular lymphocytic
HL - many lymphocytes
Good prognosis
Lymphocyte rich
HL - few lymphocytes
Bad prognosis
Lymphocyte depleted
