Lymphoma 2 Flashcards
how is lymphoma diagnosed and staged?
- lymph node biopsy & histology
- FDG-PET* or CT scan
+/-BM biopsy
+/-Lumbar puncture
- fluorodeoxyglucose
what is the epideiology of HL?
Bimodal age incidence
Most common age 20-29, young women NS subtype
Second smaller peak affecting elderly >60 years old
What is always a worry in lymphoma?
Fatal hep b reactivaction!
what ar long teerm side effects of ABVD for HL?
Pulmonary fibrosis
cardiomyopathy - most deadly SE.
what is survival in HL?
Only 50% of stage IV patients are cured
s1-2: 80%
what is the treatment dilemma in HL?
Intensify therapy (chmo + radio): more cures & more secondary cancers
Reduce Therapy: less cures & less secondary cancer
how is nhl managed ?
A. histology
B. staging: pet/ct
C. prognostic markers: LDH/
HIV! - immunocompromise
Hep B - fatal reactivation risk
performance status
D. therapy:
Urgent chemotherapy ?
Monitor only {watch & wait} ?
Sub type specific eg Antibiotic eradication H.Pylori gastric MALT lymphoma) ?
what is median survival for burkitts lymphoma and t/b LL Without Rx?
Weeks 2-5
very aggressive
which are the indolent NHL?
Follicular NHL
Marginal zone lymphoma :
Gastric mucosa associated NHL (MALT lymphoma)
Thyroid (thyroiditis) Parotid (Sjogren’s)
what is the rx for DLBCL ?
R-CHOP (Rituximab-CHOP):
( 6-8 cycles - advanced. 3 if localised)
this is combination chemotherapy + antiCD20 rituximab
relpase: Autologous Stem Cell transplant salvage
how is folliculart NHL managed?
At presentation Watch and wait only treat “if clinically indicated”:
Nodal extrinsic compression: bowel, ureter, vena cava
Massive painful nodes,
recurrent infections
Treatment
combination Immuno-chemotherapy R-Bendamustine or R-COP
Treatment is not curative - cant cure
how is Enteropahy Associated T cell lymphoma (EATL) managed?
avoid gluten
poor response to chemo - fatal
what is Chronic Lymphocytic Leukaemia (CLL) ?
• Proliferation of mature CD5+ve/CD19+ve
B-lymphocytes
most common leukaemia in western world
also cd20, cd5 present on cell
the following findings are consistent with?
- Lymphocytosis between 5 and 300 x 109/l
- Smear cells
- Normocytic normochromic anaemia
- Thrombocytopenia
- Bone marrow: will see Lymphocytic replacement of normal bone marrow elements
Chronic Lymphocytic Leukaemia (CLL)
what does the following mean :
Binet stage C, IgH unmutated, 17p del/p53mutated CLL
worse prognosis CLL
thesee are prognostic indicators
binet - clinical prognostic scoree
IgH - Immunoglobulin heavy chain gene mutation status:
Laboratory/malignant cell based prognostics. beter to be mutated
p53 & chromosome deletions - cytogenetic prosnotics
increased risk of infection - hypogammaglobulinaemeia
Richter transformation
WARM autoimmune haemolytic anaeemia
all togethr present in which leukaemia?
CLL
what are complications of CLL?
how do we treat them?
Transformation to high grade lymphoma
{DLBCL subtype}
Richter’s syndrome: Treat as high grade lymphoma with R-CHOP
Acquired auto-immune haemolytic anaemia
rx: steroids
how is CLL treated?
Prophylaxis:
Aciclovir
PCP prophylaxis for those receiving chemotherapy
IVIG is recommended for those with hypogammaglobulinemia and recurrent chest infections
Immunisation against pneumococcus, and seasonal flu
Avoid live vaccines (herpes zoster)
Watch and wait - unless contraindicated
Chemo - wont cure
Allogeneic SCT or CAR-T cells (chimaeric antigen receptor-T cells) - curative
list some contraindications for watch and wait for CLL
Progressive lymphocytosis
lymphocyte doubling time <6 months
Progressive marrow failure
Hb < 100, platelets <100, neutrophils <1
Massive or progressive lymphadenopathy/splenomegaly
Systemic symptoms (B symptoms)
why is TP53 status important in CLL?
if p53 is intact -> chemo + antiCD20
if there is 17p del/T p53 mutated CLL:
WONT respond to chemo
Need targeted therapy:
- BCR tyrosine Kinase Inhibitors
- BCL2 inhibitors
- Experimental Cell Based Therapies: CAR-T
what is the risk of BCL2 inhibitor use in leukaemia?
tumour lysis syndrome
how do Bcl2 inhibitors work
promote apoptosis
by blocking cells that regulate apoptosis
because the role of BCL2 (gene) is to make BCL2 proteins which have anti-apoptosis properties ->
they inhibit BAX/BAK at the mitochondria to stop apoptosis.
how would you identify the cd cells present on lymphocytes?
on CLL?
immunophenotype - via flow cytometry
in CLL specifically use PERIPHERAL blood
what is the role of FISH in CLL and leukaemias?
identifies chromosomal abnormalities eg mutations eeg
p53 deletions
