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Year 3 > Lymphoid Malignancy > Flashcards

Lymphoid Malignancy Flashcards

(53 cards)

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1
Q

what can cancers of lymphoid origin present with?

A 
enlarged lymph nodes
or 
extranodal involvelment
or 
bone marrow involvement
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2
Q

systemic symptoms of lymphoid cancers

A 
weight loss > 10% in 6 months
swinging fever
drenching night sweats
pruritis
fatigue
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3
Q

what is the only way to classify lymphomas and leukaemias?

A

bone marrow of lymph node biopsy

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4
Q

list the lymphoproliferative disorders from most to least common

A 
Non-hodgkin lymphoma high grade
Non-hodgkin lymphoma low grade
chronic lymphocytic leukaemia
hodgkin lymphoma
acute lymphoblastic leukemia
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5
Q

what cells are affected in ALL?

A

lymphoblasts

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6
Q

what percentage of lymphoblasts must be present in bone marrow to make a diagnosis of ALL?

A

> 20%

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7
Q

75% of cases of ALL occur in at what age?

A

<6

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8
Q

75-90% of cases of ALL are of what lineage?

A

b cell

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9
Q

presentation of ALL

A

2-3 week Hx of bone marrow failure or bone/joint pain

sometimes infection

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10
Q

survival rate for <10s in ALL without bone marrow transplant?

A

90%

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11
Q

standard treatment of ALL

A

induction combination chemo
consolidation therapy
CNS directed treatment
maintenance for 18 months

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12
Q

what is the purpose of induction treatment in ALL?

A

to achieve remission

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13
Q

if high risk of recurrence what can you give to ALL patients?

A

stem cell transplantation

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14
Q

are adults or children more likely to relapse with ALL?

A

adults

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15
Q

name the newer treatments for ALL

A

Bispecific T cell engagers (BiTe molecules) - blinatumumab

CAR (chimeric antigen receptor T cells)

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16
Q

describe treatment with CAR for ALL

A

§ Patient/healthy 3rd party T cells harvested
§ Transfected to express a specific T cell receptor expressed on leukaemia cells
(CD19)
§ Expanded in vitro
§ Re-infused into patient
§ Long term survival

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17
Q

what can T-cell immunotherapy reult in?

A

cytokine release syndrome

neurotoxicity

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18
Q

what is cytokine release syndrome?

A

fever
hypotension
dyspneoa
CAR T cell effect correlated to presence of CRS

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19
Q

symptoms of neurotoxicity as a result of T cell immunotherapy in ALL

A

confusion with normal conscious level

sizure, headache, focal neurology, coma

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20
Q

poor prognostic factors for ALL

A 
• Increasing age
• Increased white cell count
• Immunophenotyped (more primitive forms)
• Cytogenetics/molecular genetics
o T(9,22); t(4,11)
• Slow/poor response to treatment
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21
Q

adult outcome of ALL

A

Complete remission rate 78-91%

o Leukaemia free survival at 5 yr. 30-35%

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22
Q

child outcome of ALL

Study These Flashcards
A

o 5 yr. overall survival 90%

o Poor risk patients (slow response to induction or Philadelphia +ve) 5 yr. OS 45%

23
Q

CLL lymphocytes in blood

24
Q

CLL lymphocytes in bone marrow

25
characteristic immunophenotyping b cell markers in CLL
CD19,20,23 | CD5+
26
M:F CLL
2:1
27
presentation of CLL
often asymptomatic
28
frequent findings in CLL
bone marrow failure (anaemia, thrombocytopenia) lymphadenopathy splenomegaly fever and sweats
29
less common findngs in CLL
hepatomegaly infections weight loss
30
associated findings in CLL
immune paresis | haemolytic anaemia
31
describe stage A of CLL
<3 lymph node areas | same survival as age matched controls
32
describe stage B of CLL
>= 3 lymph node areas | 8 years survival
33
describe stage C of CLL
stage B + anaemia or thrombocytopenia | 6 years survival
34
what is the name of the classification system used for CLL?
Binet
35
indications for treatment in CLL
* Progressive bone marrow failure * Massive lymphadenopathy * Progressive splenomegaly * Lymphocyte doubling time < 6 months or >50% increase over 2 months * Systemic symptoms * Autoimmune cytopenias
36
treatment of CLL
• Cytotoxic chemotherapy e.g. fludarabine, bendamustine • Monoclonal antibodies e.g. rituximab, obinutuzamab • Novel agents o Bruton tyrosine kinase inhibitor e.g. ibrutinib – well tolerated and effective o PI3K inhibitors e.g. idelalisib o BCL-2 inhibitor e.g. venetoclax
37
poor prognostic factors of CLL
• Advanced disease (Binet stage B or C) • Atypical lymphocyte morphology • Rapid lymphocyte doubling time (< 12 months) • CD 38+ expression • Loss/mutation p53; del 11q23 (ATM gene) o P53 is poor prognostic factor in almost every cancer cell, it is a tumour suppressor gene • Unmutated IgBH gene status
38
presentation of lymphoma
lymphadenopathy/hepatosplenomegaly extranodal disease B symptoms bone marrow involvement
39
how is non-hodgkin lymphoma classified?
Lineage (B/T cell) grade of disease histological features
40
what lineafe are the majority of non-hodgkins lymphomas?
B cell
41
describe low grade non-hodgkin lymphoma
indolent, often asymptomatic | responds to chemo but incurable
42
describe high grade non-hodgkin lymphoma
aggressive, fast growing require combination chemotherapy can be cured
43
what is the commonest subtype of lymphoma?
diffuse large B-cell lymphoma
44
is diffuse large B-cell lymphoma high or low grade?
high
45
what is the 2nd commonest subtype of lymphoma?
follicular lymphoma
46
is follicular lymphomahigh or low grade?
low grade
47
treatment of diffuse large B cell lymphoma and follicular lymphoma
combination chemo - typically anti CD20 monoclonal antibody (rituximab) and chemo
48
what does a biopsy in hodgkin lymphoma show?
normal cells with a hodgkin cell in the middle
49
what percentage of lymphomas are hodgkin lymphoma ?
30%
50
describe the age distribution of hodgkin lymphoma
bimodal | 15-35 and later in life
51
M:F hodgkin lymphoma
1.9:1
52
what is hodgkin lymphoma associated with?
EBV familial geographical clustering
53
treatment of hodgkin lymphoma
o Combination chemotherapy (ABVD) o +/- radiotherapy o Use of PET scan to assess response to treatment and to limit use of radiotherapy

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