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Year 3 > Lymphoid Malignancy > Flashcards

Lymphoid Malignancy Flashcards

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

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

A

> 5x10^9/l

24
Q

CLL lymphocytes in bone marrow

A

> 30%

25
Q

characteristic immunophenotyping b cell markers in CLL

A

CD19,20,23

CD5+

26
Q

M:F CLL

A

2:1

27
Q

presentation of CLL

A

often asymptomatic

28
Q

frequent findings in CLL

A

bone marrow failure (anaemia, thrombocytopenia)
lymphadenopathy
splenomegaly
fever and sweats

29
Q

less common findngs in CLL

A

hepatomegaly
infections
weight loss

30
Q

associated findings in CLL

A

immune paresis

haemolytic anaemia

31
Q

describe stage A of CLL

A

<3 lymph node areas

same survival as age matched controls

32
Q

describe stage B of CLL

A

> = 3 lymph node areas

8 years survival

33
Q

describe stage C of CLL

A

stage B + anaemia or thrombocytopenia

6 years survival

34
Q

what is the name of the classification system used for CLL?

A

Binet

35
Q

indications for treatment in CLL

A
  • Progressive bone marrow failure
  • Massive lymphadenopathy
  • Progressive splenomegaly
  • Lymphocyte doubling time < 6 months or >50% increase over 2 months
  • Systemic symptoms
  • Autoimmune cytopenias
36
Q

treatment of CLL

A

• 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
Q

poor prognostic factors of CLL

A

• 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
Q

presentation of lymphoma

A

lymphadenopathy/hepatosplenomegaly
extranodal disease
B symptoms
bone marrow involvement

39
Q

how is non-hodgkin lymphoma classified?

A

Lineage (B/T cell)
grade of disease
histological features

40
Q

what lineafe are the majority of non-hodgkins lymphomas?

A

B cell

41
Q

describe low grade non-hodgkin lymphoma

A

indolent, often asymptomatic

responds to chemo but incurable

42
Q

describe high grade non-hodgkin lymphoma

A

aggressive, fast growing
require combination chemotherapy
can be cured

43
Q

what is the commonest subtype of lymphoma?

A

diffuse large B-cell lymphoma

44
Q

is diffuse large B-cell lymphoma high or low grade?

A

high

45
Q

what is the 2nd commonest subtype of lymphoma?

A

follicular lymphoma

46
Q

is follicular lymphomahigh or low grade?

A

low grade

47
Q

treatment of diffuse large B cell lymphoma and follicular lymphoma

A

combination chemo - typically anti CD20 monoclonal antibody (rituximab) and chemo

48
Q

what does a biopsy in hodgkin lymphoma show?

A

normal cells with a hodgkin cell in the middle

49
Q

what percentage of lymphomas are hodgkin lymphoma ?

A

30%

50
Q

describe the age distribution of hodgkin lymphoma

A

bimodal

15-35 and later in life

51
Q

M:F hodgkin lymphoma

A

1.9:1

52
Q

what is hodgkin lymphoma associated with?

A

EBV
familial
geographical clustering

53
Q

treatment of hodgkin lymphoma

A

o Combination chemotherapy (ABVD)
o +/- radiotherapy
o Use of PET scan to assess response to treatment and to limit use of radiotherapy

Year 3 (164 decks)

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