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Y3 immunology and haematology > lymphoproliferative disorders > Flashcards

lymphoproliferative disorders Flashcards

1
Q

what is leukaemia

A

“white blood”

generally used to describe a cancer that you can see in the blood

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2
Q

what is lymphoma and what can they present w/

A

cancers of lymphoid origin

can present w/ lymphadenopathy or extranodal involvement or w/ bone marrow involvement

systemic (B) symptoms: weight loos (>10% in 6mths), fever, night sweats, pruritus, fatigue

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3
Q

diagnosing a leukaemia/lymphoma

A

> 70 different types, defined by the malignant cell characteristics

  • biopsy - tells us what type it is (THIS IS HOW THE DIAGNOSIS IS MADE)
  • clinical examination and imaging - tells us where it is (STAGING)
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4
Q

staging of lymphoma/leukaemia

A

location and extent of the disease

information about prognosis

sometimes influences treatment

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5
Q

lymphocyte differentiation

A
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6
Q

when can malignant conditions occur in the process of lymphocyte differentiation

A

bone marrow: earliest stages of lymphoid cell development e.g. acute lymphoblastic leukaemia

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7
Q

classifications of lymphomas

A

Hodgkin lymphoma is a specific disease

Non-Hodgkin lymphoma is everything else (~70 subtypes)
- divided into high and low grade

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8
Q

key lymphoproliferative disorders (common to least common)

A

Non-Hodgkin lymphoma
- high grade (diffuse large B cell lymphoma), low grade (follicular, marginal zone)

Chronic lymphocytic leukaemia (CLL) - presents in a similar way to low grade NHL

Hodgkin lymphoma

Acute lymphoblastic leukaemia (ALL)

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9
Q

how common are the different lymphoproliferative disorders

A
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10
Q

what is ALL

A

cancerous disorder of lymphoid progenitor cells

no differentiation, instead there is rapid and uncontrolled growth and accumulation

usually in bone marrow but they can go anywhere

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11
Q

normal lymphoid progenitor cells

A

immature

rapidly proliferating cells that differentiate into lymphocytes

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12
Q

what condition is this

A

ALL

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13
Q

how common is ALL

  • incidence
  • age
  • what cell lineage
A

1-2/100 000 pop/yr

75% cases occur in children <6y/o

75-90% cases are of B cell lineage

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14
Q

how does ALL present

A

2-3wk hx of bone marrow failure or bone/joint pain

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15
Q

typical ALL hx

A

17y/o male
1mth impaired vision (both eyes)
1/2 stone weight loss
SOB on minimal exertion

fundoscopy: retinal haemorrhages

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16
Q

blood count for ALL

A

low Hb
high WCC
low plts

bone marrow - 90% B lymphoblasts

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17
Q

what can be seen here

A

normal bone marrow

white circles = fat

normal mix of different types of blood cells and platelets

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18
Q

what can be seen here

A

abnormal bone marrow

hypercellular and uniform cells

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19
Q

ALL cells characteristics

A

large cells

express CD19
CD34, TDT

haven’t had the chance to develop and mature

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20
Q

what is CD19

A

marker expressed by all B cells

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21
Q

what do CD34 and TDT indicate

A

markers of very early immature cells

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22
Q

treatment for ALL

A

induction chemotherapy to obtain remission
consolidation therapy
CNS directed treatment
maintenance treatment for 18mths

stem cell transplantation - if high risk of relapse

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23
Q

newer therapies for ALL

A

bi-specific T cell engagers (BiTe molecules)

CAR T cells

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24
Q

example of bi-specific T cell engagers

A

blinatumumab

25
how do bi-specific T cell engagers work
binds to tumour cells (CD19) and activates and recruits pts own T cells to attack the leukaemia cells
26
what are CAR T cells
chimeric antigen receptor T cells
27
how are CAR T cells made and used
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 can be curative in pts w/ very resistant disease but very expensive
28
key side effects of T cell immunotherapy
cytokine release syndrome neurotoxicity
29
T cell immunotherapy: cytokine release syndrome
fever, hypotension, SOB CAR T cell effect correlated to presence of CRS - sig. number require ITU support
30
T cell immunotherapy: neurotoxicity features
confusion w/ normal conscious level seizure, headache, focal neurology, come
31
ALL poor risk factors
increasing age increased WCC cytogenetics/molecular genetics: t(9;22), t(4;11) slow/poor response to treatment
32
ALL outcome
adults: - complete remission rate ~90% - leukaemia free survival at 5y 30-35% children - 5y overall survival ~90% - poor risk pts (slow response to induction or philadelphia +ve) 5y OS 45%
33
what happens to the cells in CLL
abnormal cells are mature - usually resemble normal, well behaved lymphocytes - grow slowly, or not at all - classic example of a low grade condition - carry many of the normal markers that B lymphocytes have
34
what does a diagnosis of CLL require
lymphocyte count >5 (normal is <4)
35
CLL incidence
``` >1700 new cases p/a UK commonest leukaemia worldwide 2M:1F occasionally familial rare in far east ```
36
CLL presentation
often asymptomatic frequently: - bone marrow failure (anaemia, thrombocytopenia) - lymphadenopathy - splenomegaly (30%) - fever and sweats (<25%) less commonly: - hepatomegaly - infections - weight loss
37
CLL associated findings
immune paresis haemolytic anaemia - 20% have +ve direct antiglobulin test - 8% clinical evidence of haemolytic anaemia
38
what is immune paresis
loss of normal immunoglobulin function
39
how is CLL staged
Binet staging system
40
CLL - Binet staging
A - <3 LN areas, median survival same as age matched controls B - ≥3 LN areas, ~8yrs med survival C - stage B + anaemia/thrombocytopenia, ~6yrs
41
CLL indications for treatment
``` progressive bone marrow failure massive lymphadenopathy progressive splenomegaly lymphocyte doubling time <6mths or >50% increase over 2mths systemic symptoms AI cytopenias ```
42
CLL treatment
often nothing - watch and wait cytotoxic chemotherapy monoclonal antibodies novel agents
43
cytotoxic chemotherapy for CLL
fludarabine | bendamustine
44
monoclonal antibodies for CLL
rituximab | obinatuzumab
45
novel agents for CLL
less immunosuppressive, oral treatments Bruton tyrosine kinase inhibitor e.g. ibrutinib PI3K inhibitor e.g. idelalisib BCL-2 inhibitor e.g. venetoclax
46
CLL poor prognostic markers
``` advanced disease (stage B/C) atypical lymphocyte morphology rapid lymphocyte doubling time (<12mth) CD38+ expression loss/mutation p53, del 11q23 (ATM gene) unmutated IgVH gene status ```
47
presentation of lymphoma
lymphadenopathy/hepatosplenomegaly extranodal disease B symptoms bone marrow invlolvement
48
assessment/staging of lymphoma
LN biopsy CT scan bone marrow aspirate and trephine
49
staging of lymphoma
I: 1 nodal site of involvement II: 2 separate nodal sites, either above or below the diaphragm but not both III: multiple nodal sites, both above and below the diaphragm IV: extranodal disease involvement A: absence of B symptoms B: fever, night sweats, weight loss
50
how is NHL classified
lineage: B or T cell (90% B cell origin) grade: high vs low
51
low grade NHL
indolent, often asymptomatic | responds to chemotherapy but incurable
52
high grade NHL
aggressive, fast growing require combination chemo can be cured
53
specific types of NHL
diffuse large B cell lymphoma: - commonest subtype of lymphoma - high grade follicular lymphoma: - 2nd commonest subtype of lymphoma - low grade - like CLL, watch and wait if not causing problems - both arise from a transformation in the germinal centre of a LN
54
how are diffuse large B cell lymphoma and follicular lymphoma treated
combination chemotherapy: | anti-CD20 monoclonal ab + chemo
55
how common is HL
30% of all lymphomas
56
age of HL | M vs F
bimodal age curve: 15-35y/o 2nd peak later in life 1.9M:1F
57
associations w/ HL
EBV | familial and geographical clustering
58
treatment of HL
``` combination chemo (ABVD - 4 different drugs) +/- radiotherapy monoclonal ab (anti-CD30) - brentuximab immunotherapy (checkpoint inhibitors) ``` PET scanning central to assessment of response to treatment

Y3 immunology and haematology (20 decks)

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