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Leukemia Flashcards

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1
Q

Leukemia is a cancer of?

A

hemopoetic cells

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2
Q

what happens to white blood cell counts in leukemia

A

elevated

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3
Q

4 types of leukemia

A

ALymphoblasticL
AML
CML
CLYMPHOCYTIC L

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4
Q

is leukemia acute or chrnoic

A

2 types acute and 2 types chronic

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5
Q

progenitor cells are also called

A

blasts

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6
Q

cancer of lymhoid progenitor or lymphoid blasts is?

A

ALL

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7
Q

cancer of mature B cell is

A

chronic LL

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8
Q

cancer of plasma cells which normally secrete antibodies

A

myeloma

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9
Q

cancer of myeloid progenitor or myeloid blasts is?

A

AML

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10
Q

cancer if differentiated myeloid progenitor (neutrophils, eosipnophils, basophils etc)

A

myeloproliferative disorder

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11
Q

cancer of b cells in germinal centre

A

lymphomas

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12
Q

where do all blood cells come from? what bone specifically?

A

bone marrow of the hip bone in adults

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13
Q

what 4 lab tool can you use to diagnose heamatological malignancies?

A
  • morphology: blood film, bone marrow biopsy
  • immunophenotyping :
    distinguishes cancerous from normal tissue
    and different types of hematological malignancy¡ies

-genetic and molecular features:
chromosome abormality, g banding and fish
mutations: pcr

mutations
changes in DNA sequende n ot chormonse
deted by sequencing technollgies

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14
Q

can you diagnose cancer based on morphology alone?

A

NO. need immunophenotyping

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15
Q

whats immunophenotyping AKA

A

flow cytometry

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16
Q

what does flow cytometry look at

A

surface antigens

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17
Q

what cell is CD20 a marker of

A

LYMPHOID –> if high percentage, suggests a lymphoid cancer.

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18
Q

for PCR do you need cells to be in metaphase

A

YES

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19
Q

for FISH do you need cells to be in metaphase

A

NO

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20
Q

one complication of intense chemotherapy

A

neutropenic sepsis

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21
Q

AML and ALL is the accumulation

A

of the blasts in the bone marrow

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22
Q

Diagnosis of AML and ALL requires what percentage of blasts in bone marrow or blood

A

20%

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23
Q

AML and ALL

A

low HB
low platelets –> bleeding
WCC low (if low: infection, if high: leucostasis)

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24
Q

treatment for AML and ALL

A

high dose myelosuppressive chemotherapy

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25
the french american british classification is for?
acute myeloid leukemia
26
leucosytosis is most commonly seen in
AML
27
What is the immunological marker for AML
CD34plus
28
common mutation in AML
FLT3
29
cytogenetics of AML
-7q
30
in what cancer can you see Auer rods (elongated structues of granules)
AML
31
what is APML
Acute Promyeloctic Leaukaemia, its a type of AML
32
what is the characteristic morphology of cells in APML
hypergranular promyelocytes
33
what genetic changes leads to APML
t15:17 translocation | fusion of PML and RARA to generate PML-RARA oncoprotein
34
treatment of APML
ATRA/arsenic/anthracyclines
35
what antibiotic do you use for prophylaxis in patients with neutropenia?
meropenem
36
treatment for leucostasis
venesection or leucopharesis
37
What dictates what treatment you give to AML patients
their risk stratified based on cytogenetics and mutations
38
if AML good risk, what is the treatment protocol?
4 cycles of intensive chemotherapy
39
If AML intermediate/poor risk, what is the treatment protocol?
chemotherapy to remission then allogenic transplant
40
what are the drugs used in the chemotheraoy of AML
daunorubicin and cytarabine
41
how do daunorubicin and cytarabine work?
antimetabolites - interfere iwth DNA synthesis
42
what is a hickman line for?
like a cannula but bigger. used to give drugs or take blood.
43
for what cancer do you use auto bone marrow transplatn
myeloma and lymphoma
44
for what cancer do you use allo bone marrow transplant
leukemia
45
what cancer correlates well with graft versus host disease
AML
46
how do you actually collect stem cells
G-CSF given to donor (or patient) subcut for 4 days – collect Day+5 * Mobilises CD34+ stem cells into peripheral blood * Collected by leucapheresis * No general anaesthetic * No evidence of late haem effects for donors
47
most common childhood cancer
ALL
48
peak incidence ALL
2-4
49
symptoms of ALL
neutropenia, thrombocytopenia, anemia, lymphadenopathy (particularlyy T-ALL) abdominal organomegaly
50
marker of ALL
CD34plus and TdT
51
what are the cytogenetics of ALL
* Hyperdiploidy common – high hyperdiploid favourable (51-65 chromosomes) * t(9;22) (Philadelphia) and t(4;11) both adverse prognostically
52
ALL treatment
o Remission induction - vincristine, prednisolone, daunorubicin, asparaginase. o Consolidation - various combinations of chemotherapeutic agents. o CNS directed therapy - high dose systemic and intrathecal methotrexate. o Maintenance therapy - vincristine, prednisolone, mercaptopurine and methotrexate for 2-3 years
53
how are chronic leukemias different from acute ones
Slower growing Don’t always require immediate treatment
54
CLL median age of presentation
65-70
55
CLL symptoms
most ofren asymptomatic but can be tiredness, night sweats, weight loss, recurrent infectims (hypogammaglobulineaemia), hepatosplenomegaly
56
CLL is the proliferation of
• Proliferation of small mature B lymphocytes in the BM and PB
57
CLL diagnosis
lymphocytosis >5 | Normochromic normocytic anemia plus minus autoimmune heamolytic aneamia
58
what is the binet classificaiton (A, B, C) used for
CLL
59
histology of CLL
lots of small mature lymphocytes with monomorphic appearance
60
CLL management and indication for treatment
Binet stage 1: observe | progressive BM failure, massive ogranomegaly, systemic symotoms
61
CLL treamtne
no benefit in treating early stage - autoimmune complications treated with steroids • Alkylating agents- chlorambucil * Purine analogues- Fludarabine * Combination Chemotherapy-FCR (fludarabine, cyclophosphamide, rituximab) * Rituximab is an anti-CD 20 mAb. * Supportive care (immunisations/blood transfusions/treatment of infections)
62
CLL poor prognostic features
Lymphocyte doubling time <12 months. * Certain chromosomal changes. * Mutations or deletions of the tumour suppressor gene TP53. Newer drugs such as Ibrutinib-targeting the B cell receptor pathway are showing promising results.
63
CML cuase
bcr-abl fusion gene | reciprocal trasnlocation of chromosomes 9 and 22
64
treatment of CML and how does it work
imatinib (glive) | blocks ATP bcr-acl binding.
65
myselodysplastic syndrome tretatent
• Supportive treatment-transfusions, treat infections, newer drugs-azacytadine (DNA demethylating agent) and bone marrow transplant.
66
• If in an exam question they mention Philadelphia chromosome or t(9:22)-
CML
67
• In patients with a raised WCC-look at the differential. If in a well patient it is mainly a lymphocytosis
likely to be CLL.

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