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Met3b > Leukemia > Flashcards

Leukemia Flashcards

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
Q

the french american british classification is for?

A

acute myeloid leukemia

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26
Q

leucosytosis is most commonly seen in

A

AML

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27
Q

What is the immunological marker for AML

A

CD34plus

28
Q

common mutation in AML

A

FLT3

29
Q

cytogenetics of AML

A

-7q

30
Q

in what cancer can you see Auer rods (elongated structues of granules)

A

AML

31
Q

what is APML

A

Acute Promyeloctic Leaukaemia, its a type of AML

32
Q

what is the characteristic morphology of cells in APML

A

hypergranular promyelocytes

33
Q

what genetic changes leads to APML

A

t15:17 translocation

fusion of PML and RARA to generate PML-RARA oncoprotein

34
Q

treatment of APML

A

ATRA/arsenic/anthracyclines

35
Q

what antibiotic do you use for prophylaxis in patients with neutropenia?

A

meropenem

36
Q

treatment for leucostasis

A

venesection or leucopharesis

37
Q

What dictates what treatment you give to AML patients

A

their risk stratified based on cytogenetics and mutations

38
Q

if AML good risk, what is the treatment protocol?

A

4 cycles of intensive chemotherapy

39
Q

If AML intermediate/poor risk, what is the treatment protocol?

A

chemotherapy to remission then allogenic transplant

40
Q

what are the drugs used in the chemotheraoy of AML

A

daunorubicin and cytarabine

41
Q

how do daunorubicin and cytarabine work?

A

antimetabolites - interfere iwth DNA synthesis

42
Q

what is a hickman line for?

A

like a cannula but bigger. used to give drugs or take blood.

43
Q

for what cancer do you use auto bone marrow transplatn

A

myeloma and lymphoma

44
Q

for what cancer do you use allo bone marrow transplant

A

leukemia

45
Q

what cancer correlates well with graft versus host disease

A

AML

46
Q

how do you actually collect stem cells

A

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
Q

most common childhood cancer

A

ALL

48
Q

peak incidence ALL

A

2-4

49
Q

symptoms of ALL

A

neutropenia, thrombocytopenia, anemia, lymphadenopathy (particularlyy T-ALL)
abdominal organomegaly

50
Q

marker of ALL

A

CD34plus and TdT

51
Q

what are the cytogenetics of ALL

A
  • Hyperdiploidy common – high hyperdiploid favourable (51-65 chromosomes)
  • t(9;22) (Philadelphia) and t(4;11) both adverse prognostically
52
Q

ALL treatment

A

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
Q

how are chronic leukemias different from acute ones

A

Slower growing

Don’t always require immediate treatment

54
Q

CLL median age of presentation

A

65-70

55
Q

CLL symptoms

A

most ofren asymptomatic but can be tiredness, night sweats, weight loss, recurrent infectims (hypogammaglobulineaemia), hepatosplenomegaly

56
Q

CLL is the proliferation of

A

• Proliferation of small mature B lymphocytes in the BM and PB

57
Q

CLL diagnosis

A

lymphocytosis >5

Normochromic normocytic anemia plus minus autoimmune heamolytic aneamia

58
Q

what is the binet classificaiton (A, B, C) used for

A

CLL

59
Q

histology of CLL

A

lots of small mature lymphocytes with monomorphic appearance

60
Q

CLL management and indication for treatment

A

Binet stage 1: observe

progressive BM failure, massive ogranomegaly, systemic symotoms

61
Q

CLL treamtne

A

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
Q

CLL poor prognostic features

A

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
Q

CML cuase

A

bcr-abl fusion gene

reciprocal trasnlocation of chromosomes 9 and 22

64
Q

treatment of CML and how does it work

A

imatinib (glive)

blocks ATP bcr-acl binding.

65
Q

myselodysplastic syndrome tretatent

A

• Supportive treatment-transfusions, treat infections, newer drugs-azacytadine (DNA demethylating agent) and bone marrow transplant.

66
Q

• If in an exam question they mention Philadelphia chromosome or t(9:22)-

A

CML

67
Q

• In patients with a raised WCC-look at the differential. If in a well patient it is mainly a lymphocytosis

A

likely to be CLL.

Met3b (3 decks)

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