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Oncology > leukaemia / lymphoma > Flashcards

leukaemia / lymphoma Flashcards

1
Q

most common childhood cancer

A

ALL

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2
Q

most common type of ALL

A

B-ALL (85%)
T-ALL (15%)

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3
Q

peak age of ALL presentation

A

2-5y

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4
Q

4 syndromes a/w ALL

A

a. Down syndrome
b. NF1
c. Bloom syndrome
d. Ataxia telangiectasia

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5
Q

biggest prognostic factor for ALL

A

response to induction!!

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6
Q

ALL: favourable vs not favourable genetics

A

favourable:
1. Hyperdiploidy (>50)
2. Trisomies 4, 10
3. ETV-RUNX protein (t12;21)

not favourable:
1. Hypodiploidy (<44)
2. Philadelphia t(9;22)

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7
Q

achieving remission after end of induction measured by?

A

MRD - must be <0.01% by D29

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8
Q

ALL risk factors

A

i. Age > 10y or <1y
ii. WCC > 50 or CSF/testicular involvement at diagnosis
iii. Cytogenetic/molecular
iv. Response to induction – biggest prognostic factor

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9
Q

for FRACP, DIC + leukaemia = what kind?

A

APML

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10
Q

very specific FRACP features for AML

A
  1. Subcutaneous nodules – ‘blueberry muffin’ lesions
  2. Infiltration of gingiva
  3. DIC (APML**)
  4. Discrete masses – chloromas, granulocytic sarcomas
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11
Q

bone marrow findings of ALL vs AML

A

ALL 85% blasts, high nucleus:cytoplasm ratio

AML 20% blasts, with auer rods

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12
Q

describe the mutation in APML, and therefore its treatment

A

t15;17 = PML-RARA: responsive to all-trans-retinoic acid (ATRA, tretinoin)

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13
Q

survival rate of ALL vs AML

A

ALL: up to 99% with favourable genetics, say 90%

AML: 60-70%

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14
Q

down syndrome: AML or ALL?

A

ALL: 20x more common EXCEPT in first 3 years of life
- worse cytogenetics, worse prognosis
- T21 more sensitive to MTX

AML: better survival in T21!

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15
Q

why are FBEs important in T21 neonates?

A

10% get transient leukaemia/MPD (high leuks, blasts, low plt/Hb)

and 20-30% will develop leukaemia by 3y

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16
Q

bcr-abl: what’s the mutation and Rx

A

t(9;22) > imatinib TK inhibitor

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17
Q

JMML syndromic risk factors

A
  1. noonan’s
  2. NF1
18
Q

most JMML have mutations in what pathway?

A

RAS/MAP kinase pathway

19
Q

key features of JMML

A
  • 1/3rd present with an URTI with hepatosplenomegaly and a rash
  • *monocytosis *
20
Q

most cases of infant leukaemia (<1y) from what mutation?

A

> 80% MLL gene (11q23 band translocation; majority t(14;11)) - and this is a shit one

21
Q

HLH: most common age group

A

birth to 18m

22
Q

pathogenesis of HLH

A

trigger > abnormal immune activation: macrophages eat up RBC and make cytokine storm, but NK and CD8 T cells can’t shut the macrophages down

23
Q

most familial HLH is caused by what kind of problem?

A

defect in perforin, so NK/CD8 can’t do their job against the macrophages

24
Q

aetiology of HLH

A
  1. genetic mutation
  2. infection - EBV**
  3. malignancy - esp lymphoid
  4. macrophage activation syndrome e.g. JIA/other rheum
25
Q

symptoms of HLH

A
  1. fever ***
  2. rash - macpap or petechiae
  3. hepsplen
  4. lymphadenopathy
  5. resp distress
  6. CNS signs

… so very non-specific really

26
Q

key Ix of HLH

A
  1. cytopaenia (Hb, plt, neuts)
  2. high ferritin
  3. high TG
  4. hepatitis
27
Q

worst prognostic factor for HLH

A

higher ferritin

28
Q

clinical presentation of lymphomas vs leukaemia

A

lymphomas less constitutional symptoms (H 1/3, NHL 10%). More often have regional lymphadenopathy

29
Q

concerning areas for lympahdenopathy

A

non-cervical and supravlacivular

30
Q

types of lymphoma

A

HL vs NHL (DLBCL, lymphoblastic lymphoma, burkitt’s, ALCL)

31
Q

presence of B symptoms matters for which cancer

A

HL (NOT NHL)

32
Q

classic biopsy finding of HL

A

Reed-Sternberg…but also seen in EBV!

33
Q

HL vs NHL

A

HL: spread continguously, rarely extra-nodal. prognosis BETTER

NHL: non-contiguous spread, often extra-nodal e.g. skin, GI

34
Q

epidemiology of HL - ages and sex

A

M:F 3 to 1
rare <5, peak 15-35y

35
Q

lymphoma and SOB - what to think of?

A

mediastinal mass (bulky >1/3 of diameter) > obstruction / SVC compression, dangerous for GA

36
Q

5-year OS for HD of all stages is…?

A

> 80%

37
Q

favourable prognostic factors for HL

A

<10 yo, female, favourable subtypes (LP and NS) and Stage I non-bulky disease

38
Q

poor prognostic factors with a HL relapse

A

<1y from completion of tx
B symptoms
extra-nodal

39
Q

which is more common in children - HL or NHL

A

NHL 60%, esp Burkitt’s younger, DLBCL adolescents

40
Q

BL vs DLBCL

A

BL - highly aggressive. germinal centre B cells. mainly abdo primary, (jaw for africans) with bone / CNS mets. “starry sky” appearance. TLS

DLBCL - aggressive. mature B cell. mainly mediastinal /abdo primary, RARELY with bone/CNS mets. TLS UNCOMMON

41
Q

types of Burkitt’s

A

endemic = African, jaw, younger, upstream of c-myc, CNS > BMA, a/w EBV

sporadic = worldwide, abdo primary, a bit older (~11y), at c-myc, BMA > CNS, no EBV

42
Q

survival rate of PTLD

A

20-35%

Oncology (4 decks)

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