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Haem/Onc > Hodgkins Lymphoma, ASPHO > Flashcards

Hodgkins Lymphoma, ASPHO Flashcards

1
Q

what are the types of classic HL?

A

LLMN

  • Nodular sclerosing
  • mixed cellularity
  • lymphocyte predominant
  • lymphocye depleted
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2
Q

What is the type of HL that is not classic?

A

Nodular Lymphocyte predominant

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3
Q

Give 5 types of NHL

A
  • Burkitt
  • Diffuse large B
  • Primary mediastinal B cell
  • Lymphoblastic
  • Anaplastic large cell
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4
Q

Give a B-cell derived, immature lymphoma

A

B-lymphoblastic

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5
Q

Give a B-cell derived mature lymphoma (4)

A

burkitt
diffuse large b
hodgkin
primary mediastinal b

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6
Q

Give a t-cell derive, mature lymphoma

A

anaplastic large cell

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7
Q

most common peds malignancies in 0-14 age range? #1-5

A 
1- leukemia
2-cns
3-lymphoma
4-neuroblastoma
5-rhabdo/STS
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8
Q

most common peds malig in age 15-19? #1-5

A 
1-lymphoma
2-germ cell
3-leuekmia
4- CNS
5- Rhabdo
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9
Q

Below the age of ___, NHL more common than HL

A

10

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10
Q

HL: classic cell?

A

Reed Sternberg= owl eye

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11
Q

describe reed sternberg

A

owl’s eye, binucleate, thick nuclear membrane, pale hcromatin, large eosinophilic nucleoli

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12
Q

Lymphocyte predom: describe cell

A

mononuclear variant of hodkgin reed sternberg cell, may have several nucleoi, convoluted irreg nucleus= popcorn

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13
Q

in HL, and LP, neoplastic cells compreise

A

<1%

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14
Q

artifcant of formulin fixation: islands…called what?

A

lacunar cells

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15
Q

Nodular sclerosing HL:; have a __ capsule

A

thick

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16
Q

NS HL tends to involve what area of body? (2)

A

neck, mediastinum

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17
Q

what = #2 most common type of classic HL?

A

mixed cellularity HL

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18
Q

mixed cellularity HL tends to be seen in what age?

A

<10

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19
Q

EBV often involved in what type of HL?

A

mixed cellularity..seen lymphocytes, histiocytes, eos

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20
Q

what type of HL is often advanced at dx?

A

mixed cellularity HL…and almost always in lymphocyte depeleted

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21
Q

lymphcoyte rich HL: see what?

A

SHEETS of lymphs!

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22
Q

lymphocyte depleted HL: see what?

A

large bizarree malig cells, few lymphocytes, disorganized fibrossi, rare in kids

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23
Q

immunophenotyping: in classic HL, what do you find?

A

CD15+, CD30+, CD45 NEG

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24
Q

immunophenotype in noedular lymphocyte predom HL, what do you see?

A

CD15 neg, CD30 neg, CD45 POS

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25
Q

what is most common histo of HL?

A

nodular sclerosing

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26
Q

NS HL becomes more common with what?

A

wiht age

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27
Q

young adults: thinking which type of HL?

A

NS

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28
Q

<10 years and not advanced: think which type of HL?

A

lymphocyte rich

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29
Q

<10 years AND ADVANCED: think which type of HL?

A

mixed cellularity HL

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30
Q

adults with HIV: think which type of HL?

A

lymphocyte depleted

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31
Q

young, male, localized: think which type of HL?

A

nodular lymphocyte predominant

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32
Q

in terms of HL, list type most seen with EBV–> least

A

Lymphocyte depleted>mixed cellularity>lypohcyte-rich (42%)>NS>nodular lympohcyte preodmaintn (rare)

33
Q

Histo subtypes of classic HL are based off what 3 thigngs>

A

tissue architectures, fibrosis, inflammatory infiltrate…not used in risk stratification

34
Q

classic HL: most common–> least common type?

A

NS>mixed cellularity>lymphocyte rich

35
Q

risk of having HL if your parent has it? sibling? monozygotic twin?

A

Parent: 3x
Sibling: 6x (more likely if sister)
Mono twin: 99x

36
Q

pateints who are immunodef: increased risk of HL– 4 egs?

A

sarcoid, ALPS (51x), Ataxia telangiectasia, HIV

37
Q

4 immune-related ways that HL can present?

A

ITP, AIHA, AI neutropenia, nephrotic syndrome

38
Q

in 0-14 age range, 3 RFs or HL?

A

low SES, larger family, early/intense expsoure to infections?

39
Q

in 15-25 age range, 4 RVFs for HL?

A

higher SES, small family/less siblings/playmates, single family house, late expsoure to infections

40
Q

what is always active in classic HL cells?

A

NFkappaB, either via LMP1 if EBV+ or IkappaBmutation

41
Q

what are the mechanisms by which HL cells resist immune system?

A

MHC 1 expression is low/absent in most HL–> less T-cell recognition; PD-1 is present on HRS cells–> T-cell anergy, growth inhibition

42
Q

Give the malignant cell of classic HL vs. nodular lympohcyte predominant HL:

A

classic: Hodgkin reed-sternberg cell; NLP: LP cells (popcorn)

43
Q

Give the origin of classic HL vs NLP

A

classic: pre-apoptotic GC B cell; NLP: GC/post-GC B cell

44
Q

give the phenotype of classic vs NLP HL

A

classic: CD15+, CD30+, CD45 neg, b-cell markers downregulated…NLP: cd15 neg, cd30 neg, cd45 pos, cd20 pos, pos ofr CD19, 20, 79a, PAX5

45
Q

clicial pres of HL?

A
  • painless cervical or supraclav LAD
  • mediastinal mass (~2/3)
  • constitutional symptoms
  • evdience of inflamm and RES activaiton (increased CRP, ESR, ferritin, anemia of chronic inflamm)
  • immune dysreg (uncommon)= AIN, AIHA, ITP, nephrotic syndrome
46
Q

which constitutional symptoms =B symptoms are prognostic in HL?

A

wt loss of 10% in 6 months, drenching night sweats, unexplained fevers >38 for 3 consecutive days

47
Q

which symptoms are NOT prognostic in HL?

A

fatigue, anorexia, mild wt loss, pain immeidately following alochol, pruritus

48
Q

NLP: what percent of HL? what % are pre-pubertal? what % male?

A

5-8%, 10-20%, 75%

49
Q

describe presentation of NLP HL

A

localized disease, no b symptoms, not bulky, not systemic, EBV negative

50
Q

good thing about NLP HL?

A

might only need surgery for stage 1A

51
Q

bad thing about NLP HL?

A

10-14% transform into DLBCL

52
Q

buzzwords for NLPL HL? 4

A

YMCA! young, male, contained, asymptomatic

53
Q

steps to eval HL?

A
  • H&P, including b sytmpoms, LAD< SVC syndrome, superior mediastinal syndrome
  • CBC, biochem, inflamm markers
  • CXR
  • excisional LN bx
  • PET-CT or PET-MRI has largely replaced BM bx
  • CT of chest to assess for lung involvemnt (MRI inadequate)
54
Q

Give 10 ddx for mediastinal mass

A
  • normal thymus
  • infection (ebv, atypical myocbacterium, histoplasmosis, toxoplasmosis)
  • lymphoprolierative disrodres
  • progressive transformaton fo the germinal centres (PTGC)
  • HL
  • Lymphobolastic lymphoma
  • DLBCL
  • Priamry mediastinal b cell lymphoma
  • anaplastic large cell lymphoma
  • germ cell tumour
  • soft tissue sarcoma
  • lymph node mets from other sites
55
Q

FDG-PET: glucose analog: 3 reasons for false +?

A

inflamm, thymic rebound, brown fat

56
Q

When do you use FDG PET for HL?

A
  • staging at dx

- response to therapy (complete metabolic response-=remission)

57
Q

what’s more sens/spec…FDG PET or CT for lymphoma?

A

PET

58
Q

is FDG PET appropriate for off therapy surveillance for recurrence?

A

No

59
Q

what’s the scale used to eval HL response to tx?

A

Deauville scale

60
Q

describe teh deauville scale

A 
1- no uptake above background
2-uptake= mediastinum
3- uptake >mediastinum but = liver
4- uptake moderately> liver
5- uptake markedly>liver or new lesions
...1,2= complete metab response...3= usually CMR but context depedent...4,5= active disease....3 at interim analysis often considered cMR
61
Q

what’s the staging used for HL?

A

Ann Arbor Staging

62
Q

Describe the stages of Ann Arbor Staging

A

Stage I: single node (I) or single extra-lymphatic organ or site (IE)
Stage II: 2 or more node regions on the same side fo the diapghram (II) or one node region and one localized lymphatic site on same side of the diaphgram (IIE)
Stage III: node regions are involved on both sides of the diaphragm (III), may include an extranodal site (IIIE) the spleen (IIIs) or both (IIISE)
Stage IV: diffuse/disseminated involement of 1 or more extranodal site or tissue (liver, lung, marrow)

63
Q

in ann arbor staging, give the stage classifications (HL):

A 
A= asymptomatic
B= b symptoms
E= invoment of extra-lympathic organ
S= splenic involvmenet
X= bulky mediastinal disease
64
Q

describe bulky disease in ann arbor staging (HL):

A

mediastinal mass: tumour >1/3 thoracic diameter on PA CXR; nodal aggregate >6 cm in the longest transverse diameter; macroscopic splenic nodules: focal defects on CT, PET, or MRI

65
Q

give 5 unfavourable prognostic factors in peds HL

A 
Advanced disease at dx
B symptoms
bulk disease
Extranodal extension
Slow/incomplete response (PET>CT)
66
Q

What qualifies as Low risk HL for COG?

A

I/IIA, no bulk

67
Q

What qualifies as Intermed risk in HL for COG?

A

I/IIA + bulk
I/IIAE
IIIA
IB, IIB no bulk

68
Q

What qualifies as High risk in HL for COG?

A

IVA
IIB+Bulk
IIIB, IVB

69
Q

does HL require LP, IT chemo, craniospinal rad?

A

NO

70
Q

survival in HL?

A

> 90% even with adv disease

71
Q

what determines tx in HL?

A

stage/prog factors at dx

objective resposne to therapy (PET>CT)

72
Q

ongoing trials in HL are designed to waht?

A

decrease chemo, decrease rad, use targeted therapy (brentuximab anti-cd 30, checkpoint inhibitors)

73
Q

radiation dose in HL?

A

20-25.5 Gy in 1.5-1.8 Gy fractions over 6-8 weeks

74
Q

trial for IR HL? chemo? radiation?

A

AHOD0031…ABVE-PC…rad not needed in RER after cycle 2, CR after 4 cycles

75
Q

tx relapsed HL how?

A

nove therapy–> high dose chemo and autologous transplant if respond…if not, do something diff

76
Q

problems with transplant for relapsed HL cases?

A
  • Late relapse (>12 months) of low stage disease don’t need autologous SCT.
  • primary refractory disease <3 months don’t do well EVEN with transplant
77
Q

targets for HL?

A
  • CD30= classic HL
  • EBV
  • CD20 (NLPHL)
  • PD-1, PD-L1, PD-L2
  • NFkappaB, JAK/STAT
  • block histone deacetylation
78
Q

late effects in HL

A

SKELETAL: decreased bone growth, AVN from radiation and steroids
CARDIAC: cardiomyoapthy, effusion, pericardiits, CHF, CAD, AMI from radiation, alkyalating agents, anthracyclines
PULMONARY: pneumonitis, fibrosis from radiation, bleo, anthracylcines
ENDO: hypot4, female infert from radiation adn alkylating agents, male infert from alkylating agents
MALIG: solid tumours from raidation, alkylating agents; AML/MDS from alkylating agnets and epipodophyllotoxins

79
Q

what’s the msot common secondary malig in HL?

A

bresat cancer in women…esp if radiation at age 10 or older for rad….decreases with age though…no excess risk in women aged 30+….the greatest RELATIVE RISK is leukemia however

Haem/Onc (30 decks)

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