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Hematology > Hematology Week 3: Lymphoma I > Flashcards

Hematology Week 3: Lymphoma I Flashcards

1
Q

Normal Lymph Node Morphology

A

1 = Paracortex

2 = Subcapsular Sinus

3 = Medulla

4 = Follicles

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2
Q

Normal Immunoarchitecture

A

A = 1

B = 2

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3
Q

Lymph Node Examination

4 Listed

A
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4
Q

Lymphoma & Leukemia Definitions

A
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5
Q

Benign and Malignant lymphadenopathies

A
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6
Q

B & T Cell maturation & Neoplastic differences

A
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7
Q

Lymphoma Pathogenesis

4 listed

A
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8
Q

Lymphotropic viruses

A
  • EBV
  • Human T cell Leukemia virus-1 (HTLV-1)
  • Human Herpes Virus 8 (HHV-8)
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9
Q

Categories of lymphomas

A

Hodgkin Lymphoma

non-Hodgkin Lymphoma

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10
Q

Hodgkin Lymphomas

A
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11
Q

Non-Hodgkin Lymphomas

A
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12
Q

Classic Hodgkin Lymphoma histological description

A
  • Reed-Sternberg cells
  • doesn’t have blue lymphoid cells
  • have a lot of pink
  • owl’s eye appearance
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13
Q

Classic Hodgkin Lymphoma Diagnostic Criteria

2 listed

A

Need both

  • Reed-Sternberg cell
  • Mixed inflammatory background
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14
Q

Reed-Sternberg cells

A
  • secrete cytokines and factors that induce accumulation of reactive cells
  • <10% of total tumor mass
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15
Q

Reed-Sternberg are derived from what cell type?

A

Derived from germinal center or post germinal center B-cells

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16
Q

Reed-Sternberg specific markers

A
  • don’t express some B-cell specific genes including immunoglobulin and CD20
  • however, they do express PAX5
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17
Q

Communication between RS cells and inflammatory cells

A
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18
Q

Do Reed-Sternberg cells express kappa or lambda?

A

NO

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19
Q

Classic Hodgkin Lymphoma Immunohistochemistry

3 listed markers

A
  • CD30+ invariably positive in Classic Hodgkin Lymphoma
  • CD15+
  • The majority are CD20-
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20
Q

EBV in Classic Hodgkin Lymphoma

2 listed

A
  • In 30-50% of Classic Hodgkin Lymphoma EBV van be detected
  • In EBV+ cases, the virus is present only in neoplastic cells not in the inflammatory background
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21
Q

Classic Hodgkin Lymphoma most Common subtype

A

Nodular Sclerosis HL

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22
Q

Nodular Sclerosis Classic Hodgkin Lymphoma Epidemiology

A

young adults

\

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23
Q

Nodular Sclerosis Classic Hodgkin Lymphoma Clinical Presentation

3 listed

A

often cervical and mediastinal LNs

Painless mass

but can cause issues such as airway obstruction

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24
Q

Nodular Sclerosis Classic Hodgkin Lymphoma Prognosis

3 listed

A
  • Excellent prognosis
  • usually low stage free of systemic manifestations
  • typically EBV is negative
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25
Q

Hodgkin Lymphoma Staging

A
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26
Q

Hodgkin Lymphoma Stage 1

A

Involvement of single lymph node region or single extralymphatic site

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27
Q

Hodgkin Lymphoma Stage 2

A
  • Involvement of two or more lymph node regions on the same side of diaphragm
  • may include localized extralymphatic
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28
Q

Hodgkin Lymphoma Stage 3

A
  • Involvement of lymph node regions on both sides of the diaphragm
  • may include spleen or localized
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29
Q

Hodgkin Lymphoma Stage 4

A

Diffuse extralymphatic disease (e.g. liver, bone marrow, lung, skin)

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30
Q

Classic Hodgkin Lymphoma prognosis low stage

A

5 year survival ~90%

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31
Q

Classic Hodgkin Lymphoma High Stage

4 listed

A
  • typically older patients,
  • B-symptoms (fever, night sweats, weight loss)
  • more often EBV+
  • 5 year disease-free survival = 60-70%
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32
Q

Classic Hodgkin Lymphoma Treatment

A

Stakes are high - Classic Hodgkin Lymphoma is curable

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33
Q

Classic Hodgkin Lymphoma Treatment Intent

A

Intent is always curative

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34
Q

Classic Hodgkin Lymphoma Treatment Regiment

4 listed

A

ABVD

  • Doxorubicin (Adriamycin)
  • Bleomycin
  • Vinblastine
  • Dacarbazine
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35
Q

Doxorubicin AKA

A

Adriamycin

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36
Q

Doxorubicin toxicities

A

Cardiac Toxicity because it is an anthracycline

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37
Q

Bleomycin toxicities

A

Pulmonary Toxicity

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38
Q

Vinblastine Toxicities

A

Vinca alkaloid so can cause Neuropathy

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39
Q

Bleomycin Drug Class

A

antineoplastic

40
Q

Bleomycin toxicity for boards

A

can cause nasty pulmonary toxicity (fibrosis)

41
Q

Brentuximab

A

Anti-CD30 (investigational in front-line therapy)

42
Q

Classic Hodgkin Lymphoma Treatment Side Effects

A
  • Very BM suppressive
  • will be neutropenic, anemic, thrombocytopenic but tolerate it because it is curable so we can put up with more side effects because the goal is curative
43
Q

Bleomycin MOA

3 listed

A
  • Antineoplastic Antibiotic
  • binds directly to DNA
  • Intercalation interfers with topoisomerase II, transcription and replication
44
Q

Bleomycin BM Suppression

A

Bleomycin does not suppress bone marrow!

45
Q

Bleomycin active locations and toxicities

A
  • inactivated except in skin and lung tissue
  • can cause skin lesions, hyperpigmentation

BUT

  • Life-threatening pulmonary fibrosis!
46
Q

Bleomycin Overview

A
47
Q

Question 1

A

D

CD30+

CD20-

CD3-

CD5-

CD15+

48
Q

Question 2

A

B Cytokines

49
Q

Question 3

A

A Stage I single lymph node droop in the right neck

50
Q

Non-Hodgkin Lymphomas

Low Grade

4 listed

A
  • Indolent
  • Natural History
  • often not curable usually disseminated
  • Typically small cells with mature features
51
Q

Non-Hodgkin Lymphomas

Intermediate/High Grade

5 listed

A
  • aggressive
  • rapid progression
  • possible cure intent with therapy
  • localized
  • often large cells or less mature cytologic features
52
Q

Non-Hodgkin Lymphomas

WHO Classification & Overview

A
53
Q

Non-Hodgkin Lymphomas

Diffuse Large B-cell Lymphoma cells arise from?

A
  • can arise fromm germinal center or post-germinal center B cells
54
Q

Non-Hodgkin Lymphomas

Diffuse Large B-cell Lymphoma

A
  • Diffuse Proliferation of large malignant b-cells
  • large vesicular cells
55
Q

Non-Hodgkin Lymphomas

Diffuse Large B-cell Lymphoma

CD20 stain

A

diffusely positive

56
Q

Non-Hodgkin Lymphomas

Most common type

A

Diffuse Large B-cell Lymphoma

57
Q

Diffuse Large B-cell Lymphoma Epidemiology

A

All ages but the median age is 60 yo

Male>Female

58
Q

Diffuse Large B-cell Lymphoma Tumor Characteristics

A
  • Rapidly growing masses
  • Nodal or extranodal (can present inside lymph nodes or outside)
59
Q

Diffuse Large B-cell Lymphoma Curability

A

40-50% cure with chemotherapy

60
Q

DLBCLs Remarkable Heterogeneity: Morphology

A

morphologically - can be round, oval, cleaved, lobulated, multinucleated or even RS like

61
Q

DLBCLs Remarkable Heterogeneity: Markers

A
  • +/- CD5, CD10, BCL2, BCL6
  • Invariably CD20+
62
Q

DLBCLs Remarkable Heterogeneity: cytogenetic and molecular features

A
  • translocations
  • mutations
  • (# of oncogenes)
  • Gene overexpression
63
Q

Flow Cytometry of DLBCL

A
64
Q

Forward scatter is a test of?

A

Cell size

65
Q

Kappa:Lambda

A

the ratio should be 1:1 if it isn’t could be monoclonal

66
Q

IGH Gene Rearrangements

A
67
Q

Different Mutations in B cell lymphomas

A
68
Q

T-cell lymphoma Histological features

4 listed

A
  • tend to have a more paracortical pattern
  • disrupts follicles
  • lymphoma is seeping into perinodal fat which is not normal
  • follicular architecture is not seen
69
Q

T Cell lymphoma CD3 and CD20 Stains

A
  • CD3 is everywhere
  • CD20 you see that B cells are rather few
70
Q

T-Cell Lymphoma Flow Cytometry

A
  • can see normal and aberrant T cell populations
  • cells that retain CD3 and CD7 are normal
  • Cells that lose CD3 and CD7 and express aberrant CD56 are abnormal
  • CD5 is expressed on all T cells
71
Q

Treatment of Non-
Hodgkin Lymphomas

4 listed

A
  • Aggressive B cell lymphoma (DLBCL) and T cell lymphomas require multiagent chemotherapy
  • CHOP - Cyclophosphamide, vincristine, doxorubicin, prednisone
  • Rituximab (antiCD20) for CD20+ diseases (R-CHOP)
  • Indolent B cell lymphomas are treated for symptoms or end-organ dysfunction
72
Q

Treatment of Non-
Hodgkin Lymphoma

Survival Curve

CHOP vs R-CHOP

A
73
Q

Langerhans Cell Histiocytosis

A

not a lymphoma this is a histiocytosis that is clonal

vesicular nuclei (coffee bean nuclei)

nuclear grooves

74
Q

Histiocytes are

A

Macrophages and dendritic cells

75
Q

The vast majority of Histiocytic Proliferations are?

A

reactive benign

(granulomas or reactive histiocytosis)

76
Q

Histiocytic proliferation types

3 listed

A
77
Q

Langerhans cell histiocytosis is thought to arise from?

A

Immature dendritic cell

BRAF mutation present in 50%

78
Q

Histiocytic or dendritic cell sarcomas prevalence?

A

Very rare

79
Q

Mutation in Langerhans cell histiocytosis

A

BRAF in 50% of cases

80
Q

Langerhans Cell Histiocytosis Overview

A
81
Q

Langerhans Cell Histiocytosis Most Serious Subtypes

2 listed

A
  • Multifocal
  • Multisystemic LCH Letterer-Siwe disease
82
Q

Langerhans Cell Histiocytosis Less Severe Subtypes

A
  • Unifocal or multifocal unisystemic LCH
  • Eosinophilic granuloma
  • Hand-Christian-Schuller
83
Q

Multifocal multisystemic LCH Letterer-Siwe survival

A

50% in 5yrs

84
Q

Multifocal multisystemic LCH Letterer-Siwe Clinical Presentations

4 listed

A
  • Skin rash- trunk, back, scalp (seborrheic)
  • Hepatosplenomegaly, lymphadenopathy, lung lesions, finally lytic destructive bone lesions
  • BM involvement -> cytopenias -> infections
  • fatal if untreated
85
Q

Multifocal multisystemic LCH Letterer-Siwe Age of onset

A

<2yo

86
Q

Multifocal or unifocal Unisystemic LCH age of onset

A

Older children, adults

87
Q

Multifocal or unifocal Unisystemic LCH Clinical Presentation

A

Indolent

may heal spontaneously or with local excision or radiation

BM cavity (ribs, femur, calvarium)

Bony masses may extend to soft tissue

88
Q

Pulmonary LCH

A

Adult smokers, regression after smoking cessation

89
Q

LCH Diagnosis

A
90
Q

LCH Immunohistochemistry

A

Dual expression of S100+ and CD1a+ can be confident of LCH

91
Q

Birbeck Granules

A

LCH

92
Q

Question 4

A

Non-Hodgkin B-Cell lymphoma because IgH gene rearrangement

large B cell lymphoma

93
Q

Question 5

A

D because 1 and 3 have a mixture whereas 2 and 4 have a clonal process

94
Q

Question 6

A

D coffee bean nuclei also

95
Q

Lymph node pathology - summary

A
96
Q

Lymph node pathology Summary

A
97
Q

Classification of lymphoid malignancy

A

Hematology (26 decks)

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