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Hematology > Hematology Week 3: Lymphoma I > Flashcards

Hematology Week 3: Lymphoma I Flashcards

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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
Hodgkin Lymphoma Staging
26
Hodgkin Lymphoma Stage 1
Involvement of single lymph node region or single extralymphatic site
27
Hodgkin Lymphoma Stage 2
* Involvement of two or more lymph node regions on the same side of diaphragm * may include localized extralymphatic
28
Hodgkin Lymphoma Stage 3
* Involvement of lymph node regions on both sides of the diaphragm * may include spleen or localized
29
Hodgkin Lymphoma Stage 4
Diffuse extralymphatic disease (e.g. liver, bone marrow, lung, skin)
30
Classic Hodgkin Lymphoma prognosis low stage
5 year survival ~90%
31
Classic Hodgkin Lymphoma High Stage 4 listed
* typically older patients, * B-symptoms (fever, night sweats, weight loss) * more often EBV+ * 5 year disease-free survival = 60-70%
32
Classic Hodgkin Lymphoma Treatment
Stakes are high - Classic Hodgkin Lymphoma is curable
33
Classic Hodgkin Lymphoma Treatment Intent
Intent is always curative
34
Classic Hodgkin Lymphoma Treatment Regiment 4 listed
**ABVD** * Doxorubicin (Adriamycin) * Bleomycin * Vinblastine * Dacarbazine
35
Doxorubicin AKA
Adriamycin
36
Doxorubicin toxicities
Cardiac Toxicity because it is an anthracycline
37
Bleomycin toxicities
Pulmonary Toxicity
38
Vinblastine Toxicities
Vinca alkaloid so can cause Neuropathy
39
Bleomycin Drug Class
antineoplastic
40
Bleomycin toxicity for boards
can cause nasty pulmonary toxicity (fibrosis)
41
Brentuximab
Anti-CD30 (investigational in front-line therapy)
42
Classic Hodgkin Lymphoma Treatment Side Effects
* 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
Bleomycin MOA 3 listed
* Antineoplastic Antibiotic * binds directly to DNA * Intercalation interfers with topoisomerase II, transcription and replication
44
Bleomycin BM Suppression
Bleomycin does not suppress bone marrow!
45
Bleomycin active locations and toxicities
* inactivated except in skin and lung tissue * can cause skin lesions, hyperpigmentation BUT * Life-threatening pulmonary fibrosis!
46
Bleomycin Overview
47
Question 1
D CD30+ CD20- CD3- CD5- CD15+
48
Question 2
B Cytokines
49
Question 3
A Stage I single lymph node droop in the right neck
50
Non-Hodgkin Lymphomas Low Grade 4 listed
* Indolent * Natural History * often not curable usually disseminated * Typically small cells with mature features
51
Non-Hodgkin Lymphomas Intermediate/High Grade 5 listed
* aggressive * rapid progression * possible cure intent with therapy * localized * often large cells or less mature cytologic features
52
Non-Hodgkin Lymphomas WHO Classification & Overview
53
Non-Hodgkin Lymphomas Diffuse Large B-cell Lymphoma cells arise from?
* can arise fromm germinal center or post-germinal center B cells
54
Non-Hodgkin Lymphomas Diffuse Large B-cell Lymphoma
* Diffuse Proliferation of large malignant b-cells * large vesicular cells
55
Non-Hodgkin Lymphomas Diffuse Large B-cell Lymphoma CD20 stain
diffusely positive
56
Non-Hodgkin Lymphomas Most common type
Diffuse Large B-cell Lymphoma
57
Diffuse Large B-cell Lymphoma Epidemiology
All ages but the median age is 60 yo Male\>Female
58
Diffuse Large B-cell Lymphoma Tumor Characteristics
* Rapidly growing masses * Nodal or extranodal (can present inside lymph nodes or outside)
59
Diffuse Large B-cell Lymphoma Curability
40-50% cure with chemotherapy
60
DLBCLs Remarkable Heterogeneity: Morphology
morphologically - can be round, oval, cleaved, lobulated, multinucleated or even RS like
61
DLBCLs Remarkable Heterogeneity: Markers
* +/- CD5, CD10, BCL2, BCL6 * Invariably CD20+
62
DLBCLs Remarkable Heterogeneity: cytogenetic and molecular features
* translocations * mutations * (# of oncogenes) * Gene overexpression
63
Flow Cytometry of DLBCL
64
Forward scatter is a test of?
Cell size
65
Kappa:Lambda
the ratio should be 1:1 if it isn't could be monoclonal
66
IGH Gene Rearrangements
67
Different Mutations in B cell lymphomas
68
T-cell lymphoma Histological features 4 listed
* 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
T Cell lymphoma CD3 and CD20 Stains
* CD3 is everywhere * CD20 you see that B cells are rather few
70
T-Cell Lymphoma Flow Cytometry
* 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
Treatment of Non- Hodgkin Lymphomas 4 listed
* **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
Treatment of Non- Hodgkin Lymphoma Survival Curve CHOP vs R-CHOP
73
Langerhans Cell Histiocytosis
not a lymphoma this is a histiocytosis that is clonal vesicular nuclei (coffee bean nuclei) nuclear grooves
74
Histiocytes are
Macrophages and dendritic cells
75
The vast majority of Histiocytic Proliferations are?
reactive benign | (granulomas or reactive histiocytosis)
76
Histiocytic proliferation types 3 listed
77
Langerhans cell histiocytosis is thought to arise from?
Immature dendritic cell BRAF mutation present in 50%
78
Histiocytic or dendritic cell sarcomas prevalence?
Very rare
79
Mutation in Langerhans cell histiocytosis
BRAF in 50% of cases
80
Langerhans Cell Histiocytosis Overview
81
Langerhans Cell Histiocytosis Most Serious Subtypes 2 listed
* Multifocal * Multisystemic LCH Letterer-Siwe disease
82
Langerhans Cell Histiocytosis Less Severe Subtypes
* Unifocal or multifocal unisystemic LCH * Eosinophilic granuloma * Hand-Christian-Schuller
83
Multifocal multisystemic LCH Letterer-Siwe survival
50% in 5yrs
84
Multifocal multisystemic LCH Letterer-Siwe Clinical Presentations 4 listed
* Skin rash- trunk, back, scalp (seborrheic) * Hepatosplenomegaly, lymphadenopathy, lung lesions, finally lytic destructive bone lesions * BM involvement -\> cytopenias -\> infections * fatal if untreated
85
Multifocal multisystemic LCH Letterer-Siwe Age of onset
\<2yo
86
Multifocal or unifocal Unisystemic LCH age of onset
Older children, adults
87
Multifocal or unifocal Unisystemic LCH Clinical Presentation
Indolent may heal spontaneously or with local excision or radiation BM cavity (ribs, femur, calvarium) Bony masses may extend to soft tissue
88
Pulmonary LCH
Adult smokers, regression after smoking cessation
89
LCH Diagnosis
90
LCH Immunohistochemistry
Dual expression of S100+ and CD1a+ can be confident of LCH
91
Birbeck Granules
LCH
92
Question 4
Non-Hodgkin B-Cell lymphoma because IgH gene rearrangement large B cell lymphoma
93
Question 5
D because 1 and 3 have a mixture whereas 2 and 4 have a clonal process
94
Question 6
D coffee bean nuclei also
95
Lymph node pathology - summary
96
Lymph node pathology Summary
97
Classification of lymphoid malignancy

Hematology (26 decks)

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