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T&D 1 > WBC Pathology > Flashcards

WBC Pathology Flashcards

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1
Q

2 methods for phenotyping

A

flow cytometry

immunohistochemistry

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2
Q

Phenotype:

immature

A

CD34

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3
Q

Phenotype:

myeloid

A

CD13
CD33
MPO

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4
Q

Phenotype:

B cell

A

CD19
CD20
kappa AND lambda light chains

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5
Q

Phenotype:

T cell

A

CD3
CD4
CD8
CD5

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6
Q

Phenotyping - other

A 
CD45 (leukocytes)
CD10 (B lyphoblasts, mature B cells, myeloid)
TdT (lymphoblasts)
CD15 (NHL)
CD30 (NHL)
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7
Q

How do cells become neoplastic? (6)

A
  • Translocation/mutation
  • inherited genetic factors
  • viruses
  • environmental factors
  • iatrogenic factors
  • smoking
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8
Q

translocation: follicular lymphoma

A

t(14;18)

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9
Q

translocation: Burkitt lymphoma

A

t(8;14)

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10
Q

translocation: Mantle cell lymphoma

A

t(11;14)

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11
Q

translocation: Acute promyelocytic leukemia (M3)

A

t(15;17)

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12
Q

translocation: Chronic myeloid leukemia

A

t(9;22)

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13
Q

How do chromosomal abnormalities occur in lymphoid neoplasms?

A

Mistakes made during Ag receptor gene rearrangement result in oncogenic rearrangements

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14
Q

In lymphoid neoplasm, how do Precursor cells become abnormal?

A

V(D)J recombinase cuts DNA at specific sites in Ig and TCR loci for Ag specificity (normal), but there is inappropriate joining of these sites next to proto-oncogenes

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15
Q

In lymphoid neoplasm, how do Mature cells become abnormal?

A

B cells go through Ig class switching / somatic hypermutation - occurs in germinal centers

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16
Q

why are B cell lymphomas more prevalent than T cell lymphomas?

A

Germinal cell B cells are more unstable due to the necessary class switching and somatic hypermutations for Ig production

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17
Q

How do chromosomal abnormalities occur in myeloid neoplasms?

A
  • translocations/inversions
  • monosomies
  • trisomies
  • deletions
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18
Q

______ chromosomal translocation creates ______ gene that interrupts normal __________. (Myeloid neoplasm)

examples

A

Structural, fusion, hematopoiesis

t(15;17)(q22;q12)
t(8;21)(q22;q22)
t(9;22)(q34;q11.2)

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19
Q

What happens when there is an acquired mutation in genes that regulate normal hematopoiesis? what are these regulatory genes? (myeloid neoplasm)

A

Imparts a survival advantage to cells

  • FLT3
  • NMPM1
  • JAK2
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20
Q

What genetic disease promotes genomic instability and increases risk for acute leukemia?

A

Fanconi anemia

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21
Q

Fanconi anemia is a genetic disease that increases the risk for what? how?

A

inc risk for Acute leukemia by promoting genomic instability

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22
Q

What two genetic diseases increase risk for childhood leukemias?

A 
Down syndrome (tri 21)
Neurofibromatosis I
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23
Q

What virus can cause Adult T cell leukemia/lymphoma?

24
Q

What virus can cause Pleural Effusion Lymphoma/Kaposi’s sarcoma?

25
Which cancers are associated with EBV?
Burkitt lymphoma Hodgkin Lymphoma Immunodeficiency associated B cell lymphomas rare NK cell lymphomas
26
What are some chronic inflammatory states that can lead to neoplasm?
- H. pylori - Hashimoto's thyroiditis - Celiac disease
27
H. plyori -->
MALT lymphomas of stomach
28
Hashimoto's thyroiditis -->
MALT lymphoma of thyroid
29
Celiac disease -->
Intestinal T cell lymphoma
30
What are the three environmental factors?
- Chronic inflammatory states - immune dysregulation - Toxins
31
What is an example of immune dysregulation? What do you see?
- HIV sustained B cell stimulation without intact T cell dependent surveillance
32
Reactive or neoplastic? | Lymphadenopathy vs Lymphadenitis
Reactive - adenopathy: LN enlargement - tender/non-tender - adenitis: LN inflammation - tender
33
What causes LN to enlarge?
- infections - AI disorders - Iatrogenic - Malignant Other
34
What are example of infections that cause lymphadenopathy?
- viral : EBV - Bacterial : Bartonella - Protozoal : Taxoplasmosis - Fungal : Histoplasma
35
What are three pathologic findings for lymphadenopathy?
- Follicular hyperplasia - due to stimuli for B cells - Paracortical hyperplasia - stimuli for T cells - Sinus histiocytosis - Nonspecific. macs within sinus, nodes draining cancer
36
What do you see in follicular hyperplasia?
- dark/light zones (normal Germinal centers) - Mantle zone with polarization (collar of resting small naiive B cells and some memory B cells) - normal bcl2 pattern (mantle stains) - tingable body macs - follicular DC
37
What are some etiologies for follicular hyperplasia?
- Toxoplasmosis - bacterial infection - early HIV - non-specific
38
What do you see in paracortical hyperplasia?
paracortical (T-cell area) expansion | - inc mature T cells, DC
39
Etiology for Paracortical hyperplasia?
- viral infections - mononucleosis - Drugs - Dilantin - Chronic skin irritation
40
Distribution of lymphadenopathy to which nodes is suspicious for malignancy?
- Supraclavicular | - retroperitoneal
41
Reactive vs neoplastic Lymphadenopathy?
Reactive: tender, mobile Neoplastic: non-tender, fixed
42
Acute nonspecific Lymphadenitis
- Tender, red, soft - Follicular hyperplasia w/ large GC and +/- neutrophils - drainage of infections - kids
43
Chronic Nonspecific Lymphadenitis
- Non-tender - Follicular hyperplasia w/ large GC and +/- neutrophils - chronic immunologic stimulation
44
Lymphoma vs Leukemia
Lymphoma - tissue Leukemia - BM/blood same neoplastic cells, regardless of where they are in the body
45
Lymphoma involves: 2/3, 1/3
- nodes (2/3) | - tissue (1/3)
46
Leukemia involves:
BM liver spleen
47
Leukemia show symptoms related to what?
Signs of BM suppression - anemia, infections, bleeding
48
Plasma cell neoplasms present as:
terminally differentiated B cells in BM, rarely in LN Bony destruction (lytic lesions)
49
What are B symptoms?
- fever, night sweats, weight loss
50
Diagnosis of lymphoid neoplasms:
disruption of both architecture and function of immune system : - infections - autoimmunity - unexplained lymphadenopathy
51
Where do neoplastic cells like to reside?
Where their normal counterparts reside
52
Diagnosis of lymphoma requires what kind of tissue for histology/phenotyping etc?
Fresh tissue
53
How do NHL and HL vary?
- differ in treatment and prognosis | - distribution, type, and number of neoplastic cells
54
How is NHL at diagnosis?
- disseminated on a molecular level
55
How is HL at diagnosis?
spreads in systemic fashion, staging important
56
which cell type is easier to identify clonality with?
B cell > T cell
57
Lymphomas are mostly ____ cell origin
B cell (85%)

T&D 1 (7 decks)

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