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T&D 1 > WBC Pathology > Flashcards

WBC Pathology Flashcards

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?

A

HTLV-1

24
Q

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

A

HHV8

25
Q

Which cancers are associated with EBV?

A

Burkitt lymphoma
Hodgkin Lymphoma
Immunodeficiency associated B cell lymphomas
rare NK cell lymphomas

26
Q

What are some chronic inflammatory states that can lead to neoplasm?

A
  • H. pylori
  • Hashimoto’s thyroiditis
  • Celiac disease
27
Q

H. plyori –>

A

MALT lymphomas of stomach

28
Q

Hashimoto’s thyroiditis –>

A

MALT lymphoma of thyroid

29
Q

Celiac disease –>

A

Intestinal T cell lymphoma

30
Q

What are the three environmental factors?

A
  • Chronic inflammatory states
  • immune dysregulation
  • Toxins
31
Q

What is an example of immune dysregulation? What do you see?

A
  • HIV

sustained B cell stimulation without intact T cell dependent surveillance

32
Q

Reactive or neoplastic?

Lymphadenopathy vs Lymphadenitis

A

Reactive

  • adenopathy: LN enlargement - tender/non-tender
  • adenitis: LN inflammation - tender
33
Q

What causes LN to enlarge?

A
  • infections
  • AI disorders
  • Iatrogenic
  • Malignant
    Other
34
Q

What are example of infections that cause lymphadenopathy?

A
  • viral : EBV
  • Bacterial : Bartonella
  • Protozoal : Taxoplasmosis
  • Fungal : Histoplasma
35
Q

What are three pathologic findings for lymphadenopathy?

A
  • Follicular hyperplasia - due to stimuli for B cells
  • Paracortical hyperplasia - stimuli for T cells
  • Sinus histiocytosis - Nonspecific. macs within sinus, nodes draining cancer
36
Q

What do you see in follicular hyperplasia?

A
  • 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
Q

What are some etiologies for follicular hyperplasia?

A
  • Toxoplasmosis
  • bacterial infection
  • early HIV
  • non-specific
38
Q

What do you see in paracortical hyperplasia?

A

paracortical (T-cell area) expansion

- inc mature T cells, DC

39
Q

Etiology for Paracortical hyperplasia?

A
  • viral infections - mononucleosis
  • Drugs - Dilantin
  • Chronic skin irritation
40
Q

Distribution of lymphadenopathy to which nodes is suspicious for malignancy?

A
  • Supraclavicular

- retroperitoneal

41
Q

Reactive vs neoplastic Lymphadenopathy?

A

Reactive: tender, mobile
Neoplastic: non-tender, fixed

42
Q

Acute nonspecific Lymphadenitis

A
  • Tender, red, soft
  • Follicular hyperplasia w/ large GC and +/- neutrophils
  • drainage of infections
  • kids
43
Q

Chronic Nonspecific Lymphadenitis

A
  • Non-tender
  • Follicular hyperplasia w/ large GC and +/- neutrophils
  • chronic immunologic stimulation
44
Q

Lymphoma vs Leukemia

A

Lymphoma - tissue
Leukemia - BM/blood

same neoplastic cells, regardless of where they are in the body

45
Q

Lymphoma involves: 2/3, 1/3

A
  • nodes (2/3)

- tissue (1/3)

46
Q

Leukemia involves:

A

BM
liver
spleen

47
Q

Leukemia show symptoms related to what?

A

Signs of BM suppression - anemia, infections, bleeding

48
Q

Plasma cell neoplasms present as:

A

terminally differentiated B cells
in BM, rarely in LN
Bony destruction (lytic lesions)

49
Q

What are B symptoms?

A
  • fever, night sweats, weight loss
50
Q

Diagnosis of lymphoid neoplasms:

A

disruption of both architecture and function of immune system :

  • infections
  • autoimmunity
  • unexplained lymphadenopathy
51
Q

Where do neoplastic cells like to reside?

A

Where their normal counterparts reside

52
Q

Diagnosis of lymphoma requires what kind of tissue for histology/phenotyping etc?

A

Fresh tissue

53
Q

How do NHL and HL vary?

A
  • differ in treatment and prognosis

- distribution, type, and number of neoplastic cells

54
Q

How is NHL at diagnosis?

A
  • disseminated on a molecular level
55
Q

How is HL at diagnosis?

A

spreads in systemic fashion, staging important

56
Q

which cell type is easier to identify clonality with?

A

B cell > T cell

57
Q

Lymphomas are mostly ____ cell origin

A

B cell (85%)

T&D 1 (7 decks)

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