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Pathology > WBC pathology > Flashcards

WBC pathology Flashcards

1
Q

● Disorders of white blood cells can be classified

into two broad categories:

A

● Proliferative disorders (↑ WBC Count)

● Leukopenia

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2
Q

○ Deficiency of leukocytes

A

Leukopenia

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3
Q

Ref val

white cells

A

4.8-10.8

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4
Q

Ref val

Granulocytes

A

40-70

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5
Q

Neutrophils

A

1.4-6.5

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6
Q

Lymphocytes

A

1.2-3.4

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7
Q

Monocytes

A

0.1-0.6

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8
Q

Eosinophils

A

0-0.5

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9
Q

○ Refers to an increase in the number of

white cells in the blood

A

Leukocytosis

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10
Q

● Peripheral blood leukocyte count is influenced by

several factors:

A

● 1.Size of myeloid and lymphoid precursor and
storage cell pools in the bone marrow, thymus,
circulation, peripheral tissues.
● 2.Rate of release of cells from the storage pools
into the circulation
● 3.Proportion of cells that are adherent to blood
vessel walls at any time (marginal pool)
● 4.Rate of extravasation of cells from blood to
tissues.

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11
Q

■ B-cell, T-cell and NK-cell origin
■ Lymphocyte class or stage of
maturation

A

Lymphoid neoplasms

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12
Q

■ Arise from early hematopoietic progenitors

A 
Myeloid neoplasms (Segmented or 
Granular lymphocytes)
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13
Q

immature progenitor cells

accumulate in the BM

A

Acute myeloid leukemias (AML)

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14
Q

associated with infective

hematopoiesis and resultant peripheral blood cytopenias

A

Myelodysplastic syndromes (MDS) -

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15
Q

increase production of one or more
differentiated myeloid elements
usually leads to elevated peripheral
blood counts

A

■ Myeloproliferative neoplasms -

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16
Q

➢ Chronic myeloid leukemia

(CML) falls under

A

Myeloproliferative neoplasms -

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17
Q 
■ Macrophages and dendritic cells
■ A special type of immature dendritic 
cell, the Langerhans cell, gives rise 
to a spectrum of neoplastic disorders 
referred to as the Langerhans cell 
histiocytoses.
A

○ Histiocytes

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18
Q

When there is mutation of the tyrosine kinase or

MYC translocation, then there is

A

a gain of function.

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19
Q

INHERITED GENETIC FACTORS

A

Bloom syndrome, Fanconi anemia, and ataxia telangiectasia (acute leukemia or lymphoma)

Down syndrome (trisomy 21) and type 1 
neurofibromatosis
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20
Q

○ Associated with nasopharyngeal
carcinoma
○ Burkitt lymphoma, Hodgkin lymphoma
(HL), B cell lymphomas

A

EBV

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21
Q

Kaposi sarcoma
herpesvirus)
○ Malignant effusion

A

Human herpesvirus-8

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22
Q

IATROGENIC FACTORS

A

Chemotherapy - Myeloid and lymphoid

neoplasms

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23
Q

SMOKING

● AML increased

A

1.3 to 2 fold in smokers

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24
Q

○ Neoplasms that present widespread
involvement of the bone marrow and the
peripheral blood

A

Leukemia

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25
Q

LYMPHOID NEOPLASMS

A

Leukemia
Lymphoma
Plasma cell neoplasms
NHLs and Hodgkin lymphomas

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26
Q

Proliferations of white cells, typically
lymphocytes, that usually present as
discrete tissue masses

A

Lymphoma

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27
Q

Two types of Lymphoma:

A

○ Hodgkin lymphoma

○ Non-Hodgkin lymphomas (NHL)

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28
Q

○ Most often arise in the bone marrow and
only infrequently involve lymph nodes or
the peripheral blood

A

● Plasma cell neoplasms

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29
Q

○ Enlarged nontender lymph nodes (often
>2cm)
○ Extranodal sites (skin, stomach or brain)

A

NHLs and Hodgkin lymphomas

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30
Q

Suppression of normal

hematopoiesis by tumor cells in the bone marrow

A

Lymphocytic leukemias

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31
Q

Neoplasm of Reed-Sternberg cells and variants

A

Hodgkin’s Lymphoma

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32
Q

Most lymphoid neoplasms resemble some

recognizable stage of

A

B- or T-cell
differentiation
○ 85-90% of lymphoid neoplasms are of B-cell origin

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33
Q 
T or F
Individuals with inherited or acquired 
immunodeficiency are at high risk of 
developing certain lymphoid neoplasms, 
particularly those caused by oncogenic 
viruses
A

T

34
Q

PRECURSOR T AND B CELL NEOPLASMS

A

ACUTE LYMPHOBLASTIC LEUKEMIA/LYMPHOMA

35
Q

● Neoplasms composed of immature B (pre-B) or T
(pre-T) cells joined together because they show
similar tumor called lymphoblasts
● Manifest as childhood acute leukemias

A

ACUTE LYMPHOBLASTIC LEUKEMIA/LYMPHOMA

36
Q

o About 85%
o childhood acute leukemia
o uncommonly presents as a mass in the skin
or a bone

A

● B-ALL

37
Q

o Less common
o Present in adolescent males as thymic
lymphomas (thymic mass)

A

T-ALL

38
Q

is the most common cancer of children

A

ACUTE LYMPHOBLASTIC LEUKEMIA/LYMPHOMA

39
Q

o B-ALL peaks at

A

age 3

40
Q

T-ALL peak in

A

adolescent

41
Q

▪ Number of normal bone marrow preB cells (cell of origin) is greatest very
early in life

A

3

42
Q

T-ALLs - mutations in

A

NOTCH1 (essential for T-cell development)

43
Q

B-ALLs - mutations in

A

PAX5, TCF3, ETV6, and
RUNX1 (genes required for proper differentiation of
early hematopoietic precursors)

44
Q

Most common numerical or structural chromosomal changes

A

hyperploidy (>50

chromosomes)

45
Q

T or F

Hyperploidy has a better prognosis than hypodiploidy
seen only in B-ALL

A

T

46
Q

Definitive diagnosis relies ________performed

with antibodies specific for B- and T-cell antigens

A

on stains

47
Q

Lymphoblasts are myeloperoxidase- (negative or positive)

A

negative

48
Q

T or f

Lymphoblasts are myeloperoxidase-negative and
contain Periodic Acid-Schiff-positive cytoplasmic
material

A

T

49
Q

Immunostaining for terminal deoxynucleotidyl
transferase (TdT), a specialized DNA polymerase that is expressed only in pre-B and pre-T lymphoblasts is
positive in >95% of cases

A

IMMUNOPHENOTYPE

50
Q

express the pan B-cell marker CD19

and the transcription factor PAX5 as well as CD10

A

Lymphoblasts

51
Q

In very immature B-ALLs, CD10 is

A

negative

52
Q

More mature “late pre-B” ALLs express

A

CD10, 19, 20,

and cytoplasmic IgM heavy chain (μ chain)

53
Q

● Characteristics of ALL are the ff:

A
  1. Abrupt stormy onset with days to few weeks of
    the first symptoms
  2. Symptoms related to depression of marrow
    function (o Fatigue due to anemia; Fever)
  3. Mass effects caused by neoplastic infiltration
    (more common in ALL) including: Bone pain, lymphadenopathy,
    splenomegaly, and hepatomegaly; testicular enlargement, Compression syndrome)
  4. Central nervous system manifestations
54
Q
  • patient
    is very red, rhetoric and
    congested
A

Compression syndrome

55
Q

Factors associated with worse prognosis:

A
  1. Age younger than 2 years
    ● strong association of infantile ALL with
    translocations involving the MLL gene
  2. Presentation in adolescence or adulthood
  3. Peripheral blood blast counts >100,000
    ● reflects a high tumor burden
56
Q

Favorable prognostic markers include:

A 
● age 2-10 years
● low WBC count
● hyperploidy
● trisomy of chromosomes 4, 7 & 10
● presence of a t(12;21)
o translocation of 12;21
57
Q

PERIPHERAL B-CELL NEOPLASMS

A

CHRONIC LYMPHOCYTIC LEUKEMIA/SMALL
LYMPHOCYTIC LYMPHOMA

FOLLICULAR LYMPHOMA

DIFFUSE LARGE B-CELL LYMPHOMA (DLBCL)

58
Q 
Chronic lymphocytic leukemia (CLL) and small 
lymphocytic lymphoma (SLL) differ only in the
A

degree of peripheral blood lymphocytosis

59
Q

Most affected patients have sufficient lymphocytosis

to fulfill the diagnostic requirement for CLL

A

absolute lymphocyte count >5000/mm3

60
Q

s the most common leukemia of adults in

the Western world

A

CLL

61
Q

The median age at diagnosis is __years, and there is a 2:1 male predominance

A

60

62
Q

T or F

CLL/SLL is much less common in Japan and other Asian countries than in the West

A

T

63
Q

In CLL/SLL, Most common genetic anomalies are deletions of

A

13q14.3, 11q, and 17p and trisomy 12q

64
Q

Molecular characterization of the region deleted on

chromosome 13 has implicated

A

2 microRNAs, miR-15a and miR-16-1, tumor suppressor genes

65
Q

Loss of these mIRs is believed to result in

A

overexpression of the anti-apoptotic protein BCL2, which is uniformly observed in CLL/SLL

66
Q

CLL/SLL morphology

Lymph nodes are diffusely effaced (being replaced) by

A

predominantly small lymphocytes 6 to 12 μm in
diameter with round to slightly irregular nuclei,
condensed chromatin, and scant cytoplasm

67
Q

are pathognomonic for CLL/SLL

A

Proliferation centers

Admixed are variable numbers of larger activated lymphocytes that often gather in loose aggregates referred to as proliferation centers that contain mitotically active cells

68
Q

a larger cell with a centrally placed nucleolus,

A

prolymphocyte

69
Q

CLL/SLL

A characteristic finding is the presence of

A

disrupted tumor cells (smudge cells)

70
Q

Tumor cells express the pan B-cell markers

A

CD19 and CD20, as well as CD23 and CD5

71
Q

eukopenia can be seen in individuals with

A

SLL

72
Q

is common and
contributes to an increased susceptibility to
infection, particularly those caused by bacteria
10% to 15% of patients develop hemolytic anemia
or thrombocytopenia due to autoantibodies made
by nonneoplastic B cells

A

Hypogammaglobulinemia

73
Q

CLL/SLL

Other variables that correlate with a worse
outcome include:

A

○ The presence of deletions of 11q and 17p
(the latter involving TP53)
○ A lack of somatic hypermutation
○ The expression of ZAP-70, a protein that augments signals produced by the Ig
receptor
○ The presence of NOTCH1 mutations

74
Q

Transformation to diffuse large B-cell

lymphoma (DLBCL) so-called

A

Richter
syndrome (approximately 5% to 10% of
patients)

75
Q

often heralded by the
development of a rapidly enlarging mass
within a lymph node or the spleen

A

Richter

syndrome

76
Q

● Most common form of indolent NHL
● It affects 15,000 to 20,000 individuals per year
● Presents in middle age and afflicts males and females
equally
● Less common in Europe and rare in Asian
populations

A

FOLLICULAR LYMPHOMA

77
Q

is strongly associated with

chromosomal translocations involving BCL2.

A

FOLLICULAR LYMPHOMA

78
Q

● Hallmark is a (14;18)
● Translocation that juxtaposes the IGH locus on
chromosome 14 and the BCL2 locus on chromosome
18.

A

FOLLICULAR LYMPHOMA

79
Q

Antagonizes apoptosis and promotes the

survival of follicular lymphoma cells

A

BCL2

80
Q

is characteristically devoid of apoptotic cells

A

Follicular lymphoma

81
Q

encodes a histone methyltransferase,
suggesting that epigenetic abnormalities such as
changes in the patterns of histone marks have an
important role in this neoplasm.

A

KMT2D

Pathology (31 decks)

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