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Hematalogy Lecture > Unit 2: Introduction to Leukemias > Flashcards

Unit 2: Introduction to Leukemias Flashcards

1
Q

-progressive, malignant disease of hematopoietic system
-Characterized by unregulated proliferation of (usually) 1 cell
line

A

Leukemia

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2
Q

Abnormal cells originate in bone marrow & then spread into peripheral blood

Leukemias are grouped by ___________ and by the maturity of affected cells (acute or chronic)

A

cell lineage

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3
Q

What is usually the cause of leukemias?
type of treatment?

A

-Cause of malignancy is usually unknown (a few exceptions)
-Not localized, but are systemic in nature. Most treatment options are systemic

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4
Q

Acute leukemia is characterized by preponderance of _____________ cells.

A

immature

-You see a gap in N.
maturation process in bone marrow The N. “pyramid” of
cell development instead has many blasts, some mature
forms, & a few intermediate stages = leukemic hiatus

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5
Q

 Sudden onset
 Short, aggressive disease pattern
 Lots of infections & hemorrhaging

A

Acute Leukemia

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6
Q

Acute leukemia:

 FAB defines by ____% blasts in bone marrow
 WHO defines by ___% blasts in bone marrow

A

> 30, >20

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7
Q

 All stages of maturation seen, with predominantly mature cells.
 Insidious onset

Insidious= slow

A

Chronic Leukemia

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8
Q

Lengthier, less aggressive disease pattern (lots of organ infiltration & massive leukocytosis).

A

Chronic Leukemia

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9
Q

Chronic Leukemia:

FAB defines by ___% blasts in bone marrow
 WHO defines by ____% blasts in bone marrow

A

< 30, <20

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10
Q

Chronic leukemia sometimes turns into acute! Called “__________”.

A

blast crisis

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11
Q

Onset of acute and chronic leukemia?

A

acute- abrupt
chronic- insidious

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12
Q

Death of acute and chronic leukemia?

A

acute- months
chronic- years

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13
Q

Patient’s age of acute and chronic leukemia?

A

acute- all ages
chronic- adults

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14
Q

WBC count with acute and chronic leukemia?

A

acute- variable (can be very low!)
chronic-high

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15
Q

Cell maturity with acute and chronic leukemia?

A

acute- immature
chronic- mature

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16
Q

Plt. count with acute and chronic leukemia?

A

acute- variable (can be very low!)
chronic- N. to increased

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17
Q

Organomegaly with acute and chronic leukemia?

Organomegaly- abnormal enlargement of organs

A

acute- mild
chronic- severe

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18
Q

system established in 1976 to provide uniform criteria for classifying acute leukemias before treatment changed their cellular morphology.

A

FAB (French-American-British) system

-FAB also wanted to aid in correlating treatment response to outcome, & to eventual prognosis.

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19
Q

FAB system is based on…

A

cell lineage and cytochemical response
 Goal was to distinguish lymphoid from myeloid leukemias.
-Worked ok for differentiating the basic acute vs. chronic and lymphocytic vs. myeloid

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20
Q

Massive information explosion, along with advent of advanced techniques, caused World Health Organization (WHO) to develop_________
system in 2001 – updated in 2008 and 2016.

A

modified FAB

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21
Q

Modified FAB system:

WHO emphasized correlation of cytogenetic & immunochemistry studies with specific leukemia
subtypes AND with _______________, in order to fine-tune treatment modalities.

FAB had difficulty with

A

clinical outcomes

FYI: FAB has difficulty classifying plt. disorders, lympho-proliferative disorders, & variant monoblastic presentations.

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22
Q

What are the four methodologies used for identifying and classifying leukemias?

A

-Morphologic review of bone marrow and Morphologic review of peripheral blood smears
-Cytochemical stains (Ex., NSE, LAP, etc.)
-Immunophenotyping
-Cytogenetic & molecular analyses

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23
Q

Methodology for identifying leukemias:

Historically most used, but really inadequate except
for differentiating acute vs. chronic! Cannot really be used by itself!

A

Morphologic review of bone marrow

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24
Q

Methodology for identifying leukemias:

What we use in lab, but of limited diagnostic utility.
Cannot ever be used by itself – send out for path review.

A

Morphologic review of peripheral blood smears

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25
Q

Methodology for identifying leukemias:

 Historically very useful.
 Identifies specific molecules in malignant cells (Ex., lipids, enzymes) that are associated with specific cell
lines.

A

Cytochemical stains (Ex., NSE, LAP, etc.)

-giving way to immunophenotyping & cytogenetic analyses . .

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26
Q

Methodology for identifying leukemias:

  • Via fluorescent Abs
  • Used for specific cell lineage &/or specific maturation stage markers.
    -Done by flow cytometry (very good for acute leukemias) using 5-color immunofluorescence.
    (Markers may be surface, cytoplasmic, or nuclear.)
A

Immunophenotyping

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27
Q

Methodology for identifying leukemias:

A
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28
Q

Immunophenotyping example:

_________ expression of ABO antigens is common in leukemias.

A

decreased

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29
Q

Immunophenotyping:

What are some flow cytometry marker examples?

Tdt

A

 Surface marker Ags/receptors – CD, HLA, etc. Certain cell
surface Ags associated with specific tumor phenotypes.
 Cytoplasmic
 Nuclear
a. Enzymes - Terminal deoxynucleotidyl Transferase (TdT) =
unique enzyme present only in early lymphoid cells. Thus ↑ levels seen in lymphoblastic leukemias (ALL), but not
typically seen in AMLs (?)
b. Aneuploidy – if tumor is aneuploid, ↑ aneuploidy = ↑risk of relapse

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30
Q

Acute myelocytic / myelogenous / myeloid /
myeloblastic / nonlymphocytic????

A

AML

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31
Q

Methodology for identifying leukemias:

the “Supreme Court of
Diagnosis”, using…
-karyotyping
-FISH
-PCR

A

Cytogenetic & molecular analyses

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32
Q

“Molecular remission” =

A

PCR negative

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33
Q

Cytogenetic & molecular analyses:

microscopic whole chromosome analysis.

A

Karyotyping

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34
Q

Cytogenetic & molecular analyses:

can use any sample type. FYI: Excellent for micro-deletion syndromes (caused by mismatch during crossing over.) (Ex., some ą-thalassemias, DiGeorge Syndrome)

A

FISH (Fluorescence In Situ Hybridization)

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35
Q

Cytogenetic & molecular analyses:

yields quantitative results; old favorite technique.
Normal gene rearrangement = NO (malignancy);
Positive translocation = YES (malignancy)

A

PCR

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36
Q

What are the 4 major types of leukemia?

A
  1. ALL - Acute Lymphoblastic
  2. CLL - Chronic Lymphocytic Leukemia
  3. AML - Acute Myeloblastic
  4. CML - Chronic Myelocytic / Myelogenous / Myeloid
    Leukemia
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37
Q

Myeloid (AML) and Lymphoid (ALL) acute or chronic?

A

acute

38
Q

What are the subtypes that fall under acute Lymphoid (ALL)?

A

-T lymphocytic
-B lymphocytic
-Null cell (?)

39
Q

What are the subtypes that fall under acute Myeloid (AML)?

A

-Myelocytic/ Myelogenous
-Promyelocytic
-Monocytic
-Myelomonocytic
(AMML)

40
Q

What are the subtypes that fall under chronic myeloid?

A

-Myelocytic/Myelogenous (CML)
-Myelomonocytic (CMML)

41
Q

What are the subtypes that fall under chronic lymphoid?

A

-Lymphocytic (CLL)
-Plasmocytic
-Hairy Cell (HCL)
-Prolymphocytic (PLL)

42
Q

For most leukemias the cause of malignancy is unknown, but with what exceptions?

A

-genetics
-Leukemogens
-Viral infections
-Radiation

43
Q

chemicals causing bone marrow depression &
aplasia predispose to leukemia later on (Ex., benzene, chloramphenicol, sulfa drugs, insecticides, antineoplastics)

A

Leukemogens

44
Q

How can viruses cause cancers?

EBV linked to

A

some retroviruses transform N. cells by
inserting their own oncogenes into host cell’s genome, causing
them to become malignant.
[EBV linked to Burkitt non-Hodgkin
lymphoma]

45
Q

Proto-oncogenes are normal genes which become altered by mutation to become ___________

A

oncogenes

46
Q

genes that cause cancer mutations.

A

Oncogenes
-Mutated version of a proto-oncogene

47
Q

Example of oncogene?

A

CML t(9;22) and Burkitt Lymphoma t(8;14)
-CML: ABL proto-oncogene on chromosome 9 is activated when fused with the BCR component of chromosome 22
-Burkitt Lymphoma:
MYC proto-oncogene on chromosome 8 is activated when fused with Ig on chromosome 14

48
Q

a chromosome number that is abnormal.

A

Aneuploid

49
Q

code for proteins which resist malignancy.

A

tumor suppressor genes

50
Q

What does laboratory evaluation include?

A

-Preliminary Workup of peripheral blood: CBC with plts. and diff.
-Second Stage Workup: bone marrow aspirate & biopsy analysis

51
Q

Laboratory evaluation:

RBCs…

A

 CBC with plts. and diff.
 RBCs – have normo-, normo- anemia (usually).
Typically this is myelophthisic anemia (?)

52
Q

Laboratory evaluation:

Plt. & WBC counts…

A

variable: mkd. ↓ in acute,
↑ in acute or chronic, to mkd. ↑ in chronic.

53
Q

Laboratory evaluation:

On differential?

A

usually see blasts & immature forms… if acute, numerous mature forms if chronic.

54
Q

Laboratory evaluation, Second Stage Workup: bone marrow aspirate & biopsy analysis:

  • Minimum ___ % blasts in bone marrow required
    for acute diagnosis in FAB system
  • Minimum ___ % blasts in bone marrow required
    for acute diagnosis in WHO system
A

30

20

55
Q

Second Stage Workup: bone marrow aspirate &
biopsy analysis:

Cytochemistry – using _____________

A

special stains

56
Q

Why do leukemia patients have hyperproliferative bone marrow?

A

due to replacement of hematopoietic tissue by
leukemic cells

57
Q

Second Stage Workup: bone marrow aspirate &
biopsy analysis:

Immunophenotyping – using ______________

A

Abs & fluorescent stains

58
Q

Second Stage Workup: bone marrow aspirate & biopsy analysis:

 Cytogenetic studies – using what techniques?

A

PCR & FISH

59
Q

cytogenetic studies are also used to detect…

A

Minimal Residual Disease (MRD) – the lowest level of disease detectable in pts. who are in continuous clinical remission

60
Q

Treatment:

the best therapy must start with…

A

an accurate diagnosis

61
Q

What are the two main goals of leukemia treatment?

A
  1. Eradicate leukemic cell mass.
  2. Provide supportive care for symptoms.
62
Q

What are factors playing roles in prognosis and treatment modalities are the pt.’s…

A

 Pretreatment health status
 Age
 Concurrent infection(s)
 Abnormal cytogenetics

63
Q

Treatment:

categories of therapy?

A
  1. chemotherapy
  2. radiation therapy
  3. supportive therapy
  4. targeted therapy
  5. stem cell transplantation
64
Q

Chemotherapy
 Typically given IV in conjunction with antibiotics;
for diffuse __________.

A

malignancies

65
Q

How are chemotherapy drugs classified?

A

by their effects on the cell
cycle and by their biochemical mechanism of
action.

 Some affect specific phases of the cell cycle
 Some affect any phase of the cell cycle

66
Q

FYI: Three stages of therapeutic strategy?

A

 Induction – of complete remission (N. bone
marrow cellularity = < 5% blasts!)
 Consolidation - low dose chemo. to prevent recurrence.
 Maintenance - of remission.

67
Q
  • Produces unstable ions that damage cancer cells’ DNA.
  • Used for localized malignancies.
A

Radiotherapy (“radiation”)

68
Q

Supportive Therapy:

 Used to support cancer patients
 Allow for more efficient and effective delivery of
chemotherapy regimens by preventing delays or dose
reductions due to low blood counts.

Examples?

A

colony stimulating factors & EPO

69
Q

Monoclonal antibodies which bind directly to affected cell, activates compliment, and cell lysis.

This is an example of what kind of treatment?

A

Targeted Therapy

70
Q

What will give best results for Bone marrow or Stem Cell Transplantation
(BMT, SCT)?

There’s been great strands in isolating

A

Pt. should be in good clinical condition & in 1st clinical
remission for best results.

(note: The effort to isolate stem cells from non-embryonic sources is making tremendous strides)

71
Q

Bone marrow or Stem Cell Transplantation (BMT, SCT):

classic approach typically requires…

A

intensive chemotherapy, then total body irradiation.

72
Q

What are the 3 types of bone marrow donors?

A

 Syngeneic
 Allogeneic
 Autologous

73
Q

Bone marrow/stem cell donor type:

identical twin donor
 Most rare and the most desired

A

Syngeneic

74
Q

Bone marrow/stem cell donor type:

donor genetically different from recipient
 Most serious transplant complication is GVHD (?
____________________), in which donor’s bone marrow T-cells destroy bone marrow & tissues of recipient.

A

Allogeneic

75
Q

Bone marrow/stem cell donor type:

patient’s own marrow or peripheral blood stem cells

A

Autologous

 Marrow is harvested, conditioned, and transplanted back in the
patient
 Requires the presence of normal stem cells and reduction of malignant cells

76
Q

Common Clinical Symptoms of All Leukemias?

A

-Myelophthisic anemia (due to bone marrow overcrowding)
-anemia: malaise, fatigue, pallor (dyspnea if severe)
-thrombocytopenia: Petechiae (pinpoint bruising),
Epistaxis (nosebleed),
Hemorrhage

77
Q

What is the 2nd main cause of death in leukemias?

A

Hemorrhage

78
Q

Common Clinical Symptoms of All Leukemias:

Due to extreme anemia:
____________________________, causing hepatosplenomegaly.

A

extramedullary hematopoiesis

NOTE: Hepatosplenomegaly may actually exacerbate anemia by inadvertently trapping RBCs (sequestration.)

79
Q

Common Clinical Symptoms of All Leukemias:

Due to neutropenia, increased incidence overwhelming
____________; this is primary cause of death in leukemia!

A

infections

80
Q

 Transient, reactive leukocytosis due to infection
 Temporary resemblance of peripheral blood
picture to “leukemic picture”
 Severe left shift & very rare nRBCs. (WBCT > 50,000/uL!)

A

Leukemoid reaction

81
Q

Leukoerythroblastic reaction aka…

A

Leukoerythroblastic anemia, or Leukoerythroblastosis)

82
Q

Leukoerythroblastic reaction:

Presence of both ________ & _____ shift in peripheral blood.

A

nRBCs, left

83
Q

Leukoerythroblastic reaction may be mild or severe, and occurs in _____ and in _________.

A

CML, lymphomas

84
Q

Caused by bone marrow damage from a malignant, “space-occupying
lesion”, with consequent extensive extramedullary hematopoiesis.

A

Leukoerythroblastic reaction

85
Q

Historically, how can you tell Leukemoid rxn. vs.
Leukoerythroblastic rxn?

A

a Leukocyte Alkaline Phosphatase (LAP) stain score

86
Q

What is Leukocyte Alkaline Phosphatase (LAP)?

A

An enzyme found in the secondary granules of neutrophils

87
Q

LAP stain score principle?

A

The substrate naphthol AS-B1 phosphate is hydrolyzed
by the enzyme at an alkaline pH, and dyed to produce a
colored precipitate

88
Q

LAP stain score:

TWO slides are obtained per patient, and activity is
graded from 0 to 4+ (performed by ____ techs, and must agree within __%)

A

2, 10

89
Q

Early leukemia:

Is LAP increased or decreased? Why?

A

-decreased
-(Ex., early CML) because leukemic neutrophils are too abnormal to express the LAP that N., mature bands & segs would. Also, you see real
leukoerythroblastosis
(Lots of nRBCs!!)

90
Q

Leukemoid reaction:

Is LAP increased or decreased? Why?

A

-increased
-due to left shift, because there are tons of bands & segs full of secondary granules containing LAP, just waiting to attack the infectious invaders – it only looks like a leukemia because of the high WBC count. Also, you see only very rare nRBCs!!

91
Q

Normal LAP score range?

A

15-170

92
Q

With the acceptance of the WHO classification, LAP score is no longer used. Instead, the presence of the
_________ gene, or _______ identifies CML.

A

BCR/ABL1, t(9;22),

Hematalogy Lecture (35 decks)

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