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Hematology > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

What is a neoplasm

A

New growth that is usually cancer or malignant

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2
Q

What are the 3 main groups of FAB classified Neoplasms

A
  1. Myeloproliferative disorders (MPD)
  2. Myelodysplastic syndromes (MDS)
  3. Acute Leukemia
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3
Q

What blast percentage makes the FAB classification acute?

A

30%

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4
Q

What are the 2 major components of bone marrow

A

Hematopoietic
vascular

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5
Q

Normal expected cellularity range equation

A

100-patient’s age +- 10%

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6
Q

In bone marrow examination what is the min cell differential

A

200
erythroid precursors and megakaryocytes are not included

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7
Q

What is the normal myeloid to erythroid ratio (M:E)

A

2-4:1

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8
Q

What are the types of Myeloproliferative disorders

A

Chronic Myelogenous leukemia (CML)
Polycythemia vera

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9
Q

General characteristics of MPD

A

Middle age (50-70)
gradual onset

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10
Q

What are MPD caused by

A

genetic defect in the HSC

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11
Q

Panhypercellularity is seen in?

A

MPD

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12
Q

What is CML

A

An unregulated proliferation of myeloid cells in the BM

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13
Q

What is CML caused by

A

Philadelphia Chromosome

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14
Q

What does myeloid refer to

A

granulocyte line of cells

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15
Q

What are the phases of CML

A

Chronic Phase
Accelerated phase
Blast crisis

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16
Q

What are the general characteristics of CML in the chronic phase

A

Middle age (50-70)
slow onset
symptoms gradually worsen
may suddenly become more aggressive

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17
Q

Symptoms of CML in the chronic phase

A

weakness
weight loss
hepatosplenomegaly
anemia due to myelophthisis
infection

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18
Q

CML in chronic phase BM lab findings

A

High WBC Count *low blast count
High PLT count
NC/NC anemia

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19
Q

What will distinguish AML from CML

A

High PLT count is only seen in CML

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20
Q

What is the M:E ratio seen in CML in the chronic phase

A

10-50:1

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21
Q

What is the blast % in CML in the chronic phase

A

<20%

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22
Q

What is happening in the BM in CML in the chronic phase

A

BM hyperplasia
Hypercellularity

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23
Q

What are the lab findings in CML Accelerated phase

A

WBC elevates further
PLT count begins to drop

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24
Q

Blast crisis in CML is analogous to what

A

Acute leukemia

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25
Q

What are the lab findings in CML Blast Crisis

A

LOW PLT count
Blast >20%
*in large clusters on smear
More severe left shift

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26
Q

Why does CML not become AML

A

CML is because of the Philadelphia Chromosome

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27
Q

What does the Philadelphia Chromosome lead to?

A

fusion of the BCR and ABL genes

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28
Q

What is the Philadelphia Chromosome translocation

A

t(9:22)

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29
Q

What is the result of the Philadelphia Chromosome in CML

A

Production of unregulated tyrosine kinase

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30
Q

What does unregulated Tyrosine Kinase do

A

Uncontrolled, fast cell division
Inhibits apoptosis
Impairs normal DNA repair

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31
Q

What are the treatment methods for CML

A

Leikapheresis
Tyrosine kinase inhibitors
Stem cell transplants

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32
Q

What is Polycythemia Vera

A

Unregulated proliferation of erythroid cells

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33
Q

What is frequently accompanied by pancytosis

A

PV

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34
Q

What is the EPO concentration in PV

A

Very low

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35
Q

What are the symptoms from the high blood viscosity in PV

A

Cardiovascular disease
Headaches
Thrombotic or hemorrhagic episodes
Hypertension

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36
Q

How many of PV patients develop acute leukemia

A

5-10%

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37
Q

What are the 3 types of PV

A
  1. Primary
  2. Secondary
  3. Relative
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38
Q

What causes Primary PV

A

Issues from HSC

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39
Q

What is Secondary PV associated with

A

Elevated EPO levels

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40
Q

What causes Secondary PV

A

Environment
-Altitude, COPD etc

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41
Q

What causes Relative PV

A

Decrease in plasma volume
-severe dehydration
-burns

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42
Q

What is the EPO concentration in Relative PV

A

Not affected

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43
Q

What are the types of Myelodysplastic Syndrome

A

Refractory Anemia
Chronic Myelomonocytic Leukemia
Therapy related MDS

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44
Q

What causes MDS

A

Genetic defect in the HSC

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45
Q

What has a higher predisposition to acute leukemia than MPD

A

MDS

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46
Q

What are the clinical findings in MDS

A

At least one type of peripheral cytopenia
Progressive decline in blood cell counts

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47
Q

What is considered Preleukemia

A

MDS
-20-40% transform

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48
Q

What is found in peripheral blood in MDS

A

Megaloblastic Anemia
Decreased retics
Basophilic stippling
Howell Jolly bodies
nRBC
Aniso
Poiko

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49
Q

Lab findings for MDS

A

Left shift
Nuclear abnormalities
Monocytosis
Variable PLT counts

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50
Q

Characteristics of Refractory Anemia

A

MEGALOBLASTIC anemia
Reticulocytopenia
Low blast count

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51
Q

How many Chronic MyeloMonocytic Leukemias turn to AML

A

30%

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52
Q

What is Therapy Related MDS

A

Secondary to chemotherapy or radiotherapy

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53
Q

What is the disease progression in Therapy Related MDS

A

Pancytopenia
More severe thrombocytopenia
Increasing presence of blasts
Development of AML

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54
Q

What is Acute Leukemia

A

A malignant proliferation of leukocytes originating in the bone marrow

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55
Q

What are the classic triad symptoms for acute leukemia

A

Anemia
Infection
Hemorrhage

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56
Q

What are the main lab findings for Acute Leukemia

A

Highly variable WBC count
Marked thrombocytopenia
Severe anemia
>20% blasts

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57
Q

How are cell lineages Identifications classified by

A

Cytochemical stains
Cytogenetics
Flow Cytometry

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58
Q

What does MPO stain

A

Peroxidase enzyme in primary granules in the myeloid line

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59
Q

What is MPO stain used for

A

Differentiate AML from ALL

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60
Q

What does Sudan Black B stain

A

the phospholipid membrane that encases the primary and secondary granules

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61
Q

What is SBB used for

A

To differentiate AML from ALL

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62
Q

What does Specific Esterase stain

A

specific esterase enzyme in primary granules of myeloid cells

63
Q

What is Specific Esterase used to stain

A

Myeloblasts

64
Q

What does Non-Specific Esterase stain

A

Non-specific esterase enzyme in monocyte precursors

65
Q

What is Combined Esterase used for

A

-Differentiate myeloblasts and monoblasts
- AML M4 vs AML M5

66
Q

What is Tartrate Resistant Acid Phosphatase (TRAP) used for?

A

To diagnose Hairy Cell Leukemia

67
Q

What is specific to cells of hairy cell leukemia

A

Isoenzyme 5

68
Q

What enzyme is present in all leukocytes

A

Acid Phosphatase

69
Q

What is TdT?

A

Terminal Deoxynucleotidyl Transferase
*a DNA polymerase

70
Q

What is TdT used for?

A

Diagnose of ALL

71
Q

What is AML M0

A

Minimally Differentiated

72
Q

Microscopic findings for AML M0

A

NO auer rods
Blasts are negative for MPO/SBB

73
Q

How are auer rods formed

A

Fusion of primary granules

74
Q

When are Auer Rods seen

A

in Neoplastic myeloblasts and promyelocytes

75
Q

If Auer Rods are seen what diagnosis is excluded

A

ALL

76
Q
A

Auer Rod

77
Q

What is AML M1

A

AML without maturation

78
Q

AML M1 has what microscopic findings

A

<10% of granulocytes mature beyond the myeloblast stage
Blasts are poorly differentiated

79
Q

What is AML M2

A

AML with Maturation

80
Q

What is the most common AML

A

AML M2
about 30%

81
Q

Common findings in AML M2

A

Myeloblasts are predominant
all stages of neutrophils
Auer Rods

82
Q

What is AML M3

A

Acute Promyelocytic Leukemia (APL)

83
Q

What is Faggot Cells

A

blasts that contain bundles of auer rods

84
Q

what is the translocation in AML M3

A

t(15;17)

85
Q

what does the AML M3 translocation do?

A

alters confirmation of retinoic acid receptors (RAR)

86
Q

What is the normal RAR function

A

RAR is a nuclear receptor for retinoic acid (Vit A)
When RA binds to the RAR DNA transcription occurs and cells are allowed to mature

87
Q

What stage do most cells not mature past in AML M3

A

Promyelocyte stage

88
Q

What is the initial presentation of APL most often

A

Abnormal bleeding and DIC

89
Q

What is the main complication from APL

A

Promyelocytes contain a large amount of tissue factor which starts the coagulation cascade

90
Q
A

AML M3

91
Q
A

AML M3

92
Q

What is AML M4

A

Acute myelomonocytic leukemia

93
Q

What is the 2nd most common AML

A

AML M4
25%

94
Q

Findings in AML M4

A

Myeloid cells
Blast nucleus may be irregular
about 20% monocytic cells
auer rods may be present

95
Q

What are the symptoms outside of the classic triad for AML M4

A

Gingival hypertrophy
Cutaneous lesions
Meningeal infiltration

96
Q
A

AML M4

97
Q

What are the two types of AML M5

A

M5a: acute monoblastic leukemia
M5b: acute monocytic leukemia

98
Q

Symptoms in addition to classic triad for AML M5

A

More extensive extramedullary involvement than AMML
Liver, spleen, skin, gums, CNS, eyes
More aggressive: >40% die

99
Q

What is AML M5a

A

Acute monoblastic leukemia (AMoL)
>80% monoblasts

100
Q

What is AML M5b

A

acute moncytic leukemia
<80% monoblasts
More promonocytes and monocytes

101
Q
A

AML M5a

102
Q
A

AML: M5b

103
Q

What are the 2 subtypes of AML M6

A

Pure Erythroid
Erythroid/myeloid

104
Q

What are characteristics of AML M6

A

Anisopoikilocytes
High # of nRBC
nRBC may be megaloblastic, bizarre, and multinucleated

105
Q

What is AML M6

A

Acute Erythroleukemia

106
Q

What is AML M7

A

Acute megakaryoblastic leukemia

107
Q

What happens in AML M7

A

proliferation of micromegakaryocytes and myeloblasts

108
Q

What AML has an increased disposition for individuals with Down Syndrome (Trisomy 21)

A

AML M7
Acute Megakaryoblastic leukemia

109
Q

What makes lymphoma different than leukemia

A

Lymphoma is hematologic cancer in lymphoid tissues while leukemia is in the BM

110
Q

What are the Acute Lymphoid Neoplams

A

B cell Malignancy
T & NK cell Malignancy

111
Q

What lymphoid neoplasms are more common

A

B cell malignancy

112
Q

What is seen in B cell Malignancy

A

May involve plasma cells
Secrete excessive Ab
Hyper viscosity syndrome
Rouleaux
May produce autoAb

113
Q

Which Acute Lymphoid Neoplasm is more aggresive

A

T & NK cell malignancy

114
Q

Where is T & NK cell malignancy involved

A

Extranodal and extramedullary sites
*skin
*CNS
*Mediastinum
*Kidneys

115
Q

What is ALL

A

Acute Lymphoblastic Leukemia
*Malignant lymphocytes

116
Q

What is the most common malignancy of childhood

A

ALL
80% of childhood leukemia

117
Q

Common complaints in ALL

A

Bone pain
Headache fatigue

118
Q

Lab findings in ALL

A

Thrombocytopenia
NC/NC anemia
excessive lymphoblasts

119
Q

What ALL subtype is the most common childhood leukemia

A

ALL L1

120
Q

What is ALL L1

A

Precursor B-cell Leukemia

121
Q

What is the most aggressive ALL

A

L2

122
Q

What ALL is more common in adults

A

ALL L2

123
Q

What mass can grow bc of ALL L2

A

Mediastinal mass from leukemic infiltration of the thymus

124
Q

What is ALL L2

A

Precursor T-cell leukemia

125
Q

What is ALL L3

A

Burkitt Leukemia

126
Q

What cell lineage is ALL L3

A

B cell lineage

127
Q

What are the chronic lymphoproliferative disorders

A

-B cell chronic lymphocytic leukemia
-Prolymphocytic leukemia
-Hairy cell leukemia
-Sezary’s syndrome

128
Q

What are the malignant lymphomas

A

Non-Hodgkin
Hodgkin

129
Q

What is the plasma cell disorder

A

Multiple myeloma

130
Q

What is Chronic Lymphocytic Leukemia

A

A B cell neoplasm
-accumulation of mature, nonfunctional memory B cells

131
Q

What is the most common leukemia in adults

A

CLL
Chronic lymphocytic leukemia

132
Q

What is Richter’s Transformation

A

When CLL progresses to aggressive prolymphocytic leukemia

133
Q

What is the % of CLL undergoing Richter’s Transformation

A

10%

134
Q

What are the symptoms of CLL

A

Swollen lymph nodes
infection
anemia
hepatosplenomegaly

135
Q

What is seen in CLL

A

smudge cells

136
Q

What is Prolymphocytic leukemia

A

Very aggressive B cell subtype

137
Q

What are lab findings in PLL

A

Extremely elevated WBC count
>55% prolymphocytes
Severe anemia and thrombocytopenia

138
Q

What is Hairy Cell Leukemia

A

A rare B-cell malignancy

139
Q

What is seen in Hairy Cell Leukemia

A

Very significant splenomegaly
Extensive BM infiltration

140
Q

What is Sezary’s Syndrome

A

A late stage variant of cutaneous T cell Lymphoma (CTCL)

141
Q
A

Sezary Cell
**look like a brain

142
Q

What is the subtype of Sezary’s Syndrome

A

Mycosis fungoides

143
Q

Characteristics of Non-Hodgkin Lymphoma

A

Originates in lymph tissue
Spreads to extranodal sites
Normal cell morphology
Older onset

144
Q

What are the B cell Non-Hodgkins lymphoma subtypes

A

Waldenstrom macroglobulinemia
Burkitt lymphoma

145
Q

What is Waldenstrom macroglobulinemia

A

A plasma cell lymphoma which produces excessive IgM Ab

146
Q

What syndrome is seen in Waldenstrom Macroglobulinemia

A

Hyper viscosity syndrome
*Protein buildup and poor circulation
*Visual impairments
*Headache
*Vertigo
*Deafness
*Rouleaux

147
Q

What are the 3 subtypes of Burkitt Lymphoma

A

Endemic
Sporadic
Adult cases

148
Q

What Burkitt Lymphoma is associated with EBV

A

Endemic

149
Q

Characteristics of Endemic Burkitt

A

African pediatric
infiltrates facial bones

150
Q

Characteristics of Sporadic Burkitt

A

North american Pediatrics
infiltrates abdominal organs

151
Q

When is Adult Cases Burkitt seen

A

HIV patients

152
Q

Characteristics of Hodgkin Lymphoma

A

Younger adults
localized malignancy - stays in lymph tissue

153
Q

What is produces in Multiple myeloma

A

Monoclonal protein production
*partial production of Ab

Hematology (4 decks)

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