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Hematology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Hematopoietic growth factors

A

Hormones that regulate the proliferation and differentiation of hematopoietic stem cells

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2
Q

Important growth factors

A

Stem cell factor and FLT3

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3
Q

Effect of deficiency of growth factors

A

Leads to aplastic anemia

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4
Q

Effect of overactivity of growth factors

A

Leads to leukemia

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5
Q

WBC Count

A

4-11 x 10^9/L

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6
Q

Leukocytosis

A

Increased WBC count above normal range

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7
Q

Leukopenia

A

Decreased WBC count below normal range

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8
Q

Neutrophils Differential Count %

A

50-70

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9
Q

Neutrophils Absolute Count

A

1500-6500

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10
Q

Lymphocyte Differential Count %

A

20-44

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11
Q

Lymphocyte Absolute Count

A

1200-3400

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12
Q

Monocyte Differential Count %

A

2-9

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13
Q

Monocyte Absolute Count

A

100-600

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14
Q

Bands Differential Count %

A

0-6

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15
Q

Bands Absolute Count

A

0-700

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16
Q

Eosinophils Differential Count %

A

0-5

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17
Q

Eosinophils Absolute Count

A

0-500

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18
Q

Basophils Differential Count %

A

0-2

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19
Q

Basophils Absolute Count

A

0-200

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20
Q

Relative cytosis or cytopenia

A

% is out of range (absolute count normal)

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21
Q

Absolute cytosis or cytopenia

A

absolute count is out of range (better reflection of health)

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22
Q

Automated WBC differential

A

instrument analyzes 10,000 cells and sorts them by size and granularity

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23
Q

Manual WBC differential

A

tech counts 100 cells on peripheral smear

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24
Q

Neutrophils

A

Phagocytic cell containing a nucleus with 2-5 lobes and pink cytoplasmic granules, Short-lived (6 days) and highly motile

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25
Q

Chemotaxis

A

Migration toward sites of infection or inflammation

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26
Q

Neutrophilia

A

increase in neutrophils

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27
Q

Leukomoid Reaction

A

an increase in white blood cell count, which can mimic leukemia

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28
Q

Left shift

A

increased numbers of less mature cells (precursors) released from the bone marrow to the peripheral blood

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29
Q

Leukocytosis is common with?

A

severe or chronic infection, severe hemolysis and metastatic cancers

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30
Q

Leukocytosis is associtated with?

A

toxic granulation (increased granulation
vacuolation (due to phagocytosed microbes)
dohle bodies (pale round to linear blue aggregates of rough endoplasmic reticulum)

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31
Q

Neutropenia

A

decrease in neutrophils

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32
Q

Selective Neutropenia Congenital Causes

A

Kostmann syndrome
Bening neutropenia
Cyclical neutropenia

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33
Q

Acquired Selective Neutropenia

A

Drug induced
Autoimmune (SLE)
Viral Infection
Some bacterial infections (Typhoid)

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34
Q

Pancytopenia

A

a decrease in all blood cells (RBCs, WBCs, and platelets)

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35
Q

Reactive Lymphocytes Features

A

increased cell size
increased cytoplasm
radial blueing
invagination around red cellS
seen most commonly with viral infections (especially EBV)

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36
Q

Lymphocytosis

A

increase in lymphocytes

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37
Q

Causes of Lymphocytosis

A

viral infection
some bacterial infection (Pertussis)
Other (Allergic drug interactions, splenectomy, metastatic carcinoma)
Chronic Lymphocytic Leukemia (CLL)
Other Lymphomas

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38
Q

Cause of Lymphocytopenia

A

bacterial or fungal sepsis
post-operative state
post steroid therapy
immunodeficiency
autoimmune disorders

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39
Q

Effect of Steroid Therapy on Lymphocytes

A

Lymphoma, because steroid melts the lymphocytes, hence it is part of all chemotherapy regiments in lymphoma

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40
Q

Monocytes

A

Large phagocytic cells with indented nucleus and fine cytoplasmic granules, Matures into different types of macrophages at different anatomical locations

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41
Q

Cause of Monocytosis

A

chronic infection
autoimmune disease
chronic neutropenia
acute leukemia
chronic myelomonocytic leukemia

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42
Q

Cause of Monocytopenia

A

Hairy cell leukemia

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43
Q

Major Functions of Eosinophils

A

anti-parasitic and bactericidal activity
immediate allergic reactions
modulating inflammatory responses

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44
Q

Causes of Eosinophilia

A

allergy and asthma
parasite infection
connective tissue disease
leukemia/lymphoma (eosinophilic leukemia, CML, AML M4)
idiopathic

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45
Q

Major Functions of Basophils

A

immediate allergic reaction
anticoagulant activity
vasodilation

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46
Q

Causes of Basophilia

A

leukemia (CML)
hypothyroidism
some viral infections
inflammatory conditions
drugs
hyperlipidemia

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47
Q

Leukoerythroblastic Picture

A

bone marrow response in which nucleated RBCs and immature WBCs are released into the peripheral blood

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48
Q

Cause of Leukoerythroblastic Picture

A

severe infection
severe hemolysis (thalassemia major)
primary myelofibrosis
metastatic tumors

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49
Q

Wright Stain

A

primary stain used on aspirate smears
combination of acid dye (eosin) and basic dye (methylene blue)

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50
Q

What does acid dye (eosin) stain?

A

erythrocytes and cytoplasmic granules

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51
Q

What does basic dye (methylene blue) stain?

A

nuclei and cytoplasmic granules

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52
Q

Prussian Blue Iron

A

second most common stain used on aspirate smear, aspirate clot
used to evaluate iron stores, sideroblasts and ringed sideroblasts

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53
Q

Iron Stores

A

macrophages store iron and return them to RBC

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54
Q

Sideroblasts

A

RBC incorporated iron into hemoglobin
usually 20-60% of RBCs

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55
Q

Ringed Sideroblasts

A

Iron accumulates in mitochondria of RBCs with disordered hemoglobin synthesis

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56
Q

Myeloperoxidase

A

stain performed on PB or aspirate smear
used in acute leukemias to confirm myeloid lineage

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57
Q

Sudan Black B

A

stain performed on PB or aspirate smear
used in acute leukemias to confirm myeloid lineage

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58
Q

Butyrate Esterase

A

stain performed on PB or aspirate smear
used in acute leukemia to distinguish neutrophilic and monocytic lineages

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59
Q

Chloroacetate Esterase

A

stain performed on PB or aspirate smear
used in acute leukemias to distinguish neutrophilic and monocytic lineages

60
Q

Periodic Acid Schiff (PAS)

A

stain performed on aspirate smear
used in the diagnosis and typing of acute leukemias

61
Q

the appearance of cells in PAS

A

normal: fine diffuse of granules
abnormal: coarse granules in acute myeloid leukemia M6

62
Q

the appearance of cells in sudan black b

A

brown/black precipitate in the cytoplasm, color intensity increases with the maturity of the cell

63
Q

the appearance of cells in butyrate esterase

A

brown pigment in monocytes

64
Q

the appearance of cells in chloroacetate esterase

A

blue pigment in neutrophils

65
Q

Terminal deoxynucleotidyl transferase (TdT)

A

various methods of detection (flow cytometry, immunofluorescent stain, immunohistochemical stain)
DNA polymerase enzyme adds nucleotides to 3’ terminus of DNA molecule
positive in ALL and some AML

66
Q

Acquired Abnormality of B12 or Folate Deficiency

A

Causes hypersegmented neutrophils (>6 lobes)

67
Q

Acquired Abnormality of Drug/toxin effect

A

dysplasia-like changes with hypogranular cytoplasm or hypolobated nuclei

68
Q

Pelger-Huet Anomaly

A

Congenital
hyposegmented neutrophils with bilobed “prince nez” or monolobated nuclei
normal cytoplasm
normal function
other white cells, red cells and platelets normal

69
Q

Pelger Huet anomaly vs Pseudo-Pelger-Huet anomaly

A

Pelger-Huet anomaly: inheritable (autosomal dominant) abnormality of nuclear segmentation, cells have a mature nucleus, and mature cytoplasm but it is a congenital condition. Also, there is no loss of cellular function.

Pseudo-Pelger Huet: Cells have a nucleus and are often hypo granular but it is an acquired condition. This is seen in underlying disorders, like myelodysplasia or myeloproliferative diseases.

70
Q

May-Hegglin Anomaly

A

decreased WBC count
all WBC have dohle bodies, blue-gray inclusions comprised of RNA, located anywhere in cytoplasm
normal function
RBC count normal
Platelet count mildly decreased (mostly large and giant platelets)

71
Q

Alder-Reilly Anomaly

A

normal WBC count
all WBC with large purple cytoplasmic inclusions
disorder polysaccharide metabolism and lysosomal accumulation of mucopolysaccharide
normal function
RBC and platelet count normal

72
Q

Features of Mucopolysaccharide disorders

A

abnormal face, skeletal dysplasia and mental retardation

73
Q

Chediak-Higashi Anomaly

A

decreased WBC count
all WBC have giant granules, representing fused lysosomes
function is abnormal
RBC and platelet count normal/decreased

74
Q

Gaucher’s Disease

A

enzyme deficiency of beta-glucocerebrosidase
accumulation of glucocerebroside
macrophage with abundant fibrillar cytoplasm (wrinkled tissue paper)

75
Q

Niemann-Pick Disease

A

enzyme deficiency of sphinogomyelinase
accumulation of sphigomyelin
macrophages with foamy cytoplasm and small uniform vacuoles

76
Q

Bone marrow cellularity of Myelodysplastic Syndromes (MDS)

A

hypercellular, would have dysplasia in one or more lineages

77
Q

peripheral cytopenias of MDS

A

pancytopenia (anemia, leukopenia, and thrombocytopenia )

78
Q

Erythropoietic changes in the bone marrow of MDS

A

megaloblastic nuclei, asymmetrical nuclear budding, and increased ring sideroblasts

79
Q

Platelet changes of MDS

A

giant or hypo-granular platelets in peripheral blood, also small megakaryocytes with non-lobated, hypolobated, or disjointed nuclei

80
Q

neutrophilic changes of MDS

A

hyposegemented nuclei or hypersegmented nuclei, or hypo-granular cytoplasm

81
Q

Auer rods

A

red, round, or rod-shaped cytoplasmic inclusions
usually present in immature granulocytes and are uncommon in immature monocytes or more mature cells.

82
Q

Indication of Auer rods

A

acute nonlymphocytic leukemia.

83
Q

Chronic Myeloid Leukemia (CML) Epidemiology

A

most common MPN
accounts for 15-20 of all leukemias
median age at diagnosis is 40-50%

84
Q

CML Clinical Presentation

A

asymptomatic in 20-40%
routine CBC: marked leukocytosis
common symptoms: fatigue, weight loss, night sweats
splenomegaly

85
Q

CML Main Differential Diagnosis

A

leukemoid reaction
other MPN or MDS/MPN

86
Q

CML vs Leukemoid Reaction

A

Differential in CML: Bands, Metamyelocytes, Myelocytes
Differential in Leukemoid: Mainly Bands

Morphology in CML: Normal
morphology in Leukemoid: Toxic

87
Q

General Feature of Myeloproliferative Neoplasm

A

Cytosis – increased number of cells​

Organomegaly (enlargement of organs, in particular, splenomegaly)​

Hypercellular bone marrow​

May progress to acute leukemia​

88
Q

Myeloproliferative Neoplasm (MPN)

A

group of diseases in which the bone marrow makes too many RBCs, WBCs, or platelet

89
Q

peripheral blood abnormalities of MPN

A

cytosis (erythrocytosis, granulocytosis, and thrombocytosis)

90
Q

bone marrow changes of MPN

A

panhypercellularity (abnormal excess of all cells in bone marrow)

91
Q

Leukocyte Alkaline Phosphatase (LAP)

A

stain performed only on PB
estimates the amount of alkaline phosphatase enzyme in each cell, used to diagnose chronic myeloid leukemia

92
Q

the appearance of cells in LAP

A

hydrolase enzyme that removes phosphate groups from molecyles
when you have chronic myeloid leukemia (CML), you have less alkaline phosphatase in your white blood cells than normal
intensity varies with concentration of enzyme un the cell

93
Q

Features of CML chronic phase

A

Leukocytosis
mainly neutrophils and myelocytes
blasts <10% and basophils <20%
stable course for years

94
Q

Peripheral Blood Features of CML Chronic Phase

A

WBC: leukocytosis due mainly to neutrophils​
myeloid cells in all stages of maturation
usually less than 2% blasts ​
absolute basophilia and eosinophilia​
RBC: mild anemia
Platelets: normal or increased

95
Q

Bone Marrow Features of CML Chronic Phase

A

hypercellular with myeloid hyperplasia
less than 10% blasts
micromegakaryocytes
pseudo-Gaucher cells and sea blue histocytes

96
Q

Characteristic of CML Accelerated Phase

A

10-19% blasts in blood or bone marrow​

> 20% basophils in blood​

Persistent thrombocytopenia <100,000 unrelated to therapy​

Persistent thrombocytosis >1,000,000 despite adequate therapy​

Increasing WBC count and spleen size​

Cytogenetic evidence of clonal evolution ​

97
Q

Characteristics of CML Blast Phase

A

> 20% blasts in blood or bone marrow​

Extramedullary proliferation of blasts​

Blast lineage may be myeloid (80%) or lymphoid (20%)​

Resembles acute leukemia​

98
Q

CML Prognosis

A

survival with treatment (5 years overall survival >90%)
first-line therapy: tyrosine kinase inhibitors like imatinib (Gleeven)
second-line therapy: stem cell transplantation

99
Q

CML Cytogenetics

A

required for diagnosis of CML
t(9;22) ​+ BCR-ABL translocation ​= Philadelphia chromosome
BCR-ABL hybrid gene has tyrosine kinase activity and enhanced phosphorylating activity resulting in altered cell growth and uncontrolled proliferation

100
Q

Polycythemia vera (PV) Epidemiology

A

median age at diagnosis is 60yrs
slight male predominance

101
Q

PV Clinical Presentation

A

Routine CBC: increased hemoglobin or red cell mass​
Increased blood viscosity (hypertension, headache, dizziness)​
Thrombosis (deep vein thrombosis, heart attack, stroke)​
Redness in face or palms​
Pruritis (itching)​
Splenomegaly (70%) and hepatomegaly (40%)​

102
Q

PV Main Differential Diagnosis

A

Secondary polycythemia​
Other MPN or MDS/MPN

103
Q

PV Polycthemic Stage Peripheral Blood Changes

A

WBC: normal or increased​
RBC: ​
Hgb >18.5 g/dl in men​
Hgb >16.5 g/dl in women​
Elevated RBC mass >25% above mean normal predicted value​
Normochromic normocytic red cells​
Low serum erythropoietin level ​
Platelets: normal or increased​

104
Q

PV Polycythemic Stage Bone Marrow Changes

A

Hypercellular with erythroid hyperplasia​
Small and giant megakaryocytes with deeply lobulated nuclei​
Absent iron stores​

105
Q

PV Spent Phase PB changes

A

anemia
leukoerythroblastic picture
anisopoikilocytosis with tear drops

106
Q

PV Spent Phase Bone Marrow Changes

A

ofter hypocellular
marked reticulin and collagen fibrosis

107
Q

PV Cytogenetics

A

no specific genetic defect
95% have JAK2 mutation
20% also have +8, +9, del(20q), del(13q) or del(9p)

108
Q

PV Prognosis

A

Without therapy, median survival is few months​
Most patients die from thrombosis or hemorrhage​
10% will develop MDS or AML​
With current therapy, median survival is 10-15 yrs​

First line therapy: Phlebotomy + aspirin​
Second line therapy: Phlebotomy + aspirin + myelosuppressive drug (hydroxyurea)​

109
Q

Essential Thrombocythemia (ET) Epidemiology

A

median age at diagnosis is 50-60yrs

110
Q

ET Clinical Presentation

A

Asymptomatic in 50%​

Routine CBC: Increased platelet count​

Thrombosis or hemorrhage​

Common symptoms: fatigue, weight loss​

Mild splenomegaly (50%) and hepatomegaly (20%)​

111
Q

ET Main Differential Diagnosis

A

Reactive thrombocytosis (iron deficiency, splenectomy, surgery, infection, autoimmune disease)​

Other MPN or MDS/MPN

112
Q

ET Peripheral Blood Changes

A

WBC: normal​

RBC: normal​

Platelet: ​

Platelet count >450,000/ul​

Anisocytosis (tiny and giant platelets)​

113
Q

ET Bone Marrow Changes

A

Hypercellular with megakaryocytic hyperplasia​

Many large to giant megakaryocytes with abundant mature cytoplasm and hyperlobulated nuclei​

Minimal reticulin fibrosis, no collagen fibrosis​

Iron stores present​

​

114
Q

ET Cytogenetics

A

No specific genetic defect

Chromosomes usually normal​

60% have JAK2 mutation

115
Q

ET Prognosis

A

Long survival with near normal life expectancy​

Less than 5% will develop MDS or AML​

Main therapy: Aspirin with or without hydroxyurea

116
Q

Primary Myelofibrosis (PMF) Epidemiology

A

median age at diagnosis is 50-60 yrs

117
Q

PMF Clinical Presentation

A

Asymptomatic in 30%​

Routine CBC: Increased WBC and platelet count​

Common symptoms: fatigue, weight loss, night sweats​

Massive splenomegaly​

118
Q

PMF Main Differential Diagnosis

A

other MPN or MDS/MPN

119
Q

PMF Prefibrotic Stage PB changes

A

WBC: mild to mod leukocytosis​

RBC: mild to mod anemia​

Platelets: mild to mod thrombocytosis

120
Q

PMF Prefibrotic Stage BM changes

A

Hypercellular with myeloid and megakaryocytic hyperplasia​

Mostly large megakaryocytes with balloon-shaped nuclei, abnormal chromatin clumping, and decreased amounts of cytoplasm​

Minimal fibrosis​

121
Q

PMF Fibrotic Stage PB Changes

A

WBC: usually decreased, left-shifted​

RBC: mod to marked anemia, marked anisopoikilocytosis with tear drops, nucleated RBC​

Platelets: usually decreased, anisocytosis, circulating megakaryocytic nuclei​

122
Q

PMF Fibrotic Stage BM Changes

A

Often hypocellular ​

Patches of hematopoietic cells separated by loose connective tissue or fat​

Prominent clusters of abnormal megakaryocytes​

Markedly increased reticulin and collagen fibrosis​

Osteosclerosis (new bone formation)​

123
Q

PMF Cytogenetics

A

no specific genetic defect, common chromosomal abnormalities (del(13q), del(20q), der(6)t(1;6), 50% have JAK2 mutation

124
Q

PMF Prognosis

A

median survival time is 3-7yrs from fibrotic stage, 10-20% develop AML

125
Q

JAK2 Mutation

A

Non receptor protein tyrosine kinase involved in signal transduction pathway
Point mutation lead to loss of auto-inhibitory control
Mutated JAK2 is in a constitutively active state

126
Q

JAK2 Mutation Progression

A

Mutation -> activation of transcriptional factors ->
increased proliferation and decreased apoptosis ->

127
Q

JAK2 Mutation Results

A

PV (95%)
ET (60%)
PMF (50%)

128
Q

Myelodysplasia

A

Dysplasia = abnormal morphology​

May be present in one or more myeloid lineages​

Seen in various conditions​

129
Q

WBC Dysplasia

A

most evident in peripheral blood neutrophils
hypo-segmented nuclei
hyper-segmented nuclei
hypogranular cytoplasm

130
Q

RBC Dysplasia

A

need to assess erythroid precursors in bone marrow
megaloblastic nuclei
asymmetrical nuclear budding

131
Q

Myelodysplastic Syndrome (MDS)

A

clonal hematopoietic stem cell disorders with abnormal maturation and ineffective hematopoiesis (cells produced in marrow but never enter circulation)

132
Q

Clinical Presentation of MDS

A

mean age at diagnosis 70yrs
peripheral cytopenia, most commonly macrocytic anemia
fatigue
no gematosplenomegaly

133
Q

MDS PB Changes

A

Pancytopenia

134
Q

MDS Bone Marrow Changes

A

hypercellular
dysplasia in one or more lineages

135
Q

MDS Cytogenetics

A

common chromosomal abnormalities: 5-, +7, +8

136
Q

MDS Prognosis

A

progression to AML ranges from 5% in MDS-SLD to 33% with MDS-EB-2
treatments includes supportive (blood products, transfusions) and chemotherapy

137
Q

Chronic Myelomonocytic Leukemia (CMML) Epidemiology

A

median age at diagnosis is 65-75 yrs old

138
Q

Clinical Presentation of CMML

A

fatigue, weight loss, night sweats
splenomegaly
history of frequent infections
bleeding

139
Q

CMML-1

A

<5% blasts in PB and <10% in BM

140
Q

CMML-2

A

5-19% blasts in PB or 10-19% blasts in BM or 20% blasts plus Auer rods

141
Q

CMML Cytogenetics

A

no specific genetic defect
common chromosomal abnormalities: +7, +8, abnormal 12p

142
Q

CMML PB Changes

A

WBC: usually increased​

Neutrophilia​

Monocytosis (>10% WBCs, abs mono count >1 x 10^9/L)​

RBC: mild anemia, normocytic or macrocytic​

Platelets: mild to mod decreased​

143
Q

CMML BM Changes

A

Usually hypercellular ​

Proliferation of granulocytes and monocytes​

Dysplastic maturation seen in all lineages​

144
Q

Myelodysplastic Syndrome vs Acute Leukemia

A

The diagnosis of MDS includes a maximum number of blasts at 19% whereas for the diagnosis of AML the minimum criterion is at least 20% blasts. The distinction between the two is based on the blast percentage. Also, there is a possibility of MDS progressing to AML, ranging from 5% in MDS-SLD to 33% with MDS-EB-2. Acute leukemia: proliferation is in precursors with reduced capacity to differentiate into mature cells. MDS is a type of chronic leukemia where proliferation is mainly in mature cells.

145
Q

Refractory Anemias

A

refers to red blood cells showing dysplasia in the bone marrow. A person with this type of MDS will also have low numbers of RBCs but a normal number of WBCs and platelets. Also, there is a normal number of blasts in the bone marrow, and <15% of ringed sideroblasts

Hematology (3 decks)

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