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Pathology > Hematology - WBC > Flashcards

Hematology - WBC Flashcards

1
Q

WBC development steps

A

Myeloblast - Promyelocyte - Myelocyte - Metamyelocyte - Band cells - Mature WBC

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2
Q

Stain used to see visualise all WBC cells

A

Wright stain

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3
Q

Most abundant WBC cells

A

Neutrophils (50-70%)

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4
Q

Nuclear lobes in neutrophils

A

2-5 nuclear lobes

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5
Q

Neutrophils levels are increased in

A

Bacterial infection
Acute inflammation
Sterile inflammation
Burns

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6
Q

Normal lymphocytes percentage

A

20-40%

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7
Q

Nucleus in Lymphocytes

A

Round nucleus

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8
Q

Lymphocytes levels are increased in

A

Viral infections (CMV,EBV)
Chronic Inflammatory conditions
Borditella pertusis infection

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9
Q

Biggest WBC in human body

A

Monocytes

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10
Q

Which WBC levels usually increases with Lymphocytes

A

Monocytes

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11
Q

Monocytes levels increases in

A

Chronic inflammation
Autoimmune disorders
IBD
TB, Malaria
Ricketssiae

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12
Q

Nuclear lobes in Eosinophil

A

2 nuclear lobes

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13
Q

Eosinophil levels increases in

A

Parasitic/worm infections
Allergy
Hodgkin’s lymphoma
Athero-embolism - Eosinophils in urine

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14
Q

Least WBC found in Blood

A

Basophils (1-2%)

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15
Q

Basophils levels increases in

A

Allergic conditions
Chronic myelogenous leukemia

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16
Q

Nucleus shape of Band neutrophils

A

Horse shoe shaped nucleus

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17
Q

Band neutrophils seen in peripheral blood due to

A

When there is increased stimulation of BM

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18
Q

Shift to left means

A

Increased leukocytes count in blood

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19
Q

Normal WBC levels

A

4,000-11,000 WBCs per microliter

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20
Q

Condition when WBC levels are more than 40-50k WBCs per microliter

A

Leukemoid reaction

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21
Q

Leukemoid reaction means

A

Increased no. Of matured Wbc cells

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22
Q

LAP score in Leukemoid reaction

A

Increases

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23
Q

Leukemoid reaction is usually seen in

A

Pneumonia
Infectious endocarditis
Septicimea

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24
Q

Leukemia means

A

Increased involvement of Bone marrow and surrounding blood vessels

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25
Q

Lymphoma means

A

Infiltration of Cancer cells in different organs of body via lymph nodes

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26
Q

In leukemia

A

Cancer cells in BM - Can suppress normal cells leads to
Decreased RBC - Anemia
Decreased WBC - Fever
Decreased platelets - Increased risk of bleeding

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27
Q

In leukemia

A

Cancer cells in BM - Can suppress normal cells leads to
Decreased RBC - Anemia
Decreased WBC - Fever
Decreased platelets - Increased risk of bleeding

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28
Q

WHO Classification of lymphoid neoplasms

A

1) Precursor B cell neoplasm
2) Peripheral B cell neoplasm
3) Precursor T cell neoplasm
4) Peripheral T cell neoplasm
5) Hodgkin’s lymphoma

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29
Q

WHO Classification of Myeloid Neoplasm

A

1) Acute myeloid leukemia
2) Myelodysplastic Syndrome
3) Myeloproliferative neoplasms

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30
Q

WHO classification of Macrophages

A

Langerhans cell histiocytosis

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31
Q

Cancers arising from precursors cells are usually

A

Multiply very rapid
Very rapid onset of symptoms

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32
Q

Cancers arising from Peripheral cells are usually

A

Slow growing
Chronic leukemia
Symptoms onset can take months to years

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33
Q

Risk factors Of Acute leukemia

A

Ionising radiation
Chemicals
Genetic factors
Infectious organisms

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34
Q

Chemicals having risk of Acute leukemia

A

Smoking
Benzene
Drugs - Anticancer drugs (Alkylating agents, Topoisomerase inhibitors)

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35
Q

Genetic factors responsible for acute leukemia

A

Down Syndrome (Trisomy 21) - ALL (MC), AML
Klinefelter’s syndrome
Neurofibromatosis
Fanconi’s anemia
Ataxia telangectasia

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36
Q

Infectious organisms responsible for acute leukemia

A

EBV (Epstien barr virus)
HTLV-1
HHV-8

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37
Q

Due to blocking of differentiation in acute leukemia

A

There is increased no. Of immature cells

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38
Q

Clinical symptoms of acute leukemia

A

Acute/sudden onset of action
Weakness, fever
Lymph nodes enlargement
Bleeding
Abdominal fullness

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39
Q

Blood exam in acute leukemia shows

A

TLC increased

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40
Q

Percentage of immature Wbc cells in normal person on BM Aspiration

A

5%

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41
Q

In case of Acute leukemia percentage of immature Wbc cells is

A

More than 20% of lymphoblasts or myeloblasts

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42
Q

If Lymphoblast >20%

A

Acute lymphoblastic leukemia(ALL)

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43
Q

Stain used to identify Lymphoblasts

A

TdT(Terminal deoxynucleotide transferase)
PAS (Periodic acid-Schiff)

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44
Q

If Myeloblast >20%

A

Acute myeloid leukemia (AML)

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45
Q

Stain used to identify Myeloblast cells

A

Myeloperoxidase
Non specific esterase

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46
Q

Flow cytometry is used to

A

See absence or presence of CD Molecules

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47
Q

Precursor cell of Acute Myelogenous leukemia (AML)

A

Myeloblast

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48
Q

Precursor cell of Acute Myelogenous leukemia (AML)

A

Myeloblast

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49
Q

Moat commonly affected population in AML

A

Elderly population (60yrs)

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50
Q

Affected myeloid cells in AML

A

Erythroblast
Megakaryoblast
Myeloblast

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51
Q

Clinical signs of AML

A

Sudden onset
Fatigue
Fever
Anorexia
Weight loss

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52
Q

AML-FAB Classification

A

M0 to M7

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53
Q

M0

A

Minimally differentiated AML

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54
Q

M1

A

AML without maturation

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55
Q

M2

A

AML With maturation

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56
Q

M3

A

Acute Promyelocytic Leukemia

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57
Q

M4

A

Acute Myelomonocytic leukemia

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58
Q

M5

A

Acute monocytic leukemia

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59
Q

M6

A

Acute erythroleukemia

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60
Q

M7

A

Acute Megakaryocytic leukemia

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61
Q

M1 to M4 AML are identified by

A

Myeloperoxidase

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62
Q

M5 AML identified by

A

Non specific esterase

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63
Q

M6 AML are identified by

A

PAS +ve

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64
Q

M7 AML is identified by

A

CD41
CD61

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65
Q

Myeloblast are stained by

A

Myeloperoxidase
Non specific esterase
PAS +ve

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66
Q

Special markers used to identify Myeloblast

A

CD41 and CD61

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67
Q

Most common AML

A

M2 - AML with maturation

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68
Q

Translocation seen in AML with maturation

A

t(8;21)

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69
Q

AML with maturation also known as

A

Granulocytic sarcoma
Myeloblastoma

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70
Q

In AMl With maturation cell deposits in

A

Retroorbital tissues - Pushes eyeball forward - Development of Proptosis

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71
Q

Markers used for AML with Maturation

A

CD45, Lysosome+ve
CD43

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72
Q

Translocation seen in Acute Promyelocytic Leukemia (M3)

A

t(15;17)

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73
Q

In M3, Due to t(15;17) there is fusion of

A

PML protein + Retinoic acid receptor fusion - can lead to vitamin A defeciency

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74
Q

In M3 AML, there is high risk of development of

A

DIC - because tumor cells release mucin - leads to extensive damage of endothelial cells

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75
Q

Aeur rods are seen in

A

Acute Promyelocytic Leukemia (M3)

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76
Q

20-30 Aeur rods together termed as

A

Faggot cell (Bundle of stick appearance)

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77
Q

Translocation seen in Acute myelomonocytic leukemia (M4)

A

t(16;16)

78
Q

Gum hypertrophy and leukemia cutis are seen in

A

Acute Myelomonocytic leukemia (M4) and Acute monocytic leukemia(M5)

79
Q

AML most commonly associated with Down Syndrome

A

Acute Megakaryocytic leukemia (M7)

80
Q

WHO classification of AML

A

AML with specific genetic defetcs
AML with Myelodysplasia related changes
AML (Therapy related)
AML not otherwise specified
Myeloid sarcoma
Myeloid profileration related to Down Syndrome

81
Q

AML with Specific genetic defetcs includes

A

t(8;21)
t(16;16)
PML-Retinoic acid receptor fusion (M3)
Nucleophosmin mutation
t(11;v)
Good prognosis

82
Q

AML with Myelodysplasia related changes includes

A

Abnormal proliferation of myeloid cells
Monosomy 5 and 7
Intermediate prognosis

83
Q

AML (Therapy related) includes

A

Alkylating agents
Topoisomerase inhibitors
Very bad prognosis

84
Q

Myeloid proliferation related to sown Syndrome includes

A

GATA1 Mutations
Transient abnormal myelopoiesis
Myeloid leukemia associated with Down Syndrome

85
Q

Most common AML subtype in Infants

A

M5

86
Q

Most common AML Subtype in childrens

A

M7

87
Q

Diagnosis of AML

A

Peripheral blood smear
BM Examination
Flow cytometry
Cytogenetics
Molecular study

88
Q

Investigation of choice in AML

A

Flow cytometry

89
Q

Most common leukemia in childrens

A

Acute Lymphoblastic leukemia (ALL)

90
Q

Clinical features of ALL

A

Sudden onset
Fatigue
Pallor
Increased risk of infection - Fever
Increased bleeding - petechiae, purpura, gum bleeding
Splenomegaly, hepatomegaly
Lymphadenopathy
Sternal tenderness
In male - enlarged testicular mass

91
Q

Cytogenetic abnormality seen in B cell ALL

A

Hyperploidy (Presence of more than 50 chromosomes)

92
Q

Translocations seen in B cell ALL

A

t(12;21) , t(9;22) , t(1;19)

93
Q

Prognosis of B cell ALL in Hyperploidy and t(12;21)

A

Good prognosis

94
Q

Prognosis of B cell ALL in hypoploidy and t(9;22) , t(1;19)

A

Bad Prognosis

95
Q

EBF and PAX-5 is required for

A

Proper B cell differentiation

96
Q

Mutations in EBF AND PAX-5 can leads to

A

Loss of function - proliferation of undifferentiated cells

97
Q

Mutations seen in T cell ALL

A

NOTCH Mutation - Gain of function mutation

98
Q

NOTCH Mutation is associated with

A

Excessive proliferation of tumor cells

99
Q

Diagnosis of ALL

A

Peripheral blood smear
BM Aspiration - greater no. Of precursor cells (Lymphoblasts)

100
Q

More common ALL

A

Pre B cell ALL

101
Q

In Pre B cell ALL which organ is involved

A

Bone marrow

102
Q

In Pre T cell ALL which organ is involved

A

Thymus

103
Q

Pre B cell ALL usually seen in which age

A

Upto 3 yrs of age

104
Q

Pre T cell ALL usually seen in which age

A

Puberty

105
Q

Prognosis of Pre B CELL ALL

A

Better prognosis

106
Q

Prognosis of T cell ALL

A

Bad Prognosis

107
Q

Good prognosis Factors in ALL

A

Hyperploidy
t(12;21)
Trisomy 4/7/10
White race
1-10 years of age
Female gender
Less blast count (<1 lakh)
Pre B cell ALL
Drug reponse
Remission <14 days

108
Q

Bad Prognosis Factors in ALL

A

Hypoploidy
MLL/KMT2A translocation
t(9;22), t(1;19) , t(4;11) , t(5;14)
Black race
<1 year ; >10 year
Male gender - testicular involved
More blast count (>1 lakh)
Pre T cell ALL
no response to drug
Remission >14 days

109
Q

Treatment of ALL

A

Anticancer drugs (Childrens tolerate well than adults)
Bone marrow transplantation
CAR-T Therapy

110
Q

CAR-T Therapy

A

Infusion of modified antigenic T cells - Targets CD19 (usually present on Tumor cells) - destroys tumor cells

111
Q

CAR-T Therapy is associated with

A

Massive release of cytokines

112
Q

Chronic myeloid lukemia is an example of

A

Myeloproliferative disorder

113
Q

CML arises from

A

Pleuripotent hematopoietic stem cells

114
Q

Risk factors of CML

A

Radiation exposure
t(9;22) - Philadelphia chromosome

115
Q

Gene present on Chromosome 9(CML)

A

ABL gene - Tyrosine kinase activity present

116
Q

Gene present on Chromosome 22(CML)

A

BCR gene

117
Q

BCR-ABL Fusion gene chromosome also known as

A

Philodelphia chromosome

118
Q

Fusion gene BCR-ABL leads to

A

Increased activity of Tyrosine kinase - needed for cell replication - due to which no. Of cells increases

119
Q

Philodelphia chromosome can be seen in

A

CML (MC)
ALL (B Cell)
Chronic neutrophilic leukemia

120
Q

Age group in risk of CML

A

25-60years , mostly >50

121
Q

Clinical features of CML

A

Non specific Clinical features - Fatigue, fever, weight loss
Extra medullary hematopoiesis - Massive splenomegaly - Abdominal fullness
Abdominal pain can be present in case of Splenic infarct

122
Q

Blood examination in CML

A

TLC increased
Hb levels low
Platelet count increases

123
Q

Peripheral smear in CML

A

Myeloid precursors increased
Basophils ++
Eosinophils +

124
Q

Differential diagnosis of Leukemoid reaction with CML

A

Benign condition
No philodelphia chromosome
TLC(40-50K) i.e; less than 1lakh
Basophilia and Eosinophilia usually not seen

125
Q

Serum B12 levels in CML

A

Increases

126
Q

LAP score in CML

A

Decreased

127
Q

BM Examination in CML

A

Cellularity increases
Reticulin +++
Sea blue histiocytes
Pseudo gaucher cells
Increased no. Of WBC precursors
Blast cells increases

128
Q

Sea blue histiocytes are seen in

A

CML

129
Q

Pseudo gaucher cells can be seen in

A

Gaucher like cells
Can be seen in - CML, Multiple myeloma, Myelodysplastic Syndrome, Thalessemia

130
Q

Difference between pseudo gaucher cells and Gaucher cells

A

PGC - No iron staining
No inclusions in cytoplasm

131
Q

Stages according to no. Of Blast cells

A

Chronic stage
Accelerated stage
Blast stage

132
Q

Chronic stage in CML

A

Asymptomatic
Blasts <10%
Philodelphia chromosome +

133
Q

Accelerated stage in CML

A

10-19% Blasts
Splenomegaly, Basophils increased
Cytogenetic changes
WBC Count increased
Platelet count increases
Response to Tyrosine kinase Inhibitors therapy

134
Q

Blast stage in CML

A

Blasts >20%
Lymphadenopathy

135
Q

Sudden increase in size of lymph nodes in CML patient indicates

A

Patient reached to Blast stage

136
Q

CML can progress t0

A

AML (70%)
ALL (30%)

137
Q

College girl appearance seen in peripheral smear in which disease

A

CML

138
Q

Philodelphia chromosome can be identified by which method

A

FISH - Fluorescent insitu Hybridization

139
Q

Fusion gene in Philadelphia chromosome is detected by

A

FISH

140
Q

mRNA in Philadelphia chromosome is detected by

A

PCR

141
Q

Treatment of CML

A

Tyrosine kinase Inhibitors - Imatinib

142
Q

Response to TKI depends on

A

1)Hematological resistance to 1st TKI
2)Hematological/cytological/molecular resistance for 2 sequential TKIs
3) >2 mutations in BCR-ABL gene if patient on TKI

143
Q

Treatment of CML In young patients

A

Allogenic BM transplantation

144
Q

Prognostic index used for CML

A

SOKAL Index
Hassford index

145
Q

SOKAL index includes factors like

A

Spleen size
% of circulating blasts
Clonal cytogenetic defects
Age
Level of platelets

146
Q

In Hassford index factors includes

A

Same as SOKAL Index Except % of Eosinophils and basophils in place of clonal defects

147
Q

Commonest blood cancer in Adults

A

Chronic lymphocytic leukemia (CLL)

148
Q

CLL Arises from

A

Peripheral B cell

149
Q

B cell mutations seen in CLL

A

11q deletion
12q Trisomy
13q deletion
17p deletion
NOTCH-1 +++
Somatic hypermutation

150
Q

ZAP-70 levels in CLL

A

Increased - tumor cell rate of replication increases

151
Q

If there is mutations in B cell it leads to

A

Formation of abnormal plasma cells - Abnormal antibodies formation

152
Q

Due to presence of abnormal antibodies in CLL

A

Decreased Immunoglobulins (Hypogammaglobunemia)
Infection frequency increases
Autoantibodies - RBC destruction

153
Q

Which protein is defected in case of CLL

A

Vimentin

154
Q

Vimentin is responsible for

A

For maintaining Lymphocytes structure

155
Q

Defect of vimentin leads to

A

Fragile tumor cells

156
Q

Clinical features of CLL

A

Non specific - Fever/weight loss/night sweats
>60 yr
Fatigue
Lymph node enlargement

157
Q

Clinical features of CLL

A

Non specific - Fever/weight loss/night sweats
>60 yr
Fatigue
Lymph node enlargement

158
Q

Blood examination in CLL

A

Anemia
Platelet count decreases
TLC Increases
DLC - Lymphocytes increases

159
Q

Absolute lymphocyte count (ALC) levels in CLL

A

> 5000/microliter

160
Q

Hypogammaglobunemia is seen in case of

A

CLL

161
Q

Peripheral smear in CLL

A

Smudge cells or parachute cells due to vimentin defect

162
Q

Convent girl appearance seen in peripheral smear of

A

CLL

163
Q

BM Examination in CLL

A

Hypercellular BM
Lymphoid precursors +++

164
Q

Lymph node biopsy or exam in CLL

A

Disturbed Lymph node appearance - due to infiltration of tumor cells

165
Q

Investigation of choice in CLL

A

Flow Cytometry

166
Q

Investigation of choice in CLL

A

Flow Cytometry

167
Q

CD molecules seen in CLL

A

CD19/20/21/23 +
CD5 +

168
Q

CD molecules seen in CLL

A

CD19/20/21/23 +
CD5 +

169
Q

Good prognostic factors in CLL

A

13q deletion
Somatic hypermutation - slow growing tumor

170
Q

Good prognostic factors in CLL

A

13q deletion
Somatic hypermutation - slow growing tumor

171
Q

Bad prognostic factors in CLL

A

11q deletion, 17p deletion, 12q Trisomy
NOTCH ++
ZAP-70 ++

172
Q

Poorest prognosis in CLL

A

17p deletion

173
Q

Poorest prognosis in CLL

A

17p deletion

174
Q

Treatment of CLL

A

Fludarabine - best
Rituximab - against CD22
B cell Tyrosine kinase Inhibitors - IBUTINIB

175
Q

If there is additional mutations in CLL Patients that leads to syndrome named as

A

Richter syndrome

176
Q

Mutations in myeloid stem cells leads to

A

Dysrerythropoiesis or abnormal erythropoiesis

177
Q

Myelodysplastic Syndrome is classified into

A

Primary - usually elderly patients (70yr)
Secondary - therapy related

178
Q

In case of therapy related myelodysplastic syndrome there is history of

A

Radiation exposure or Cytotoxic drugs

179
Q

Epigenetic factors responsible for Myelodysplastic Syndrome

A

DNA methylation
Histone modification

180
Q

Genetic factors responsible for MDS

A

Epigenetic factors
Nuclear transcription factors
RNA Splicing defects

181
Q

Commonest mutation in adults in MDS

A

5q deletion

182
Q

Commonest genetic defect in childrens resulting to MDS

A

Monosomy 7

183
Q

Most common genetic mutation responsible for MDS in India

A

Complex karyotype

184
Q

Effect on RBCs due to defective myeloid stem cells

A

Abnormal nuclear budding
Megaloblastic changes
Ring Sideroblast - Prussian blue stain

185
Q

Effect on WBCs due to defective myeloid stem cells

A

Neutrophils - 2 lobule - Pseudo-pelger huet Anomaly

186
Q

Effect of defective myeloid stem cells on Platelets in MDS

A

Divided multiple nuclear lobes - PAWN BALL Megakaryocytes

187
Q

Due to additional mutations CLL Or SLL can progress to

A

Diffuse large B cell Lymphoma(DLBCL)

188
Q

Clinical features of MDS

A

Pancytopenia
Weakness/ Fatigue
Increased risk of infection
Bleeding tendency increases

189
Q

BM Examination in MDS

A

Hypercellular BM
Blasts <20%

190
Q

Peripheral smear in MDS

A

Cell count relatively decreases
Nuclear lobe budding
Ringed sideroblast
Pseudo-pelger huet cells - WBC
PAWN BALL Megakaryocyte - Platelets

191
Q

Management in MDS

A

Young - Allogenic BM Transplantation
Symptomatic treatment
Decitabine - inhibits DNA methylation
LENALIDOMIDE - 5q deletion

192
Q

Further mutations in myeloid cells can progress to

A

AML

Pathology (14 decks)

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