Hematology - WBC Flashcards
1
Q
WBC development steps
A
Myeloblast - Promyelocyte - Myelocyte - Metamyelocyte - Band cells - Mature WBC
2
Q
Stain used to see visualise all WBC cells
A
Wright stain
3
Q
Most abundant WBC cells
A
Neutrophils (50-70%)
4
Q
Nuclear lobes in neutrophils
A
2-5 nuclear lobes
5
Q
Neutrophils levels are increased in
A
Bacterial infection
Acute inflammation
Sterile inflammation
Burns
6
Q
Normal lymphocytes percentage
A
20-40%
7
Q
Nucleus in Lymphocytes
A
Round nucleus
8
Q
Lymphocytes levels are increased in
A
Viral infections (CMV,EBV)
Chronic Inflammatory conditions
Borditella pertusis infection
9
Q
Biggest WBC in human body
A
Monocytes
10
Q
Which WBC levels usually increases with Lymphocytes
A
Monocytes
11
Q
Monocytes levels increases in
A
Chronic inflammation
Autoimmune disorders
IBD
TB, Malaria
Ricketssiae
12
Q
Nuclear lobes in Eosinophil
A
2 nuclear lobes
13
Q
Eosinophil levels increases in
A
Parasitic/worm infections
Allergy
Hodgkin’s lymphoma
Athero-embolism - Eosinophils in urine
14
Q
Least WBC found in Blood
A
Basophils (1-2%)
15
Q
Basophils levels increases in
A
Allergic conditions
Chronic myelogenous leukemia
16
Q
Nucleus shape of Band neutrophils
A
Horse shoe shaped nucleus
17
Q
Band neutrophils seen in peripheral blood due to
A
When there is increased stimulation of BM
18
Q
Shift to left means
A
Increased leukocytes count in blood
19
Q
Normal WBC levels
A
4,000-11,000 WBCs per microliter
20
Q
Condition when WBC levels are more than 40-50k WBCs per microliter
A
Leukemoid reaction
21
Q
Leukemoid reaction means
A
Increased no. Of matured Wbc cells
22
Q
LAP score in Leukemoid reaction
A
Increases
23
Q
Leukemoid reaction is usually seen in
A
Pneumonia
Infectious endocarditis
Septicimea
24
Q
Leukemia means
A
Increased involvement of Bone marrow and surrounding blood vessels
25
Lymphoma means
Infiltration of Cancer cells in different organs of body via lymph nodes
26
In leukemia
Cancer cells in BM - Can suppress normal cells leads to
Decreased RBC - Anemia
Decreased WBC - Fever
Decreased platelets - Increased risk of bleeding
27
In leukemia
Cancer cells in BM - Can suppress normal cells leads to
Decreased RBC - Anemia
Decreased WBC - Fever
Decreased platelets - Increased risk of bleeding
28
WHO Classification of lymphoid neoplasms
1) Precursor B cell neoplasm
2) Peripheral B cell neoplasm
3) Precursor T cell neoplasm
4) Peripheral T cell neoplasm
5) Hodgkin's lymphoma
29
WHO Classification of Myeloid Neoplasm
1) Acute myeloid leukemia
2) Myelodysplastic Syndrome
3) Myeloproliferative neoplasms
30
WHO classification of Macrophages
Langerhans cell histiocytosis
31
Cancers arising from precursors cells are usually
Multiply very rapid
Very rapid onset of symptoms
32
Cancers arising from Peripheral cells are usually
Slow growing
Chronic leukemia
Symptoms onset can take months to years
33
Risk factors Of Acute leukemia
Ionising radiation
Chemicals
Genetic factors
Infectious organisms
34
Chemicals having risk of Acute leukemia
Smoking
Benzene
Drugs - Anticancer drugs (Alkylating agents, Topoisomerase inhibitors)
35
Genetic factors responsible for acute leukemia
Down Syndrome (Trisomy 21) - ALL (MC), AML
Klinefelter's syndrome
Neurofibromatosis
Fanconi's anemia
Ataxia telangectasia
36
Infectious organisms responsible for acute leukemia
EBV (Epstien barr virus)
HTLV-1
HHV-8
37
Due to blocking of differentiation in acute leukemia
There is increased no. Of immature cells
38
Clinical symptoms of acute leukemia
Acute/sudden onset of action
Weakness, fever
Lymph nodes enlargement
Bleeding
Abdominal fullness
39
Blood exam in acute leukemia shows
TLC increased
40
Percentage of immature Wbc cells in normal person on BM Aspiration
5%
41
In case of Acute leukemia percentage of immature Wbc cells is
More than 20% of lymphoblasts or myeloblasts
42
If Lymphoblast >20%
Acute lymphoblastic leukemia(ALL)
43
Stain used to identify Lymphoblasts
TdT(Terminal deoxynucleotide transferase)
PAS (Periodic acid-Schiff)
44
If Myeloblast >20%
Acute myeloid leukemia (AML)
45
Stain used to identify Myeloblast cells
Myeloperoxidase
Non specific esterase
46
Flow cytometry is used to
See absence or presence of CD Molecules
47
Precursor cell of Acute Myelogenous leukemia (AML)
Myeloblast
48
Precursor cell of Acute Myelogenous leukemia (AML)
Myeloblast
49
Moat commonly affected population in AML
Elderly population (60yrs)
50
Affected myeloid cells in AML
Erythroblast
Megakaryoblast
Myeloblast
51
Clinical signs of AML
Sudden onset
Fatigue
Fever
Anorexia
Weight loss
52
AML-FAB Classification
M0 to M7
53
M0
Minimally differentiated AML
54
M1
AML without maturation
55
M2
AML With maturation
56
M3
Acute Promyelocytic Leukemia
57
M4
Acute Myelomonocytic leukemia
58
M5
Acute monocytic leukemia
59
M6
Acute erythroleukemia
60
M7
Acute Megakaryocytic leukemia
61
M1 to M4 AML are identified by
Myeloperoxidase
62
M5 AML identified by
Non specific esterase
63
M6 AML are identified by
PAS +ve
64
M7 AML is identified by
CD41
CD61
65
Myeloblast are stained by
Myeloperoxidase
Non specific esterase
PAS +ve
66
Special markers used to identify Myeloblast
CD41 and CD61
67
Most common AML
M2 - AML with maturation
68
Translocation seen in AML with maturation
t(8;21)
69
AML with maturation also known as
Granulocytic sarcoma
Myeloblastoma
70
In AMl With maturation cell deposits in
Retroorbital tissues - Pushes eyeball forward - Development of Proptosis
71
Markers used for AML with Maturation
CD45, Lysosome+ve
CD43
72
Translocation seen in Acute Promyelocytic Leukemia (M3)
t(15;17)
73
In M3, Due to t(15;17) there is fusion of
PML protein + Retinoic acid receptor fusion - can lead to vitamin A defeciency
74
In M3 AML, there is high risk of development of
DIC - because tumor cells release mucin - leads to extensive damage of endothelial cells
75
Aeur rods are seen in
Acute Promyelocytic Leukemia (M3)
76
20-30 Aeur rods together termed as
Faggot cell (Bundle of stick appearance)
77
Translocation seen in Acute myelomonocytic leukemia (M4)
t(16;16)
78
Gum hypertrophy and leukemia cutis are seen in
Acute Myelomonocytic leukemia (M4) and Acute monocytic leukemia(M5)
79
AML most commonly associated with Down Syndrome
Acute Megakaryocytic leukemia (M7)
80
WHO classification of AML
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
AML with Specific genetic defetcs includes
t(8;21)
t(16;16)
PML-Retinoic acid receptor fusion (M3)
Nucleophosmin mutation
t(11;v)
Good prognosis
82
AML with Myelodysplasia related changes includes
Abnormal proliferation of myeloid cells
Monosomy 5 and 7
Intermediate prognosis
83
AML (Therapy related) includes
Alkylating agents
Topoisomerase inhibitors
Very bad prognosis
84
Myeloid proliferation related to sown Syndrome includes
GATA1 Mutations
Transient abnormal myelopoiesis
Myeloid leukemia associated with Down Syndrome
85
Most common AML subtype in Infants
M5
86
Most common AML Subtype in childrens
M7
87
Diagnosis of AML
Peripheral blood smear
BM Examination
Flow cytometry
Cytogenetics
Molecular study
88
Investigation of choice in AML
Flow cytometry
89
Most common leukemia in childrens
Acute Lymphoblastic leukemia (ALL)
90
Clinical features of ALL
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
Cytogenetic abnormality seen in B cell ALL
Hyperploidy (Presence of more than 50 chromosomes)
92
Translocations seen in B cell ALL
t(12;21) , t(9;22) , t(1;19)
93
Prognosis of B cell ALL in Hyperploidy and t(12;21)
Good prognosis
94
Prognosis of B cell ALL in hypoploidy and t(9;22) , t(1;19)
Bad Prognosis
95
EBF and PAX-5 is required for
Proper B cell differentiation
96
Mutations in EBF AND PAX-5 can leads to
Loss of function - proliferation of undifferentiated cells
97
Mutations seen in T cell ALL
NOTCH Mutation - Gain of function mutation
98
NOTCH Mutation is associated with
Excessive proliferation of tumor cells
99
Diagnosis of ALL
Peripheral blood smear
BM Aspiration - greater no. Of precursor cells (Lymphoblasts)
100
More common ALL
Pre B cell ALL
101
In Pre B cell ALL which organ is involved
Bone marrow
102
In Pre T cell ALL which organ is involved
Thymus
103
Pre B cell ALL usually seen in which age
Upto 3 yrs of age
104
Pre T cell ALL usually seen in which age
Puberty
105
Prognosis of Pre B CELL ALL
Better prognosis
106
Prognosis of T cell ALL
Bad Prognosis
107
Good prognosis Factors in ALL
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
Bad Prognosis Factors in ALL
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
Treatment of ALL
Anticancer drugs (Childrens tolerate well than adults)
Bone marrow transplantation
CAR-T Therapy
110
CAR-T Therapy
Infusion of modified antigenic T cells - Targets CD19 (usually present on Tumor cells) - destroys tumor cells
111
CAR-T Therapy is associated with
Massive release of cytokines
112
Chronic myeloid lukemia is an example of
Myeloproliferative disorder
113
CML arises from
Pleuripotent hematopoietic stem cells
114
Risk factors of CML
Radiation exposure
t(9;22) - Philadelphia chromosome
115
Gene present on Chromosome 9(CML)
ABL gene - Tyrosine kinase activity present
116
Gene present on Chromosome 22(CML)
BCR gene
117
BCR-ABL Fusion gene chromosome also known as
Philodelphia chromosome
118
Fusion gene BCR-ABL leads to
Increased activity of Tyrosine kinase - needed for cell replication - due to which no. Of cells increases
119
Philodelphia chromosome can be seen in
CML (MC)
ALL (B Cell)
Chronic neutrophilic leukemia
120
Age group in risk of CML
25-60years , mostly >50
121
Clinical features of CML
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
Blood examination in CML
TLC increased
Hb levels low
Platelet count increases
123
Peripheral smear in CML
Myeloid precursors increased
Basophils ++
Eosinophils +
124
Differential diagnosis of Leukemoid reaction with CML
Benign condition
No philodelphia chromosome
TLC(40-50K) i.e; less than 1lakh
Basophilia and Eosinophilia usually not seen
125
Serum B12 levels in CML
Increases
126
LAP score in CML
Decreased
127
BM Examination in CML
Cellularity increases
Reticulin +++
Sea blue histiocytes
Pseudo gaucher cells
Increased no. Of WBC precursors
Blast cells increases
128
Sea blue histiocytes are seen in
CML
129
Pseudo gaucher cells can be seen in
Gaucher like cells
Can be seen in - CML, Multiple myeloma, Myelodysplastic Syndrome, Thalessemia
130
Difference between pseudo gaucher cells and Gaucher cells
PGC - No iron staining
No inclusions in cytoplasm
131
Stages according to no. Of Blast cells
Chronic stage
Accelerated stage
Blast stage
132
Chronic stage in CML
Asymptomatic
Blasts <10%
Philodelphia chromosome +
133
Accelerated stage in CML
10-19% Blasts
Splenomegaly, Basophils increased
Cytogenetic changes
WBC Count increased
Platelet count increases
Response to Tyrosine kinase Inhibitors therapy
134
Blast stage in CML
Blasts >20%
Lymphadenopathy
135
Sudden increase in size of lymph nodes in CML patient indicates
Patient reached to Blast stage
136
CML can progress t0
AML (70%)
ALL (30%)
137
College girl appearance seen in peripheral smear in which disease
CML
138
Philodelphia chromosome can be identified by which method
FISH - Fluorescent insitu Hybridization
139
Fusion gene in Philadelphia chromosome is detected by
FISH
140
mRNA in Philadelphia chromosome is detected by
PCR
141
Treatment of CML
Tyrosine kinase Inhibitors - Imatinib
142
Response to TKI depends on
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
Treatment of CML In young patients
Allogenic BM transplantation
144
Prognostic index used for CML
SOKAL Index
Hassford index
145
SOKAL index includes factors like
Spleen size
% of circulating blasts
Clonal cytogenetic defects
Age
Level of platelets
146
In Hassford index factors includes
Same as SOKAL Index Except % of Eosinophils and basophils in place of clonal defects
147
Commonest blood cancer in Adults
Chronic lymphocytic leukemia (CLL)
148
CLL Arises from
Peripheral B cell
149
B cell mutations seen in CLL
11q deletion
12q Trisomy
13q deletion
17p deletion
NOTCH-1 +++
Somatic hypermutation
150
ZAP-70 levels in CLL
Increased - tumor cell rate of replication increases
151
If there is mutations in B cell it leads to
Formation of abnormal plasma cells - Abnormal antibodies formation
152
Due to presence of abnormal antibodies in CLL
Decreased Immunoglobulins (Hypogammaglobunemia)
Infection frequency increases
Autoantibodies - RBC destruction
153
Which protein is defected in case of CLL
Vimentin
154
Vimentin is responsible for
For maintaining Lymphocytes structure
155
Defect of vimentin leads to
Fragile tumor cells
156
Clinical features of CLL
Non specific - Fever/weight loss/night sweats
>60 yr
Fatigue
Lymph node enlargement
157
Clinical features of CLL
Non specific - Fever/weight loss/night sweats
>60 yr
Fatigue
Lymph node enlargement
158
Blood examination in CLL
Anemia
Platelet count decreases
TLC Increases
DLC - Lymphocytes increases
159
Absolute lymphocyte count (ALC) levels in CLL
>5000/microliter
160
Hypogammaglobunemia is seen in case of
CLL
161
Peripheral smear in CLL
Smudge cells or parachute cells due to vimentin defect
162
Convent girl appearance seen in peripheral smear of
CLL
163
BM Examination in CLL
Hypercellular BM
Lymphoid precursors +++
164
Lymph node biopsy or exam in CLL
Disturbed Lymph node appearance - due to infiltration of tumor cells
165
Investigation of choice in CLL
Flow Cytometry
166
Investigation of choice in CLL
Flow Cytometry
167
CD molecules seen in CLL
CD19/20/21/23 +
CD5 +
168
CD molecules seen in CLL
CD19/20/21/23 +
CD5 +
169
Good prognostic factors in CLL
13q deletion
Somatic hypermutation - slow growing tumor
170
Good prognostic factors in CLL
13q deletion
Somatic hypermutation - slow growing tumor
171
Bad prognostic factors in CLL
11q deletion, 17p deletion, 12q Trisomy
NOTCH ++
ZAP-70 ++
172
Poorest prognosis in CLL
17p deletion
173
Poorest prognosis in CLL
17p deletion
174
Treatment of CLL
Fludarabine - best
Rituximab - against CD22
B cell Tyrosine kinase Inhibitors - IBUTINIB
175
If there is additional mutations in CLL Patients that leads to syndrome named as
Richter syndrome
176
Mutations in myeloid stem cells leads to
Dysrerythropoiesis or abnormal erythropoiesis
177
Myelodysplastic Syndrome is classified into
Primary - usually elderly patients (70yr)
Secondary - therapy related
178
In case of therapy related myelodysplastic syndrome there is history of
Radiation exposure or Cytotoxic drugs
179
Epigenetic factors responsible for Myelodysplastic Syndrome
DNA methylation
Histone modification
180
Genetic factors responsible for MDS
Epigenetic factors
Nuclear transcription factors
RNA Splicing defects
181
Commonest mutation in adults in MDS
5q deletion
182
Commonest genetic defect in childrens resulting to MDS
Monosomy 7
183
Most common genetic mutation responsible for MDS in India
Complex karyotype
184
Effect on RBCs due to defective myeloid stem cells
Abnormal nuclear budding
Megaloblastic changes
Ring Sideroblast - Prussian blue stain
185
Effect on WBCs due to defective myeloid stem cells
Neutrophils - 2 lobule - Pseudo-pelger huet Anomaly
186
Effect of defective myeloid stem cells on Platelets in MDS
Divided multiple nuclear lobes - PAWN BALL Megakaryocytes
187
Due to additional mutations CLL Or SLL can progress to
Diffuse large B cell Lymphoma(DLBCL)
188
Clinical features of MDS
Pancytopenia
Weakness/ Fatigue
Increased risk of infection
Bleeding tendency increases
189
BM Examination in MDS
Hypercellular BM
Blasts <20%
190
Peripheral smear in MDS
Cell count relatively decreases
Nuclear lobe budding
Ringed sideroblast
Pseudo-pelger huet cells - WBC
PAWN BALL Megakaryocyte - Platelets
191
Management in MDS
Young - Allogenic BM Transplantation
Symptomatic treatment
Decitabine - inhibits DNA methylation
LENALIDOMIDE - 5q deletion
192
Further mutations in myeloid cells can progress to
AML
