PRELIM LEC: QUANTITATIVE AND QUALITATIVE Flashcards
(212 cards)
1
Q
Does not involve malignancy
A
QUANTITATIVE
2
Q
reaction of the immune system against certain invading pathogens
A
REACTIVE:
2
Q
increase in WBCs
A
LEUKOCYTOSIS
3
Q
increase in WBC count as a response to pathologic infection/inflammation physiologic condition
A
REACTIVE LEUKOCYTOSIS
4
Q
Total WBC count will increase
A
NEUTROPHILIA
5
Q
Only _____ cannot affect WBC count even if it increases.
A
basophil
6
Q
Criteria to diagnose ______
➔ Relative count: increase > 10%
➔ Absolute count: ≥ 7 x 10^9 /L (Children: 8.5 x 10^9 /L)
A
neutrophilia
7
Q
Causes of neutrophilia:
A
- Catecholamine
- Increase in Bone Marrow production
- Transfer from bone marrow pool to circulating pool (↑ demand = ↑ production). Leads to increased number of immature cell
(band/metamyelocyte)
8
Q
● Not a leukemia
● Not malignant
● Should be differentiated from malignancy
● Leukemia like status particularly Chronic Myeloid Leukemia
A
LEUKEMOID REACTION
9
Q
LEUKEMOID REACTION DIFFERENTIATION:
A
CYTOGENETIC TESTING
CYTOCHEMICAL STAINING
10
Q
Detection of mutated chromosomes (C9 and
C22)
- Positive: CML
- Negative: LR
A
CYTOGENETIC TESTING
11
Q
- Leukocyte Alkaline Phosphatase (LAK) Test
- ↑ score: LR
- ↓ score: CML
A
CYTOCHEMICAL STAINING
12
Q
Bacterial infections
A
TRUE NEUTROPHILIA
13
Q
Immature WBCs
(Leukoerythroblastic Reaction)
A
PERSISTENT NEUTROPHILIA
14
Q
Decrease in neutrophil count
A
NEUTROPENIA
14
Q
● Complete history and physical examination
● Assess CBC and ESR
● Bone marrow examination (to rule out malignancy)
A
NEUTROPHILIA WORK-UP
15
Q
Agranulocytes = neutrophils <0.5 x 10^9 /L
A
NEUTROPENIA
16
Q
PATHOLOGIC CAUSES OF NEUTROPENIA:
A
Aplastic Anemia
General Pancytopenia
Ineffective Hematopoiesis
17
Q
occurs when there is aplasia in the bone marrow; all cell types are affected. Red marrow is replaced by yellow marrow (adipocytes)
A
Aplastic Anemia
18
Q
due to megaloblastic anemia
- ↓ Vit B12 and B9 = ↓DNA Synthesis
A
Ineffective Hematopoiesis
19
Q
Other causes of neutropenia
A
● Severe infection
● Increase destruction of neutrophils
Two types:
1. Immune-mediated/immune mechanism
(autoimmune)
2. Increase sequestration of the spleen
(overactive/overstimulated)
19
Q
Occurrence of neutropenia starting at infancy with period’s alteration of neutrophil count from normal to neutropenic levels followed by a recovery phase
A
CYCLIC NEUTROPENIA
20
Q
- Reduced Bone Marrow Reserve Pool
- Reduced Mitotic Pool
A
CHRONIC NEUTROPENIA
21
Q
- Inability to release mature granulocytes from the bone marrow to circulation
- Myelokathexis type
A
CONGENITAL NEUTROPENIA
22
NEONATAL NEUTROPENIA
Accelerated:
1. Immune-mediated
2. Sepsis
23
NEONATAL NEUTROPENIA
Diminished:
1. Hemolytic disease of the newborn
2. Problem in the bone marrow
3. Infection that is reoccurring.
24
Neonatal alloimmune neutropenia
IMMUNE NEUTROPENIA
25
Occurs when maternal IgG (Type 3) crosses
placenta and binds to paternal human neutrophil antigens on fetal leukocytes leads to the destruction of neutrophils.
ALLOIMMUNE
26
- IgG antibodies against 1 or more Human Neutrophil Antigen (HNA)
- Self-limiting
AUTOIMMUNE NEUTROPENIA
27
DRUGS THAT CAN CAUSE NEUTROPENIA:
CHEMOTHERAPEUTIC AGENT
ANTI-INFLAMMATORY DRUGS
ANTI-THYROID DRUG
ANTI-BACTERIAL
PHENOTHIAZINES
28
➢ Kills **normal and malignant cells**
➢ Preparation of bags of platelets and
agranulocytes
CHEMOTHERAPEUTIC AGENT
29
➢ Neutropenia developed as an **idiosyncratic**
reaction
- Unusual or unpredictable effect
- No apparent mechanisms/reason
- Influenced by genetic makeup
ANTI-INFLAMMATORY DRUGS
30
**Destruction** of immature neutrophils
ANTI-THYROID DRUG
31
➢ Some causes **aplasia** in the Bone Marrow
➢ Such as Chloramphenicol
ANTI-BACTERIAL
32
**Direct toxic effect **on granulocyte precursors
PHENOTHIAZINES
33
Increase >0.4 x 10^9/L
EOSINOPHILIA
34
Large production of IL4 (recruits eosinophils from the BM)
and IL3
EOSINOPHILIA
35
Not uncommon to expect CHARCOT-LEYDEN
CRYSTALS (Other name: **LYSOPHOSPHOLIPASE**)
EOSINOPHILIA
36
OTHER CAUSE OF EOSINOPHILIA
HYPERIMMUNOGLOBULIN E SYNDROME
37
JOB’S SYNDROME (other name)
HYPERIMMUNOGLOBULIN E SYNDROME
38
Eosinophil has a high affinity in IgE due to the
mutation in the STAT 3 gene
HYPERIMMUNOGLOBULIN E SYNDROME
39
↑ IgE = ↑ Eosinophils
HYPERIMMUNOGLOBULIN E SYNDROME
40
Abnormal chemotactic ability of neutrophils
HYPERIMMUNOGLOBULIN E SYNDROME
41
Encodes for IL6 and IL10
STAT 3 GENE
42
necessary for development of Th17, which
kills extracellular bacteria and fungi)
IL6
43
has anti-inflammatory effect
IL10
44
TRIAD OF JOB’S SYNDROME
1. EOSINOPHILIA
2. Increase serum IgE of >2000 IU/mL
3. Recurrent skin and pulmonary infection
45
A STRESS RELATED due to increase production of GLUCOCORTICOID HORMONES
EOSINOPENIA
46
EOSINOPENIA INCREASE GLUCOCORTICOID:
1. Affects EOSINOPHIL **CHEMOTAXIS**
2. Affects EOSINOPHIL **ADHERENCE**
47
BASOPHILIA
Factors causing basophilia:
1. Time of the day - **CD2O3C** (receptor for allergen including pollen but has circadian rhythm)
2. Age
3. Physical activity
4. Hormones
48
HORMONES AFFECTING BASOPHILIA
1. ACTH - Can induce leukocytosis
2. PROGESTERONE - Hypothyroidism can induce HIGH BASOPHIL COUNT and migration of leukocytes in general.
3. THYROID HORMONES
49
Adults: >1.0 x 10^9 /L
MONOCYTOSIS
50
Neonates: >3.5 x 10^ /L
MONOCYTOSIS
51
Does not independently occur, increase with other cells
MONOCYTOSIS
52
MONOCYTOSIS Drugs:
1. Colony Stimulating Factors
2. Olanzapine
53
Causes:
● Monocytes of <2.2 x 10^9 /L
● Associated with other lineage cytopenia
●** Steroid therapy**
● Certain viral infection (EBV)
**● Listeria monocytogenes**
MONOCYTOPENIA
54
**Inversely proportional with neutrophils**, to give way to other WBCs that are in demand.
LYMPHOCYTOSIS
55
It is a **non-specific response** to inflammation
LYMPHOCYTOSIS
56
EBV: Infection that can cause lymphocytosis
LYMPHOCYTOSIS
57
Called atypical due to its abnormal morphological appearance (very delicate
cytoplasm), squeezed by neighbouring RBCs. Resembles big monocytes, scalloped appearance.
Atypical Lymphocytes:
58
1. Children: >10 x 10^9 /L
2. Adults: >5 x 10^9 /L
LYMPHOCYTOSIS
59
- AKA Kissing disease
- Caused by Epstein-Barr Virus
INFECTIOUS MONONUCLEOSIS
60
- One of the most common cause congenital/viral infection in the US
- Cell with **Owl-Eye appearance**
- Slight lymphocytosis
- 20% variant lymphocytes
CYTOMEGALOVIRUS
61
- Caused by Toxoplasma gondii
- Presence of variant lymphocytes
- Resembles IM
- Sx: Chills, fever, headache, and lymphadenopathy
TOXOPLASMOSIS
62
- Whooping cough
-Bacteria is transmitted through aerosol droplets
BORDETELLA PERTUSSIS
63
50 x 10^9 /L
LYMPHOCYTOSIS
64
100 x 10^9 /L
LEUKOCYTOSIS
65
➔ Adults: <1 x 10^9 /L
➔ Children: <2 x 10^9 /L
LYMPHOCYTOPENIA
66
Other causes:
1. In response to stress
2. Pathologic causes :
a. Decrease production
b. Mechanical loss
c. Increase destruction
d. Functional abnormalities
LYMPHOCYTOSIS
67
HIV infect CD4+ cells, which release IL2 necessary for CD8 proliferation (immunosuppressed)
t
68
● Atypical morphology
● Nucleus is indented and larger
● Cytoplasm is also indented
● Scalloped appearance
REACTIVE LYMPHOCYTOSIS
69
● Morphologic alteration
● Nuclear alteration
1. Hyposegmented
2. Hypersegmented
● Cytoplasmic
1. Deposition of accumulated substance (inclusion bodies)
QUALITATIVE
70
Hypolobulation of
PELGER-HUET ANOMALY (PHS)
71
Nucleus is not that segmented/lobulated
PELGER-HUET ANOMALY (PHS)
72
2 lobules
PELGER-HUET ANOMALY (PHS)
73
All PMNs are affected
PELGER-HUET ANOMALY (PHS)
74
More than half of the neutrophils are **hypolobulated**
PELGER-HUET ANOMALY (PHS)
75
Seen in **Myelodysplastic Syndrome** (<50% of the cells)
PELGER-HUET ANOMALY (PHS)
76
PELGER-HUET ANOMALY (PHS)
TYPES:
1. Pince-Nez
2. Peanut
3. Dumbbell
4. Spectacle
77
Cause: Mutation of Lamin B - Receptor Gene
PELGER-HUET ANOMALY (PHS)
78
Integral protein found in inner nuclear membrane of the WBC
LAMIN B- RECEPTOR GENE
79
Seen in the long arm of CHROMOSOME I
LAMIN B- RECEPTOR GENE
80
Normal Function: Maintains **nuclear shape** of the WBC
LAMIN B- RECEPTOR GENE
81
Mutated: Leads to problem in NUCLEAR SHAPE and lack
of SEGMENTATION
LAMIN B- RECEPTOR GENE
82
● Only **1 copy **of C1 has mutated
● Clinically **normal**
● Neutrophils are usually **bilobed**
● **Pince nez** appearance
HETEROZYGOUS PHS
83
● **2 copies **of chromosome 1
● Presents **cognitive impairmen**t, heart
defect and skeletal abnormalities
● Neutrophils are **mononuclear**
NOTE: Some pelgeroid neutrophils resemble immature neutrophils and needs to be differentiated.
HOMOZYGOUS PHS
84
Acquired because of other disease:
● Restricted Neutrophils
➔ Exception myelodysplastic syndrome
● Clinical correlation needed
➔ For differentiation of Pseudo PHA and True PHA
● Less than 50% of the neutrophils are affected
● Neutrophils are hypogranular
➔ But it is also present in myelodysplastic
syndrome
85
# *
is seen in malignancy, while true PHA is present on its own.
Pseudo PHA
86
is present in chemotherapy and other
myeloproliferative diseases except Myelodysplastic syndrome.
Pseudo PHA
87
**Hypersegmentation** of neutrophils
UNDRITZ ANOMALY
88
>5 lobes are present
UNDRITZ ANOMALY
89
Cause: Megaloblastic anemia cannot proceed to G2 of cell cycle leads to continuous cell growth without division
UNDRITZ ANOMALY
90
Increase segmentation of nucleus
UNDRITZ ANOMALY
91
No megaloblastic anemia
HEREDITARY NEUTROPHIL HYPERSEGMENTATION
92
No clinical problems/non-pathologic
HEREDITARY NEUTROPHIL HYPERSEGMENTATION
93
**Retention** of neutrophils in the Bone Marrow
MYELOKATHEXIS
93
Caused by CXCR4 Mutation
MYELOKATHEXIS
94
# *
Neutropenia despite the increase of neutrophils in the bone marrow
MYELOKATHEXIS
95
**Pyknotic **neutrophil nucleus
MYELOKATHEXIS
96
Hypersegmentation of nucleus
MYELOKATHEXIS
97
Nuclear filaments is **EXTREMELY LONG**
MYELOKATHEXIS
98
**Receptor in the neutrophil** precursors and mature neutrophils
CXCR4
99
Homing of **neutrophils** in the bone marrow
CXCR4
100
If mutated, there is **hyperactivity** that will lead to inability of the neutrophil to be released in the circulation
CXCR4
101
Only seen in neutrophils of females
BARR BODY
102
**Not a nuclear **segmentation
BARR BODY
103
Nuclear appendages present at the **end** of the nucleus
BARR BODY
104
Normally seen in **61 out of 500 PMNs**
BARR BODY
105
Cause: **Inactivated chromosome** present in somatic cell, caused by lyonization (i**nactivation of extra copy of X chromosome)**
BARR BODY
106
Barr body is seen in males
KLINEFELTERS SYNDROME (XXY) (chromosome alteration)
107
BARR BODY
THREE VARIANTS:
1. Drumstick = **without** hollow center
2. Racquet = **with** hollow center
3. Sessile nodule = **no** filament
108
● Seen in **lymphocytes**
● Inactivated chromosome is present
DAVIDSON’S
109
Large **poorly stained** metachromic granules in leukocytes
ALDER-REILEY ANOMALY
110
Can be evident in all leukocytes
ALDER-REILEY ANOMALY
111
Granules are made up of **MUCOPOLYSACCHARIDE**
ALDER-REILEY ANOMALY
112
May resemble toxic granules
ALDER-REILEY ANOMALY
113
Seen in GARGOYLISM or HURLER SYNDROME or MPS 1
ALDER-REILEY ANOMALY
114
Due to defect in **ALPHA LEVO-IDURONIDASE,** which leads incomplete degradation of heparan sulfate and dermatan sulfate → aggregation of mucopolysaccharide
ALDER-REILEY ANOMALY
115
ALDER-REILEY ANOMALY Symptoms:
- Mental retardation
- Cloudy (corners of the eye)
- Dwarfism
116
ALDER-REILEY ANOMALY Cure:
Stem Cell Transplant, enzyme therapy **(primary mode of treatment in the MTS)**
117
TOXIC GRANULES
118
Can be mistaken as Alder-Reiley Anomaly
TOXIC GRANULES
119
**LARGE PRIMARY GRANULES** primarily containing
PEROXIDASE
TOXIC GRANULES
120
Impaired cytoplasmic maturation due to IMMATURE RELEASE
TOXIC GRANULES
121
Found in severe infections, cancer, hematoma, tissue undergoing necrosis
TOXIC GRANULES
122
MYH9 mutation
MAY-HEGGLIN ANOMALY
123
Macrothrombocytopenia
MAY-HEGGLIN ANOMALY
124
Inclusion: Myosin heavy chain
MAY-HEGGLIN ANOMALY
125
Large dohle-like body inclusions
MAY-HEGGLIN ANOMALY
126
important fo cytoskeletal protein production for normal release of platelets. If mutated, leads to less shedding → macrothrombocytopenia
Myosin Heavy Chain (MYH9 gene)
127
Intracytoplasmic **pale blue round** inclusions
DOHLE BODIES
128
# *
Can also be seen normally in small amounts
DOHLE BODIES
129
Remnants of rRNA
DOHLE BODIES
130
If increased with toxic vacuolation or
granulation = infection or inflammation.
DOHLE BODIES
131
can be used as markers of immature release of neutrophils in bone marrow
Dohle bodies and toxic granules
132
Ribosomal RNA
DOHLE BODIES
133
Round, elongated with round ends
DOHLE BODIES
134
Toxic, granulation vacuolation
DOHLE BODIES
135
Remnants of myosin heavy chain
MAY-HEGGLIN
ANOMALY
136
Spindle in shape
MAY-HEGGLIN
ANOMALY
137
Macrothrombocytopenia
MAY-HEGGLIN
ANOMALY
138
Mutation of CHS1 LYST Gene
CHEDIAK HEGASHI GRANULES
139
codes for normal **lysosomal traffickin**
CHS1 LYST Gene
140
**Giant cytoplasmic granules **(bigger granules than toxic granulation and alder-reilly bodies; that are also useless) in all granule-containing cells
CHEDIAK HEGASHI GRANULES
141
Abnormal platelets
CHEDIAK HEGASHI GRANULES
142
EDTA samples more than 2 hours becomes yellow (acidic), which reflects autophagy
CHEDIAK HEGASHI GRANULES
143
Inability to combine with lysosomes and phagosomes (phagolysosome). This leads to:
1. Bleeding
2. Albinism
3. Recurrent Infection
144
Seen in sepsis. Not normal in
granulocytes
Toxic vacuoles
145
Seen in Septic conditions and toxemia respectively
PYKNOSIS
PYKNOSIS AND RINGED CELLS
146
**Ringed cells are seen earlier **than pyknosis (seen after 2
hours)
PYKNOSIS AND RINGED CELLS
147
**Shrunken nuclei **due to nuclear water loss or apoptosis
PYKNOSIS AND RINGED CELLS
148
Seen in s (?) conditions and poor preparation
techniques
PYKNOSIS AND RINGED CELLS
149
Lupus Erythematosus (LE)
LE CELLS
150
Neutrophil or monocyte engulfing nuclei of other cells (in vitro phenomenon)
LE CELLS
151
Engulfing of cells due to **Anti-Nuclear Antibodies**
- Leads to depolarization of DNA
LE CELLS
152
Used to test suspected patients. Blood
samples (**should be ABO compatible**) from leukemic patients (their lymphocytes are fragile). The floating nucleus is engulfed by LE cells.
LE Cell test
153
Factors for LE cells:
- Presence of living polymorphonuclear
- Dead cell nucleus
- Serum of patient that has antinuclear antibody
154
Monocytes or macrophages ingesting other cell’s** unaltered nucleus **(no Coating of ANA)
TART CELLS (PSEUDO-LE CELLS/ NUCLEOPHAGOCYTES)
155
Unaltered nucleus
TART CELLS (PSEUDO-LE CELLS/ NUCLEOPHAGOCYTES)
156
**Physiological** phenomenon
TART CELLS (PSEUDO-LE CELLS/ NUCLEOPHAGOCYTES)
157
Actually seen as an **artifact**
TART CELLS (PSEUDO-LE CELLS/ NUCLEOPHAGOCYTES)
158
Aggregates of immunoglobulins in the plasma cell
➔ Morula cell / Berry cell / Grape cell / Mott cell
RUSSELL BODIES
159
Formed due to abnormal increase in the production of immunoglobulins found in gammopathy
RUSSELL BODIES
160
codes for mucin production, if mutated there
will be no production of mucin → aggregation of **immunoglobulins** in the plasma cell.
MUC1 gene
161
secreted with immunoglobulins
Mucin
162
Autofluorescent
ROMANOWSKY STAIN
163
Eosinophilic inclusions
H&E
164
Orange
PAPANICOLAU STAIN
165
Periodic Acid Schiff (PAS)
Positive
166
**Invagination** of intracellular immunoglobulins aggregates
to the nucleus
DUTCHER BODIES
167
Similar to Russell bodies but its inclusion is inside the
nucleus.
DUTCHER BODIES
168
PAS (+)
DUTCHER BODIES
169
Firstly associated with **Waldenstrom’s Macroglobulinemia**
(Gammopathy)
DUTCHER BODIES
170
Atypical plasma cells characterized by the **fiery fingers**
FLAME CELLS
171
Formed because of immunoglobulins, due to the **dilation** of rough endoplasmic reticulum that leads to the obstruction of cytoplasm.
FLAME CELLS
172
Red-purple color is due to **IgA.**
FLAME CELLS
173
Can be seen in:
- IgE myeloma
- Other plasma cell dysplasia
FLAME CELLS
174
Used to classify different types of:
- Reactive / atypical / effector / plasmacytoid
transformed lymphocytes
- Formed when stimulated by antigens
DOWNY LYMPHOCYTE CLA
175
Heterogeneous population of cells
● Seen in:
- Infectious Mononucleosis
- Viral infection
- Toxoplasmosis
- Severe anemia
DOWNY LYMPHOCYTE CLA
176
**Turk** irritation cell / **Plasmacytoid** Lymph
TYPE I
177
Origin: B CELL
TYPE I
178
Seen: severe anemia, **Rubella**, chronic infection
TYPE I
179
Cytoplasm: moderately basophilic,
vacuolated, **foamy appearance**
TYPE I
180
Nucleus: indented or oval, **dense locks of** chromatin
TYPE I
181
# *
● Infectious mononucleosis: EPSTEIN BARR VIRUS
TYPE II
182
Origin: T CELL
TYPE II
183
Cytoplasm: **BALLERINA SKIRT** APPEARANCE, resembling a** fried egg** (bluish in color)
TYPE II
184
Nucleus: **round mass **of chromatin (less condense)
TYPE II
185
Origin: T&B CELL
TYPE III
186
Cells in transition: undergoing changes
in order
TYPE III
187
Transformed lymphocytes / Reticular L
TYPE III
188
Cytoplasm: vacuolated with
ABUNDANT BASOPHILIA, CLEAR
PERINUCLEAR AREA
TYPE III
189
Nucleus: finely reticulated nuclear
TYPE III
190
**Smudge** cell or Shadow cells of **Grurpecht**
BASKET CELL
191
Product of lymphocyte degradation
BASKET CELL
192
**FRAGILE CELLS** THAT ARE DAMAGED DURING
SMEAR
BASKET CELL
193
If increased, sign for Chronic Lymphocytic Leukemia
BASKET CELL
194
22% Bovine Albumin
BASKET CELL
195
Pathognomonic
HAIRY CELL
196
Lymphocytes with HAIRY-LIKE PROJECTIONS
HAIRY CELL
197
# *
Origin: B CELL
HAIRY CELL
198
TRAP (Tartrate Resistant Acid Phosphatase) positive
HAIRY CELL
199
HAIRY CELL LEUKEMIA
HAIRY CELL
200
Medium sized
HAIRY CELL
201
Nucleus: round to oval
HAIRY CELL
202
LARGE, BILOBED NUCLEUS or TWO NUCLEI with
eosinophilic nucleoli
REED-STERNBERG CELLS
203
Nucleotide abundant cytoplasm [OWL’S EYE
APPEARANCE similar to cytomegalovirus)
REED-STERNBERG CELLS
204
Formed by clonal transformation of B CELL
REED-STERNBERG CELLS
205
Derived from apoptotic GERMINAL CELLS
REED-STERNBERG CELLS
206
**Benefits: adds specificity** and variation of the antibody
production.
GERMINAL CELLS
207
Cons: Gateway for malignancies to happen; Easily mutated (easy to become malignant cells)
GERMINAL CELLS
208
Pathognomonic > HODGKIN’S LYMPHOMA
GERMINAL CELLS
