Leukemias Flashcards
(197 cards)
1
Q
Four Methodologies Used for Identifying & Classifying Leukemias
A
A. Morphologic review of bone marrow
B. Morphological review of peripheral blood smears
C. Cytochemical stains (Ex. → NSE, LAP, etc.)
D. Immunophenotyping
E. Cytogenetic & molecular analyses
2
Q
“Supreme Court of Diagnosis”
A
Cytogenetic & molecular analyses
3
Q
ALL
A
Acute lymphoblastic (less specifically, lymphocytic) Leukemia
4
Q
CLL
A
Chronic lymphocytic leukemia:
5
Q
AML
A
Acute myeloblastic (less specifically, Myelocytic or Myeloid) Leukemia; aka ANLL (Acute Nonlymphocytic Leukemia)
6
Q
CML
A
Chronic myelocytic/Myelogenous/Myeloid Leukemia
7
Q
Acute Myeloid (AML)
A
Myelocytic/Myelogenous
Promyelocytic
Monocytic
Myelomonocytic (AMML)
Erythrocytic (AEL)
Megakaryocytic (AMegL)
8
Q
Acute Lymphoid (ALL)
A
T-Lymphocytic
B-Lymphocytic
Null Cell (?)
9
Q
Chronic Myeloid
A
Myelocytic/
Myelogenous (CML)
Myelomonocytic (CMML)
10
Q
Chronic Lymphoid
A
Lymphocytic (CLL)
Plasmacytic
Hairy Cell (HCL)
Prolymphocytic (PLL)
11
Q
Hundreds of genetic defects now known to cause cancers. Usually somatic translocations and aneuploidy
A
Genetics
12
Q
Chemicals causing bone marrow depression and aplasia predispose to leukemia later on (Ex. benzene, chloramphenicol, sulfa drugs, insecticides, antineoplastics)
A
Leukemogens
13
Q
Some retroviruses transform N. cells by inserting their own oncogenes into host cells genome, causing them to become malignant. [EBV linked to Burkitt non-hodgkin lymphoma]
A
Viral infections
14
Q
Transient, reactive leukocytosis due to infection
Temporary resemblance of peripheral blood picture to “leukemic picture”
Severe left shift & very rare nRBCs (WBCT > 50,000/uL)
A
Leukemoid reactions:
15
Q
Presence of both nRBCs & left shift in peripheral blood
Caused by bone marrow damage from a malignant, “space-occuping lesion”, with consequent extensive extramedullary hematopoiesis
May be mild or severe, & occurs in CML & in lymphomas
A
Leukoerythroblastic reaction (aka. Leukoerythroblastic anemia, or Leukoerythroblastosis)
16
Q
Presence of the BCR/ABL1 gene, or t(9;22), identifies CML
A
Leukemoid reaction vs Leukoerythroblastic reaction
17
Q
Normal LAP scores
A
range from 15-170
18
Q
LAP ↓ in early leukemia
A
(Ex → early CML) because leukemic neutrophils are too abnormal to express the LAP that normal mature bands & segs would
19
Q
Lap ↑ in leukemoid reaction due to left shift
A
because there are tons of band & segs full of secondary granules containing LAP, just waiting to attack the infectious invaders – it only looks like leukemia because of the high WBC count.
20
Q
Process of replacing active marrow by fat tissue during development; results in restrictive active marrow sites
A
Retrogression
21
Q
- In patients with solid malignant tumors
- Example → lymphomas, carcinomas and sarcomas, with possible “mets” to bone marrow - As part of initial workup of unexplained ↑ or ↓ in RBCs, WBCs, and/or platelets
- As part of differential diagnosis workup for infections that manifest clinically as “fevers of unknown origin”
A
Three main reasons for performing a bone marrow evaluation
22
Q
Posterior iliac crest (adults and children)
Sternum (adults)
Vertebrae (in adults)
Tibia (children <1 year old)
A
Four preferred locations for bone marrow tap (in order of preference):
23
Q
- Developing hematopoietic cells (blasts of all types, normally at overall 5% cellularity)
- Macrophages or histiocytes: large cells, with abundant cytoplasm & debris-filled vacuoles, and irregular, “spreading” shape.
- Megakaryocytes: involved in platelet formation through endometriosis
- Osteoblasts: part of bone marrow stroma; specialized bone matrix-synthesizing cells
- Osteoclasts: huge (>100 u), multi-nucleated cells with ruffled border; formed from fusion of mono and macrophages!
A
Five types of normal bone marrow cells:
24
Q
a. Positive in which AMLs? M1-M4
b. Positive cells show gray-black or red-brown cytoplasmic granules
c. Stain reacts w/ lysosomal enzyme primary granules of myeloid and (to lesser extent) of monocytic cells
d. Mature granulocytes give strongest (+) reaction; monos and immature granulocytes show less (+) (scattered pattern)
A
Myeloperoxidase (MPO or MPX)
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Since _____ is NOT found in lymphoid cells, it is best used for differentiating between AML and ALL!
Myeloperoxidase (MPO or MPX)
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a. stains lipoproteins and phospholipids
b. Found in primary (azurophilic) & secondary granules of mature and immature neutrophils (& in eos, & slightly in monos and monoblasts)
c. Negative for lymphs, megakaryocytes, and erythroid precursors
d. Results parallel those for MPO!
e. Positive in which AMLs? M1-M4
Sudan Black B (SBB)
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This stain is also best for differentiating AML from ALL
Sudan Black B (SBB)
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______ faster, but ____ more stable and can be run on older specimens
MPO, SBB
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a. Pos in AMLs? → M1 - M4
b. Pos cells show reddish staining of cytoplasmic granules
c. Useful in separating monocyte precursors from granulocyte precursors
d. Present in 1° granules of neutrophils (& mast cells), but shows a negative or weak positive reaction in monocytes of lymphocytes
Specific Esterase
30
Auer rods of AML myelocytes strongly +1 why?
Because they're fused 1° granules and contain SE (specific esterase)
31
____ (+) in monocytic cells, and T-cells
____ (-) in myeloid cells and megakaryocytes
Nonspecific Esterase (alpha-Napthyl Butyrate Esterase, NBE)
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The NSEs primarily are used to differentiate _____ leukemias from monocytic ones!
Myeloid
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More sensitive than NBE
Positive cells show brownish appearance
(NAE) Nonspecific esterase (Alpha-Napthyl acetate esterase, NAE)
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____ strongly (+) in monocytes, T-cells, and megakaryocytes
NAE
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"Fluoride inhibition" NaFl inhibits enzymatic activity in ______… other cells are unaffected
monocytes
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____ stain is positive in these 4 disease states
80% ALL (chunky or block pattern)
CLL
Gaucher’s disease
Some AML (AMol, AEL, AMegL)
PAS
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stains glycogen
Periodic Acid Schiff (PAS)
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Used to diagnose Hairy cell Leukemia (HCL) because only these cells strongly + with this modified stain
TRAP stain
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Add L-Tartaric acid, then stain. Normal cells will not retain acid phosphatase activity; however, HCL cells do retain this activity, because they have a different acid phosphatase isoenzyme: thus called “TRAP +”.
Acid phosphatase (ACP)
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Positive cells show red ppt. With fast red violet stain; show black ppt. With fast blue violet stain
Leukocyte Alkaline Phosphatase (LAP)
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a. Only neutrophils contain this enzyme (in varying amounts) in their secondary granules
b. Used to help differentiate early CML from other conditions like leukemoid reactions or PV (at a screening level only)
Leukocyte Alkaline Phosphatase (LAP)
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Polycythemia vera
Leukemoid reaction
Bacterial infections
3rd trimester pregnancy
Steroid therapy
Chronic granulocytic leukemias
Blast crises
Chronic neutrophilic leukemias
CML w/ infectious
Myelofibrosis
Increased LAP (>110)
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Late CML
CML in remission
Secondary erythrocytosis
Normal LAP
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Early CML
PNH
Sideroblastic anemia
Marked eosinophilia
Sickle cell anemia
Improper technique
Myelodysplastic disorders
PNH
Viral infections
Decreased LAP <15
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ACD
Hemochromatosis
Sideroblastic anemia
3 conditions with increased bone marrow [Fe]
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Principle: Fe3+ (ferric) + potassium cyanide → ferricyanide (blue-green ppt.)
Used to evaluate RBC Fe stores; reported semi-quantitatively
(Perl’s) Prussian blue iron stain
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T lymphoblasts and megakaryocytic precursors
Acid phosphatase stain
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Mature neutrophils
Leukocyte alkaline phosphatase (LAP)
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Granulocytes; slight in monos
Sudan Black B (SBB)
50
Abnormal blast cells
Periodic acid-schiff (PAS)
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- Most common type of adult leukemia (incidence increases with age)
- All are rapidly fatal if left untreated
- Involves a defect of HSC (CD34+)
Acute Myeloid Leukemia
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- Hyperuricemia due to increased cell turnover
- Hyperphosphatemia due to cell lysis
- Hypokalcemia due to progressive bone destruction
AML Lab Findings
These are all signs of tumor lysis syndrome- a group of metabolic complications that can occur in patients with a malignancy
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abnormal hyperproliferation of bizarre granulocyte and/or monocyte precursors
Dysmyelopoiesis
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- Makes up 5% of AMLs; found in children and adults younger than 60 yp
- WBCs have functional problems (With phago-cytosis and chemotaxis)
AML w/ t(8;21) (q22:q22)
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- Blasts are large with abundant, dysplastic cytoplasm and numerous primary granules and Auer rods. Sometimes exhibit Pseudo-Pelger Huet
- MBO & SBB 1+
- PAS neg
- SE +
- (+/-) Auer rods
AML w/ t(8;21) (q22:q22)
56
- Rare: 5-8% of all AMLs and occurs at any age (usually young)
- Myeloblasts, monoblasts, and promyelocytes observed
- Also eosinophilia with dysplastic changed
Remission rate is good but only ½ are cured
AML w/ inv(16)(p13.1p22)
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- Makes up 8% of AMLs
- Abnormal hypergranular promyelocytes with Auer rods
- Granules can obscure nucleus with abundant cytoplasm and variable nucleus size and shape
AML w/ t(15;17) (q22;q12)- Acute promyelocytic leukemia (APL)
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Leukemic cells also have defective retinoic acid receptor (RARa gene), so can be treated with ____
ATRA (All Trans Retinoic Acid -- Vit A derivitive
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ATRA pushes ____ into finishing maturation, thus causing remission!
Pros
60
Unusual susceptibility to bleeding (hemorrhage) due to a defect in the system of coagulation
“bleeding diathesis”
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- Strongly associated with DIC
- A promyelocytes primary granules are rich in thromboplastin-like substances… which trigger a “bleeding diathesis”
Acute promyelocytic leukemia (APL)
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cells look agranular if only light microscopy used -- what subtype of leukemia is this?
Microgranular APL
63
bundles of auer rods
faggot cells in Acute Promyelocytic Leukemia
64
- Prolonged clotting time tests
- ⬇ plt. Count (because plts. Used up making clots)
- MPO and SBB= 2+ pos.
- PAS neg
- SE pos
- Both NSEs neg
- auer rods, can be in bundles
Lab findings of APL
65
Peripheral blood absolute monocytosis (>20%); many circulating blasts, pros, immature granulocytes and monos!
Acute myelomonocytic leukemia (aka. AMML)
66
- MBO and SBB still +
- Both NSEs now start to be +
- SE still +
- PAS still (-)
- (+/-) Auer rods
- CD 11b, CD 4, CD 36, and CD 64
Acute myelomonocytic leukemia (aka. AMML)
67
CND and soft tissue involvement
Ex. gum hypertrophy and skin lesions
AMML -- Acute myelomonocytic leukemia
68
Usually CD4 and CD64 pos (“gold std.”)
Acute monocytic leukemia (aka. AMoL)
69
Makes up 5-8% of AMLs
When >80% leukemic cells are monocytic
Acute monocytic leukemia (aka. AMoL)
70
Bone marrow shows some granulocytes, but majority composition is monoblasts, promonocytes, and monocytes
Acute monocytic leukemia (aka. AMoL)
71
Increased serum and urinary lysozyme - why?
Because this is enzyme found in greatest amounts in monos
72
- MPO and SBB +/- (most frequently NEG)
- Both NSEs pos (NBE 3+!)
- PAS pos (finally)
- Very rare Auer rods (most frequently NEG)
Acute Monocytic leukemia - AMoL
73
Makes up only 3% of AMLs
Only AML with marked erythroid precursor hyperplasia
Acute erythroid leukemia (AEL)
74
Leukemia that is frequently preceded by a myelodysplastic syndrome
Acute erythroid leukemia (AEL)
75
abnormal proliferation of bizarre RBC precursors, with reverse M:E ratio due to huge # of abnormal erythroblasts, and even a few ringed sideroblasts
dyserythropoiesis
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- Bone marrow shows dyserythropoiesis
- Peripheral blood- nRBCs with marked aniso, poikilocytosis and schistocytosis due to the dyserythropoiesis
- Lots of myeloblasts
Acute Erythroid Leukemia
77
- >50% bizarre, multinucleated, megaloblastoid nRBCs!! (with few ringed sideroblasts)
- Both NSEs+
- PAS +
Acute erythroid leukemia
78
Early, abnormal erythroblasts are PAS + in “______” or “blocky” pattern. Later, abnormal erythroblasts + in “_____” pattern
Granular; diffuse
79
Rarest form of AML!! (makes up <1% of AMLs)
Frequently associated with Down’s syndrome
Acute megakaryocytic/megakaryoblastic leukemia (AMegL)
80
dry tap upon bone marrow aspiration due to myelofibrosis
AMegL
81
⬆ #s of megakaryocyte precursors, include megakaryoblasts, atypical megakaryocytes (with “blebbing”), and giant platelets
dysmegakaryopoiesis
82
Few myeloblasts can look lymphoid or undifferentiated
Little accompanying dyserythropoiesis
Can be associated with t(3;21) and t(1;22)
AMegL Lab findings
83
MPO and SBB neg
NBE neg., but NAE pos
AMegL
84
- May plt.- specific receptors, such as GPIIb/IIIa receptor +
- Acid phosphatase pos
AMegL
85
Leukemia that is ACP positive
T-Cell ALL
86
Normo- normo- anemia, neutropenia, & thrombocytopenia due to bone marrow overcrowding
Acute Lymphoid Leukemia (ALL)
87
increased numbers of smudge cells (>12/100 WBCs)
ALL
88
- Bone pain from infiltration
- Account for 75% of childhood leukemias
ALL
89
Acute Lymphocytic Leukemia can be classified into:
B-ALL
T-ALL
90
- Small size is most common with distinct nucleoli
- Large type is 2-3 times larger than lymphocyte with distinct nucleoli
Morphology of Lymphoblasts
91
CD10 marker
Intermediate (common) B-All
92
CALLA - Common Acute Lymphoblastic Leukemia
CD10
93
CD2
CD3
CD4
CD5
CD7
CD8
TdT
T-ALL
94
movement of cytoplasmic CD22 to surface (sCD22)
Mature B-ALL
95
CD34
CD19
Cytoplasmic CD22 (cCD22)
TdT
Early B-ALL (pro/pre-pre)
96
CD34
CD19
CD10*
cCD22
TdT
Intermediate (common) B-ALL
97
CD19
cCD22
TdT (variable)
Pre-B-ALL
98
CD19
Surface CD22 (sCD22)
Mature B-ALL
99
mutations involving the NOTCH1 gene
T-ALL (majority of them)
100
B-ALL with the t(9;22); BCR-ABL1 mutation
worst prognosis
101
B-ALL with t(12;21);ETV6-RINX1 translocation
Excellent prognosis in children
102
_______ is common in B-ALLs with good prognosis in children, bad for adults and children
Hyperdiploidy
103
Poor prognosis
More common in adult & late teen males
Frequently seen with mediastinal mass (thymomegaly) in teenage boys
Treated with very aggressive chemo
T-cell ALL
104
Three Chronic Lymphoproliferative Leukemias
Chronic Lymphocytic Leukemia (CLL)
Prolymphocytic Leukemia (PLL)
Hairy Cell Leukemia (HCL)
105
This is the MOST COMMON leukemia occurring in ELDERLY PATIENTS
CLL/SLL (small lymphocytic leukemia)
106
- Many smudge cells in peripheral blood due to marked cytoplasmic fragility (also seen in ALLs)
- Report smudge cells as number per 100 WBCs diffed
CLL/SLL lab findings
107
95% cases are B-cell → CD 5, 19, 20, & 23 +
5% cases are T-cell → CD 2, 4, 5, 6, 8 +
CLL/SLL
108
Most Common Leukemia/lymphoma in Western Hemisphere
CLL/SLL
109
- Malignant, monoclonal proliferation of small lymphoid cells
- Mature-looking, but functionally immature, B cells
- Cells are so immature, they don’t respond to Ag
CD5, CD19, CD20, CD23, IgM and IgD+ B-cells
CLL/SLL
110
_____ involves lymph nodes and organ infiltration
SLL
111
- Lymphs usually appear mature & mostly normal
- Diagnosis based on Monoclonal B-lymphs > 5,000/uL
CLL/SLL
112
Appear “hypermature” → some have “soccer ball” appearance ⚽
CLL/SLL Lab Findings
113
Prognosis based upon genetic mutations
CLL treatment
114
Punched out nucleolus is characteristic finding
Prolymphocytic Leukemia (PLL)
115
Lymph Node involvement is mostly seen with ____
T-cell PLL
116
Rare, mature lymphoid leukemia (both B- and T-cell involvement)
PLL - Prolymphocytic Leukemia
117
Most common in men in their 60’s
Very poor prognosis, mean survival ~3 years w/ B-cell
PLL
118
- Immature-looking, but functionally intermediate maturity, prolymphocyte B cells in peripheral blood
- Large pros, moderately coarse chromatin, 1-2 large nucleoli, agranular & lightly basophilic cytoplasm
PLL
119
- Absolute lymphocytosis in peripheral blood
- ALC = 25,000 - 1,000,000/uL
- Cells will look more mature than lymphoblasts, but yet more immature than a regular “resting lymph”
- CD20, CD19, CD22, and FMC7
PLL Lab Finding
120
Acute onset of common symptoms
Also gross splenomegaly with sweats, fevers, and weight loss
PLL Clinical Symptoms
121
Presence of sweats and fevers in PLL make it important to rule out _____
HIV
122
- Malignant, monoclonal proliferation
- Atypical-looking, but functionally intermediate to fully mature, B-cells, in with “hair” cytoplasmic projections
Hairy Cell Leukemia (HCL)
123
- RARE → accounts for only 2% of all leukemias
- More common in middle-aged men
HCL
124
Characteristic pancytopenia & “dry tap” on bone marrow aspiration
HCL
125
Cells contain unusual isoenzyme of acid phosphatase that is not inhibited by tartaric acid → Tartrate-Resistant Acid Phosphatase, or TRAP
HCL
126
______ are TRAP +
Hairy Cells
127
PAS, SBB, and MPO → negative
Positive for CD19, CD20, CD22, CD25, and CD103
HCL
128
- Malaise and fatigue
- Hugely enlarged spleen → in 90% of the patients
HCL Clinical Symptoms
129
- Considered completely incurable in the past
- Now, however, its relatively easy to control with chemotherapy and splenectomy
- Good remission rates possible
HCL Treatment
130
Preponderance of immature cells. You see a gap in the normal maturation process in the bone marrow.
Acute Leukemia
131
- All stages of maturation seen, with predominantly mature cells
- Insidious onset
- Lengthier, less aggressive disease pattern
Chronic Leukemia
132
Sudden onset
Short, aggressive disease pattern
Lots of infections & hemorrhaging
Acute Leukemia
133
- FAB defines by > 30% blasts in bone marrow
- WHO defines by > 20% blasts in bone marrow (-blastic)
Acute Leukemia
134
- FAB defines by <30% blasts in bone marrow
- WHO defines by < 20% blasts in bone marrow (-cytic)
Chronic Leukemia
135
Chronic sometimes turns into acute! → Called ____
blast crisis
136
- Historically most used, but really inadequate except for differentiating acute vs. chronic
- Cannot really be used by itself
Morphologic review of bone marrow
137
What we use in the lab, but of limited diagnostic utility. Cannot ever be used by itself – send out for path review.
Morphological review of peripheral blood smears
138
Historically very useful
Identifies specific molecules in malignant cells that are associated with specific cell lines
Example → lipids, enzymes
Giving way to immunophenotyping & cytogenetic analyses
Cytochemical stains (Ex. → NSE, LAP, etc.)
139
Via fluorescent Abs
Used for specific cell lineage and/or specific maturation stage markers
Immunophenotyping
140
Markers may be:
Surface
Cytoplasmic
Nuclear
141
the “Supreme Court of Diagnosis”
Cytogenetic & molecular analyses
142
- Karyotyping
- FISH (Fluorescence in Situ Hybridization)
- PCR
Cytogenetic & molecular analyses
143
Molecular remission” = PCR _____
Negative
144
- Excellent for microdeletion syndromes (caused by mismatch during crossing over)
- Example → some a-thalassemias, DiGeorge Syndrome
FISH (Fluorescence in Situ Hybridization)
145
- yields quantitative results; old favorite technique
- Normal gene rearrangement →NO (malignancy)
- Positive translocation → YES (malignancy)
PCR
146
can use any sample type
FISH
147
microscopic whole chromosome analysis
Karyotyping
148
4 major types of leukemia
ALL
CLL
AML
CML
149
- Myelocytic/Myelogenous
- Promyelocytic
- Monocytic
- Myelomonocytic (AMML)
- Erythrocytic (AEL)
- Megakaryocytic (AMegL)
AML
150
- T-Lymphocytic
- B-Lymphocytic
- Null Cell
ALL
151
- Myelocytic/Myelogenous (CML)
- Myelomonocytic (CMML)
Chronic Myeloid
152
- Lymphocytic (CLL)
- Plasmacytic
- Hairy Cell (HCL)
- Prolymphocytic (PLL)
Chronic Lymphoid
153
a chromosome number that is abnormal
Aneuploid
154
- Produces unstable ions that damage cancer cells’ DNA
- Used for localized malignancies
Radiotherapy (“radiation”)
155
- Used to support cancer patients
- Allow for more efficient and effective delivery of chemotherapy regimens by preventing delays or dose reductions due to low blood counts
- Examples are colony stimulating factors 7 EPO
Supportive Therapy
156
Monoclonal antibodies which bind directly to affect cell, activates complement, and cell lysis
Targeted Therapy
157
- Typically given IV in conjunction with antibiotics; for diffuse malignancies
- Drugs can be classified by their effects on the cell cycle and by their biochemical mechanism of action
Chemotherapy
158
- of complete remission
- Normal bone marrow cellularity - < 5% blasts
Induction
159
low dose chemo. To prevent recurrence
Consolidation
160
of remission
Maintenance
161
Patient should be in good clinical condition & in 1st clinical remission for best results
Bone Marrow or Stem Cell Transplantation
162
- bone marrow overcrowding
- anemia
- thrombocytopenia
- extreme anemia
-neutropenia
Clinical Symptoms of all leukemias
163
______ may actually exacerbate anemia by inadvertently trapping RBCs (sequestration)
Hepatosplenomegaly
164
Due to extreme anemia:
Extramedullary hematopoiesis
165
- Transient, reactive leukocytosis due to infection
- Temporary resemblance of peripheral blood picture to “leukemic picture”
- Severe left shift & very rare nRBCs
Leukmoid Reaction
166
- Presence of both nRBCs & left shift in peripheral blood
- Caused by bone marrow damage from a malignant, “space-occuping lesion”, with consequent extensive extramedullary hematopoiesis
- May be mild or severe, & occurs in CML & in lymphomas
Leukoerythroblastic reaction
167
How do you tell Leukoerythroblatic reaction apart from Leukmoid reaction
LAP (Leukocyte alkaline phosphatase) stain score
168
LAP
An enzyme found in the secondary granules of neutrophils
169
LAP ____ in early leukemia
↓ Decrease
- because leukemic neutrophils are too abnormal to express the LAP that normal mature bands & segs would
170
Lap ____ in leukemoid reaction due to left shift
↑ Increased
- because there are tons of band & segs full of secondary granules containing LAP, just waiting to attack the infectious invaders – it only looks like leukemia because of the high WBC count.
171
Normal LAP scores
range from 15-170
172
the presence of the BCR/ABL1 gene, or t(9;22), identifies _____
CML
173
t(9;22) is also called
Philadelphia chromosome
174
Hematopoietic sites
Sternum
Skull
Proximal end of large bones
Vertebrae
Illiac crest
175
Fat cell conversion
Yellow marrow
176
Spoke like pattern of venous sinuses and cords of hematopoioetic tissue
Red marrow
177
Process of replacing active marrow by fat tissue during development >> results in restrictive active marrow sites
Retrogression
178
- Patients with solid malignant tumors
- As part of initial workup of increased or decreased RBCs, WBCs, and/or platelets
- As part of differential diagnosis workup for infections that manifest clinically as "fevers of unknown origin"
Three main reasons for a bone marrow evaluation
179
Fat droplets
Bone spicules
Very immature hematopoietic cells
Three findings used to verify bone marrow has been extracted rather than p.b.
180
1. Developing hematopoietic cells
2. Macrophages or histiocytes
3. Megakaryocytes
4. Osteoblasts
5. Osteoclasts
5 normal cells found in bone marrow
181
Part of bone marrow stroma >> specialized bone matrix-synthesizing cells
Rare in normal adult bone marrow
Osteoblasts
182
- Multinucleated cells with ruffed border
- Formed from the fusion of monocytes and macrophages
- Responsible for bone de-mineralization and resorption
Osteoclasts
183
1. Cellularity
2. Differential cell count
3. Type and concentration of abnormal aggregates
4. Number & morphology of megakaryoctyes
5. Presence & degree of fibrosis
6. Presence of abnormal intra- or extracellular material
7. Presence of abnormal changes in bony ultrastructure
7 aspects of routine bone marrow evaluation
184
- Judged as normal
- Increased (hyperplastic)
- Decreased (hypoplastic)
- ALL evaluated on 10x
Cellularity
185
Ratio of fat cells to hematopoietic cells
1:2 in adults normally
186
- Evaluated on 100x oil immersion
- Requires counting 500-100 cells
- After counts M:E ratio ranges from 2:1 -4:1 and is slightly higher in infants
Differential cell count
187
Normal M:E ratio for adults
1.2:1 to 5:1
2:1 to 4:1
188
Normal M:E raio for infants
5:1 - 6:1
189
#1 stain for bone marrow
Wright stain
190
Leukemia is characterized by
unregulated proliferation
191
Abnormal cells originate in ____ and then spread into peripheral blood
bone marrow
192
Leukemias are grouped by ______ and by the maturity of _______ cells.
Cell lineage; affected
193
Leukemias are not localized but are _____ in nature
systemic
194
Preponderance of immature cells. You see a gap in the normal maturation process in the bone marrow. The normal pyramid of cell development instead of many blasts, some mature forms, and a few intermediate stages
Immature cells
195
Acute leukemia has ____ onset
sudden
196
Chronic leukemia has ____ onset
insidious
197
When chronic leukemia turns into acute it is called _______.
blast crisis
