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Hematology II > Leukemias > Flashcards

Leukemias Flashcards

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

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2
Q

“Supreme Court of Diagnosis”

A

Cytogenetic & molecular analyses

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3
Q

ALL

A

Acute lymphoblastic (less specifically, lymphocytic) Leukemia

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4
Q

CLL

A

Chronic lymphocytic leukemia:

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5
Q

AML

A

Acute myeloblastic (less specifically, Myelocytic or Myeloid) Leukemia; aka ANLL (Acute Nonlymphocytic Leukemia)

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6
Q

CML

A

Chronic myelocytic/Myelogenous/Myeloid Leukemia

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7
Q

Acute Myeloid (AML)

A

Myelocytic/Myelogenous
Promyelocytic
Monocytic
Myelomonocytic (AMML)
Erythrocytic (AEL)
Megakaryocytic (AMegL)

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8
Q

Acute Lymphoid (ALL)

A

T-Lymphocytic
B-Lymphocytic
Null Cell (?)

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9
Q

Chronic Myeloid

A

Myelocytic/
Myelogenous (CML)
Myelomonocytic (CMML)

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10
Q

Chronic Lymphoid

A

Lymphocytic (CLL)
Plasmacytic
Hairy Cell (HCL)
Prolymphocytic (PLL)

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11
Q

Hundreds of genetic defects now known to cause cancers. Usually somatic translocations and aneuploidy

A

Genetics

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12
Q

Chemicals causing bone marrow depression and aplasia predispose to leukemia later on (Ex. benzene, chloramphenicol, sulfa drugs, insecticides, antineoplastics)

A

Leukemogens

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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

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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:

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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)

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16
Q

Presence of the BCR/ABL1 gene, or t(9;22), identifies CML

A

Leukemoid reaction vs Leukoerythroblastic reaction

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17
Q

Normal LAP scores

A

range from 15-170

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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

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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.

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20
Q

Process of replacing active marrow by fat tissue during development; results in restrictive active marrow sites

A

Retrogression

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21
Q
  1. In patients with solid malignant tumors
    - Example → lymphomas, carcinomas and sarcomas, with possible “mets” to bone marrow
  2. As part of initial workup of unexplained ↑ or ↓ in RBCs, WBCs, and/or platelets
  3. 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

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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):

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23
Q
  1. Developing hematopoietic cells (blasts of all types, normally at overall 5% cellularity)
  2. Macrophages or histiocytes: large cells, with abundant cytoplasm & debris-filled vacuoles, and irregular, “spreading” shape.
  3. Megakaryocytes: involved in platelet formation through endometriosis
  4. Osteoblasts: part of bone marrow stroma; specialized bone matrix-synthesizing cells
  5. 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:

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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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25
Q

Since _____ is NOT found in lymphoid cells, it is best used for differentiating between AML and ALL!

A

Myeloperoxidase (MPO or MPX)

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26
Q

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

A

Sudan Black B (SBB)

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27
Q

This stain is also best for differentiating AML from ALL

A

Sudan Black B (SBB)

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28
Q

______ faster, but ____ more stable and can be run on older specimens

A

MPO, SBB

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29
Q

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

A

Specific Esterase

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30
Q

Auer rods of AML myelocytes strongly +1 why?

A

Because they’re fused 1° granules and contain SE (specific esterase)

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31
Q

____ (+) in monocytic cells, and T-cells
____ (-) in myeloid cells and megakaryocytes

A

Nonspecific Esterase (alpha-Napthyl Butyrate Esterase, NBE)

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32
Q

The NSEs primarily are used to differentiate _____ leukemias from monocytic ones!

A

Myeloid

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33
Q

More sensitive than NBE
Positive cells show brownish appearance

A

(NAE) Nonspecific esterase (Alpha-Napthyl acetate esterase, NAE)

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34
Q

____ strongly (+) in monocytes, T-cells, and megakaryocytes

A

NAE

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35
Q

“Fluoride inhibition” NaFl inhibits enzymatic activity in ______… other cells are unaffected

A

monocytes

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36
Q

____ stain is positive in these 4 disease states
80% ALL (chunky or block pattern)
CLL
Gaucher’s disease
Some AML (AMol, AEL, AMegL)

A

PAS

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37
Q

stains glycogen

A

Periodic Acid Schiff (PAS)

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38
Q

Used to diagnose Hairy cell Leukemia (HCL) because only these cells strongly + with this modified stain

A

TRAP stain

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39
Q

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 +”.

A

Acid phosphatase (ACP)

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40
Q

Positive cells show red ppt. With fast red violet stain; show black ppt. With fast blue violet stain

A

Leukocyte Alkaline Phosphatase (LAP)

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41
Q

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)

A

Leukocyte Alkaline Phosphatase (LAP)

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42
Q

Polycythemia vera
Leukemoid reaction
Bacterial infections
3rd trimester pregnancy
Steroid therapy
Chronic granulocytic leukemias
Blast crises
Chronic neutrophilic leukemias
CML w/ infectious
Myelofibrosis

A

Increased LAP (>110)

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43
Q

Late CML
CML in remission
Secondary erythrocytosis

A

Normal LAP

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44
Q

Early CML
PNH
Sideroblastic anemia
Marked eosinophilia
Sickle cell anemia
Improper technique
Myelodysplastic disorders
PNH
Viral infections

A

Decreased LAP <15

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45
Q

ACD
Hemochromatosis
Sideroblastic anemia

A

3 conditions with increased bone marrow [Fe]

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46
Q

Principle: Fe3+ (ferric) + potassium cyanide → ferricyanide (blue-green ppt.)
Used to evaluate RBC Fe stores; reported semi-quantitatively

A

(Perl’s) Prussian blue iron stain

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47
Q

T lymphoblasts and megakaryocytic precursors

A

Acid phosphatase stain

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48
Q

Mature neutrophils

A

Leukocyte alkaline phosphatase (LAP)

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49
Q

Granulocytes; slight in monos

A

Sudan Black B (SBB)

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50
Q

Abnormal blast cells

A

Periodic acid-schiff (PAS)

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51
Q
  • Most common type of adult leukemia (incidence increases with age)
  • All are rapidly fatal if left untreated
  • Involves a defect of HSC (CD34+)
A

Acute Myeloid Leukemia

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52
Q
  • Hyperuricemia due to increased cell turnover
  • Hyperphosphatemia due to cell lysis
  • Hypokalcemia due to progressive bone destruction
A

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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53
Q

abnormal hyperproliferation of bizarre granulocyte and/or monocyte precursors

A

Dysmyelopoiesis

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54
Q
  • Makes up 5% of AMLs; found in children and adults younger than 60 yp
  • WBCs have functional problems (With phago-cytosis and chemotaxis)
A

AML w/ t(8;21) (q22:q22)

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55
Q
  • 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
A

AML w/ t(8;21) (q22:q22)

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56
Q
  • 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
A

AML w/ inv(16)(p13.1p22)

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57
Q
  • Makes up 8% of AMLs
  • Abnormal hypergranular promyelocytes with Auer rods
  • Granules can obscure nucleus with abundant cytoplasm and variable nucleus size and shape
A

AML w/ t(15;17) (q22;q12)- Acute promyelocytic leukemia (APL)

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58
Q

Leukemic cells also have defective retinoic acid receptor (RARa gene), so can be treated with ____

A

ATRA (All Trans Retinoic Acid – Vit A derivitive

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59
Q

ATRA pushes ____ into finishing maturation, thus causing remission!

A

Pros

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60
Q

Unusual susceptibility to bleeding (hemorrhage) due to a defect in the system of coagulation

A

“bleeding diathesis”

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61
Q
  • Strongly associated with DIC
  • A promyelocytes primary granules are rich in thromboplastin-like substances… which trigger a “bleeding diathesis”
A

Acute promyelocytic leukemia (APL)

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62
Q

cells look agranular if only light microscopy used – what subtype of leukemia is this?

A

Microgranular APL

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63
Q

bundles of auer rods

A

faggot cells in Acute Promyelocytic Leukemia

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64
Q
  • 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
A

Lab findings of APL

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65
Q

Peripheral blood absolute monocytosis (>20%); many circulating blasts, pros, immature granulocytes and monos!

A

Acute myelomonocytic leukemia (aka. AMML)

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66
Q
  • 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
A

Acute myelomonocytic leukemia (aka. AMML)

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67
Q

CND and soft tissue involvement
Ex. gum hypertrophy and skin lesions

A

AMML – Acute myelomonocytic leukemia

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68
Q

Usually CD4 and CD64 pos (“gold std.”)

A

Acute monocytic leukemia (aka. AMoL)

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69
Q

Makes up 5-8% of AMLs
When >80% leukemic cells are monocytic

A

Acute monocytic leukemia (aka. AMoL)

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70
Q

Bone marrow shows some granulocytes, but majority composition is monoblasts, promonocytes, and monocytes

A

Acute monocytic leukemia (aka. AMoL)

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71
Q

Increased serum and urinary lysozyme - why?

A

Because this is enzyme found in greatest amounts in monos

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72
Q
  • MPO and SBB +/- (most frequently NEG)
  • Both NSEs pos (NBE 3+!)
  • PAS pos (finally)
  • Very rare Auer rods (most frequently NEG)
A

Acute Monocytic leukemia - AMoL

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73
Q

Makes up only 3% of AMLs
Only AML with marked erythroid precursor hyperplasia

A

Acute erythroid leukemia (AEL)

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74
Q

Leukemia that is frequently preceded by a myelodysplastic syndrome

A

Acute erythroid leukemia (AEL)

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75
Q

abnormal proliferation of bizarre RBC precursors, with reverse M:E ratio due to huge # of abnormal erythroblasts, and even a few ringed sideroblasts

A

dyserythropoiesis

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76
Q
  • Bone marrow shows dyserythropoiesis
  • Peripheral blood- nRBCs with marked aniso, poikilocytosis and schistocytosis due to the dyserythropoiesis
  • Lots of myeloblasts
A

Acute Erythroid Leukemia

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77
Q
  • > 50% bizarre, multinucleated, megaloblastoid nRBCs!! (with few ringed sideroblasts)
  • Both NSEs+
  • PAS +
A

Acute erythroid leukemia

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78
Q

Early, abnormal erythroblasts are PAS + in “______” or “blocky” pattern. Later, abnormal erythroblasts + in “_____” pattern

A

Granular; diffuse

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79
Q

Rarest form of AML!! (makes up <1% of AMLs)
Frequently associated with Down’s syndrome

A

Acute megakaryocytic/megakaryoblastic leukemia (AMegL)

80
Q

dry tap upon bone marrow aspiration due to myelofibrosis

81
Q

⬆ #s of megakaryocyte precursors, include megakaryoblasts, atypical megakaryocytes (with “blebbing”), and giant platelets

A

dysmegakaryopoiesis

82
Q

Few myeloblasts can look lymphoid or undifferentiated
Little accompanying dyserythropoiesis
Can be associated with t(3;21) and t(1;22)

A

AMegL Lab findings

83
Q

MPO and SBB neg
NBE neg., but NAE pos

84
Q
  • May plt.- specific receptors, such as GPIIb/IIIa receptor +
  • Acid phosphatase pos
85
Q

Leukemia that is ACP positive

A

T-Cell ALL

86
Q

Normo- normo- anemia, neutropenia, & thrombocytopenia due to bone marrow overcrowding

A

Acute Lymphoid Leukemia (ALL)

87
Q

increased numbers of smudge cells (>12/100 WBCs)

88
Q
  • Bone pain from infiltration
  • Account for 75% of childhood leukemias
89
Q

Acute Lymphocytic Leukemia can be classified into:

A

B-ALL
T-ALL

90
Q
  • Small size is most common with distinct nucleoli
  • Large type is 2-3 times larger than lymphocyte with distinct nucleoli
A

Morphology of Lymphoblasts

91
Q

CD10 marker

A

Intermediate (common) B-All

92
Q

CALLA - Common Acute Lymphoblastic Leukemia

93
Q

CD2
CD3
CD4
CD5
CD7
CD8
TdT

94
Q

movement of cytoplasmic CD22 to surface (sCD22)

A

Mature B-ALL

95
Q

CD34
CD19
Cytoplasmic CD22 (cCD22)
TdT

A

Early B-ALL (pro/pre-pre)

96
Q

CD34
CD19
CD10*
cCD22
TdT

A

Intermediate (common) B-ALL

97
Q

CD19
cCD22
TdT (variable)

98
Q

CD19
Surface CD22 (sCD22)

A

Mature B-ALL

99
Q

mutations involving the NOTCH1 gene

A

T-ALL (majority of them)

100
Q

B-ALL with the t(9;22); BCR-ABL1 mutation

A

worst prognosis

101
Q

B-ALL with t(12;21);ETV6-RINX1 translocation

A

Excellent prognosis in children

102
Q

_______ is common in B-ALLs with good prognosis in children, bad for adults and children

A

Hyperdiploidy

103
Q

Poor prognosis
More common in adult & late teen males
Frequently seen with mediastinal mass (thymomegaly) in teenage boys
Treated with very aggressive chemo

A

T-cell ALL

104
Q

Three Chronic Lymphoproliferative Leukemias

A

Chronic Lymphocytic Leukemia (CLL)
Prolymphocytic Leukemia (PLL)
Hairy Cell Leukemia (HCL)

105
Q

This is the MOST COMMON leukemia occurring in ELDERLY PATIENTS

A

CLL/SLL (small lymphocytic leukemia)

106
Q
  • Many smudge cells in peripheral blood due to marked cytoplasmic fragility (also seen in ALLs)
  • Report smudge cells as number per 100 WBCs diffed
A

CLL/SLL lab findings

107
Q

95% cases are B-cell → CD 5, 19, 20, & 23 +
5% cases are T-cell → CD 2, 4, 5, 6, 8 +

108
Q

Most Common Leukemia/lymphoma in Western Hemisphere

109
Q
  • 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
110
Q

_____ involves lymph nodes and organ infiltration

111
Q
  • Lymphs usually appear mature & mostly normal
  • Diagnosis based on Monoclonal B-lymphs > 5,000/uL
112
Q

Appear “hypermature” → some have “soccer ball” appearance ⚽

A

CLL/SLL Lab Findings

113
Q

Prognosis based upon genetic mutations

A

CLL treatment

114
Q

Punched out nucleolus is characteristic finding

A

Prolymphocytic Leukemia (PLL)

115
Q

Lymph Node involvement is mostly seen with ____

A

T-cell PLL

116
Q

Rare, mature lymphoid leukemia (both B- and T-cell involvement)

A

PLL - Prolymphocytic Leukemia

117
Q

Most common in men in their 60’s
Very poor prognosis, mean survival ~3 years w/ B-cell

118
Q
  • 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
119
Q
  • 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
A

PLL Lab Finding

120
Q

Acute onset of common symptoms
Also gross splenomegaly with sweats, fevers, and weight loss

A

PLL Clinical Symptoms

121
Q

Presence of sweats and fevers in PLL make it important to rule out _____

122
Q
  • Malignant, monoclonal proliferation
  • Atypical-looking, but functionally intermediate to fully mature, B-cells, in with “hair” cytoplasmic projections
A

Hairy Cell Leukemia (HCL)

123
Q
  • RARE → accounts for only 2% of all leukemias
  • More common in middle-aged men
124
Q

Characteristic pancytopenia & “dry tap” on bone marrow aspiration

125
Q

Cells contain unusual isoenzyme of acid phosphatase that is not inhibited by tartaric acid → Tartrate-Resistant Acid Phosphatase, or TRAP

126
Q

______ are TRAP +

A

Hairy Cells

127
Q

PAS, SBB, and MPO → negative
Positive for CD19, CD20, CD22, CD25, and CD103

128
Q
  • Malaise and fatigue
  • Hugely enlarged spleen → in 90% of the patients
A

HCL Clinical Symptoms

129
Q
  • Considered completely incurable in the past
  • Now, however, its relatively easy to control with chemotherapy and splenectomy
  • Good remission rates possible
A

HCL Treatment

130
Q

Preponderance of immature cells. You see a gap in the normal maturation process in the bone marrow.

A

Acute Leukemia

131
Q
  • All stages of maturation seen, with predominantly mature cells
  • Insidious onset
  • Lengthier, less aggressive disease pattern
A

Chronic Leukemia

132
Q

Sudden onset
Short, aggressive disease pattern
Lots of infections & hemorrhaging

A

Acute Leukemia

133
Q
  • FAB defines by > 30% blasts in bone marrow
  • WHO defines by > 20% blasts in bone marrow (-blastic)
A

Acute Leukemia

134
Q
  • FAB defines by <30% blasts in bone marrow
  • WHO defines by < 20% blasts in bone marrow (-cytic)
A

Chronic Leukemia

135
Q

Chronic sometimes turns into acute! → Called ____

A

blast crisis

136
Q
  • Historically most used, but really inadequate except for differentiating acute vs. chronic
  • Cannot really be used by itself
A

Morphologic review of bone marrow

137
Q

What we use in the lab, but of limited diagnostic utility. Cannot ever be used by itself – send out for path review.

A

Morphological review of peripheral blood smears

138
Q

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

A

Cytochemical stains (Ex. → NSE, LAP, etc.)

139
Q

Via fluorescent Abs
Used for specific cell lineage and/or specific maturation stage markers

A

Immunophenotyping

140
Q

Markers may be:

A

Surface
Cytoplasmic
Nuclear

141
Q

the “Supreme Court of Diagnosis”

A

Cytogenetic & molecular analyses

142
Q
  • Karyotyping
  • FISH (Fluorescence in Situ Hybridization)
  • PCR
A

Cytogenetic & molecular analyses

143
Q

Molecular remission” = PCR _____

144
Q
  • Excellent for microdeletion syndromes (caused by mismatch during crossing over)
  • Example → some a-thalassemias, DiGeorge Syndrome
A

FISH (Fluorescence in Situ Hybridization)

145
Q
  • yields quantitative results; old favorite technique
  • Normal gene rearrangement →NO (malignancy)
  • Positive translocation → YES (malignancy)
146
Q

can use any sample type

147
Q

microscopic whole chromosome analysis

A

Karyotyping

148
Q

4 major types of leukemia

A

ALL
CLL
AML
CML

149
Q
  • Myelocytic/Myelogenous
  • Promyelocytic
  • Monocytic
  • Myelomonocytic (AMML)
  • Erythrocytic (AEL)
  • Megakaryocytic (AMegL)
150
Q
  • T-Lymphocytic
  • B-Lymphocytic
  • Null Cell
151
Q
  • Myelocytic/Myelogenous (CML)
  • Myelomonocytic (CMML)
A

Chronic Myeloid

152
Q
  • Lymphocytic (CLL)
  • Plasmacytic
  • Hairy Cell (HCL)
  • Prolymphocytic (PLL)
A

Chronic Lymphoid

153
Q

a chromosome number that is abnormal

154
Q
  • Produces unstable ions that damage cancer cells’ DNA
  • Used for localized malignancies
A

Radiotherapy (“radiation”)

155
Q
  • 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
A

Supportive Therapy

156
Q

Monoclonal antibodies which bind directly to affect cell, activates complement, and cell lysis

A

Targeted Therapy

157
Q
  • 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
A

Chemotherapy

158
Q
  • of complete remission
  • Normal bone marrow cellularity - < 5% blasts
159
Q

low dose chemo. To prevent recurrence

A

Consolidation

160
Q

of remission

A

Maintenance

161
Q

Patient should be in good clinical condition & in 1st clinical remission for best results

A

Bone Marrow or Stem Cell Transplantation

162
Q
  • bone marrow overcrowding
  • anemia
  • thrombocytopenia
  • extreme anemia
    -neutropenia
A

Clinical Symptoms of all leukemias

163
Q

______ may actually exacerbate anemia by inadvertently trapping RBCs (sequestration)

A

Hepatosplenomegaly

164
Q

Due to extreme anemia:

A

Extramedullary hematopoiesis

165
Q
  • Transient, reactive leukocytosis due to infection
  • Temporary resemblance of peripheral blood picture to “leukemic picture”
  • Severe left shift & very rare nRBCs
A

Leukmoid Reaction

166
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

167
Q

How do you tell Leukoerythroblatic reaction apart from Leukmoid reaction

A

LAP (Leukocyte alkaline phosphatase) stain score

168
Q

LAP

A

An enzyme found in the secondary granules of neutrophils

169
Q

LAP ____ in early leukemia

A

↓ Decrease
- because leukemic neutrophils are too abnormal to express the LAP that normal mature bands & segs would

170
Q

Lap ____ in leukemoid reaction due to left shift

A

↑ 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
Q

Normal LAP scores

A

range from 15-170

172
Q

the presence of the BCR/ABL1 gene, or t(9;22), identifies _____

173
Q

t(9;22) is also called

A

Philadelphia chromosome

174
Q

Hematopoietic sites

A

Sternum
Skull
Proximal end of large bones
Vertebrae
Illiac crest

175
Q

Fat cell conversion

A

Yellow marrow

176
Q

Spoke like pattern of venous sinuses and cords of hematopoioetic tissue

A

Red marrow

177
Q

Process of replacing active marrow by fat tissue during development&raquo_space; results in restrictive active marrow sites

A

Retrogression

178
Q
  • 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”
A

Three main reasons for a bone marrow evaluation

179
Q

Fat droplets
Bone spicules
Very immature hematopoietic cells

A

Three findings used to verify bone marrow has been extracted rather than p.b.

180
Q
  1. Developing hematopoietic cells
  2. Macrophages or histiocytes
  3. Megakaryocytes
  4. Osteoblasts
  5. Osteoclasts
A

5 normal cells found in bone marrow

181
Q

Part of bone marrow stroma&raquo_space; specialized bone matrix-synthesizing cells
Rare in normal adult bone marrow

A

Osteoblasts

182
Q
  • Multinucleated cells with ruffed border
  • Formed from the fusion of monocytes and macrophages
  • Responsible for bone de-mineralization and resorption
A

Osteoclasts

183
Q
  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
A

7 aspects of routine bone marrow evaluation

184
Q
  • Judged as normal
  • Increased (hyperplastic)
  • Decreased (hypoplastic)
  • ALL evaluated on 10x
A

Cellularity

185
Q

Ratio of fat cells to hematopoietic cells

A

1:2 in adults normally

186
Q
  • 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
A

Differential cell count

187
Q

Normal M:E ratio for adults

A

1.2:1 to 5:1
2:1 to 4:1

188
Q

Normal M:E raio for infants

189
Q

1 stain for bone marrow

A

Wright stain

190
Q

Leukemia is characterized by

A

unregulated proliferation

191
Q

Abnormal cells originate in ____ and then spread into peripheral blood

A

bone marrow

192
Q

Leukemias are grouped by ______ and by the maturity of _______ cells.

A

Cell lineage; affected

193
Q

Leukemias are not localized but are _____ in nature

194
Q

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

A

Immature cells

195
Q

Acute leukemia has ____ onset

196
Q

Chronic leukemia has ____ onset

197
Q

When chronic leukemia turns into acute it is called _______.

A

blast crisis

Hematology II (8 decks)

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