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106 Cards in this Set

  • Front
  • Back
fx of reactiv neutrophilia
toxic granulation, vacuolization and dohle bodies
fx of MPD
persistent neutrophilia, basophilia, lack of toxic changes, myelocyte bulge, LAP score increased unless CML where decreased
fx of GM-CSF
leukocytosis (prominent toxic granulation)
abnl nuclear segmentation
morphologically unremarkable heretidary wbc d/o
- Chronic granulomatous disease
– Leukocyte adhesion deficiency
– Myeloperoxidase deficiency
gene mutation in chediak-higashi syndrome
LYST mutation- defect in lysosome formation
which causes ↓ phagocytosis and
defective microtubule polymerization

defect in granules
dz states in chediak-higashi (5)
- Abnormal WBC & LGL cause infections
– Melanosomes cause occulocutaneous albinism
– Neurons cause neuropathy
– Platelets cause bleeding
– Accelerated phase, hemophagocytic-like triggered by viral infection (EBV)
inclusions in chediak-higashi
coarse (large) granules - made of primary and secondary granules
bottom line chediak-higashi
lysomes, LYST, coarse granules, multisystem
myh9 related syndromes
- May Hegglin Anomaly
– Sebastian Syndrome
– Fletchner Syndrome
– Epstein Syndrome
made-hegglin (dohle bodies and enlarged plts)
myh9 disorder fx
getcha early
enlarged plts
hearing loss
alder-reilly anomaly
what is alder reilly anomaly
Dense ametachromatic azurophilic granules in all WBCs, PAS+

"azurophilics retained"
specific diseases where see alder-reilly anomaly
lysozymal enzymes to break down mucopolysaccharides
– Mucopolysaccharidoses (Hurlers, Hunters)
mutations in pelger huet anomaly
Autosomal dominant disorder with lamin B receptor mutation

peLger Buet
what is gaucher
Glucocerebroside Accumulation
Like GAucher
what is niemann-pick
sphIEngomyelin accumulation
hypogranularity of pmn
MDS! or understaining :)
expression of LGLs
what are hematogones and where found; flow results
recovering marrow, peds cases
maturing B cell
CD20, CD10, CD34, Tdt+
how distinguish between ALL and hematogones on flow
hematogones show a range of maturation (both those with CD10 expression and those without); in ALL, all have CD10 expression!!!
hantavirus pulmonary syndrome
Hb concentration, pulmonary edema, increase immunoblastic morphology, lack of toxic granulation,
who gets persisent polyclonal B lymphocytosis
female smokers, HLA-Dr7
pertussis findings in peripheral smear
clefted lymph nuclei, reider cells
molting monocytes
malaria, listeria, tb
if see monocytes and promonocytes and splenomegaly, what should you think
neoplasm (monocytic
cytokine relatively specific for eosinophils
what is loeffler pneumonia
eosinophilic pneumonia
what is churg-strauss syndrome
eosinophilic vasculitis
three fx that distinguish MDS
ineffective hematopoiesis (with a frequently hypercellular marrow)
often see dyspoeisis in myeloid lineage
if see gingival hyperplasia, what should you think of
monocytic leukemia
what are auer rods
fusion of primary (azurophilic) granules
exceptions to 20% rule for blasts
1. M6 - can be made below this threshold
2. certain cytogenetic findings (e.g. t(8;21)
3. Monoblastic leukemias (can include promyelocytes and promonocytes)
in counts, how many are "enough" to count to get blast in marrow and PB
marrow - 500
blood - 200
four most common immunophenotypic markers for AML
HLA-DR (not seen on APML)

usu do not see lymphoid markers but can see 20% have CD7
shared fx of AML with t(8;21) and inv (16)
- younger patients
- good chemo response
- both translocations involve a chain of core binding factor (CBF) - 8;21 has AML1 gene which is CBFa
the inv 16 involves CBFb
morphology of 8:21 blasts (and Ihc)
M2: so AML with maturation; pronounced azurophilic granularity, having large granules and Auer rods

so really interesting ihc that could alone s/o this diagnosis: CD34 (early marker) and aberrant CD15 (late marker)
others: CD34, CD13, CD33 and HLA-Dr (as expect)
if have CD56, worse prognosis
monocytic markers (6!)
CD4, CD11b, CD14, CD24, CD64, CD68
t(8;21) genes
inv(16) genes
less common AML with recurrent translocations
t(9;11) genes
t(6;9) genes
aml with mutated npm1
aml with mutated cebpa
t(9;11) genes: mllt3-mll3
t(6;9) genes: DEK-NUP214
inv 3 RPN1:EV1
erythroid markers
glycophorin and hemoglobin A
megakaryocytic markers
CD42 (gpIb/IX)
CD41 (gpIIb/IIIa)
CD61 (gpIIIa),
CD36 (gpIIIb/IV)
block positivity for lymphoblasts with PAS
three histochemical stains for myeloid markers
-MPO (deteriorates with time)
- NSE (two: alpha napthyl esterase, alpha napthyl butyrate)
- sudan black B (marks lipid)
strict criteria for M4
– >20% blasts including
– >20% neutrophils and precursors
– >20% monocytes and precursors
strict criteria for M5 (acute monoblastic and monocytic leukemia)
>80% of cells are monocytic cells
– M5a-- >80% of monocytic cells are monoblasts
– M5b-- <80% of monocytic cells are monoblasts
strict criteria for M6
Erythroleukemia M6a
> 50% of all nucleated cells erythroid cells
• >20% of non-erythroid cells are myeloblasts
Pure erythroid leukemia M6b (rare)
– >80% erythroblasts
strict criteria for M7
> 20% blasts, 50% are megakaryoblasts
what, with M7 morphology, is excluded from M7 diagnosis
Excludes t(1;22), inv(3), t(3;3) and Down syndrome-related cases
of the three common aml cytogenetics, order them in prognosis
t(15;17) best
strict criteria for M3
> 20% (blasts + abnormal promyelocytes)
what are the variant APML and why do we care
resistant to ATRA
- T(5;17)(q23;q12) • 5 – nucleophosmin gene
– t(11;17)(q13;q21) • 11- nuclear matrix association
– t(11;17)(q23;q21) • 11 – ZBTB16 (previously PLZF)
good: APML, microgranular variant
pertinent fx in t(9;11)(p22q23) AML
involves MLL
monocytic differentiation
often get secondary abnormalities (ex. trisomy 8)
details on t(6;9)(p23q34) AML
poor prognosis
more on inv(3)
• Dysplastic small hypolobated megakaryocytes
more on t(1;22)
• Restricted to infants and children <3 years old
• Megakaryoblasts
name three alkylating agents
Busulfan, chlormabucil, cyclophosphamide
name some topo II inhibitors
timing and prognosis of aml due to alk agents
5-6 years, poor
timing and prog of topo II inhibitors
2-3 years, not related to MDS, better prognosis
often monocytic
various conclusions about aml mutations NPM1 and CEBPA
NPM1 mutation with concurrent FLT-3 wild-type
status is prognostically favorable.
• NPM1 mutation with concurrent FLT-3 mutation is
not prognostically favorable
• CEBPA mutation is prognostically favorable
B-ALL phenotypic markers
• Blasts, TdT and CD34
• B markers: CD19 usually +, CD20 often –
• CD10+/-
• Surface immunoglobulin usually negative
special phenotypic findings with t(4;11) B-ALL
T(4;11) CD10-, CD15+
special phenotypic markers with T(1;19)
CD10+, CD34+ ALL
b cell development
staining for PAX - pattern
staining for Tdt
staining for CD10
staining for CD34
seven (!) B ALL with recurrent translocations
B LBL w t(9;22)(q34;q11.2); BCR-ABL1
2. B LBL w t(v;11q23); MLL rearranged
3. B LBL w t(12;21)(p13;q22);TV6/RUNX1
4. B LBL w hyperdiploidy
5. B LBL w hypodiploidy
6. B LBL w t(5;14)(q31;q32);IL3-IGH
Assoc with eosinophilia
7. B LBL w t(1;19)(q23;p13.3)E2A-PBX1
three good prognostic indicators for BALL
- t(12;21) or ETV6-RUNX6 fusion
• Hyperdiploid > 50
• Age 1-10
5 poor prognostic factors in B-ALL (3 specific)
- Hypodiploid
• t(9:22); BCR/ABL
• 11q23; MLL; t(4;11) MLL/AF4 fusion
• RUNX1 amplification
• Complex abnormalities
infant B-ALL
4-11; "inf"ormation
child ALL translocation
adult B-ALL translocation
T-all location and lab findings
mediastinal mass, hypercalcemia
B-ALL phenotype
CD34, HLA-DR, CD99
often can have dim myeloid ag - don't let that deter you!
ALL with t(1;19) immunophenotype
CD34- CD20-
CD19+, CD9+, CD10+
precursory T ALL immunophenotype
CD34+, CD99+
CD7+ (important)
CD2, CD3, CD5 (either double positive or double neg CD4/8)
note: neg for HLA-DR
progn for 1;19
special immunophenotypic markers and cytogenetics for infant type ALL
t(4;11); CD15+, lack of CD10
what is one of the most specific markers for myeloid derivation
some mutations in T-ALL
affect czomes 7 (BG) and 14 (AD) where tcr are

some partner genes:
Myc (8q24)
– TAL1(1q32)
– RBTN1(11p15), RBTN2 (11p13)
– HOX11(10q24)
mutations in PV
this is the really significant JAK2 dz
Jak2 (V617F) - most and JAk2 (exon 12)
also Tet2 (16%) and IDH1/2 (a/w blast transformation)
peripheral blood findings for PV
-increased rbcs (hct >60%), hb>18.5m, >16.5f, inc mcv
-panymyelosis (increased plts, wbcs)
- teardrop rbcs

(note in BM: hypercellular, megas are big)
fx of ET
most common MPN
- largely restric to megas/plts (large mega, increased plts to >450/600)
stains for ET
CD61 (gbIIIa)
and CD64
mutations for ET
jak2 and mpl
which is the bad myeloproliferative d/o
primary myelofibrosis
findings in primary MF
teardrop rbcs
more mega "atypia"
inreased likelihood of blast transformation
another name for teardrop cells
cytogenetics in CML
i(17q), trisomy 8 and 19

if eosinophilia, PDGRA, B and FGFR
findings in CML
decreased LAP score
myelocyte bulge
sea blue histiocytes
hypolobated megas
basophilia, eos
most common bcr-abl in cml, cnl and all
cml- 210
cnl - 230
all - 190
cytopenias in mds
- Hb <10g/dL, macrocytic anemia
– Neutrophil count <1800/uL
– Platelet count <100,000/uL
some cytogenetics in MDS
-5, 5q-, -7, +8, 20q-, +9, -18, -19, +21
good prognostic markers in MDS
Normal, -Y, del(5q), del(20q), TET2 mutations
poor prognostic markers in MDS
Complex (>3 abnormalities) or chr 7
flow testing for MDS
- Coexpression of CD7, CD56, CD10, CD11b or CD15 on blasts
- Absence of CD33, CD13 or HLADR on blasts
- Abnormal CD56, CD19, CD7 or CD5 on myeloid cells
- hypogranularity of PMNs
- loss of CD13/16 maturation (nike swoop)
findings in mds with isolated 5q-
Hypolated megas & thrombosis
– RPD14 deficiency,
cell lines most affect in childhood refractory cytopenia
-neutropenia and thrombocytopenia
Pediatric MPD/MDS
• Poor prognosis
• increased HbF
• increased sensitivity to GM-CSF
• RAS/NF1/CBL/PTPN11 mutations
who has an increase in JMMoL
• ↑ in patients with neurofibromatosis 1 or
Noonan syndrome