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Hem > 120214 intro to WBC disorders > Flashcards

120214 intro to WBC disorders Flashcards

1
Q

leukemoid rxn

A

benign, exaggerated response to an infec
absolute leukocyte count over 50,000/uL
may involve neutrophils, lymphocytes, or eosinophils

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2
Q

etiology of leukemoid rxn

A 
perforating appendicitus (neutrophils)
whooping cough (lymphocytes)
cutaneous larva migrans-nematodes (eosinophils)
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3
Q

neutrophilia

A

neutrophil count over 7,000/uL

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4
Q

causes of neutrophilia

A

infection
sterile inflam w necrosis (acute MI)
drugs

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5
Q

causes of neutropenia

A

chemo
aplastic anemia
immune destruction (lupus)
septic shock

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6
Q

eosinophilia etiology

A

type I hypersensitivity
invasive helminths
hypocortisolism
neoplasms (Hodgkin’s lymphoma)

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7
Q

basophilia etiology

A

CML (and other chronic myeloproliferative neoplasms)

chronic kidney disease

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8
Q

leukemia

A

proliferation of neoplastic cells primarily in bone marrow and peripheral blood

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9
Q

lymphoma

A

proliferation of neoplastic cells primarily in LNs and extramedullary lymphoid tissue

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10
Q

myeloid neoplasms–list them

A

myeloproliferative neoplasms
meylodysplastic syndromes
acute myeloid leukemia

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11
Q

MPN-what do you see in bone marrow

A

hypercellular with effective hematopoeisis (increased peripheral blood granulocytes, RBCs and/or platelets)

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12
Q

general features of MPN

A

hypercellular bone marrow w effective hematopoeisis
splenomegaly or hepatomegaly

potential for progression (bone marrow fibrosis or acute leukemia)

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13
Q

MPN vs MDS –their similarities

A

both are due to deranged stem cell

both–see hypercellular bone marrow (lot of precursors in bone marrow)

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14
Q

MPN vs MDS-differences?

A

MPN is hypercellular BM with effective hematopoiesis

MDS is hypercellular BM with INeffective hematopoiesis (decreased periph bl counts). why does this happen? b/clonal abnormalities in bone marrow promote cell death

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15
Q

ex of myeloproliferative neoplasms

A

CML, BCR-ABL positive
polycythemia vera
primary myelofibrosis
essential thrombocythemia

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16
Q

BCR-ABL fusion gene produces what?

A

protein with increased tyrosine kinase activity

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17
Q

what cytogenetics is associated with CML?

A

philadelphia chromosome t(9;22) –BCR-ABL

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18
Q

basophilia is seen in

A

CML

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19
Q

therapy for CML

A

BCR-ABL tyrosine kinase inhibitors:

Gleevec (imatinib mesylate)

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20
Q

polycythemia vera

A

increase in RBCs, granulocytes, platelets

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21
Q

what cytogenetics is assoc w polycythemia vera?

A

JAK2 mutation (JAK pathway promotes proliferation and survival)

22
Q

clinical findings for PV

A

splenomegaly
thrombotic events b/c of hyperviscosity
gout (increased uric acid b/c of increased cell breakdown)
signs of increased histamine (mast cells)-ruddy face, pruritis after bathing, peptic ulcer disease

23
Q

lab findings for PV

A

increased RBC mass

decreased EPO

24
Q

primary myelofibrosis

A

rapid development of BONE MARROW FIBROSIS and EXTRAMEDULLARY HEMATOPOIESIS in spleen, liver, LNs

25
Q

clinical findings for primary myelofibrosis

A

splenomegaly

splenic infarcts with left sided pleural effusions

26
Q

what do you see in BM with primary myelofibrosis

A

fibrosis and clusters of atypical megakaryocytes

27
Q

what is assoc w JAK2 kinase mutation

A

PV
essential thrombocythemia
myelofibrosis

28
Q

teardrop cells

A

myelofibrosis

29
Q

essential thrombocythemia

A

neoplastic stem cell disorder with proliferation of megakaryocytes. hypercellular BM with abnormal megakaryocytes

30
Q

peripheral blood of essential thrombocythemia

A

large hypogranular platelets

31
Q

tx for essential thrombocythemia

A

alkylating agents or similar drugs to lower platelet count

32
Q

myeloblasts for myelodysplastic syndromes (peripheral blood or bone marrow)

A

under 20%

33
Q

MDS is due to

A

chromosomal abnormalities in 50% cases

34
Q

findings for MDS

A

cytopenias (uni, bi, or pan)
dysplastic features
hypercellular bone marrow
ring sideroblasts (iron around nucleus)

35
Q

monosomy 7

A

MDS

36
Q

MDS progresses to what in 30% of cases

A

AML

37
Q

therapy for MDS

A

supportive-blood products, antibiotics, growth factors

hypomethylating agents-decitabine, azacitidine

allogeneic stem cell transplant

38
Q

acute leukemia

A

neoplastic proliferation of immature cells (blasts)

39
Q

ALL is most common in

A

children, but may be seen in adults

40
Q

compare AML and ALL blasts

A

see slide 80

41
Q

Auer rods

A

in 60-70% of AML cases

42
Q

how to put cytochemical stains to use?

A

MPO–in myeloblasts

NSE (non specific esterase)–monocytic blasts in AMLs with monocytic differentiation

43
Q

markers of immaturity

A

useful for acute leukemia

CD34 (AML and ALL)
TdT (mostly seen in ALL)
CD117 (AML)
CD1a (restricted to immature T cells)

44
Q

general outcome for AML

A

poor

45
Q

clinical features of AML

A

related to cytopenias–weakness, fatigue, petechiae, infections

46
Q

diagnostic criterion for AML

A

greater than 20% myeloid blasts in blood or marrow

47
Q

acute leukemia–what happens to blasts’ number in BM and blood stream?

A

increased blasts make it harder to have normal hematopoiesis in BM

blasts normally go into the blood stream–causing increased WBC count

48
Q

AML with recurrent cytogenetic abnormalities–prognosis?

A

generally favorable

49
Q

ex of recurrent cytogenetic abnormalities for AML

A

t(8,21)
inv(16)
t(15;17)
the above all have favorable prognoses

11q23 rearrangment–intermediate or unfavorable

50
Q

acute promyelocytic leukemia

A

AML with t(15;17)
Faggot cells (single cells with multiple Auer rods)
there’s risk for DIC
responds to all-trans retinoic acid (ATRA)

51
Q

Langerhans cell histiocytosis

A

histiocytic neoplasm

CD1a, langerin--typical markers
Birbeck granules (tennis racket appearance on EM)
52
Q

hemophagocytic lymphohistiocytosis/hemophagocytic syndrome

A

hyperinflam condition

primary HLH
secondary HLH: EBV, lymphomas

VERY HIGH FERRITIN

Hem (10 decks)

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