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Heme Midterm 3 > Leukemias > Flashcards

Leukemias Flashcards

1
Q

how do we diagnose leukemias?

A

by whether they are chronic or acute

by what the prominent cell type is and the stage of maturation

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2
Q

what does a bone marrow biopsy give you that is important?

A

architecture and pattern of involvement

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3
Q

T cell CD markers

A

1,2,3,4,5,7,8

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4
Q

CD13/15 cell

A

granulocyte

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5
Q

CD14 cell

A

monocyte

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6
Q

B cell CD markers

A

19,20,21,22,23

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7
Q

CD34 marker

A

stem cell

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8
Q

CD33 marker

A

myeloid

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9
Q

in flow cytometry what does side scatter measure?

A

complexity of the molecule…so if the cell has tons of antigens will have higher side scatter

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10
Q

in flow cytometry what does forward scatter measure?

A

how big is the cell

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11
Q

what can fluorescence tell you in flow cytometry?

A

can be used to label for specific cell markers and determine the cell type based on these

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12
Q

CML

A

chronic myelogenous leukemia

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13
Q

CML classification and disease associations

A

myeloproliferative disorder
P vera
essential thrombocytosis
primary myelofibrosis

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14
Q

what specific cell has gone awry in CML?

A

hematopoietic progentior cell…with a mutation that pushes it to the myeloid side and not lymphoid

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15
Q

common symptoms and presentation of CML

A

fever, weight loss, early satiety, sweats, fatigue

often an asymptomatic patient with high white count

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16
Q

PE findings for CML

A

splenomegaly and hepatomegaly

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17
Q

common lab findings in CML (3)

A

leukocytosis with basophils eosinophils and PMNs
Anemia
thrombocytosis

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18
Q

what will you see on the bone marrow aspirate in CML? and what about biopsy?

A

increased M:E ratio
hypercellular

not much fat…lots of granulocytes

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19
Q

what to see on smear with CML?

A

immature granulocytes and basophilia

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20
Q

what genetic change is required for CML?

A

Philadelphia chromosome…translocation (9;22) Bcr-Abl regions together

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21
Q

how do we see the t(9;22)??

A

either with FISH or cytogenetics (karyotyping)

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22
Q

how else can we pick up the t(9;22)?

A

quantitative PCR for the Bcr-Abl regions

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23
Q

CML phases

A

chronic-3-5 years
accelerated- 6-9 months (luekocytosis, splenomegaly)
blast crisis- survival about 5 months

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24
Q

blast crisis of CML characteristics

A

worsening symptoms with leukocytosis
cytopenias cause issues like anemia and infection
extramedullary diseases

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25
Q

is the blast crisis of CML, AML or ALL?

A

can actually be either because the progenitor cell will pass on to both the myeloid and lymphoid cell lines

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26
Q

best treatment for CML?

A

Abl tyrosine kinase inhibitors…Imatinib mesylate

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27
Q

CLL

A

chronic lymphocytic leukemia

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28
Q

what cell is CLL a malignancy of?

A

mature B cells…homogeneous population of mature B lymphocytes

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29
Q

What is the most common adult leukemia?

A

CLL

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30
Q

risk factor for CLL?

A

having a family member with CLL

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31
Q

symptoms of CLL at presentation

A

fevers, sweats, fatigue, weight loss, early satiety

FREQUENT INFECTIONS

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32
Q

4 lab findings in CLL

A

luekocytosis high lymphocytes
anemia
thrombocytopenia
hypogammaglobulinemia

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33
Q

hypogammaglobulinemia in CLL, why?

A

because malignant B cells are being made and they are not cranking out the good immunoglobulins

34
Q

PE findings for CLL

A

hepatomegaly, splenomegaly and lymphadenopathy

35
Q

autoimmune disorders in CLL

A

autoimmune hemolytic anemia and immune thrombocytopenia

36
Q

smear findings in CLL

A

tons of lymphocytes…diagnostic

37
Q

aspirate findings in CLL

A

lots of maturing lymphocytes, loss of heterogeneity

38
Q

flow cytometry markers for CLL

A

will have one of either kappa or lambda light chains

will have CD5 and CD23 cell markers

39
Q

stage 0 of CLL

A

lymphocytosis…15 yrs

40
Q

stage 1 of CLL

A

lymphocytosis and lymphadenopathy…8 yrs

41
Q

stage 2 of CLL

A

lymphocytosis and splenomegaly…6 yrs

42
Q

stage 3 of CLL

A

lymphocytosis and anemia…3 yrs

43
Q

stage 4 of CLL

A

lymphocytosis and thrombocytopenia…2 yrs

44
Q

what is treatment for CLL?

A

it is not a treatable disease…not curable and if you do treat it is seen to have same outcome as no treatment so dont give the patient toxic drugs for no effect

45
Q

AML

A

acute myeloid leukemia

46
Q

AML cell with issue

A

committed myeloid progenitor cell

47
Q

what happens with myeloid development in AML ?

A

they myeloid cells lose ability to differentiate so you get a homogeneous mixture of myeloblasts

48
Q

what percent blasts do you need for AML classification?

A

20% in blood or bone marrow

49
Q

Auer rods

A

little rod like things seen in myeloblast…MEAN YOU HAVE AML

50
Q

clinical manifestations of AML with blood counts (3)

A

sever anemia, thrombocytopenia and neutropenia

51
Q

Hyperleukocytosis in AML

A

leads to infiltrates on X ray in lung and mental state changes, due to blood stasis

52
Q

how to get AML?

A

can be from MDS or MPD…can be from genetic mutations

treatment related…radiation therapy causes it

53
Q

what is the common good cytogenetic abnormality in AML and common bad one in AML??

A

t(15;17) (PML/RARa)…acute promyelocytic leukemia is good

deletion of chromosome 5 and 7 is bad

54
Q

is AML from MDS or MPD good or bad prognosis?

A

bad

55
Q

is treatment caused AML good or bad prognosis?

A

bad

56
Q

induction treatment for AML

A

7+3
7 days o pyrimidine analog (cytarabine)
3 days of anthracycline

this gives complete remission

57
Q

consolidation treatment of AML, when and what drugs?

A

in younger adults where you want better than just remission…shooting for cure

high dosage of cytarabine for many cycles

58
Q

if you have a high risk AML…what is something to consider if you get patient to remission?

A

allogenic stem cell transplant

59
Q

treatment for APL

A

induction chemo from AML…plus all trans retinoic acid

60
Q

what does all trans retinoic acid do for APL?

A

it releases the block on cell differentiation…allowing myeloid cells to differentiate again

61
Q

FLT3 mutation in AML with normal cytogenetic

A

is a tyrosine kinase…leads to bad prognosis…in lots of de novo AML

62
Q

ALL

A

acute lymphoblastic leukemia

63
Q

ALL cell type affected

A

the committed lymphoid progenitor cell (pre T or B)

64
Q

ALL cell differentiation?

A

ability to differentiate is lost so you get a population of lymphoblasts accumulating

65
Q

Which of the luekemias is the kid cancer?

A

ALL

66
Q

3 risk factors for ALL

A

familial syndromes like downs
prior radiation
prior chemo

67
Q

how does ALL present on blood count?

A

usually leukocytosis with increased blasts in the blood

68
Q

aleukemic in ALL?

A

when marrow is packed and not circulating the lymphocyte blasts into the blood

69
Q

B cell ALL

A

better prognosis than T cell…in kids mainly

70
Q

T cell ALL

A

presents in teenage years with mediastinal mass or soft tissue mass

much higher risk than B ALL

71
Q

5 clinical presentations of ALL

A

anemia, neutropenia, thrombocytopenia, hepatosplenomegaly, tumor lysis syndrome

72
Q

tumor lysis syndrome

A

manifestation of high cell turnover leading to hyperuricemia, hyperkalemia hypocalcemia, high LDH

can lead to uric acid in kidneys and renal failure

73
Q

are lymph nodes invoved in ALL ?

A

yes, more than in AML

74
Q

two common places for ALL to get involved

A

CNS and testicular in males, must prevent CNS relapse with therapy

75
Q

prognosis based on age in ALL

A

if you are less than 1 it is bad, and if you are more than 10 it is bad ( T cell)

76
Q

what white cell count signals bad prognosis in ALL?

A

greater than 50x10^9

77
Q

what is the genetic change with bad prognosis in ALL

A

t(9;22) same as CML, hypodiploidy

78
Q

what is the genetic change with good prognosis in ALL

A

t(12;21) and hyperdiploidy

79
Q

cell markers for ALL

A

CD19 CD10 no surface light chain

TdT

80
Q

What is TdT and why is it a marker for ALL?

A

it is an early marker for lymphocytes so since ALL arrests the lymphoblasts you get these markers present

Heme Midterm 3 (10 decks)

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