Ch. 6 - Acute and Chronic Leukemias Flashcards

1
Q

What type of leukemia do pts of 0-14 years get?

A

ALL

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2
Q

What type of leukemia do pts of 15-59 years get?

A

AML

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3
Q

What type of leukemia do pts of 40-60 years get?

A

AML/CML

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4
Q

What type of leukemia do pts of >60 years get?

A

CLL

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5
Q

In acute myelogenous leukemia, maturation of the (blank) is arrested

A

granulocyte

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6
Q

Evidence of marrow failure shows as what type of changes in lab work?

A

Anemia
thrombocytopenia
neutropenia
leukocytosis with increased blasts

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7
Q

Evidence of marrow failure shows as what type of clinical symptoms?

A

Fatigue
bleeding/ecchymosis
DIC
monocytic gum infiltration

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8
Q

What is done with a bone marrow BIOPSY>

A

sent to histology

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9
Q

what is done with a bone marrow ASPIRATE?

A
  1. flow cytometry
  2. peripheral smear
  3. cytogenetics including FISH and karyotype
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10
Q

csome issues including t(15;17)(q22;q12) corresponding to FAB M3, presenting in decades 3-5 is what leukemia?

A

Acute promyelocytic leukemia

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11
Q

How quickly does APL replicate?

A

Quickly. That’s how quickly. rapid doubling time, baby.

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12
Q

T/F: APL has low numbers of Auer rods

A

false; large numbers

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13
Q

What is the two item treatment for APL?

A

All-trans retinoic acid (ATRA) and an alkylating agent

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14
Q

T/F: APL has a remission rate above 80%

A

true

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15
Q

T/F: Acute monocytic leukemia presents with large numbers of auer rods

A

false; they are rare

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16
Q

Gum infiltration is common in which leukemia

A

acute monocytic leukemia

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17
Q

How do you Dx Acute monocytic leukemia?

A

immunophenotype

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18
Q

Which leukemia is caused by the t(9;22) BCR-ABL fusion product, aka the PHILADELPHIA CSOME

A

Chronic Myelogenous leukemia

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19
Q

T/F: the chronic phase of AML can last years before converting to a blast crisis

A

true

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20
Q

What are the risk factors that lead to CML?

A

radiation or benzene exposure

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21
Q

T/F: The Philly csome is specific for CML

A

false!!!!

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22
Q

The BCR-ABL fusion protein on the Philly csome produces a constitutively active (blank), leading to dysregulation of proliferation and apoptosis

A

tyrosine kinase

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23
Q

The ABL portion of the fusion protein comes from csome (9/22)

A

9

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24
Q

the BCR portion of the fusion protein comes from csome (9/22)

A

22

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25
Q

The BCR-ABL fusion protein activates what intracellular cascade pathway?

A

STAT pathway

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26
Q

What is the WBC count in CML?

A

> 5

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27
Q

A differential of a pt with CML would show (full/inhibited) granulocyte differentiation

A

full

28
Q

What are the clinical findings of someone with CML?

A

fever, night sweats, wt. loss, splenomegaly, bleeding.ecchymoses

29
Q

CML leads to an increase in (one/all) myeloid products

A

all

30
Q

A blast crisis has greater than (blank) percent blasts

A

20%

31
Q

What is the the cause of death in a blast crisis?

A

hyperviscous blood leading to heart failure, lung infiltrates, kideny injury from rapidly dying cells.

Short story: multi organ failure

32
Q

CML is treated with (blank) type drugs–think about what the Philly csome produces

A

tyrosine kinase inhibitor

33
Q

Gleevec is a drug used to treat (blank)

A

CML

34
Q

With allogenic (stem cell/bone marrow) transplant, 5 year progression free survival of CML is 80-95%

A

stem cell

35
Q

What is the most common leukemia in children?

A

B cell ALL

36
Q

What percent of ALLs are B cell?

A

80-85%

37
Q

75% of B cell ALL cases involve children under the age of (blank)

A

6

38
Q

What two markers do B cell ALLs express?

A

CD10 and tdt

39
Q

B cell ALLs are caused by (differentiated/undifferentiated) lymphoblasts

A

primitive undifferentiated

40
Q

What is the most common secondary site of ALL involvement?

A

THE CNS

also seen in the lymph nodes, spleen, liver and testis

41
Q

What age group gives a favorable prognosis for B cell ALL?

A

1-10

42
Q

What genetic markers give a favorable impression for ALL?

A

t(12;22)/ETV/RUNX1

and hyperdiploidy of the cancer cells

43
Q

What type of leukemia often presents with a mediastinal mass?

A

T cell ALL

44
Q

How do T cell ALL markers differ from B cell ALL markers?

A

B cell: CD10 and tdt POS

T cell: CD10 - and tdt +

45
Q

CD3 is a pan-(blank) cell marker

A

T cell

46
Q

(blank) is a clonal B cell neoplasms caused by a light chain restriction

A

chronic lymphocytic leukemia

47
Q

Overall, what is the most common human leukemia?

A

CLL

48
Q

What is the most common leukemia of the elderly?

A

CLL

49
Q

what two markers does CLL express?

A

CD5 and CD23

50
Q

What two markers do the virgin mature B cells express in CLL?

A

CD19 and CD20

51
Q

What is the blast percent in CLL

A
52
Q
Name the disease:
WBC 10-100
small mature lymphs
clumped chromatin/TORTOISE SHELL appearance
Smudge cells
A

CLL

53
Q

T/F: There is a T cell variant of CLL

A

false

54
Q

T/F: CLL warrants aggresive chemotherapy

A

false

55
Q

What drug is given if Tx is warranted for CLL?

A

Chlorambucil

56
Q

A mutated (blank) gene is extremely favorable in CLL with a median survival of 293 months

A

Ig Variable heavy chain– IGVH

57
Q

ZAP-70 and CD38 expression in CLL are (favorable/unfavorable)

A

unfavorable

58
Q

What is the Richter transformation?

A

transition from CLL to DLBCL; median survival less than one year–formation of lymphocytic lymphoma solid tumors

59
Q
What is this disease?
CD11c, CD25, CD103
Neoplasm of memory B cells
Older Caucasian males
Indolent disease
Pancytopenia, monocytopenia
Splenomegaly
A

Hairy cell leukemia

60
Q

What is unique about where hairy cell leukemia sets up shop in the spleen?

A

sequesters in the RED pulp

61
Q

In hairy cell leukemia the bone marrow has a distinct (blank) appearance

A

fried egg

62
Q

The dense (blank) network in hairy cell leukemia leads to a dry tap during bone marrow aspiration

A

reticulun

63
Q

Adult T cell leukemia is caused by what virus?

A

HTLV-1

64
Q

Where is HTLV endemic?

A

Japan, West Afrika, Carribean

65
Q

What cancer has floret or clover leaf cells?

A

Adult T cell leukemia