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House Hemat > Acute Leukemias > Flashcards

Acute Leukemias Flashcards

1
Q

ACUTE LEUKAEMIAS: INTRODUCTION

______ of hematopoietic precursor cells, characterized by the accumulation of _______ in the ______

A

Neoplasms

excess blasts

bone marrow.

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2
Q

ACUTE LEUKAEMIAS: INTRODUCTION

Malignant _______ and _____ of ______ haemopoietic cells.

A

proliferation and accumulation

immature

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3
Q

ACUTE LEUKAEMIAS: INTRODUCTION

They are usually of (slow or rapid?) onset & are (slowly or rapidly?) fatal.

A

Rapid

rapidly

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4
Q

ACUTE LEUKAEMIAS: INTRODUCTION

They are subdivided into acute _______ and acute __________

A

lymphoblastic leukaemia (ALL)

myeloblastic leukaemia (AML).

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5
Q

ALL and AML can be further classified into subtypes

T/F

A

T

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6
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Pathophysiology follows:
1.______ failure due to _________ of its normal elements

2.________ of other _____

  1. leuko______

4.________ symptoms

5.other

A

Marrow failure; infiltration/ replacement

infiltration; organs

Stasis

Constitutional

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7
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Symptoms onset over _____ to ____ typically

A

days to weeks

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8
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Pathophysiology follows:

Marrow failure-

_______
————
________

A

anaemia
thrombocytopenia
neutropenia

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9
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Pathophysiology follows:Infiltration of other organs

-_____,______ ,______ (particularly in ALL): - _____,______ ,_______ , _____ masses (T-ALL)

  • gums: -________(_____ subtype of ____)

-_____ pain especially in children with ____

  • any organ or tissue
A

liver, spleen, lymph nodes; hepatomegaly, splenomegaly, lymphadenopathy

mediastinal

gum hypertrophy; monocytic; AML

bone; ALL

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10
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Pathophysiology follows: leukostasis

•only seen with WBC&raquo_space;____ x 109/L

•in CNS: - ______

• in lungs: - ______,______

A

50

strokes

pulmonary infiltrates, hypoxemia

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11
Q

PATHOPHYSIOLOGY OF CLINICAL FEATURES of Acute leukemias

Pathophysiology follows: Constitutional symptoms

-______,_____are common

-_______ is relatively uncommon

A

fevers, sweats

weight loss

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12
Q

LABORATORY & DIAGNOSTIC INVESTIGATIONS of acute leukemia

Approach:

______ tests
_______ test
_______ tests

A

Initial

Confirmatory

Further

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13
Q

LABORATORY & DIAGNOSTIC INVESTIGATIONS of acute leukemia
Approach

Initial tests: ______ and __________ to determine ______ and the presence of _____

A

Complete blood count

peripheral blood smear

WBC count; blasts

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14
Q

LABORATORY & DIAGNOSTIC INVESTIGATIONS of acute leukemia

Approach

Confirmatory test: _______ and ______ to examine morphology, histochemistry, cytogenetics, and immunophenotyping

A

bone marrow aspiration and biopsy

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15
Q

LABORATORY & DIAGNOSTIC INVESTIGATIONS of acute leukemia

Approach

Further tests: if ______ is suspected (e.g., _____, _____ analysis, biochemistry – renal and liver function tests etc)

A

organ involvement

imaging

CSF

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16
Q

LABORATORY FEATURES: Hematologic indices:

Leukocytes: The white blood cell count (WBC) may be elevated, normal, or low and is a reliable diagnostic marker.

T/F

A

F

It is not

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17
Q

LABORATORY FEATURES : Hematologic indices

Anaemia – usually _____cytic

A

normo

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18
Q

LABORATORY FEATURES : Hematologic indices

Peripheral blood smear: presence of _____

A

blasts

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19
Q

LABORATORY FEATURES: Hematologic indices:

Coagulation studies: to rule out ____ especially in the _____ subtype _______ leukemia.

A

DIC

AML

promyelocytic

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20
Q

Features of acute leukaemia on bone marrow:

__________ marrow

Excess number of ______

A

Hypercellular

blasts

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21
Q

Acute Leukaemia is diagnosed when over _____% of nucleated cells in the bone marrow are blasts.

A

20

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22
Q

Although blasts are often readily identifiable in the peripheral blood, the key investigation to make the diagnosis of acute leukaemia before committing the patient to chemotherapy is __________________________

A

the bone marrow investigation

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23
Q

LABORATORY FEATURES

Bone marrow aspiration & biopsy is also helpful to:

_________ acute leukaemia

Obtain samples for _______

A

Sub-classify

cytogenetic analysis

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24
Q

Bone marrow aspirate and biopsy have only diagnostic value but no prognostic value

T/F

A

F

They have prognostic value in addition to diagnostic value

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25
Q

LABORATORY FEATURES
Other lab findings:
Electrolytes and metabolic markers:

___ PO42-
___ Ca2+
___ K+
___ Lactate dehydrogenase
____ uric acid

A

↑

↓

↑

↑

↑

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26
Q

LABORATORY FEATURES
Other lab findings:

X-ray may show ________ and _________ due to enlargement of the ____ and/or ________ in ALL

A

lytic bone lesions and mediastinal mass

thymus

mediastinal lymph nodes

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27
Q

DISTINCTION BETWEEN ALL
AND AML

Who has Auer rods
Who has cytoplasmuc granules

A

only AML blasts
only AML blasts

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28
Q

DISTINCTION BETWEEN ALL AND AML

-ALL is primarily a (pediatric or adult?) disease

-AML is primarily a (pediatric or adult?) disease

A

pediatric

adult

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29
Q

DISTINCTION BETWEEN ALL AND AML: Histochemistry

PAS
TdT
Myeloperoxidase

A

Positive ; negative
Positive ; negative
Negative ; positive

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30
Q

DISTINCTION BETWEEN ALL AND AML: morphology

Auer Rods
granules
Nucleoli

A

None; present

Coarse; fine

Inconspicuous; fine

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31
Q

ALL

Immunophenotyping by flow cytometry

B-ALL is usualy positive for ??

T-ALL is usualy positive for ???

A

B-ALL is usualy positive for CD10 (CALLA), CD19, and CD20

T-ALL is usualy positive for CD2-CD8, especialy CD3

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32
Q

AML

Immunophenotyping by flow cytometry

A

The majority of subtypes are positive for CD13, 33. 34, 117, and HLA-DR

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33
Q

ACUTE LYMPHOID LEUKAEMIA (ALL)

A malignant transformation of a clone of ___________ cells leading to a proliferation and accumulation of _________.

A

lymphoid stem

lymphoblasts

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34
Q

ALL can occur both in adult and children.

T/F

A

T

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35
Q

_______ is the most common malignancy of childhood constituting about _____% of childhood leukaemias.

A

ACUTE LYMPHOID LEUKAEMIA (ALL)

80

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36
Q

ALL - Aetiology

____________ cause or risk factors in most cases

A

No identifiable

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37
Q

ALL - Aetiology

Environmental risk factors - prior bone marrow damage due to _______, ________ and electromagnetic fields

A

alkylating chemotherapy

ionizing radiation

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38
Q

ALL - Aetiology

Adult T-cell leukemia/lymphoma is linked to infection with ______

A

HTLV

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39
Q

ALL - Aetiology

Genetic or chromosomal factors

•Down syndrome - risk of ALL is ___-___ times higher in patients with Down syndrome

•—————- type 1

•___________

A

10–20

Neurofibromatosis

Ataxia telangiectasia

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40
Q

ALL Classification
Classification may be based on

______
_________
The current ____ Classification (2016)

A

Morphology

Immunological markers -

WHO

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41
Q

ALL Classification
Classification may be based on

Morphology - the __________________ classification of ALL

A

French-American-British (FAB) historical

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42
Q

ALL Classification
Classification may be based on

Immunological markers -

Immunophenotype classification of ALL: based on the ____ (B cell or T cell) and _____ of the leukemic cells

A

origin

Maturity

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43
Q

ALL Classification
Classification may be based on

The current WHO Classification (2016) classifies ALL into subtypes of _________________/________ based on ______ and _______ factors

A

precursor lymphoblastic leukaemia/lymphoma

morphologic and genetic

44
Q

ALL Morphologic classification (FAB)
L1: Blasts are ___genous, (small, larger or large?) , with (scant or prominent?) nucleoli and ___ nucleo-cytoplasmic ratio.

L2: Blasts are (small, larger or large?), ____geneous with (scant or prominent?) nucleoli and _______ cytoplasm

L3: Blasts are (small, larger or large?) with ____philic cytoplasm and cytoplasmic vacuoles

A

homo; small; scant ; high

Larger; hetero; prominent ; more abundant

Large; baso

45
Q

ALL Morphologic classification (FAB)
L1: ___-__% ALL

L2: ____% ALL

L3:____% ALL

A

20-30

70

1-3

46
Q

ALL - Immunologic classification
1. _______ types

2._____ ALL
3. _____ ALL

A

Precursor B-cell

B-cell

T-cell

47
Q

ALL - Immunologic classification
1. Precursor B-cell types

•Pro B (CD ____)

•Early Pre B (CD ___)

•Pre B (CD ____, intracytoplaasmic μ+)

A

10-

10+

10+/-

48
Q

ALL - Immunologic classification

B-cell ALL

  • ____ immunoglobulin (Sig+)

– related to __________ (Mature B-cell ALL)

A

surface

Burkitt’s lymphoma

49
Q

ALL - Immunologic classification

T-cell ALL

  • (CD__/ CD__)

– Adolescent (males or females?) , thymic mass
Early (pro-T) ALL
Intermediate-T ALL
Mature T-cell ALL

A

3; 7+

Males

50
Q

ALL - Incidence

•Common in ____ with incidence highest at ___-___ years.

•The ____, early pre-B (CD10+) is most usual in _____ and has _____ incidence.

•T – ALL has a (male or female?) preponderance.

•In adults, the peak incidence is in those older than ____ years.

A

Children; 3 – 7

cALL; children; equal sex

Male

65

51
Q

Laboratory investigations of ALL

Cytochemical staining: - Strongly ______ PAS stain and ______ sudan black & peroxidase reaction.

A

positive

negative

52
Q

In Laboratory investigations: Biochemical tests for ALL, ______ and ______ tests are preformed as baseline investigations before treatment begins.

A

Renal and liver functions

53
Q

Laboratory investigations of ALL: Radiology

Ultrasound may show organ infiltrates

T/F

A

T

54
Q

ALL – Morphology (FAB ___ ) is the leukemic counterpart of Burkitt’s lymphoma

A

L3

55
Q

ALL – Morphology (FAB L3)

Is endemic in parts of ______

_____ sized cells with ____ colored vacuolated cytoplasm

Express _____ immunoglobulin ____ chain (usually _____)

t(__:__), c-myc oncogene

A

Africa

Large; blue

monoclonal; light; gamma

8:14

56
Q

ALL Cytochemistry

______ for TdT

_______ for Myeloperoxidase

A

Positive

Negative

57
Q

ALL Cytogenetics

90% have ______ abnormality

Hyperdiploidy (>___ chromosomes)

________ (eg t(9;22 )

A

chromosomal

50

Translocation

58
Q

ALL Cytogenetics has no Prognostic significance

T/F

A

F

It does

59
Q

Only B-ALL cells express TdT

T/F

A

F

Both T-ALL and B-ALL cells express TdT (terminal deoxynucleotidyl transferase) a marker present early in T and B cell development.

60
Q

TdT is involved in _______ of the T cell receptor (TcR) and immunoglobulin (Ig) genes.

A

somatic mutations

61
Q

B-ALL variably expresses CD__ , and CD___

A

10

19

62
Q

CD ____ is a a pan-B cell marker.

A

19

And maybe 10?

63
Q

B-ALL cells do not express surface immunoglobulin except _______

A

mature B-ALL.

64
Q

T-ALL cells variably express T-cell related antigens CD___, CD__, CD__, and CD__, in addition to Tdt

A

1a

7

4

8

65
Q

T-ALL cells express the T cell receptor on their surface.

T/F

A

F

They do not

66
Q

ALL Management

_____,______,________

A

Supportive, Definitive & Curative

67
Q

ALL Management

Supportive
Administration of _____,_____,______, and _____

Manage ____________ with ______ and ______ support

______ to prevent ______ and _____ induced nephropathy

A

fluid, antibiotics, red cell and platelet transfusion

side effects of drugs; antiemetics, nutritional support

Allopurinol; hyperuricemia and urate

68
Q

ALL Management

Initial therapy may be complicated by _____ syndrome which is characterized by rapid development of hyper____, hyper____, hyper________, hypo____, ______ nephropathy and acute renal failure.

The patient should therefore be given ______ before starting therapy and be well hydrated.

A

tumour lysis

uricaemia; kalaemia

phosphataemia; calcaemia

uric acid

allopurinol

69
Q

ALL Management Definitive - divided into:
1._____ therapy (Remission induction)
2. ____/_____
3._________
4.______ prophylaxis

A

Induction

Consolidation /Intensification

Maintenance

CNS

70
Q

ALL Management Definitive -

  1. Induction therapy (Remission induction)–

• ____ weekly and ______ daily.

•High dose ______

•Give until ___________ and Patient is clinically ____.

Haematological values return to normal. Less than ___% blasts in the bone marrow. _____ in the peripheral blood.

A

vincristine; prednisolone

chemotherapy

patient goes into full remission; normal

5; No blast

71
Q

ALL Management

Consolidation /Intensification:- it makes use of (low or high?) dose of _____ therapy.
Patient may need a lot of supportive care. Drugs include cytosine arabinoside, daunorubicin, vincristine etc.

A

High

Multidrug

72
Q

ALL Management

Maintenance- ________,_______ for ___yrs in adults and girls and ___ yrs in males.

A

6-mercaptopurine, methotrexate

2

3

73
Q

ALL Management

CNS prophylaxis: ____________ or_________

A

intrathecal methotrexate or radiation.

74
Q

ALL Management

Curative treatment – _______________

A

Allogeneic Stem cell transplantation.

75
Q

ALL is curable in (children or adults ?) but difficult to treat in (children or adults?)

A

Children

Adults

76
Q

ALL Prognosis : Prognostic factors –

Haematological factors - poor with very _____,_______, and ______ involvement

Sex – poor in _____ due to _____ involvement

A

high WBC, low platelet count and CNS involvement

males; testicular

77
Q

ALL Prognosis
Prognostic factors –

Race – Poor in _______

Genetics: Hyperdiploidy (more than ___ chromosomes in metaphase) is associated with a ____ prognosis, while the presence of the _____ chromosome t(9;22);BCR/ABL is associated with a very ____ outcome.

A

blacks

46; better

Philadelphia; poor

78
Q

The Philadelphia chromosome is more frequent in (childhood or adult?) than (childhood or adult?) B-ALL.

A

Adult

Childhood

79
Q

B-ALL is generally a ____ prognosis leukaemia in children.

A

good

80
Q

B-ALL

___% of children with this disease can be cured with multi-agent intravenous, oral, and intrathecal (in the cerebrospinal fluid)

Chemotherapy given over a period of _____ years

The cure rate among adults is (lower or higher?) at about ______%. This is owing to the presence of __________

A

80

three

Lower; 30

less favourable cytogenetics.

81
Q

T-ALL in childhood is not treated as high risk disease

T/F

A

F

It is

82
Q

Prognostic factors in ALL( good , bad)

Age
WBC

A

2-10 years ; less than 2 or greater than 10

10k or less; more than 50k

83
Q

Prognostic factors in ALL( good , bad)

Gender

Type

A

Female; male

L1/CALL; L3/BALL

84
Q

Prognostic factors in ALL( good , bad)

Cytogenetics
Remission
Extra medullary disease

A

Hyperdiploidy; Philadelphia Chromosome, Hypodiploidy

Early; late

Absent; present

85
Q

ACUTE MYELOID LEUKAEMIA (AML)

Accumulation of _____ cells.

A

primitive myeloid

86
Q

ACUTE MYELOID LEUKAEMIA (AML)

A (benign or malignant?) transformation of a clone of myeloid stem cells leading to a proliferation and accumulation of _____.

A

malignant

myeloblasts

87
Q

ACUTE MYELOID LEUKAEMIA (AML)

AML constitutes ____% of adult leukaemias and about _____% of childhood leukaemias.

A

80

15 – 20

88
Q

ACUTE MYELOID LEUKAEMIA (AML)

There are two types of AML:

_______ AML

_______ AML

A

Denovo

Secondary

89
Q

ACUTE MYELOID LEUKAEMIA (AML)

There are two types of AML:
Denovo AML – _______________

Secondary AML – following _____, _____ disorders or following treatment of haematological malignancies with ______ e.g. busulphan, melphalan etc

A

No pre-existing disease

MDS; myeloproliferative

chemotherapy

90
Q

CML can cause AML

T/F

A

T

91
Q

AML - Classification
Classification –Two types of classification exist:

_________ and ______

A

FAB Classification and WHO Classification

92
Q

AML - FAB classification
This is a morphological classification

M0 -_______________ leukaemia

M1 - ______ leukaemia _____
M2 - ______ leukaemia ______

M3 - ______________ leukaemia
M4 - _________ leukaemia

M4Eo - Variant: Increase in abnormal marrow ______
M5 - ______ leukaemia

M6 - _____leukemia (_______ disease)
M7 - ___________ leukaemia

A

minimally differentiated

Myeloblastic ; without maturation

Myeloblastic; with maturation

Hypergranular promyelocytic

Myelomonocytic; eosinophils

Monocytic ; Erythro; DiGuglielmo’s

Megakaryoblastic

93
Q

DiGuglielmo’s disease is ______leukemia( M__)

A

Erythro

M6

94
Q

AML Incidence

The vast majority of AML occur in (children or adults?) ,with the median age being ___ years.
AML represents ___% of all cancer deaths.

A

Adults

60

1.2

95
Q

AML Clinical features is Essentially same as ALL

T/F

A

T

96
Q

AML Haematological investigations is same as in ALL

T/F

A

T

97
Q

AML Laboratory investigations

Lumbar Puncture is frequently done

T/F

A

F

Not done in many cases except when you suspect CNS disease which is commonly seen in M4 and M5.

98
Q

AML’s Biochemical test is As with ALL

T/F

A

T

99
Q

AML Laboratory investigations - diagnosis

Cytochemistry
Periodic acid-schiff (PAS )–______ or _______

Sudan black and peroxidase – ______

Non specific esterase – ______ in ____ and ——-

A

Negative or weakly positive

positive

Positive

M4 and M5

100
Q

AML Laboratory investigations - diagnosis

Immunophenotype – myeloid cells have the following CD – CD ___ & CD ____

A

13

33

101
Q

AML Cytochemistry

Myeloperoxidase -______

TdT -_______

A

Positive

Negative

102
Q

AML Immunology

Positive for myelo/monocytic antigens CD ____ and ___

Negative for B-lineage antigens CD__ and __

Negative for T lineage antigens CD__ and __

A

13 and 33

10 and 19

3 and 7

103
Q

AML M3 (Promyelocytic)

-Neoplastic ____
-____ Auer rods
-treated with _______

A

Promyelocytes

Many

Retinoic acid

104
Q

AML Prognosis

Good
•BM response : ____% blasts after first course
•Age - <___ years

Bad
• BM response -____% blasts after first course.
Age - > ___ years.

A

<5; 60

> 20; 60

105
Q

Most common translocation in ALL

Philadelphia chromosome translocation

Translocation in M3

Translocation in M2

Translocation in L3

A

15:21

9:22

15:17

8:21

8:14

106
Q

Mo morphologicallu resembles ______

A

L2

House Hemat (29 decks)

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