Acute leukemia Flashcards

1
Q

What is acute leukemia

A

A heterogenous group of malignant disorders that is characterised by uncontrotrolled clonal and accumulation of blast cells in the bone marrow and body tissues

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2
Q

Acute leukemias are classified as

A

ALL and AML

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3
Q

A cute lymphoid leukemia mainly occurs in

A

Children and is curable in 70% of them

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4
Q

ALL gender distribution

A

Found in more males than females

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5
Q

All in adults

A

Found less in adults and only curable in minority of them

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6
Q

Acute myeloid leukemia is found mainly in

A

Adults and is curable in minority of them

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7
Q

AML gender distribution

A

M>F

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8
Q

Causes of acute leukemia

A
Idiopathic
Underlying hematologic disorders
Chemicals, drugs
Ionizing radiation
Viruses i.e HTLV 1, EBV,HIV
Heredetary genetic conditions like fanconis anemia, down syndrome, ataxia telangectasia
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9
Q

Pathophysiology of acute leukemia

A

Blast cells are arrested in the early phase from maturation and also begin to proliferate rapidly due to an abnormal expression of genes often as a result of chromosomal translocations.

Blast cells overtake the bone marrow leading to decreased production of other cells causing anemia, thrombocytopenia and neutropenia

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10
Q

invasion of vital organs in AL

A

varies according to subtype

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11
Q

Hyperluekocytosis in AL

A

This occurs due to the uncontrolled increase in the number of blast cells which prevents the increase in other cells lines.

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12
Q

Effects of hyperleukocytosis

A

increase in blood viscosity
predisposes one to microthrombi or acute bleeding
Can cause decreased organ perfusion

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13
Q

IN AL there can be hidden site relapse in

A

testes

meninges

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14
Q

Metabolic manifestations of AL

A

Hyponatremia due to vasopressin released by myeloblast

Hypokalemia due to lysozyme released by myeloblast

Hyperurecimea - due to lysis of leukemic blast cells

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15
Q

Hypokalemia die to lysozyme release usually seen in

A

AML M5

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16
Q

Symptoms of AL

A
Marrow failure
leukostasis
tissue infiltration
constitutional symptoms like fever, weight loss
DIC

Lasts for a short duration

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17
Q

Signs of AL

A
Gum hypertrophy
Lymph adenopathy
Hepatosplenomegaly
petechiae
Confusion
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18
Q

Types of blasts in acute lymphocytic leukemia

A

L1 -85%
l2-14%
L3-1% (Burkitts lymphoma)

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19
Q

L1 blast

A

small homogenous blasts,
single inconspicuous nucleolus
Regular nuclear outline

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20
Q

L2 blasts

A

Larger sized blasts

More pleomorphic

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21
Q

L3 burkitt cell type

A

Basophilic and vacuolated cytoplasm

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22
Q

M3 acute promyelocytic leukemia features

A

Hypergranular;promyelocytes

Auer rods/faggot cells seen

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23
Q

classical M3 FEATURES

A

Hypergranular, 80% leucopeanic (low WBC)

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24
Q

Variant M3 features

A

hypogranular

leokocytosis

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25
Q

GRanules in M3 contain

A

Thromboplastin like Procoagulants leading to massive DIC

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26
Q

Diagnostic feature of M3

A

t(15;17)

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27
Q

M4- acute myelomonocytic leukemia features

A

Monocytes

promonocytes

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28
Q

M4 is involved with the part of the body

A

CNS

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29
Q

Variant M4

A

M4 with eosinophilia

30
Q

Variant M4 prognosis

A

good

31
Q

AML M5 divided into

A

M5a - acute monoblastic leukemia

M5b - acute monocytic leukemia

32
Q

AML associated with

A

Infiltration into gums and skin

33
Q

Variant M4 associated with

A

Deletions and inversions on chromosome 16q

34
Q

Symptoms of AML M5

A

Weakness
bleeding
diffuse erythematous skin rash

35
Q

50% or more of nucleated marrow cells are

A

erythroid precursors and cause M6 erythroleukemia

36
Q

30 % or more of non erythrod cells are

A

myeloblasts

37
Q

Acute megarkaryoblastic leukemia M7 associated with

A

fibrosis of bone marrow

38
Q

M7 blasts have

A

cytoplasmic blebs and pseudopod formation

39
Q

Precursor B cells for ALL

A

t(9,22)

t(11q23)

t(1,19)

t(12,21)

40
Q

Precursor T cell ALL

A

Burkitt-cell leukemia

41
Q

Diagnosis and classification of aml requires

A
morphological assessment
immunophenotyping
cytogenic analysis
molecular analysis
clinical assessment
42
Q

AML definition

A

A type of cancer of the bone marrow with more than 20 percent blast cells

43
Q

WHO classification of AML

A

AML with genetic abnormalities
AML with multilineage dysplasia
AML therapy related
AML not otherwise categorised

44
Q

What distinguishes AML from ALL

A

in light microscopy, AML has auer rods, cytoplasmic granules. ALL doesnt have them

Flow cytometry for immunophenotyping

Special stains

45
Q

Blast size comparison

A

small in ALL large in AML

46
Q

Cytoplasm comparison

A

Scanty in ALL Moderate in AML

47
Q

Chromatin material

A

Dense in ALL, Fine lacy in AML

48
Q

Nucleoli comparison

A

Indistinct in ALL, prominent in Aml

49
Q

AUer rods comparison

A

Found in AML, not founD IN ALL

50
Q

cytochemical staining with peroxidase

A

negative in ALL, positive with AML

51
Q

Periodic acid schiff stain

A

Positive ALL, negative AML

52
Q

Acid phospahtase test is

A

POsitive in all

53
Q

What is immunophenotyping

A

Identification of antigens present on blast cells to identify if leukemia is lymphoid or myeloid

Also differentiates T-ALL and B-ALL

To identify the subtype of leukemia i.e AML-M7 has a specific marker of CD-61

54
Q

Common antigens in AML

A

CD 13,33,117

55
Q

Common antigens in ALL

A
B-ALL
T-ALL
CD-10
CD-19
CD-22
CD-3
CD-7
56
Q

Cytogenics and molecular studies will

A

Detect abnormalities in leukemic clone

And provide prognostic value

57
Q

Cytogenics and molecular studies will

A

Detect abnormalities in leukemic clone

And provide prognostic value

58
Q

A biochemical screening that shows leucocytosis will cause

A

renal impairment

hyperuriceamia

59
Q

chest radiography that shows mediastinal mass

A

present in 70% of T-ALL patients

60
Q

ALL bone lesions seen in

A

childhood

61
Q

Diagnostic feature of AML with maturation M2

A

t(8,21)

62
Q

Diagnostic feature of ALL,CML

A

t(9,22)

63
Q

Diagnostic feature of B-ALL

A

t(8,14)

64
Q

Phases of ALL treatment

A

induction
intensification
CNS prophylaxis
maintenance

last 3 are post remission therapy

65
Q

Phases of ALL treatment

A

Induction

consolidation– post remission therapy

66
Q

Principles of treatment in AL

A
  1. combination chemotherapy ; complete remission and prevent future relapse
  2. supportive care ; transfusion, antibiotics, nutrition
  3. Psychosocial support
67
Q

Age as a poor prognostic factor

A

in ALL if your’e less than 1 and in aml if youre greater than 60

68
Q

total white blood cell count poor prognosis

A

if greater than 50*10^9/L

69
Q

CNS and poor prognosis

A

if present in both AML and ALL though rare in AML

70
Q

Sex and poor prognosis

A

In male who have ALL

IN both male and females who have AML

71
Q

Poor prognostic factors cytogenic

A

for ALL T(9,22)

IN AML monosomy 5,7