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Semester 5 April > Types of leukaemia > Flashcards

Types of leukaemia Flashcards

0
Q

Classification of acute leukaemia based on..

A 
Morphology
Cytochemistry 
Immunophenotype (flow cytometry)
Genetic abnormalities (karyotype,FISH,PCR)
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1
Q

Define acute leukaemia

A

Presence of at least 20% blasts in the PB or BM

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2
Q

What is most common malignancy in children

A

ALL

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3
Q

Most common secondary leukaemia

A

AML

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4
Q

Morphology in AML

A

Large blasts
Primitive nuclei
Granules
Auer rods

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5
Q

AML cytochemistry

A

Sudan black B pos

MPO pos

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6
Q

AML flow cytometry

A

CD13

CD33

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7
Q

Cytogenetics of AML

A

t(8:21)
t(15:17)
inv(16)

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8
Q

Morphology ALL

A

Scanty cytoplasm
Primitive nuclei
No granules
No auer rods

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9
Q

Cytochemistry of ALL

A

Sudan black neg

MPO neg

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10
Q

Flow cytometry ALL

A

B - CD10, CD 19

T - CD7, CD3

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11
Q

Cytogenetics ALL

A

t(4:11)

t(12:21)

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12
Q

Markers for immature cells

A

CD34

HLA-DR

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13
Q

Myeloid marker

A

CD13

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14
Q

T cell marker

A

CD 2

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15
Q

B cell markers

A

CD 19, CD 10

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16
Q

How to prevent infections

A 
Single room (reverse isolation)
Regular hand washing
Avoid contact with any sick person
No fresh fruit or raw veg
Antibiotics and anti fungal prophylaxis
Careful oral care
Care of IV lines
17
Q

Translocations of Burkitt’s

A

t(8:14)
t(2:8)
t(8:22)

8=myc oncogene
14,2,22 = immunoglobulin chain

18
Q

Types of Burkitt’s

A

Endemic - jaw mass
Sporadic - abdo mass, ascites
Immunodeficiency associated - advanced

19
Q

Egs of chronic myeloproliferative disorders

A

CML
Polycythemia Vera
Essential Thrombocytopenia
Primary myelofibrosis

20
Q

Cytogenetic finding in CML

A

t(9:22) Philadelphia chr

9 - BCR/ABL. 22 - light chain

21
Q

What does increase BCR/ABL cause

A

Increase tyrosine kinase activity
Increased cell proliferation
Decreased apoptosis
Adherence of BM cells to stroma

22
Q

Course of CML

A
  1. Initial chronic stable phase
  2. Accelerated phase
  3. Blast phase
23
Q

Rx of CML

A 
Tyrosine kinase inhibitors (not cure)
BM transplant (cure)
24
Q

Underlying pathology on BCR/ABL neg

A

JAX2 mutation = unregulated proliferation of granulocytes, megakaryocytes and erythrocytes

25
Q

Causes of increased RBC other than PV

A

1ry familial polycythemia
Ectopic EPO production
Chronic tissue hypoxia
Relative - dehydration, burns

26
Q

Lab findings in PV

A

Increase:
RBC, Hb, hematocrit, platelet, blood viscosity

Abnormal megs - hypersegmented nuclei

27
Q

Rx of PV

A

Repeated venesection
Long term warfarin
Aspirin
Cytoreductive agents

28
Q

Course of PV

A

Prodromal, prepolycythemic phase
Overt polycythemic phase
Spent/ postpolycythemic phase

29
Q

Reactive causes of thrombocytosis

A
  1. Infection/inflammation
  2. Chronic haemorrhage
  3. Fe def
  4. Post surgery
  5. Malignancy
30
Q

Why can ET present with bleeding despite increased platelets

A

Platelets are mostly non functional

31
Q

Rx of ET

A

Control platelet count
Cytoreductive agents
Aspirin

32
Q

Define primary myelofibrosis

A

Progressive generalized reactive fibrosis of BM with haemopoiesis in liver and spleen. BM fibrosis due to megakaryocytes proliferation -> PDGF.

33
Q

Course of primary myelofibrosis

A

Prefibrotic phase

Fibrotic phase

34
Q

Rx of primary myelofibrosis

A

Palliative
Reduce anaemia HSM
In kids BM transplant may cure

35
Q

Chronic B cell leukaemic types

A

CLL
Hairy cell leukaemia
B prolymphocytic leukaemia

36
Q

Chronic T cell leukaemic types

A

T prolymphocytic leukaemia
Large granular lymphocytic leukaemia
Adult T leukaemia/Lymphoma

37
Q

Presentation of hairy cell leukaemia

A

Severe infection
Anaemia
Splenomegaly

38
Q

Clinical picture with multiple myeloma

A

BM infiltration - bone pain, fractures, amaemia, infection, bleeding, osteolytic lesions -> renal calcification
Monoclonal proteins - renal failure (high calcium, urea, light chains) hyperviscosity, peripheral neuropathy, amyloidosis, high ESR

39
Q

Diagnosis of multiple myeloma

A 
Monoclonal Ig
Immunotyping
Hence Jones proteins in urine
Many plasma cells in aspirate
(X-ray, ESR)
NB exclude other causes of monoclonal Ig
40
Q

Define amyloidosis

A

Deposition of protein extracellularly that disrupts tissue/organ function.

41
Q

Organs affected by systemic amyloidosis that generally show clinically

A

Heart - failure
Nerves - neuropathy, carpal tunnel
Kidneys - failure
Tongue - macroglossia

Semester 5 April (17 decks)

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