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Hugh's MD2 Core Conditions and Presentations > Leukemia > Flashcards

Leukemia Flashcards

1
Q

What is the only way to cure CLL?

A

Allograph

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2
Q

How is flow cytometry used outside of diagnosis?

A

Follow up detection of clearance of leukaemic cells

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3
Q

What is the first line therapy of CLL?

A

FCR

F - Fludarabine

C - Cyclophosphamide

R - Rituximab

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4
Q

How is CML monitored?

A

Measure bcr-abl transcript in blood

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5
Q

What are the second generation tyrosine kinase inhibitors? When are they used?

A

Dasatinib

Nitolinib

Resistant to imatinib

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6
Q

Cytologically, what is unique about APML?

A

Faggot cells with lots of auer rods

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7
Q

What is the common leukaemia in adults?

A

CLL

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8
Q

What is the first line therapy for CML?

A

Tyrosine kinase inhibitors - Imatinib

Virtually eliminated the need for transplantation

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9
Q

How is leukaemia diagnosed on bone marrow?

A

Blasts make up >20% of nucleated cells

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10
Q

What are the three stages of CML?

A

Chronic

Accelerated

Blast

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11
Q

How does risk effect treatment in AML?

A

Good risk don’t require transplant

Adverse risk require transplant

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12
Q

How do you stratify intermediate risk patients from cytogenetics?

A

Molecular testing

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13
Q

What are symptoms of acute leukemia?

A

Symptoms of anaemia - lethargy, SOB, pallor, presyncope

Neutropenia - fever, rigors, infections

Thrombocytopenia - bruising, bleeding

B symptoms - fevers, sweats, weight loss

Lymphadenopathy, hepatosplenomegaly

Symptoms of hyperleucocytosis

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14
Q

How are leukemia classified?

A

Acute vs chronic

Myeloid vs lymphoid

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15
Q

What are auer rods classic of?

A

Acute myeloid leukaemia

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16
Q

How is CLL diagnosed with Ix?

A

Morphology on blood film and marrow

  • Small mature lymphocytes, smear cells
  • Cytopenia

Immunophenotype

  • cells expressing CD5
17
Q

What is the natural history of CML?

A

Chronic phase: asymptomatic, up to 5 years

Accelerated: symptoms develop, cytopenias, hepatosplenomegaly

Blast phase: acute leukaemia, full range of myelo-development present on blood film

18
Q

What is the diagnostic feature of CML?

A

9;22 philadelphia chromosome and BCL-ABL protein

19
Q

The philadelphia chromosome and BCR-ABL phenotype is in which type of leukaemia?

A

CML

20
Q

When is CLL treated?

A

Only when they become symptomatic

(LNs, cytopenias, B symptoms)

21
Q

What is the critical drug used in ALL?

A

L-asparaginase

22
Q

What are the mainstays of treatment on AML in Aus?

A

Cytarabine and anthracycline

1x Induction (high dose)

2x Consoliation (lower dose)

23
Q

Why do you do cytogenetics in CLL?

A

You want to know the genetype as

Because 17p deletion doesn’t response to FCR treatment

And deletion of 13p has an indolent course

24
Q

How does treatment of APML differ from other acute leukaemia?

A

It’s medical emergency

DIC common

25
Q

Which cohort of people get CLL?

A

Elderly

26
Q

How do you investigate acute leukemia?

A

FBE and film

Bone marrow biopsy

Immunophenotyping

Cytogenetics

Molecular studies

27
Q

What is the etiology of leukemia?

A

Mostly unknown

Other risk factors:

  • Previous cytotoxic theray eg adriomycin
  • Ionizing radiation
  • Chemical exposure
  • Infections - adult T cell leukemia lymphoma and HTLV-1 (not common in Aus)
  • Genetic - trisomy 21
  • Rare familial syndromes
28
Q

Which cytogenetic type has the worst prognosis in CLL?

A

17p deletion

Or other TP53 mutation (that isn’t a 17p deletion)

29
Q

How are chronic leukaemias usually diagnosed?

A

On screening FBE for other conditions

30
Q

How do you manage APML acutely?

A

Correct coagulopathy with platelets, cryoprecipitiate and fibrinogen

And all trans retinoic acid (ATRA) and arsenic as soon as possible - this very curative (98%, 5 yearly survival)

31
Q

When is blasts in the peripheral blood normal?

A

Never

Hugh's MD2 Core Conditions and Presentations (67 decks)

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