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Cancer Care > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

Describe the steps from developing an acute leukaemia to bone marrow failure

A

malignant transformation of haematopoeitic stem cells ——–> cells proliferate but don’t differentiate ——-> accumulation of leukaemic blast cells in marrow —–> marrow failure

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2
Q

What cells are affected by AML?

A

Red Blood Cells
Monocytes
Granulocytes
Megakaryocytes

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3
Q

What cells are affected by ALL?

A

B Cells

T Cells

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4
Q

What do you look for in a cytochemical stain in acute leukaemias?

A

TdT+ in lymphoblasts - ALL

Myeloperoxidase in myeloblasts - AML

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5
Q

What supportive measures are given for all leukaemias?

A

Blood products - irradiated

Allopurinol

GCSF

Antibodies

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6
Q

How is philadelphia + ALL managed?

A

Stem cell transplant

Imatinib

TKI’s - tyrosine kinase inhibitors

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7
Q

What is APL? What genetics is it associated with?

A

Acute Promyelocytic Leukaemia

translocation of chromosome 15 and 17 t(15;17)

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8
Q

How does APL normally present? Describe the pathophysiology of this

A

Younger than AML and it’s other subtypes (age 25 ish)

build up of promyelocytes –> lots of Auer rods –> high coagulation risk –> DIC

Medical Emergency!

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9
Q

How is APL treated?

A

It responds to retinoic acid (ATRA)

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10
Q

What is myelodysplastic syndrome?
What would the bone marrow look like?
How would it present?

A

Condition which is a precursor of AML

Blasts build up in marrow but <20%

Same signs - cytopaenia, bruising etc.

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11
Q

How is myelodysplastic syndrome managed?

A

<5% blasts - conservative management with transfusions and antibiotics

> 5% blasts - treat like AML - chemo or bone marrow transplant

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12
Q

Describe the age presentation of ALL vs AML

A

ALL is childhood (2-5)

AML is adults (65)

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13
Q

How does ALL present?

A 
Penia symptoms 
Bone pain
Hepatosplenomegaly 
Fever
Testicular enlargement 
mediastinal involvement = airway obstruction
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14
Q

What are the blood results in ALL?

A

normocytic, normochromic anaemia
thrombocytopenia
leukocytosis but with neutropenia
reduced reticulocytes

Renal failure: raised K and phosphate

raised LDH

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15
Q

What is the bone marrow like in ALL?

A

hypercellular

blast cell infiltration

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16
Q

On cytochemical staining, what is seen in ALL? Compare this to AML?

A

blasts are TDT+ve

In AML it is myeloperoxidase +ve

17
Q

What are the poor prognostic factors for ALL?

A

male
non white
age <2 or >10
chromosomal translocations eg Philadelphia
high WCC
B or T cell surface makers (seen on immunophenotyping flow cytometry)

18
Q

Describe how anaemia, thromboyctopenia, neutropenia and leukocytosis present

A

anaemia: tired, SOB, pale, weak
thrombocytopenia: bleeding and bruising
neutropenia: recurrent infections
leukocytosis: pro-thrombotic

19
Q

How does AML present?

A 
Similar to AML:
Penia symptoms
Bone pain
Splenomegaly
\+ gingival hyperplasia
\+ purple skin nodules
20
Q

What is seen on the blood film of AML?

A

Blast cells with Auer rods

21
Q

Characteristics of the bone marrow in AML?

A

Hypercellular

>20% Blast cells

22
Q

Poor prognostic features of AML?

A

> 60
20% blasts after first chemo
chromosome deletions

23
Q

What is CLL?

A

a type of low grade B cell non-hodgkins lymphoma

24
Q

How does CLL present?

A 
often asymptomatic and picked up as incidental lymphocytosis
\+ lymphadenopathy
\+ B symptoms
\+ penia symptoms 
\+ splenomegaly
25
Q

What are the blood test results of CLL?

A

Lymphocytosis (Raised WCC)
anaemia
thrombocytopenia

26
Q

What is seen on a blood film in CLL?

A

Smudge/smear cells
Lymphocytosis
NOT blasts

27
Q

What are the complications of CLL?

A

Hyperviscosity = thrombotic events
Warm autoimmune haemolytic anaemia
Hypogammaglobulinaemia = infections
Richter Transformation

28
Q

What is hypogammaglobulinaemia and what does it lead to?

A

It results in a lack of antibodies and therefore infections

29
Q

What is Richter transformation? What is the pathophysiology? How does it present?

A

Transformation of CLL to a high grade lymphoma
Due to leukaemia cells infiltrating the lymph node

SUDDEN deterioration of symptoms

  • B symptoms
  • lymph node swelling
  • abdo pain and nausea
30
Q

How does CML present?

A

Massive splenomegaly = abdo discomfort
B symptoms
Penia symptoms

31
Q

Blood results seen in CML?

A

+++ leukocytosis
normocytic, normochromic anaemia
Thrombocytosis progresses to penia

32
Q

What is seen on a blood film of CML? and what is seen in the bone marrow?

A

Granulocytes at all different stages of development

BM: hypercellular with ++ granulocytes

33
Q

What cytogenetic findings suggest CML?

A

Philadelphia!! Seen in 95% of patients with CML

34
Q

What is the Philadelphia chromosome?

A

Translocation of the long arm of 9 and 22. This leads to a BCR-ABL gene. This codes for +++tyrosine kinase activity

35
Q

How is CML managed?

A

Imatinib: tyrosine kinase inhibitor

Leukophoresis

36
Q

What are the complications of CML?

A

Thrombotic event

Blast transformation to an acute leukaemia

Cancer Care (25 decks)

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