Leukaemia Flashcards

1
Q

State the five key aspects of normal haemopoiesis

A
Self-renewal 
Proliferation 
Differentiation 
Maturation 
Apoptosis
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2
Q

How does malignancy arise?

A

Increased proliferation
Lack of differentiation
Lack of maturation
Lack of apoptosis

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3
Q

How does acute leukaemia arise?

A

Proliferation of abnormal progenitors with block of differentiation/maturation

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4
Q

How does chronic myeloid leukaemia arise?

A

Proliferation of myeloid cells but no differentiation/maturation block

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5
Q

What causes leukaemia?

A

Multifactorial

Acquired somatic mutations in regulatory genes (driver mutations)

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6
Q

What do driver mutations do?

A

Select clones and confer a growth advantage

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7
Q

What is a clone?

A

Population of cells derived from a single parent cell

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8
Q

Is malignancy polyclonal or monoclonal?

A

Monoclonal

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9
Q

Name four factors that help determine the subtype of malignancy

A

Lineage
Developmental stage within lineage
Anatomical site
Histology/presentation

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10
Q

What are the two key lineages?

A

Myeloid

Lymphoid

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11
Q

What are the two main anatomical site of haematological malignancy?

A

Blood - leukaemia

Lymph nodes - lymphoma

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12
Q

Describe the characteristics of a high grade tumour

A
Large cells 
High nucleus to cytoplasm ratio 
Prominent nucleoli 
Rapid proliferation 
Rapid progression of symptoms
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13
Q

In acute leukaemia what type of cells are in excess?

A

Blasts

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14
Q

Name two types of acute leukaemia

A

Acute myeloid

Acute lymphoblastic

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15
Q

Describe ALL

A

Disease of primitive lymphoid cells - lymphoblasts. Most common childhood cancer

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16
Q

How will ALL present?

A

Marrow failure - anaemia, infection, bleeding
Leukaemia effects
Bone pain

17
Q

What is meant by leukaemic effects?

A

High count with obstruction of circulation and involvement of areas outwit the marrow/blood

18
Q

Name two common extra-medullary sites

A

CNS, testes

19
Q

Describe AML

A

More common in elderly >60 years old

De novo or secondary

20
Q

How does AML present?

A

Similar to ALL with dominant marrow failure

21
Q

Name two subgroups of AML

A

DIC in acute promyelocytic leukaemia

Gum infiltration

22
Q

What investigations should be done in acute leukaemia?

A
Blood count and film 
Coagulation screen 
D dimer and fibrinogen - DIC 
Bone marrow aspirate
Immunophenotyping 
Cytogenic analysis 
Trephine biopsy
23
Q

What will a blood film of leukaemia show?

A
Reduced Hb
Neutrophils 
Platelets 
Increased WCC
Blasts 
Aner Rods
24
Q

What are Aner rods?

A

Cytoplasmic inclusions seen in AML

25
Q

How does immunophenotyping work?

A

Lineage specific proteins on cell surface

Definitive diagnosis - important for treatment

26
Q

How is leukaemia treated?

A

Multi-agent chemotherapy

27
Q

How long may ALL last?

A

2-3 years

28
Q

How is AML treated?

A

2-4 cycles of chemo followed by 2-4 weeks recovery. Intensive therapy requires prolonged hospitalisation

29
Q

Name the type of long term central venous access used

A

Hickman Line

30
Q

Where is the tip of Hickman Line?

A

SVC - right atrium junction

31
Q

What are the complications of leukaemia treatment?

A

Anaemia
Neutropenia - infections
Thrombocytopenia

32
Q

Which infections are common in leukaemia patients?

A

Gram negative bacteria from large bowel can cause fulminant life threatening sepsis
Fungal infections can also occur

33
Q

After culture what must be done in leukaemia patients with infection?

A

Broad spec antibiotics

34
Q

How will thrombocytopenia present and what is the treatment?

A

Bleeding
Petechiae
Requires platelet transfusion

35
Q

Name the side effects of chemotherapy

A
Nausea/vomiting 
Hair loss 
Liver/renal dysfunction 
Tumour lysis syndrome 
Infection (bacterial, fungal, protozoal - PJC)
Late effects - infertility/cardiotoxic