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MBChB3 > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

Describe features of acute leukaemia

A
  • Clonal disorder
  • blast proliferation in bone marrow with maturation arrest
  • rapid onset
  • serious compromise of normal marrow constituents (normal counts fall)
  • death within days/weeks if untreated
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2
Q

Causes of leukaemia

A

Largely unknown
- genetics
- antecedent blood disorders
- infection
- chemicals/chemo/radiotherapy

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3
Q

Describe the presentation of acute leukaemia

A
  • rapid onset of symptoms
  • lethargy
  • infection
  • bleeding and bruising
  • bone pain
  • gum swelling
  • lymphadenopathy
  • skin rash
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4
Q

What do the blood results and blood film show in acute leukaemia?

A
  • anaemia
  • neutropenia
  • thrombocytopenia
  • blasts (diagnosis when >20%)
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5
Q

What technique is used to determine the type of leukaemia a patient has?

A
  • flow cytometry
  • Karyotyping
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6
Q

What are the treatment options for acute leukaemia?

A
  • intensive chemotherapy with/without stem cell transplant (for younger patients)
  • low dose chemotherapy
  • supportive care only (for elderly patients or those with major co-morbidities)
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7
Q

What are the effects of chemotherapy?

A
  • high morbidity, bleeding and infection
  • hair loss, infertility, mucousitis
  • prolonged in-patient stays
  • psychological element
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8
Q

Describe a typical presentation of acute lymphocytic leukaemia

A
  • limping child
  • purpuric rash
  • unexplained bone pain
  • lumpy liquid presentation of bone marrow
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9
Q

What is the treatment of acute lymphocytic leukaemia?

A
  • chemotherapy + steroids
  • CNS directed treatment
  • initial aggressive therapy then oral maintenance
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10
Q

What treatment can be given as supportive care for acute leukaemia?

A
  • blood transfusion (helps symptoms and improves QOL)
  • fresh frozen plasma (for coagulopathy)
  • platelet transfusions (to help bleeding)
  • antibiotics
  • growth factors
  • granule yes (refractory infections)
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11
Q

What types of leukaemia patients are considered for bone marrow transplant?

A
  • relapsed patients
  • refractory patients (not in complete remission after 2 cycles of chemotherapy)
  • high risk profile patients
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12
Q

Describe possible presentations for chronic leukaemia

A
  • no symptoms
  • lethargy, night sweats, weight loss
  • symptoms of anaemia
  • lymphadenopathy
  • infection
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13
Q

What determines a diagnosis of chronic leukaemia?

A
  • Clonal population of mature abnormal B lymphocytes above 5x10^9/L
  • expression of surface markers
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14
Q

How are leukaemias staged?

A

BINET system:
- A = less than 3 lymph node groups involved (10y survival)
- B = over 3 nodes involved, liver, spleen (7y survival)
- C = anaemia/thrombocytopenia (2y survival)

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15
Q

What is the effect of a 17p deletion on chronic lymphocytic anaemia?

A
  • causes aggressive disease due to the loss of p53 (important tumour suppressor gene)
  • refractory to chemotherapy treatment
  • may respond to steroids and antibody treatment
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16
Q

What are the possible immune complications of chronic lymphocytic anaemia?

A
  • autoimmune haemolytic anaemia
  • autoimmune thrombocytopenia
17
Q

How does having chronic lymphocytic leukaemia lead to a significant increase in risk of infection?

A
  • hypogammaglobulinaemia (low antibody levels)
  • cell mediated immunity is impaired
  • neutropenia
  • defects in complement activation
18
Q

What are the indications for treatment in chronic lymphocytic leukaemia?

A
  • if symptomatic
  • if signs of bone marrow failure
19
Q

What is the treatment for chronic lymophocytic leukaemia?

A
  • chemotherapy
  • targeted therapy
20
Q

What can be seen in a blood film of a CML patient?

A

Variety of cells at all stages of maturation. Higher nuclear to cytoplasmic ratio in some blood cells.

21
Q

Describe a possible presentation of CML

A
  • asymptomatic
  • weight loss
  • night sweats
  • abdominal discomfort
  • splenomegaly
22
Q

Describe the triphasic process of CML if left untreated

A
  • chronic phase: variety of myeloid precursors, low numbers of blasts and leukaemia cells
  • accelerated phase: more blasts leading to blast crisis (20%)
  • myeloid blast phase
23
Q

Describe the genetic mechanism behind CML

A

When a BCR gene fuses with an ABL gene it encodes an oncoprotein that drives proliferation of myeloid cells in the marrow and upregulates proliferative pathways. BCR-ABL sign for diagnosis.

24
Q

Treatment for BCR-ABL CML

A
  • imatinib: turns off oncogene preventing development of CML
25
Q

What are the possible complications of CML?

A
  • imatinib resistance/tolerance
  • need for 2nd/3rd line TKI inhibitors (type of chemo)
  • accelerated blast phase/blast crisis (if patient presents too late)

MBChB3 (100 decks)

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