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Haematology > Leukaemias > Flashcards

Leukaemias Flashcards

1
Q

What types of leukaemia are there?

A
  • Acute myeloid leukaemia
  • Acute lymphoblastic leukaemia
  • Chronic myeloid leukaemia
  • Chronic lymphocytic leukaemia
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2
Q

What defines acute leukaemias?

A

They are fast and rapidly progressing, and have the main feature of immature blast cells.

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3
Q

What are the main clinical features of acute leukaemias?

A

As they are failures of the bone marrow, there is a pancytopaenia, causing:

  • Anaemia (pallor, SOB, lethargy)
  • Thrombocytopaenia (bleeding)
  • Neutropaenia (infections)

Other symptoms can be variable:

  • Splenomegaly
  • Hepatomegaly
  • Lymphadenopathy (more in ALL)
  • Skin/gum deposits (more in AML)
  • CNS involvement (more in ALL)
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4
Q

What is the lineage of the cells of the blood?

A

A haematopoietic stem cell can either differentiate into a myeloid stem cell of a lymphoid stem cell. Myeloid stem cells can differentiate into platelets, red blood cells, and white blood cells. Lymphoid stem cells will differentiate into T or B cells.

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5
Q

What is the underlying cause of acute leukaemias?

A

While the actual pathophysiology is largely unknown, there are some appreciated familial conditions and associations (Down’s, chemotherapy, radiotherapy, smoking).

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6
Q

What are the molecular defects in acute leukaemias?

A

Largely, they are a combination of suppression of apoptosis (Type 1), and a suppression of differentiation (Type 2).

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7
Q

What is the epidemiology surrounding AML?

A

This is more commonly a disease of adulthood, with increasing age indicating a worsened prognosis.

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8
Q

What is acute promyelocytic leukaemia?

A

It is caused by a translocation of chromosomes 15 and 17. It is associated with DIC and fibrinolysis. On microscopy, multiple Auer rods can be seen in the cytoplasm of the blast cells.

This can be cured.

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9
Q

What investigations are performed for any case of acute leukaemia?

A
  • Bloods: FBC, U&Es, LFTs
  • Microscopy +/- cytochemistry
  • Immunophenotyping and flow cytometry
  • Cytogenetics/molecular genetics
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10
Q

What would investigations show for AML?

A
  • High white cell count (blasts)
  • Auer rods and granules on microscopy
  • Flow cytometry: CD34, MP
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11
Q

On flow cytometry, what does CD34, CD3, CD19 and MPO mean?

A

CD34: precursor cells/stem cells
CD3: B cells
CD19: T cells
MPO: myeloid peroxidase (myeloid cells)

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12
Q

What are the treatment principles of AML?

A

Chemotherapy is used, usually for 4-5 courses. If they have acute promyelocytic leukaemia, ATRA is used as a cure.

Supportive measures are given as well (blood products, antibiotics, allopurinol, fluids, electrolytes)

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13
Q

What is the prognosis of AML?

A

There is a 30-40% 5yr survival

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14
Q

What is the epidemiology surrounding ALL?

A

This is the most common cancer in children.

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15
Q

What would investigations show for ALL?

A
  • High white cell count (blasts)
  • High lymphocytes or precursors
  • Flow cytometry: CD34 and CD3/CD19
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16
Q

What are the treatment principles for ALL?

A

Remission Induction:
- Chemotherapy with steroids

Consolidation:
- Multiple chemotherapy agents to maximise effects

Maintenance:
- 2 years for girls and adults, 3 years of boys (testes act as a store)

CNS treatment as leukaemia can extend into CSF

Supportive measures are given as well (blood products, antibiotics, allopurinol, fluids, electrolytes)

17
Q

What is CLL?

A

Chronic lymphocytic leukaemia a cancer causing a very high lymphocyte count, that is more chronic than ALL.

18
Q

What is the epidemiology surrounding CLL?

A

It mainly affects the elderly (>65) and affects males more than females

19
Q

What are the clinical features of CLL?

A
  • May be asymptomatic and found on routine bloods (80% of cases)
  • Symmetrical painless lymphadenopathy
  • BM failure: anaemia, infection, bleeding
  • B symptoms: weight loss, fever, night sweats
  • Autoimmunity: AIHA, ITP
  • Can progress to lymphoma (Richter’s transformation DLBC)
20
Q

What investigation results can be found on patients with CLL?

A
  • A very high lymphocyte count: >5
  • A low serum immunoglobulin
  • Smear cells
  • Abnormal BM (lymphocyte replacement)
21
Q

What are the good and bad prognostic factors for CLL?

A

Good:

  • Hypermutated immunoglobulin gene
  • Low ZAP-70 expression
  • 13q14 deletion

Bad:

  • Raised LDH
  • CD38 positive
  • 11q13 deletion
  • p53 deletion
22
Q

What in the Binet staging of CLL?

A

Stage A:

  • <3 nodes affected
  • High WBC
  • Usually no treatment is required here

Stage B:
- >3 nodes affected

Stage C:
- Anaemia or thrombocytopaenia

Stage C has lower survival

23
Q

What are the treatment principles of CLL?

A

Supportive:
- Vaccines (flu, pneumo, HiB)

Watchful waiting until:

  • Lymphocyte doubling in <6 months
  • BM failure
  • Severe lymphadenopathy
  • B symptoms
  • Autoimmune cytopaenia

Tyrosine Kinase inhibitors:
- Ibrutinib

24
Q

What is CML?

A

Chronic myeloid leukaemia, where there is proliferation of the myeloid cells.

25
Q

What is the epidemiology surrounding CML?

A

It affects the middle aged and men are more at risk. It usually affects those aged 40-60 and carries a mean survival of 3-5 years.

26
Q

What are the clinical features of CML?

A
  • Usually found on routine examination
  • Lethargy
  • Thrombotic event/sudden blindness
27
Q

What investigation results are found in CML?

A
  • Philadelphia chromosome positive t(9;22)
  • BCR-ABL fusion gene
  • WBC (neutrophilia to above 50)
  • Hb and platelets are preserved
  • Hypercellular BM with immature and mature cells
28
Q

What are the phases of CML?

A

Chronic phase:

  • <5% blasts, WBC slowly increase over years
  • Imatinib is extremely effective here
  • Prognosis 3-5 years

Accelerated phase:

  • Blasts 10-19%
  • Manifestations: splenomegaly
  • Less responsive to therapy
  • Prognosis 9-12 months

Blast phase:

  • Blast cells >20%
  • Resembles acute leukaemia
  • Possible try SCT
  • Prognosis 3-6 months
29
Q

What are the treatment options for CML?

A

1) Imatinib
2) 2nd or 3rd generation tyrosine kinase inhibitors
3) Allogeneic stem cell transplant

Haematology (13 decks)

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