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Leukaemia (CH) Flashcards

1
Q

What is leukaemia?

A

Uncontrolled proliferation of immature WBCs that then accumulate in the blood or bone marrow

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2
Q

Describe how haematopoietic stem cells –> blood cells (recap)

A
  • multipotential haematopoietic stem cell –> common myeloid progenitor + common lymphoid progenitor
  • common myeloid progenitor –> megakaryocyte (–> thrombocytes), erythrocyte, mast cell, myeloblast (–> basophil, neutrophil, eosinophil, monocyte–>macrophage)
  • common lymphoid progenitor –> natural killer cell (large granular), small lymphocyte –> T lymphocyte + B lymphocyte–>plasma cell
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3
Q

What are the four types of leukaemia?

A
  • acute lymphoblastic leukaemia (ALL)
  • acute myeloid leukaemia (AML)
  • chronic lymphocytic leukaemia (CLL)
  • chronic myeloid leukaemia (CML)

Acute = problem with progenitors
Chronic = problem with mature cells

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4
Q

What are the typical symptoms of leukaemia? (11)

A
  • fatigue
  • weight loss
  • fever
  • pallor
  • ecchymoses
  • petechiae
  • bleeding
  • dyspnoea
  • dizziness
  • palpitations
  • recurrent infections
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5
Q

What does the management of leukaemia generally involve? (2)

A
  • chemotherapy +/- radiotherapy
  • stem cell transplantation
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6
Q

What is acute lymphoblastic leukaemia (ALL)?

A

Lymphoid progenitor cell becomes genetically altered and undergoes uncontrolled proliferation

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7
Q

Who does acute lymphoblastic leukaemia (ALL) occur most in?

A

Children 2-5 years old –> most common malignant disease in children

M>F

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8
Q

What condition increases the risk of acute lymphoblastic leukaemia (ALL)?

A

Down syndrome

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9
Q

What do most patients with acute lymphoblastic leukaemia (ALL) usually have on presentation?

A

Signs and symptoms related to cytopenias (e.g. fatigue, easy bruising) and enlarged lymph nodes

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10
Q

What is acute lymphoblastic leukaemia (ALL) characterised by?

A

Early lymphoid precursors replacing the normal HSCs of the bone marrow and further infiltrating various body organs

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11
Q

What are the clinical features of acute lymphoblastic leukaemia (ALL)? (9)

A
  • bone pain (secondary to BM infiltration)
  • lymphadenopathy
  • hepatomegaly
  • splenomegaly
  • fever
  • testicular swelling
  • anaemia - lethargy and pallor
  • thrombocytopenia - ecchymoses, petechiae, epistaxis, menorrhagia
  • neutropenia - recurrent infections
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12
Q

What distinguishes ALL from AML?

A

Lymphadenopathy and fevers (not seen in AML)

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13
Q

What investigations do we do for acute lymphoblastic leukaemia (ALL)? (3)

A
  • FBC - neutropenia, thrombocytopenia, anaemia (normocytic), leukocytosis
  • peripheral blood smear - lymphoblasts (immature WBCs)
  • bone marrow aspiration and biopsy (confirms diagnosis) - hypercellular marrow with >20% of cells being lymphoblasts
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14
Q

How do we manage newly diagnosed acute lymphoblastic leukaemia (ALL)? (2)

A
  • dexamethasone
  • cyclophosphamide
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15
Q

How do we manage acute lymphoblastic leukaemia (ALL) with positive Philadelphia chromosome?

A

Tyrosine kinase inhibitor (imatinib)

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16
Q

How do we manage acute lymphoblastic leukaemia (ALL) in remission?

A

Cyclophosphamide, stem cell transplant

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17
Q

How do we manage a relapse of acute lymphoblastic leukaemia (ALL)?

A

Salvage chemotherapy (blinatumomab), stem cell transplantation

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18
Q

What is chronic lymphocytic leukaemia (CLL)?

A

Low-grade B-cell lymphoma caused by a monoclonal proliferation of well-differentiated lymphocytes which are almost always B cells

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19
Q

What is the median age at diagnosis of chronic lymphocytic leukaemia (CLL)?

A

70-72 years old - most common leukaemia in adults

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20
Q

What is a rare complication of chronic lymphocytic leukaemia (CLL)?

A

Richter transformation - sudden transformation of CLL into a significantly more aggressive form of large cell non-Hodgkin’s lymphoma

  • lymph node swelling
  • fever
  • weight loss
  • night sweats
21
Q

What cells do you see in chronic lymphocytic leukaemia (CLL)?

A

Smudge cells - remnant of cells that have no identifiable plasma membrane or nuclear structure

22
Q

How is chronic lymphocytic leukaemia (CLL) often found?

A

Incidental finding

23
Q

What are the clinical features of chronic lymphocytic leukaemia (CLL)? (7)

A
  • B symptoms - weight loss, fever, anorexia
  • lymphadenopathy - more marked than CML
  • splenomegaly / hepatomegaly
  • pruritus
  • thrombocytopenia = bleeding
  • recurrent infections (hypogammaglobulinaemia)
  • anaemia - SOB, fatigue
24
Q

Why do patients often have a late diagnosis of chronic lymphocytic leukaemia (CLL)?

A

Many cases remain asymptomatic for a long period of time - incidental finding

25
Q

What investigations do we do for chronic lymphocytic leukaemia (CLL)? (3)

A
  • FBC - persistent lymphocytosis with high % of small, mature lymphocytes, anaemia, thrombocytopenia
  • blood smear - smudge/smear cells (and spherocytes and polychromasia if haemolysis)
  • features on bloods of anaemia - warm AIHA, IgG
26
Q

How do we manage chronic lymphocytic leukaemia (CLL)?

A
  • asymptomatic early stage - watchful waiting
  • advanced/symptomatic - chemotherapy
  • relapse - allogenic stem cell transplant
27
Q

What is acute myeloid leukaemia (AML)?

A

Life-threatening haematological malignancy caused by clonal expansion of myeloid blasts in the BM, peripheral blood and/or extramedullary tissues

28
Q

Who does acute myeloid leukaemia (AML) occur most in?

A

65 years old - most common acute leukaemia in adults

29
Q

What is the most common cause of acute myeloid leukaemia (AML)?

A

Pre-existing haematopoietic disorders e.g. aplastic anaemia, myeloproliferative disorders like polycythaemia vera

30
Q

What usually progresses to acute myeloid leukaemia (AML)?

A

1/3 of myelodysplasia progresses to AML

31
Q

What is seen on cytology in acute myeloid leukaemia (AML)?

A

Auer rods - large pink/red stained needle-like structures

32
Q

What condition is acute myeloid leukaemia (AML) associated with?

A

Down syndrome

33
Q

What are the clinical features of acute myeloid leukaemia (AML)?

A
  • anaemia - fatigue, pallor, weakness
  • neutropenia (despite high WCC) - frequent infection
  • thrombocytopenia - epistaxis, bleeding gums, petechiae, purpura, easy bruising
  • splenomegaly - ‘early satiety’
  • bone pain
34
Q

What investigations are done for acute myeloid leukaemia (AML)?

A
  • FBC - neutropenia, thrombocytopenia, anaemia, leukocytosis
  • peripheral blood smear - myeloblasts (immature WBCs) and Auer rods
  • bone marrow aspiration and biopsy (confirms diagnosis) - >20% blasts, Auer rods
35
Q

How do we manage acute myeloid leukaemia (AML)?

A
  • hydration, hydroxycarbamide, allopurinol
  • chemotherapy, cytarabine, stem cell transplant
36
Q

What indicates poor prognosis in acute myeloid leukaemia (AML)? (3)

A
  • age >60
  • > 20% blasts after first chemotherapy
  • depletion of chromosomes 5 or 7
37
Q

What is chronic myeloid leukaemia (CML)?

A

Overexpression of cells of myeloid lineage, especially granulocytes

38
Q

When is peak incidence of chronic myeloid leukaemia (CML)?

A

50-60 years old

39
Q

What chromosome is seen in chronic myeloid leukaemia (CML)?

A
  • Philadelphia chromosome in >95%
  • reciprocal translocation between chromosome 9 and 22
  • resulting BCR-ABL gene codes for a fusion protein that has tyrosine kinase activity in excess of normal
40
Q

What are the clinical features of chronic myeloid leukaemia (CML)? (5)

A
  • B symptoms - weight loss, fever, night sweats
  • massive splenomegaly
  • anaemia
  • hyperviscosity symptoms - increased thrombotic risk
  • gout
41
Q

What investigations do we do for chronic myeloid leukaemia (CML)? (4)

A
  • FBC - leukocytosis, thrombocytosis, basophilia, eosinophilia, high band cells
  • blood film - left shift (immature granulocytes) –> granulocytosis + myeloblasts
  • decreased leukocyte alkaline phosphatase (LAP)
  • cytogenic testing - for confirmation of Philadelphia chromosome
42
Q

What is the first-line treatment for chronic myeloid leukaemia (CML)?

A

Tyrosine kinase inhibitors (Imantinib)

43
Q

What is a complication of treatment with chemotherapy (leukaemia)?

A

Tumour lysis syndrome: PUKE calcium (E = elevated)

  • hyperPhosphataemia
  • hyperUricaemia
  • hyperKalaemia
  • hypercalcaemia
44
Q

How do we diagnose tumour lysis syndrome?

A
  • PUKe calcium +
  • increased serum creatinine OR
  • cardiac arrhythmia OR
  • seizure
45
Q

What can be used as prophylaxis against tumour lysis syndrome?

A

Allopurinol

46
Q

Give an example of a patient who would need immediate specialist referral for urgent FBC (leukaemia)?

A

0-24 years old with unexplained petechiae or hepatosplenomegaly

47
Q

How can we interpret bloods in leukaemia?

A
  1. look at lymphocytes
  2. look at WBC
  3. others - blasts, bands

E.g.
1. low lymphocytes = AML or CML
2. WBC>100 = chronic = consider CML
3. presence of band cells = confirm CML

48
Q

How can we differentiate between acute and chronic myeloid leukaemias?

A
  • blasts = AML
  • bands = CML
49
Q

Summary of the four types of leukaemia.

A
  • AML - immature myeloid WBCs - anaemia, spontaneous bleeding - adults and children
  • CML - myeloid stem cells - anaemia, low platelets, splenomegaly - rare in children
  • ALL - immature B/T cells and macrophages - disturb BM function - children
  • CLL - lymphoid B/T cell - lymphadenopathy, splenomegaly - over 55s

Year 3 (211 decks)

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