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Year 3 - Haematology > Introduction to leukemias > Flashcards

Introduction to leukemias Flashcards

1
Q

What are leukemias?

A

A group of blood cancers associated with an increase in white blood cells

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2
Q

What would the Buffy coat look like in someone with a leukemia?

A
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3
Q

What are the acute leukemias?

A

Acute myeloid leukemia (AML)
Acute lymphoblastic leukemia (ALL)

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4
Q

What are the chronic leukemias?

A

Chronic lymphocytic leukemia

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5
Q

What are the malignancies of the primitive compartment?

A

Acute myeloid leukemia (AML)
Acute lymphoblastic leukemia (ALL)
Chronic myeloid leukemia (CML)

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6
Q

What is the malignancy of the less primitive compartment?

A

Chronic lymphocytic leukemia (CLL)

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7
Q

What is the likely diagnosis?

A

Acute leukemia

An excess of blasts in the blood originating from the marrow suggests acute leukemia

Additional support for this diagnosis:
- Reduction in normal cells (Hb/RBC, platelets and neutrophils) suggests absence of maturation
Immunphenotyping can help clarify if AML or ALL

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8
Q

Describe the difference between blast crisis of CML vs the chronic phase

A

Blast crisis - presents as acute leukemia
In chronic phase of CML - differentiation and maturation preserved so there is usually neutrophils and thrombocytosis

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9
Q

What are the missing words?

A

Chronic lymphocytic leukemia

A persistent small to medium sized lymphocytosis for years that is asymptomatic is most likely CLL.

IF there is predominant involvement of lymph nodes with cells that by immunohistochemsitry are identified CLL, then the term lymphoma would be used

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10
Q
A

Untreated chronic lymphocytic leukemia

Indolent low grade lymphoproliferative (lymphoid) disorder that is asymptomatic and stable in many patients with no indication for treatment. In contrast, acute leukemias are rapidly fatal without treatment

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11
Q
A

Autoimmune thrombocytopenia

CLL is known to be associated with autoimmune thrombocytopenia (ITP) in a proportion of patients, and the stability of the remainder of the counts makes a peripheral (autoimmune) reason for thrombocytopenia more likely rather than a central (marrow failure) cause.

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12
Q

What is the pathophysiology of chronic myeloid leukemia?

A

Clonal stem disorder - primitive compartment

Philadelphia chromosome (BCR-ABL1 re arrangement)

In chronic phase - excessive proliferation with maturation

Excessive production of granulocytes and precursors

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13
Q

What change can chronic myeloid leukemia undergo?

A

Blast transformation - when it resembles acute leukemia

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14
Q

Draw out how chronic phase chronic myeloid leukemia behaves and what cells are generated

A
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15
Q

What cancer is seen here?

A

Chronic myeloid leukemia (Chronic phase)

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16
Q

Acute leukemias can be described as what process?

A

Proliferation with blocked differentiation / maturation

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17
Q

Draw out how acute myeloid leukemia would present and what cells would be made

A

Acute myeloid leukemia (proliferation with blocked differentiation / maturation)

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18
Q

What can be seen here?

A
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19
Q

Draw out how acute lymphoblastic leukemia presents and what cells it would make

A
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20
Q

What cancer do we see here?

A

Acute lymphoblastic leukemia (proliferation with blocked differentiation / maturation)

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21
Q

What is the process by which acute leukemia occurs?

A

Rapidly progressive clonal malignancy of the marrow / blood with maturation dfects

Defined as an excess of “blasts” (>=20%) in either peripheral blood or bone marrow

Decrease / loss of normal haemopoeitic reserve

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22
Q

What is the pathophysiology process of acute leukemia?

A

Acute leukaemia is an aggressive clonal malignancy of the bone marrow and therefore blood, with increased proliferation but blocked differentiation of primitive progenitor or stem cells that have undergone leukaemic transformation

As a result, there is an excess of primitive looking cells called blasts that exceed 20% in the blood or bone marrow. Due to the aggressive proliferation of leukaemic cells, normal marrow function suffers and normal blood cell production stops.

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23
Q

What are the types of acute leukemia?

A

Acute myeloid leukemia (AML)
Acute lymphoblastic leukemia (ALL)

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24
Q

What is the pathophysiology of acute lymphoblastic leukemia (ALL)?

A

A malignant disease of primitive lymphoid cells resulting in an excess of lymphoblasts

25
Who does acute lymphoblastic leukemia typically affect?
Most common childhood cancer
26
What is the clinical presentation of acute lymphoblastic leukemia?
Due to marrow failure - anaemia, infections, bleeding Leukaemia effects - high count with obstruction of circulation, involvement of areas outside the marrow and blood (extra-medullary) e.g. CNS, testis Bone pain
27
What is the pathophysiology of acute myeloid leukemia?
Malignant disease of primitive myeloid cells (an excess of myeloblasts)
28
Who does acute myeloid leukemia typically affect?
More common in older age group (>60 years)
29
What is the presentation of acute myeloid leukemia?
Marrow failure - anaemia, infections, bleeding Subgroups of AML have characteristic presentation - coagulation defect (DIC in acute promyelocytic leukemia); gum infiltration
30
What investigations can we do for acute leukemia?
Morphology (blood count and film) Coagulation screen - DIC Bone marrow aspirate, from this: - Morphology - Immunophenotyping by flow cytometry - Cytogenetics & molecular genetics - Trephine (piece of bone)
31
What can we see on morphology of acute leukemia?
White cell count does not always need to be raised, patients may have pancytopenia Reduction in normal cells Presence of abnormal cells (not always seen) Note the abnormal cells ("Blasts") with a high nuclear:cytoplasmic ratio, "open chromatin, nucleolus"
32
What investigation will most patients go if there is suspicion of acute leukemia?
Bone marrow aspiration
33
What would be seen on morphology of acute leukemia from bone marrow aspirate?
And the aspirate will be fixed and stained like a blood film for CLICK morphological assessment. In the image shown CLICK, there are few normal marrow cells as these have been replaced by a monotonous or similar-looking population of cells with high-grade features that I described earlier – so, these cells are large, with a high nucleus: cytoplasmic ratio and prominent nucleoli.
34
What do we do after bone marrow morphology?
Immunophenotyping - by flow cytometry The next step is to work out the lineage of the malignancy and immunophentyping is used to distinguish between acute myeloid and acute lymphoblastic leukaemia even if there are Auer rods present in the blasts. CLICK In this flow-cytometry plot, you will see the expression of CD33, usually a myeloid antigen, with CD34 in the top right quadrant of the graph to indicate an acute myeloid leukaemia.
35
What is CD33 a marker of?
Usually an antigen of myeloid
36
What is CD34 an indicator of?
Usually a sign of acute myeloid leukemia
37
Even if cells from AML and ALL look alike, they will express lineage associated proteins. What investigation is required for a definitive diagnosis?
Immunophenotyping (has large replaced cytochemistry)
38
Why are cytogenetics and molecular genetics (NGS, WGS) used in acute leukemia?
Diagnostic utility Prognostic significance
39
What is trephine used for?
Piece of bone which enables better assessment of cellularity and helpful when aspirate is sub-optimal
40
How do we treat acute leukemia?
Supportive care - blood products, antibiotics Definitive anti-leukemic therapy: multi agent chemotherapy
41
How do we treat ALL?
Can last up to 2-3 years Different phases of treatment of varying intensity Targeted treatments in certain genetic subsets CNS directed treatment Immunotherapy
42
How do we treat AML?
Intensive chemotherapy (3-4 cycles) - prolonged hospitalisation Less intensive therapy (non curative in most)
43
What can be done after chemotherapy in acute leukemia?
Allogenic stem cell transplantation in some
44
What is a Hickman line?
A Hickman Line is a hollow silicone tube which is inserted into one of the large blood vessels through a small cut in your upper chest
45
What are problems of marrow suppression (disease or treatment related)?
Anaemia Neutropenia - infections Thrombocytopenia - bleeding (purpura, petechiae)
46
What bacteria can cause fulminant life threatening sepsis in neutropenic patients?
Gram negative bacteria
47
Bacterial infections are common in bone marrow suppression but what other infections are patients susceptible to?
Fungal infections
48
What are complications of anti leukaemia treatment?
Nausea + vomiting Hair loss Liver, renal dysfunction Tumour lysis syndrome (during first course of treatment) Infection Late effects (loss of fertility, cardiomyopathy with anthracyclines)
49
Describe what infections can happen in patients using anti leukaemia treatment
Bacterial - empirical treatment with broad spectrum antibiotics (particularly covering gram negative organisms) as soon as neutropenic fever Fungal (e.g. aspergillum if prolonged neutropenia and persisting fever unresponsive to antibacterial agents) Pneumocystis jirovecci pneumonia (more relevant in ALL therapy)
50
What chemotherapy can cause cardiomyopathy?
Anthracyclines
51
Is acute leukemia treatment worth the effort?
Many patients will go into remission (<5% marrow blasts with recovery of normal haemopoeisis) Unfortunately remissions may not be durable depending on type of acute leukemia and many patients relapse Some patients die of treatment related toxicity
52
What is the pathophysiology of chronic lymphocytic leukemia?
A clonal (malignant) lymphoproliferative disorder of the mature B lymphoid compartment
53
Describe epidemiology of CLL
Most prevalent type of adult leukemia in some parts of world Median age of diagnosis is 72 years
54
Describe what parts CLL affects
Slower pace of disease than acute leukemia and "low grade", less primitive cells Frequently involves lymph nodes, liver and spleen
55
What are symptoms of CLL?
Often none (Even when WCC is 500 x 10^9/L) Non specific (night sweats, fever, fatigue, weight loss) Related to lymph node or spleen enlargement Related to bone marrow infiltration (Cytopenia) Infections (immunocompromised) Autoimmune cytopenia - Autoimmune haemolysis (direct antibody (Coombs) test positive) - Autoimmune thrombocytopenia (ITP)
56
What transformation can happen in CLL?
Richter transformation to a different lymphoma, often high grade
57
How do we test for CLL?
Morphology Immunophenotyping - for clonal B cell population expressing markers of CLL Genetic testing including TP53 gene mutations Immunoglobulin levels, direct antibody test (DAT) CT - chest, abdomen, pelvis
58
How do we treat CLL?
Supportive care - blood products, antibiotics
59
Kinase inhibitors can cause what side effects
Inhibit platelet function (implications pre surgery / dental work) Be associated with cardiac arrhythmias

Year 3 - Haematology (35 decks)

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