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Haematology & Transfer Practice > Introduction to Haematological Malignancies > Flashcards

Introduction to Haematological Malignancies Flashcards

1
Q

What is a malignancy?

A
  • presence of cancerous cells or tumors that have the potential to spread to other parts of the body.
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2
Q

What causes Haemopoiesis

A

Rapidly dividing cells more prone to cytogenetic abnormalities (mutations) during division.
Ionising radiation
Chemicals/drugs
Genetics
Viruses

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3
Q

Consequences of acquired mutations

A
  • Abnormal Maturations
  • Uncontrolled proliferation and abnormal maturation
  • Uncontrolled proliferation: Increased cellular division and reduced cell death
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4
Q

Consequences of uncontrolled proliferation

A
  • Malignant cells crowd out the bone marrow
  • Normal cells cant compete for space of nutrients
  • Reduction in production of normal cells
  • Malignant cells spill out into the peripheral circulation but they are functionally incompetent.
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5
Q

Common features of Anemia

A

Lethargy
Pallor

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6
Q

Common features of Leucopenia

A

Infections

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7
Q

Common features of thrombocytopenia

A
  • Easy bruising
  • Bleeding
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8
Q

Secondary symptoms of hematological malignancies

A

Splenomegaly
Bone pain (myeloma)
Weight loss
Extramedullary haemopoiesis
Night sweats

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9
Q

What kind of proliferation causes acute leukemia?

A

Haemopoietic stem cell with abnormal clones causes proliferation with minimal or no differentiation.

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10
Q

What kind of proliferation causes Myelodysplastic Syndromes?

A

Haemopoietic stem cell with abnormal clones causes proliferation with abnormal differentiation

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11
Q

What kind of proliferation causes Myeloproliferative Disorder?

A

Haemopoietic stem cell with abnormal clones causes proliferation with differentiation

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12
Q

Myeloproliferative Neoplasms

A

Caused by clonal proliferation of haemopoietic cells leading to excess production of one or more cell lines.

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13
Q

Examples of Myleoproliferative Neoplasms (MPs)

A

Polycythaemia vera (PV)
Essential thrombocythemia (ET)
Primary myelofibrosis

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14
Q

What can MPs turn into

A

these disroders are closely related to each other sharing clinical/ morphological/ ,olecular features
can transform into each other - e,g JAK2 mutations or can transform into acute myeloid leukemia

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15
Q

Myelodysplasia / Myelodysplastic Syndrome (MDS)

A

Clonal disorder of haemopoetic stem cells characterised by production of abnormal cells (dysplasia)
Low incidence ( 2-12 cases per 100000) each year
patients are usually > 60 years old at diagnosis
Numerous subtypes

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16
Q

Myelodysplasia / Myelodysplastic Syndrome (MDS) - clinical pathogenesis

A

Bone marrow is hypercellular
- blood shows pancytopenia due to disturbed maturation and inability to replace the cells
- Retarded maturation and cell death in bone marrow causes ineffective cell production

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17
Q

What is panytopenia

A

reduction in the number of all three major types of blood cells (RBC, WBC, Platelets)

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18
Q

Myelodysplasia / Myelodysplastic Syndrome (MDS) - Diagnosis

A

Via microscopy and mrophology

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19
Q

Leukemia

A

characterised by the abnormal proliferation of haemopoeitic cells that progressively infiltrate the bone marrow and lymphatic tissues compromising the production of normal blood cells.
accounts for 4% of deaths from malignant disease

20
Q

Initial classification of leukaemia - Difference between myeloid and lymphoid

A

Myeloid: originates in the myeloid cells (precursors to main blood cells) except lymphocytes
Lymphoid : originates in the lymphoid cells, which are precursors to lymphocytes. Affects lymphoblast’s and lymphocytes

21
Q

Initial classification of leukaemia - Chronic or acute

A

Chronic Leukaemia - progress slowly over time (months to years) with the cells produced by the bone marrow being partially mature with improper function causing the accumulation of dysfunctional cells in the blood stream.
Acute Leukemia - rapid progression ( weeks to months) with immature abnormal cells (blasts) multiplying quickly and crowding out healthy cells in the bone marrow causing a rapid onset of symptoms.

22
Q

acute leukaemia: AML

A

acute myeloid leukemia (AML).
More common in adults w- peak incidence at 60+ years
Causes majority of adult leukemia

23
Q

Acute Leukaemia - ALL

A

More common in children
Peak incidence of 3 years of age for B-ALL

15-20 years of age for T-ALL

24
Q

Chronic Leukemia - CML

A

Chronic Myeloid Leukaemia
Peak incidence of 50-60 years of age
Chronic phase -> accelerated phase -> Blast crisis

25
Q

Chronic Leukaemia -> CLL

A

chronic lymphocytic leukemia (CLL)
- peak incidence in over 50s
about 25% of leukaemias

26
Q

Types of lymphoid malignancies

A

Lekuaemia: Originates in the bone marrow in singular cells
Lymphoma: originates in the lymph nodes causing a solid network of cells?

27
Q

What is multiple myeloma

A

type of cancer that originates from plasma cells,

28
Q

How does classifying malignancies help the patients?

A
  • Identifying most at risk patients
  • Identifying patients who need to be treated sooner
  • I dentifying the most effective treatments
29
Q

How does classifying malignancies help research?

A
  • Aids understanding of underlying mechanisms: targets for new therapies
  • Helps researchers communicate effectively with each other
30
Q

Classification of Leukaemia - French American British (FAB) system advantages and limitations

A

Advantages: Quick, Cheap, Helps to identify medical emergencies
Disadvantages: Limited prognostic information, no predictive information

31
Q

WHO Classification of Haematological Malignancies advantages

A

-Includes subcategories that have predictable clinical outcomes.
-Includes immunophenotyping, cytogenetic and molecular characteristics.
-Accurate and precise with clearly defined criteria makes classification less subjective.
-Allows international collaboration on research
-Subtypes of AML respond differently to standard treatment: Cytogenetics and molecular abnormalities help identify subgroups with good or bad prognosis
-Treatment may now be tailored to genetic abnormality e.g. the use of all‐trans retinoic acid in acute promyelocytic leukaemia with t(15;17)

32
Q

Lab Diagnosis of Leukaemia - Immunotyping

A

Performed using flow cytometry as immature cells are difficult to differentiate morphologically
Detects different cell markers that cells express at different stages of maturation
- Confirms which cell type has been affected and at what stage of maturation the affected clone has been trapped

33
Q

Samples taken for immunotyping

A

Peripheral Blood
Bone Marrow Aspirate

34
Q

Immunohistochemistry types

A

Indirect/direct
immunofluorescence

35
Q

Immunohistochemistry samples

A

Bone marrow trephine
Lymph nodes biopsies

36
Q

Types of Cytogenetics (with increasing resolutions)

A

Karyotyping
FISH
Genomic Microarray
NGS

37
Q

Karyotyping: Euploidy chromosome error

A

Normal chromosome complement
Diploid in autosomal cells (2n)
46 chromosomes

38
Q

aneuploidy

A

More or less of a chromosome than normal.
Monosomy (2n-1)
Trisomy (2n+1)

39
Q

Polyploidy

A

Multiple sets of chromosomes
Triploidy (3n-69 chromosomes)
Tetraploidy (4n – 92 chromosomes

40
Q

Karyotyping: chromsomal structural abnormalities

A

-Additions
- Insertions
- Duplications
- Deletions
- Translocations
- Inversions

41
Q

FISH

A
  • Identifies specific sequences using a probe (complementary piece of DNA strand attached to a flourescent marker)
  • Doesn’t need live cells or cell culture
  • Quick turn around time (less than 24 hrs)
  • Can only detect specific mutations
42
Q

Genomic Microarray

A

Tests for copy number variation (deletions and duplications) across the genome.

43
Q

Genomic Microarray Advantages and Limitations

A

Advantages: High resolution, no cell culturing, global.
Limitations: Cant detect balanced structural abnormalities or repetitive DNA sequences.
Considerations: Incidental findings

44
Q

NGS advantages

A

High specificity and sensitivity

45
Q
A

Haematology & Transfer Practice (13 decks)

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