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AP0509 Component 2 Exam > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

Neoplasm

A
  • abnormal new growth
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2
Q

Benign tumour

A
  • remain localised, don’t metastasize
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3
Q

Malignant tumour

A
  • metastasize through lymphatic channels or blood vessels to lymph nodes and other tissues in the body
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4
Q

Primary tumour

A
  • tumour growing at the anatomical site where tumour progression began and proceeded to yield this mass
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5
Q

Metastatic tumour

A
  • tumour forming at one site in body, cells (metastases) of

which derive from a tumour located elsewhere in the body

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6
Q

Carcinomas

A
  • constitute 90% of cancers

- cancers of epithelial cells

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7
Q

Sarcomas

A
  • rare and consist of tumours of connective tissues (connective tissue, muscle, bone etc.)
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8
Q

Leukaemias and lymphomas

A
  • constitute 8% of tumours
  • aka liquid tumours
  • leukaemias arise from blood forming cells
  • lymphomas arise from cells of the immune system (T and B cells)
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9
Q

Proto-oncogenes

A
  • over 100
  • proteins that promote cell cycle
  • mutations lead to oncogenes, promote cell growth regardless of circumstances
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10
Q

Tumour suppressor genes

A
  • proteins that inhibit cell cycle

- mutations lead to cell cycle not stopping even when it should (p53 and Rb genes)

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11
Q

DNA repair genes and apoptosis genes

A
  • DNA repair genes repair any mutated genes

- apoptosis genes kill mutated genes

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12
Q

Proto oncogenes that code for leukaemia

A
  • BCR-ABL (tyrosine kinase)

- MYC (transcription factor)

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13
Q

Tumour suppressor genes that codes for leukaemia

A
  • NF-1

- inhibitor of Ras, a protein that stimulates cell division

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14
Q

Leukaemia vs Lymphoma

A
  • Leukaemia: neoplasm originates from haemopoietic stem cells in bone marrow w/widespread movement in peripherical blood
  • Lymphoma: neoplasm originates from lymphocytes, which are in lymph nodes, spleen, thymus and bone marrow
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15
Q

Symptoms of leukaemia

A
  • weight loss
  • fever
  • frequent infections
  • shortness of breath
  • muscular weakness
  • pain/tenderness in bones or joints
  • fatigue
  • loss of appetite
  • swelling of lymph nodes
  • spleen/liver enlargement
  • night sweats
  • easy bruising
  • purplish patches or sports
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16
Q

Malignant haematopoiesis

A
  • cell of origin of leukaemia undergoes mutations
  • become leukaemia stem cells
  • block in differentiation causes them to divide and become blasts
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17
Q

Oncogenic drivers of granulocyte macrophage progenitor

A
  • MLL-ENL
  • MLL-AF9
  • MOZ-TIF2
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18
Q

Oncogenic drivers of common myeloid progenitor

A
  • MLL-ENL
  • MLL-AF9
  • MOZ-TIF2
  • MN1
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19
Q

Oncogenic drivers of common lymphoid progenitor

A
  • MLL-ENL

- MLL-AF9

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20
Q

Oncogenic drivers from haematopoietic stem cell

A
  • MLL-ENL
  • MLL-AF9
  • MOZ-TIF2
  • MN1
  • CALM-AF10
  • MLL-GAS7
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21
Q

General mechanisms of leukemic transformation

A
  • impaired differentiation
  • increased cell survival
  • increased proliferation
  • increased self-renewal
  • genomic instability
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22
Q

Metastasis of leukaemia

A
  • Leukaemia-derived exosomes transfer pro-angiogenic molecules toward ECs
  • enhances angiogenesis through stimulating factors
  • Leukemic cells-derived exosomes cause metastasis
    to lymph nodes through blood circulation
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23
Q

Leukaemia clonal disorder

A
  • Haematological malignancies are clonal disorders

- the malignant cells all share the same basic genetic or molecular abnormalities

24
Q

Key genetic/biochemical steps in leukaemia (aetiology)

A
  • genetic mutation/oncogene activation leading to
  • increased proliferation rate
  • reduced apoptosis
  • block in differentiation
25
Q

Physical, chemical and biological agents in activation of oncogenes or mutations

A
  • heredity
  • chromosomal abnormalities
  • chemical agents/drugs e.g benzene
  • ionising radiation
  • viruses
26
Q

Chromosomal abnormalities in leukaemia

A
  • deletions: deletion of entire, or part of, a chromosome, therefore effect on cell function
  • inversions: rearrangement in which a segment of a chromosome is reversed
  • translocations: exchange of genetic material between chromosomes
27
Q

Four main types of leukaemia

A
  • acute lymphoblastic (lymphocytic) leukaemia (ALL)
  • acute myeloid (myelogenous) leukaemia (AML)
  • chronic lymphocytic leukaemia (CLL)
  • chronic myeloid leukaemia (CML)
28
Q

Acute (ALL and AML) vs Chronic (CLL and CML) leukaemias

A
  • acute: made of immature blast cells
  • ALL most common in children
  • AML most common in adults
  • chronic have no blast cells
29
Q

General features of leukaemia

A
  • most common neoplastic disease of white cells
  • 9 per 100,000 population
  • expansion of bone marrow + infiltration by neoplastic white cells is common
  • neoplastic proliferation of marrow cells forming one or more cell lines.
  • Circulation of neoplastic cells in peripheral blood in most cases.
  • Anaemia
  • Low platelets
  • Bone marrow appearance becomes ‘monotonous’ as it is replaced by abnormal cells
30
Q

Acute leukaemias

A
  • uncontrolled proliferation of poorly differentiated blast cells (>20%)
  • marrow replacement by blast cells causes anaemia, increase in infection, and an increased tendency towards bleeding.
  • Patients develop fever, malaise, bleeding and mouth ulcers due to infections.
  • increased white cell count (including blast cells) in about 50% of cases. Could also be normal or reduced
    • Diagnosis is based on the bone marrow aspirate.
    • frequently show infiltration of many organs, especially the brain
31
Q

French-American-British (FAB) Scheme of Classification of AML (M0, M1, M2)

A
  • M0 Undifferentiated
  • M1 AML without maturation
  • M2 AML with granulocytic maturation
32
Q

French-American-British (FAB) Scheme of Classification of AML (M3, M4)

A
  • M3 Acute promyelocytic leukaemia

- M4 Myelomonocytic leukaemia

33
Q

French-American-British (FAB) Scheme of Classification of AML (M5, M6, M7)

A
  • M5 Monoblastic or monocytic leukaemia
  • M6 Erythroleukaemia
  • M7 Megakaryocytic leukaemia
34
Q

Auer rods

A
  • large, crystalline cytoplasmic inclusion bodies
35
Q

Bone marrow failure in acute leukaemias

A
  • pallor and lethargy, due to reduction in erythropoiesis.
  • Fever, malaise, infections of the mouth, throat, skin and respiratory tract - due to
    the reduction in production of normal WBC’s.
  • Spontaneous bruising, purpura, bleeding gums etc, usually due to
    thrombocytopaenia.
36
Q

Organ infiltration in acute leukaemias

A
  • Bone pain.
  • Lymphadenopathy in ALL
  • Moderate splenomegaly and hepatomegaly, especially in ALL
  • Infiltration of the gums and skin is particularly seen in myelomonocytic (M4) and
    monocytic (M5) types
37
Q

Lab findings in acute leukaemias

A
  • Normochromic, normocytic anaemia
  • Total WBC count may be decreased or normal but it is often increased to >200 x 10^9
    /l, with variable numbers of blast cells.
  • In AML the blast cells may contain Auer Rods.
  • Thrombocytopaenia is present in most acute leukaemias, and is marked in AML.
  • Hypercellularity of the bone marrow
38
Q

Chloroacetate esterase in acute leukaemias

A
  • leucocyte isoenzymes of esterases 1,2,7 and 8 can be stained using a-naphthyl AS-D chloroacetate.
  • main application of this stain is in the differentiation of granulocytic cell lines (CE positive) and monocytic cell lines (negative)
39
Q

Peroxidase and Sudan Black B

A
  • Peroxidase is for myeloperoxidase which is
    present in granulocyte and monocyte cell lines.
    • Sudan Black B stains neutral fats, phospholipids and lipoprotein and the reaction
    patterns are closely equivalent to the peroxidase reaction.
  • These stains are therefore most useful in distinguishing between ALL and AML (M1
  • M6)
40
Q

Non-specific esterase in acute leukaemias

A
  • many substrates which can be used to identify and localise isoenzymes of esterases 3,4,5, and 6.
  • main use of this stain is to differentiate between granulocytic and monocytic cell lines.
  • monocytic cell lines are NSE positive
41
Q

Acid phosphatase in acute leukaemias

A
  • Acid phosphatase is present in lysosomes of haemopoietic cells.
  • The most significant application isthe classification of lymphoproliferative diseases.
  • In T- cell ALL the reaction is localised to an area of the cytoplasm which is occupied by the Golgi apparatus
42
Q

Terminal deoxynucleotidyl transferase (TdT) in acute leukaemias

A
  • TdT is a DNA polymerase activity which is present at high levels in lymphoid cells.
  • It is an early marker for B and T cell acute lymphoblastic leukaemia
43
Q

Lysozyme in acute leukaemias

A
  • Greatly increased levels of serum lysozyme are seen in monocytic leukaemias, with smaller increases seen in myeloblastic leukaemias
44
Q

Immunological markers in acute leukaemias

A
  • particularly used in identification of subgroups of ALL presence or absence of cell surface marker molecules.
  • The advent of McAbs has allowed identification of cells at varying stages of their
    differentiation
45
Q

FAB classification of ALL

A
  • L1 small, monomorphic
  • L2 large, heterogeneous
  • L3 Burkitt-cell type
46
Q

Acute Lymphoblastic Leukaemia (ALL)

A
  • Accumulation of lymphoblasts in bone marrow
  • Incidence of ALL is highest at 3–7 years
  • Some cases initiated by genetic mutations that occur during development in utero
47
Q

Chronic leukaemias

A
  • malignant cells are relatively well differentiated
  • Identifiable morphologically by the use of conventional Romanowski staining procedures.
  • 2 major classifications of chronic leukaemia are CML and CLL.
48
Q

Chronic myeloid leukaemia (CML)

A
  • aka chronic granulocytic leukaemia CGL.
  • malignant proliferation of granulocytes in bone marrow and other haemopoietic organs
  • characterised by the presence of a chromosomal marker, the Philadelphia (Ph) chromosome, in the haemopoietic cells
49
Q

Philadelphia chromosome

A
  • Translocation t(9;22)(q34;q11)
  • The Philadelphia chromosome is 22
  • This is where the ABL-BCR (tyrosine kinase) fusion is
50
Q

Incidence of CML

A
  • 20% of all leukaemias
  • 1 per 100,000 population
  • between 20 and 60 years of age.
51
Q

Clinical features of CML

A
  • Anaemia: pallor, lethargy, especially in the later stages
  • Splenomegaly and hepatomegaly - former is almost always present and often massive, latter is fairly common.
  • Bleeding: haemorrhage or bruising is common, due to abnormal platelet function.
  • Hypermetabolism: an increase in the basal metabolic rate is common, resulting in fever, night sweats and weight loss.
  • Bone pain - hypercellularity of marrow.
  • Prolonged infections
52
Q

Lab findings in CML

A
  • Normochromic/normocytic anaemia
  • WBC count between 50-300 x10^9/l, but may be higher
  • A complete range of myeloid cells seen in the peripheral blood, majority of cells being myelocytes, metamyelocytes, band forms and mature
    neutrophils
  • A few myeloblasts and promyelocytes may be seen
53
Q

Features in CML

A
  • Thrombocytosis common in the early stages, platelet counts of >1000 x10^9/l may be reached
  • platelets are larger than normal and reduced function.
  • Hypercellularity of marrow, with many cells of granulocyte series.
  • most cases show increased level of LDH. Serum B12 levels may be up to 15x normal level, due to increased synthesis of
    transcobalmins I and III by leukaemic granulocytes.
  • Philadelphia Chromosome: Chromosomal analysis of
    haemopoietic cells reveals the Ph chromosome.
  • An abnormally small chromosome which results from translocation of a portion of the long arm of ch 22 to
    ch 9. This is considered as a diagnostic indicator of
    CML.
54
Q

Incidence of CLL

A
  • disease of the elderly, rare in patients <40 years old

- male:female ratio of 2:1

55
Q

Clinical features of CLL

A
  • Anaemia isn’t an obvious symptom in most cases, especially in the early stages
  • About 10% of casesdevelop an haemolytic anaemia
  • Splenomegaly and hepatomegaly are common
  • Lymphadenopathy.
  • Bruising and purpura - due to thrombocytopaenia
  • Infections are common: bacterial, fungal, viral infections may present
56
Q

Lab findings of CLL

A
  • anaemia may be present later
  • 10% of cases develop autoimmunity.
  • Total WBC is >15 x 10^9/l and may be 300 x 10^9/l or higher.
  • Between 70-99% of cells are small mature lymphocytes.
  • Smear cells are common, fragile cells which are disrupted when making the blood film.
  • mature cells are B-cells in 90% of cases.
  • relatively rare T-CLL tends to be much more aggressive
  • Thrombocytopaenia - usually in later stages
  • bone marrow biopsy isn’t usually required for diagnosis, marrow is 30-50% infiltrated by lymphocytes.

AP0509 Component 2 Exam (21 decks)

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