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DMD2 sem 2 > Haematology 2 > Flashcards

Haematology 2 Flashcards

1
Q

What causes leukaemias?

A

Unknown but associated with:

Radiation

Chemical agents (benzene)

Oncogenic viruses

Smoking

Genetic predisposition

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2
Q

How are leukaemias classified?

A

Based on primary haematopoietic cell line affected (myeloid or lymphoid)

Based on clinical behaviour (Acute or chronic leukaemia)

Simplest 4 categoried:

Acute Myelogenous leukaemia (AML)

Acute Lymphocytic Leukaemia (ALL)

Chronic Myelogenous leukaemia (CML)

Chronic Lymphocytic Leukaemia (CLL)

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3
Q

How can leukaemia be diagnosed?

A

FBC

Bone marrow biopsy

Additional methods (Flow cytochemical staining)

Cytometric immunophenotyping

Genetic analysis

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4
Q

What would a FBC show in a case of leukaemia?

A

Peripheral granulocyte cound increase in chronic leukaemia

Increase or decrease or normal in acute leukaemia

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5
Q

What are the types of myeloid neoplasms?

A

Acute myeloid leukaemia

Myeloproliferative disorders:
Chronic myelogenous leukaemia (CML)
Polycythemia vera
Essential thrombocythemia
Systemic mastocytosis
Chronic eosinophilic leukaemia
Stem cell leukaemia

Myelodysplastic syndromes

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6
Q

What is acute myelogenous leukaemia?

A

Clonic proliferation of immature WBC (blasts) in the bone marrow and subsequently in the blood.

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7
Q

What percentage of leukaemias are AML?

A

1/3 of all leukaemia

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8
Q

Who gets AML most often?

A

Adults increases in incidence with age (mean age 65yo)

Male to Female ratio 5:3

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9
Q

What causes AML?

A

De novo

Environmental causes: Tobacco, benzene containing compound, chemotherapy

Consequence of myelodysplastic syndrome (30% of MDS-es progress to AML)

Genetic factors (Translocations and rearrangement of gases. Down syndrome, klinefeller syndrome, fanconi anaemia, recklinghausen

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10
Q

What are the clinical signs of AML?

A

Anaemia related: Shortness of breath, weakness, dyspnea on exertion

Physical findings: Pallor, bleeding/bruising, hepatomegaly, and/or splenomegaly.

Otherwise unexplained headache or focal neurological complaints.

Pancytopaenia save for WBC

Accumulation of leukemic forms in the peripheral blood, bone marrow and/or other tissues

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11
Q

How is AML diagnosed?

A

> 20% BM cellular component = myeloid blasts/promyelocytes

Myeloblasts: Delicate nuclear chromatin, 3 to 5 nucleoli, fine azurophilic cytoplasmic granules.

Auer rods

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12
Q

What are auer rods?

A

Red staining rod-like structures. Numerous in acute promyelocytic leukaemia. Specific for neoplastic myeloblasts

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13
Q

How is AML treated?

A

Phases of therapy include:

Induction therapy: Intensive combination chemotherapy to achieve a CR through reducing the number of leukaemia cells and restoring normal bone marrow function.

Post-remission therapy: Chemotherapy, targeted therapies, and autologous or allogenic haematopoietic cell transplantation

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14
Q

What is CML?

A

Myeloproliferative neoplasm with dysregulated production and uncontrolled proliferation of mature and maturing granulocytes with fairly normal differentiation

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15
Q

What happens in CML?

A

BCR (chromosome 22) fuses with ABL1 (Chromosome 9) creating a philadelphia chromosome and a protein results from this leading to elevated and constitutive kinase activity leading to CML

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16
Q

How can CML be diagnosed?

A

FISH allows visualization of the BCR-ABL gene

17
Q

How common is CML?

A

Accounts for approximately 15 - 20% of adult leukaemias in adults.

Annual incidence of 1 to 2 cases per 100k

Slight male predominance

Median age is 50 years

18
Q

What are the risk factors for CML?

A

No known familial dysposition (except familial CML on JAK2 and Ph chromosome)

Only risk factor known is ionizing radiation.

19
Q

How does CML present?

A

Triphasic or biphasic clinical course:

Chronic phase: Present at the time of diagnosis.

Accelerated phase: Progressively impaired neutrophil differentiation and difficulty in controlling leukocyte counts with treatment.

Blast crisis: Resembling acute leukaemia

20
Q

What are the clinical findings associated with CML?

A

Asymptomatic in 20 - 50% of cases

In symptomatic patients: Fatigue (34%), malaise, weight loss, excessive sweating, abdominal fullness, and bleeding episodes

21
Q

How is CML treated?

A

Imatinib blockes BCR-ABL

22
Q

Why is imatinib relevant to dentists?

A

imatinib may lead to mucosal pigmentation of a grey blue colour,

23
Q

What Condition has overlapping clinical symptoms with acute lymphoblastic leukaemia?

A

Acute lymphoblastic lymphoma

24
Q

What happens in ALL /LBL?

A

Clonal proliferation of lymphoid cells that have undergone maturational arrest in early differentiation.

Both pre-B and pre-T cell tumours take on the clinical appearance of ALL during their course.

25
Q

What cells are most commonly involved in B/T-ALL/LBL?

A

Precursor to B lymphocytes (85%)

T lymphocytes in 10 - 15%

Uncommon variants in <1% (early T and NK cells)

26
Q

Who most commonly gets B/T-ALL/LBL?

A

Most common in children

2500 to 3500 new cases of ALL/LBL are diagnosed in children each year.

3.4 cases per 100000

Peak incidence at 2 - 5 years

More common in boys

Incidence is increasing

27
Q

What are the risk factors for ALL/LBL?

A

Unknown cause

Genetic and environmental influence

Advanced paternal age and maternal foetal loss

Increased birth weight

Not a familial disease

28
Q

How is ALL diagnosed?

A

Characteristic morphology

Diagnostic immunohistophenotype of cells from:

Peripheral blood

Bone marrow

Lymph node

Other involved tissue

Markers:

B-lymphoblasts: CD19, cytoplasmic CD79a, and cytoplasmic CD22

T-lymphoblasts: CD3

29
Q

What is the prognosis of B/T-ALL/LBL?

A

Poor prognosis for ages =<1 and >=10 yo, leukocyte count >=50000/microL, race, and male

30
Q

What is the treatment for ALL/LBL?

A

Administration of a multidrug regimen: Induction, consolidation, and maintenance. Takes 2 - 3 years to complete.

Transfusion support

Treatment of proven and suspected infections

Correction of metabolic imbalances

Leukopheresis (rarely)

31
Q

How is the induction treatment carried out for ALL/LBL?

A

90% of children achieve complete remission at the end of induction.

initial treatment in BCR-ABL1 positive ALL is imatinib

Weekly vincristine (3 - 4 weeks), Daily corticosteroids and asparaginas in BCR-ABL negative

32
Q

What is different for children with down-syndrome in terms of ALL?

A

Susceptible to adverse events and treatment-related mortality
• Severe mucositis in response to MTX
• Increased risk of infection
• Reduced intensity chemo

33
Q

What are the goals for post remission therapy?

A

Started soon after CR

Goal:

Prevent leukaemic regrowth

Reduce residual tumour burden

Prevent the emergence of drug-resistance in the remaining leukaemic cells

34
Q

How long does consolidation last? What drugs does it include?

A

4 - 8 months

Includes:

Cytarabine

Methotrexate

Anthracyclines

Alkylating agents (Cyclophosphamide, ifosfamide)

Epipodophyllotoxins

DMD2 sem 2 (97 decks)

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