S31 Acute Leukemias Flashcards

1
Q

CD34 is expressed on

A

most stem cells

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2
Q

TdT expression defines a

A

lymphoid lineage

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3
Q

AML is characterized by what immunological markers usually

A

CD13, CD33, CD117

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4
Q

B-ALL is characterized by what immunological markers

A

TDT, CD10, CD19, cCD22

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5
Q

T-ALL is characterized by what markers

A

TdT, CD2, CD3, CD7

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6
Q

AML can occur with what recurrent genetic abnormalities

A

t(8;21) inv(16) t(15;17)(q22;q12); PML-RARA

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7
Q

AML with recurrent genetic abnormalities and diagnostic criteria

A

detections of genetic abnormalities means that bone marrow blast cell count does not need to exceed 20% in order to make a diagnosis. have good prognosis.

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8
Q

AML with myelodypslasia-related changes

A

AML associated with microscopic features of dysplasia in a least 50% of cells in at least two lineages.

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9
Q

Therapy-related myeloid neoplasms (t-AML)

A

arises in patients who have been previously treated with drugs such as etoposide or alkylating agents commonly exhibit mutations in MLL gene. clinical response usually poor.

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10
Q

AML, not otherwise specified

A

absence of cryogenic abnormalities and comprises around 30% of all cases. Mutations in NPM! and FLT3 genes r more freq in those with normal cryogenetics

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11
Q

Myeloid sarcoma

A

rare refers to disease resembles a solid tumor but is composed of myeloid blast cells

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12
Q

Myeloid proliferations related to down’s syndrome

A

children w/ Down’s syndrome increased risk of acute leukemia two myeloid variants recognized: - transient abnormal myelopoiesis, self-limiting leucocytosis -AML

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13
Q

Mixed phenotype acute leukaemia

A

express two markers for both myeloid and lymphoid differentiation either on same blast cells or on two different cell populations. poor prognosis.

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14
Q

Clinical features of AML

A

down marrow failure due to accumulation of malignant cells within marrow infections- frequent profound anaemia and thrombocytopenia promyelocytic variant for AML: bleeding tendency due to thrombocytopenia and disseminated intravascular coagulation (DIC) Tumour cells infiltrate variety of tissues Myelomonocytic (involves a proliferation of CFU-GM myeloblasts and monoblasts) and monocytes subtypes: Gum hypertrophy and infiltration by leukemia cells, skin involvement and CNS disease

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15
Q

Favorable cytogenetics for AML

A

t(15:17), t(8;21), inv(16), Trisomy 8 No FLT3 mutation Nucleophosmin-1 mutation CEBPa mutation

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16
Q

Unfavorable cytogenetics for AML

A

11q23 abnormality - MLL gene deletions of chromosome 5 or 7 TP53 mutated Abnormal (3q) t(6;11), (10;11), (9;22) FLT3 internal tandem repeat

17
Q

AML treatment overview

A

supportive and specific Induction- determine by age, cytogenetics and performance status CR 66-85% no maintenance CNS treatment - neuro deficit or headache - M4, M5 supportive care Hematopoietic cell transplantation: High risk disease, relapsed disease

18
Q

AML treatment drugs

A

most commonly used drugs: cytosine arabinoside and daunorubicin Idarubicin, mitoxantrone ALL-trans retinoid acid (ATRA) and Arsenic trioxide is used in promyelocytic leukemia (presents with bleeding)

19
Q

Neutropenia

A

decreased number of circulating neutrophils

20
Q

Causes of Neutropenia

A

Drug Toxicity (e.g. chemotherapy with alkylating drugs): damage to stem cells results in decreased production of WBCs, especially neutrophils

Severe infection (e.g., gram-negative sepsis)- Increased movement of neutrophils into tissues results in decreased circulating neutrophils

21
Q

What can be used a treatment to boost granulocyte production

A

GM-CSF

G-CSFf

22
Q

lymphopenia

A

decreased number of circulating lymphocytes

23
Q

Lymphopenia is caused by

A

Immunodeficiency (e.g. DiGeorge syndrome or HIV)

High cortisol state (exogenous corticosteroids, or cushing syndrome): induces apoptosis of lymphocytes

Autoimmune destruction (systemic lupus erythematosus)

Whole Body radiation- lymphocytes are highly sensitive to radiation; lymphopenia is earliest change to emerge after whole body radiation.

24
Q
A