Lecture 9: Haematological Malignancies (Parts 1-4) Flashcards

1
Q

Compare AML and ALL:

A

AML:
Myeloid lineage (CD13+, CD33+)
Auer rods on blood film
Peak in adults
t(15;17) PML-RARA (APL)

ALL:
Lymphoid lineage (CD10+, CD19+)
Agranular blasts with high N:C ratio
Peak in children (3-7 years)
t(12;21) TEL-AML1 (good prognosis)

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2
Q

Key FBC findings in AML?

A

↓Hb, ↓platelets, ↑WBC (blasts), neutropenia.

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3
Q

What is the first-line treatment for ALL?

A

Induction chemotherapy (vincristine, dexamethasone, asparaginase) + CNS prophylaxis.

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4
Q

What defines CML?

A

Philadelphia chromosome t(9;22) → BCR-ABL1 fusion → constitutive tyrosine kinase activity.

Blood film: Myeloid precursors (metamyelocytes, basophilia).

Treatment: Tyrosine kinase inhibitors (imatinib).

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5
Q

How is CLL diagnosed?

A

Lymphocytosis (>5×10⁹/L), smudge cells on film, CD5+/CD19+/CD23+ on flow cytometry.

Binet staging: Determines prognosis (Stage A: >13 years survival).

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6
Q

Which translocation is diagnostic for CML?

A

t(9;22)(q34;q11) → BCR-ABL1.

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7
Q

What immunophenotypic markers distinguish B-ALL from T-ALL?

A

B-ALL: CD10, CD19, TdT.

T-ALL: CD3, CD7, TdT.

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8
Q

What is the significance of Auer rods?

A

Pathognomonic for AML (seen in myeloblasts).

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9
Q

Classic symptoms of CLL?

A

Fatigue, lymphadenopathy, recurrent infections, hepatosplenomegaly.

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10
Q

How is APL (AML-M3) treated?

A

ATRA (All-Trans Retinoic Acid) + arsenic trioxide (targets PML-RARA fusion).

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11
Q

Why is imatinib used in CML?

A

Inhibits BCR-ABL1 tyrosine kinase → halts proliferation.

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