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ALL Flashcards

1
Q

What is acute lymphoblastic leukemia (ALL)?

A

A malignant proliferation of lymphoid precursor cells (lymphoblasts) in the bone marrow, blood, and other tissues.

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2
Q

What are the two main subtypes of ALL?

A

B-cell ALL (most common).

T-cell ALL.

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3
Q

What age groups are most affected by ALL?

A

Most common cancer in children (peak incidence: 2–5 years).

Smaller peak in adults, particularly >50 years.

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4
Q

Name some risk factors for ALL.

A

Genetic predisposition (e.g., Down syndrome, Klinefelter syndrome).

Prior chemotherapy or radiation therapy.

Exposure to high doses of ionizing radiation.

Certain infections (e.g., Epstein-Barr virus in some cases of T-cell ALL).

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5
Q

What is the underlying pathophysiology of ALL?

A

Genetic mutations in lymphoid precursor cells result in uncontrolled proliferation and a failure to mature, crowding out normal hematopoiesis.

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6
Q

What cytogenetic abnormalities are associated with ALL?

A

t(9;22): Philadelphia chromosome (BCR-ABL1 fusion, poor prognosis).

t(12;21): ETV6-RUNX1 fusion (common in children, good prognosis).

t(4;11): MLL rearrangement (poor prognosis, common in infants).

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7
Q

What are the common symptoms of ALL?

A

Symptoms of bone marrow failure: Fatigue, pallor, infections, bleeding/bruising.

Organ infiltration: Bone pain, lymphadenopathy, hepatosplenomegaly, testicular swelling.

CNS involvement: Headache, vomiting, cranial nerve palsies.

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8
Q

What are B-symptoms in ALL?

A

Fever, night sweats, and unintentional weight loss.

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9
Q

How does T-cell ALL often present?

A

With a mediastinal mass, causing symptoms like cough, dyspnea, or superior vena cava syndrome.

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10
Q

What are the key diagnostic steps for ALL?

A

Complete blood count (CBC) with peripheral smear: Blasts, anemia, thrombocytopenia, leukopenia, or leukocytosis.

Bone marrow biopsy: Hypercellular marrow with >20% lymphoblasts (diagnostic).

Immunophenotyping/flow cytometry: Identifies B-cell or T-cell lineage.

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11
Q

What markers are used to identify B-cell ALL?

A

CD19, CD20, CD22, CD79a.

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12
Q

What markers are used to identify T-cell ALL?

A

CD3, CD4, CD8, CD7.

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13
Q

What cytogenetic studies are critical in ALL?

A

Fluorescence in situ hybridization (FISH) or polymerase chain reaction (PCR) for specific chromosomal translocations like t(9;22).

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14
Q

How is CNS involvement diagnosed in ALL?

A

Lumbar puncture with cerebrospinal fluid (CSF) analysis for blasts.

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15
Q

What are the key phases of ALL treatment?

A

Induction therapy: Achieve remission by eradicating detectable leukemia.

Consolidation therapy: Eliminate residual disease and prevent relapse.

Maintenance therapy: Prolong remission and eradicate minimal residual disease.

CNS prophylaxis: Prevent CNS relapse using intrathecal chemotherapy or cranial irradiation.

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16
Q

What drugs are commonly used in the treatment of ALL?

A

Chemotherapy: Vincristine, prednisone, asparaginase, anthracyclines.

Tyrosine kinase inhibitors (TKIs) for Philadelphia chromosome-positive ALL (e.g., imatinib).

Methotrexate and cytarabine for CNS prophylaxis.

17
Q

When is hematopoietic stem cell transplantation (HSCT) considered?

A

For high-risk or relapsed ALL.

18
Q

What supportive therapies are needed during ALL treatment?

A

Blood product transfusions for anemia and thrombocytopenia.

Prophylactic antibiotics and antifungals to prevent infections.

Allopurinol or rasburicase for tumor lysis syndrome.

19
Q

What factors influence the prognosis of ALL?

A

Age: Better prognosis in children; worse in adults and infants.

Cytogenetics: Good prognosis with t(12;21), poor with t(9;22).

White blood cell count at diagnosis: Higher counts indicate poorer outcomes.

Response to induction therapy: Minimal residual disease (MRD) negativity indicates better prognosis.

20
Q

What are common complications of ALL and its treatment?

A

Infection: Due to neutropenia and immunosuppression.

Tumor lysis syndrome: Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia.

CNS relapse: Neurological deficits due to leukemic infiltration.

Long-term: Secondary malignancies, cardiotoxicity (anthracyclines), growth retardation (cranial irradiation).

21
Q

What is the mechanism of action of vincristine?

A

Vincristine binds to tubulin and inhibits microtubule formation, preventing mitotic spindle assembly and arresting cell division at metaphase.

22
Q

What is the mechanism of action of anthracyclines (e.g., doxorubicin, daunorubicin)?

A

Intercalate into DNA, inhibiting topoisomerase II and preventing DNA replication.

Generate free radicals, causing oxidative damage to DNA and cell membranes.

23
Q

How does asparaginase work in ALL?

A

Asparaginase depletes asparagine, an amino acid essential for leukemic cell survival, leading to apoptosis.

24
Q

What is the mechanism of action of methotrexate?

A

Methotrexate inhibits dihydrofolate reductase, blocking folate metabolism and DNA synthesis, particularly in rapidly dividing cells.

25
Q

How does cytarabine (Ara-C) work?

A

Cytarabine is a nucleoside analog that inhibits DNA polymerase, halting DNA synthesis and repair in dividing cells.

26
Q

What is the mechanism of action of imatinib in Philadelphia chromosome-positive ALL?

A

Imatinib selectively inhibits BCR-ABL tyrosine kinase, preventing phosphorylation of proteins needed for leukemic cell proliferation and survival.

27
Q

Why is methotrexate used intrathecally in ALL?

A

Methotrexate penetrates the cerebrospinal fluid (CSF), preventing or treating leukemic infiltration of the CNS.

28
Q

How does allopurinol prevent tumor lysis syndrome in ALL?

A

Allopurinol inhibits xanthine oxidase, reducing uric acid formation from purine breakdown during cell lysis.

29
Q

What is the mechanism of action of rasburicase in tumor lysis syndrome?

A

Rasburicase catalyzes the conversion of uric acid to allantoin, a more soluble compound, rapidly reducing serum uric acid levels.

30
Q

Why are glucocorticoids (e.g., prednisone, dexamethasone) used in ALL?

A

Glucocorticoids induce apoptosis in lymphoid cells by binding to glucocorticoid receptors and altering gene transcription.

Haematology (2 decks)

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