AML Flashcards

1
Q

What is Acute Myeloid Leukemia (AML)?

A

A clonal hematopoietic malignancy characterized by the accumulation of immature myeloid cells (blasts) in the bone marrow, peripheral blood, or other tissues.

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2
Q

What are the hallmark features of AML?

A

Bone marrow failure (anemia, neutropenia, thrombocytopenia).

Rapid proliferation of myeloid blasts.

Organ infiltration (e.g., hepatosplenomegaly).

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3
Q

How is AML classified?

A

Based on morphology (FAB classification).

Molecular and genetic abnormalities (WHO classification).

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4
Q

What are the common risk factors for AML?

A

Genetic predispositions: Down syndrome,

Fanconi anemia, and Bloom syndrome.

Previous chemotherapy/radiation therapy (therapy-related AML).

Environmental exposures: Benzene, smoking, pesticides.

Myelodysplastic syndrome (MDS) or other hematologic disorders.

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5
Q

What are common genetic abnormalities associated with AML?

A

Translocations: t(8;21), inv(16), t(15;17) (associated with APL).

FLT3 mutations: Poor prognosis.

NPM1 mutations: Favorable prognosis when no FLT3 mutation is present.

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6
Q

What causes AML?

A

Mutations in hematopoietic stem cells disrupt normal differentiation, leading to the accumulation of immature myeloid blasts that impair normal hematopoiesis.

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7
Q

How does AML lead to bone marrow failure?

A

Replacement of normal bone marrow with blasts suppresses normal hematopoiesis, causing anemia, neutropenia, and thrombocytopenia.

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8
Q

What are the common presenting symptoms of AML?

A

Fatigue and weakness (anemia).

Fever and infections (neutropenia).

Easy bruising or bleeding (thrombocytopenia).

Bone pain or discomfort.

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9
Q

What are common signs of AML on physical examination?

A

Pallor.

Petechiae or ecchymoses.

Hepatosplenomegaly or lymphadenopathy (less common).

Gum hypertrophy (monocytic AML).

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10
Q

What is leukostasis, and how does it present in AML?

A

A medical emergency caused by high blast counts (>100,000/μL), leading to impaired microcirculation and symptoms like headache, dyspnea, or visual changes.

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11
Q

How is AML diagnosed?

A

Peripheral blood smear: Presence of blasts.

Bone marrow biopsy: Hypercellularity with >20% myeloid blasts.

Cytogenetic analysis: To identify chromosomal abnormalities.

Flow cytometry: To confirm lineage and immunophenotype.

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12
Q

What are characteristic findings in AML on a blood smear?

A

Blasts with Auer rods (specific for AML).

Anemia, thrombocytopenia, and variable leukocyte counts.

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13
Q

What laboratory findings are commonly seen in AML?

A

Elevated lactate dehydrogenase (LDH).

Hyperuricemia.

Disseminated intravascular coagulation (DIC) in acute promyelocytic leukemia (APL).

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14
Q

What is the French-American-British (FAB) classification for AML?

A

Based on morphology and cytochemistry, includes subtypes M0 to M7 (e.g., M3: APL, M5: Monocytic AML).

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15
Q

What is the primary treatment approach for AML?

A

Induction therapy: To achieve remission (e.g., “7+3” regimen: cytarabine and daunorubicin).

Consolidation therapy: To eliminate residual disease (e.g., high-dose cytarabine or allogeneic stem cell transplantation).

Targeted therapies: For specific mutations (e.g., FLT3 inhibitors, IDH inhibitors).

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16
Q

How is acute promyelocytic leukemia (APL) managed?

A

All-trans retinoic acid (ATRA) combined with arsenic trioxide or chemotherapy.

Monitor for differentiation syndrome (a potential complication).

17
Q

What supportive treatments are critical in AML?

A

Transfusions (RBCs, platelets).

Prophylactic antimicrobials.

Allopurinol or rasburicase for tumor lysis syndrome.

Leukapheresis in leukostasis.

18
Q

What factors affect the prognosis of AML?

A

Age: Younger patients have better outcomes.

Cytogenetics: Favorable (e.g., t(8;21)), intermediate, or poor (e.g., complex karyotypes).

Performance status and comorbidities.

Molecular mutations (e.g., FLT3, NPM1).

19
Q

What is differentiation syndrome, and how is it treated?

A

A complication of APL therapy (with ATRA), characterized by fever, dyspnea, and fluid overload. Treated with corticosteroids.

20
Q

What are common complications of AML?

A

Leukostasis (in hyperleukocytosis).

Tumor lysis syndrome.

DIC (especially in APL).

Opportunistic infections during immunosuppression.