Acute Myeloid Leukemia

What are common presenting signs of bone marrow failure disorders such as Acute Myeloid Leukemia (AML)?

Fatigue, dyspnea on exertion, infections from neutropenia, bleeding/petechiae from thrombocytopenia, and symptomatic anemia due to marrow replacement by blasts.

How does AML cause pancytopenia?

Myeloblasts proliferate uncontrollably and crowd out normal hematopoiesis, preventing maturation of RBCs, platelets, and neutrophils. Bone marrow gets hyperplastic

What is the goal of AML induction chemotherapy?

To induce remission by eliminating visible leukemia blasts and allowing normal hematopoiesis to recover.

What drugs are used in standard AML induction therapy?

Cytarabine for 7 days plus daunorubicin for 3 days (“7+3” regimen).

Why do AML patients remain hospitalized for weeks during induction?

Severe neutropenia, anemia, and thrombocytopenia require continuous supportive care including antibiotics, transfusions, and monitoring for tumor lysis and organ toxicity.

What supportive care is required during AML induction?

Broad‑spectrum antibiotics, pRBC transfusions, platelet transfusions, Tumer Lysis Syndrome prevention(end organ damage due to billions of CA cells dying and imbalance of electrolytes released from cytoplasm), electrolyte monitoring, and management of chemo toxicities (GI, hepatic, renal, cardiac).

How do clinicians assess response to AML induction therapy?

A day‑14 bone marrow biopsy (“nadir marrow”) is performed to check for residual blasts

What happens if blasts remain on the day‑14 marrow?

Additional chemotherapy is required (e.g., “5+2” or alternative regimen), resetting the recovery timeline.

What is the purpose of AML consolidation therapy?

To eradicate residual microscopic leukemia and reduce relapse risk after remission is achieved.

What drugs are used in AML consolidation therapy?

High‑dose cytarabine (HiDAC) given in multiple cycles as outpatient or short inpatient stays.

Why do AML patients often return to the hospital during consolidation?

Neutropenic fevers requiring IV antibiotics and monitoring.

What cytogenetic abnormality defines Acute Promyelocytic Leukemia (APL)?

t(15:17)

Why is APL associated with Disseminated Intravascular Coagulopathy?

Promyelocytes release procoagulant granules, causing consumptive coagulopathy and high early hemorrhage risk.

What drug promotes differentiation of Acute Promyelocyte Leukemia (APL) promyelocytes?

ATRA (all‑trans retinoic acid), which overcomes the differentiation block caused by PML‑RARα.

How does ATRA work in APL?

It binds the altered retinoic acid receptor, restoring promyelocyte differentiation into mature neutrophils.

What is the second major drug used in APL therapy? MOA?

Arsenic trioxide, which also promotes differentiation and apoptosis of leukemic promyelocytes.

What major toxicity is associated with arsenic trioxide?

QTc prolongation requiring ECG and electrolyte monitoring.

Why is APL treated differently from other AML subtypes?

Its unique PML‑RARα fusion makes it highly responsive to differentiation therapy rather than cytotoxic chemotherapy.

What are 3 general causes of bone marrow failure?

Bone marrow is EMPTY (ex: aplastic anemia), Bone marrow hematopoietic elements are NOT MATURING (ex: myelodyspastic syndrome), and Bone marrow space is REPLACED with only one type of cell (ex: leukemias +other malignancies).

What cell is in excess in Acute Myeloid Leukemia?

Myeloblasts

What are Acute Myeloid Leukemia risk factors?

Prior chemotherapy, prior radiation, exposure to benzenes(long term, high conc), preceding myelodysplastic syndrome (MDS), AGE(bc it is a cell division problem)

Laboratory values that suggest Acute Myeloid Leukemia (AML)?

Elevated WBC, low ANC(absolute neutrophil count) that is proportionall very low to other cells on diff, anemia, and thrombocytopenia

How many blasts are required on smear for AML diagnosis? Needed for determining lineage?

>20% of blasts, auer rods are essentially pathologic in AML. Use flow cytometry to determine lineage

What is leukostasis in Acute Myeloid Leukemia (AML)? Sx? Treatment?

Myeloblasts are so big and high amount of them they begin to stick together leading to occlusive obstructions sx: chest pain, SOB, heacaches, blurry vision

Tx: Emergent leukopheresis to filter out big sticky cells + add hydroxyurea to slow down production

What cell line is altered in Acute Promyelocytic Leukemia?

Promyelocytes