Acute Leukemias Flashcards

1
Q

Etiologies of AML

A
  • Antecedent MDS (rarely MPS)
  • Inherited syndromes (Downs)
  • Drugs (chemos)
  • Chemicals/Radiation
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2
Q

Clinical presentation of AML

A
  • Symptoms less than 3 mos

- Fever, bleeding, fatigue, SOB

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3
Q

WBC counts of AML?

A

Not always elevated - about 1/3 of patients will actually have a leukopenia

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4
Q

Characteristic peripheral smear of AML

A

Polys and blasts but no intermediate forms (“leukemic hiatus”)

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5
Q

What is required to diagnose AML?

A

BM biopsy

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6
Q

Treatment for AML (NOT including APL)

A
  • Induction therapy: 7 days of Cytarabine (continuous IV) and 3 days of Daunorubicin (an anthracycline)
  • Intensive supportive therapy
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7
Q

How to treat AML if induction therapy has not resulted in complete remission?

A
  • Treat again
  • Switch to salvage regimen (e.g. high dose cytarabine)
  • If this fails, consider allogeneic HSCT
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8
Q

How should AML patients over 70 yo be treated?

A

Most cannot tolerate standard tx

  • Low dose Decitabine
  • Reduced intensity conditioning regimens w/allo-HSCT
  • Intensive supportive therapy
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9
Q

Clinical presentation of APL

A

Presents similar to other acute leukemia BUT bleeding and thrombosis are common

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10
Q

Why do APL patients present with bleeding/thrombosis?

A

Due to disseminated intravascular coagulation (DIC)

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11
Q

Prognosis of APL

A

85% of pts will be cured with modern treatment (there used to be a lot of early mortality due to ICB and DIC)

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12
Q

Typical APL patients

A

Younger and RARELY preceded by MDS

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13
Q

What does BM biopsy of APL look like?

A

Large and granular promyelocytes frequently with prominent Auer rods

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14
Q

What is the most distinguishing feature of APL?

A

Mutation of retinoic acid receptor gene (can try to treat with high doses of Vitamin A)

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15
Q

Treatment of APL

A
  • All-trans Retinoic Acid (ATRA, component of Vitamin A, NOT myelosuppressive)
  • Arsenic trioxide
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16
Q

How does ATRA treat APL?

A
  • Component of Vitamin A
  • Will induce APL promyelocytes to differentiate into mature myeloid cells
  • Induces CR in over 90% of pts
17
Q

CR of APL is defined as:

A
  • Less than 5% blasts in BM
  • Resolution of cytogenetic/molecular abnormalities in BM
  • CBC with ANC over 10^3 and platelets over 10^5
18
Q

Who is MC affected by ALL?

A

Children and young adults

19
Q

General classes of ALL

A

B cell and T cell

20
Q

Etiology of ALL

A
  • Trisomy 21 (Down)
  • Radiation exposure (T cell type)
  • Many cases UNKNOWN
21
Q

Common PE findings of ALL

A
  • Lymphadenopathy

- Hepatosplenomegaly

22
Q

Treatment of ALL

A
  • Vincristine (NOT myelosuppressive) and prednisone: rapidly reduces ALL blasts
  • Intensification treatment (similar to induction tx of AML - 7/3 of cytarabine and anthracycline)
23
Q

Maintenance treatment of ALL

A

6-MP (oral) and weekly MTX for 2-3 years

24
Q

Prognosis of pediatric ALL

A

Over 90% survival rate

25
Q

Prognosis of adult ALL

A

Long term survival is approx 35% pts