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IHO Week 4 > Acute Leukemia: Clinical Cases and Correlates > Flashcards

Acute Leukemia: Clinical Cases and Correlates Flashcards

1
Q

What is AML?

A
  • Uncontrolled clonal proliferation and accumulation of neoplastic hematopoietic precursor cells of myeloid lineage
  • –Inhibition of normal hematopoiesis
  • –Defective maturation
  • –Dissemination into blood and other tissues
  • –20% myeloblasts in BM (WHO) or 30% myeloblasts in BM (FAB)
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2
Q

What is the #1 thing to think about with leukemia? (EXAM)

A

What are the cytogenetics? This drives prognosis and treatment

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3
Q

What are you thinking if you see a patient with fever, chills and swollen glands under neck?

A

Viral illness

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4
Q

What are you thinking if you see fever, chills, and diffuse adenopathy (all over body)?

A

HIV, AML (leukemia) (BAD STUFF)

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5
Q

Who is at increased risk for acute myelogenous leukemia? (EXAM)

A

-Down Syndrome, Ataxia telangiectasia, Fanconi anemia, Li Fraumeni syndrome, Wiskott-Aldrich, familial leukemia, myelodysplasia, PNH

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6
Q

What can cause secondary AML (acute myelogenous leukemia)?

A

Prior chemotherapy, radiation exposure, benzene

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7
Q

What is the median age of diagnosis for AML? How many cases in the US?

A
  • Median age: 63 (80% > 15) - mostly adults
  • 7,400 deaths in US in 2002
  • 10,600 new cases in US in 2002
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8
Q

What can AML do the the mouth? (EXAM)

A

Can cause gums to hypertrophy

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9
Q

What are the clinical features associated with AML?

A
  • Pancytopenia (red cells, white cells & platelets reduced)
  • –Anemia (often asymtomatic in elderly)
  • –Neutropenia
  • –Thrombocytopenia
  • B symptoms: fever, night sweats, chills, malaise, weight loss
  • Extremedullary disease - outside of the blood & bone marrow!
  • –Monocytic leukemias are most common (infiltration of leukemia in the gums)
  • –Skin, CNS, orbits, bone, lung, kidney, spleen, liver, ovary
  • Hyperleukocytosis
  • –>100,000 blast count/ml
  • –APML, moncytic AML, inv(16), 11q23
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10
Q

How should you treat AML?

A

Promptly with hydroxyurea, leukopheresis, chemotherapy

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11
Q

What are the two methods of classification of AML?

A

FAB

WHO

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12
Q

What does AML look like on a blood film?

A
  • Monocytic blast
  • Cleft in the nucleus of monocytes
  • You’ll also see an auer rod
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13
Q

What is the FAB classification?

A
  • > 30% BM myeloblasts
  • M0 (undifferentiated myeloid leukemia)
  • M1 (acute myeloid leukemia without maturation)
  • M2 (acute myeloid leukemia with maturation)
  • M3 (acute promyelocytic leukemia)
  • M4 (acute myelomonocytic leukemia)
  • M5 (acute monocytic leukemia)
  • M6 (acute erythroleukemia)
  • M7 (acute megakaryocytic leukemia)
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14
Q

What is the WHO classification of AML?

A
  • > 20% BM myeloblasts
  • AML with recurrent cytogenetic abnormalities
  • –ex: t(8;21), t(15;17), t(inv16), 11q23
  • AML with multilineage dysplasia
  • AML and MDS, therapy-related
  • AML not otherwise categorized
  • –similar to FAB list
  • Acute biphenotypic leukemia
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15
Q

What is the MAJOR PROGNOSTIC FACTOR for AML?

A

CYTOGENETICS - major and most important thing in terms of prognosis and treatment

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16
Q

What are favorable features of the AML? (good prognostic indicators)

A

-Age

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17
Q

What are unfavorable features of AML? (poor prognostic indicators)

A
  • Poor risk cytogenetics
  • Age >60
  • Presence of infection or sepsis
  • Poor performance status
  • Presence of prior MDS
  • Secondary AML
  • Extreme leukocytosis
  • Extramedullary disease (enlarged lymph nodes all over - adenopathy all over)
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18
Q

WHAT IS THE SINGLE MOST IMPORTANT PROGNOSTIC FACTOR FOR AML?

A

CYTOGENETICS

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19
Q

What cytogenetic outcomes have a favorable risk?

A

t(8;21) (best), t(16;16), t(15;17)

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20
Q

What cytogenetic outcomes have an intermediate risk?

A

(Normal karyotype)

-NPM1+/Flt3- genotype most favorable

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21
Q

What cytogenetic outcomes have an unfavorable risk?

A

del 5, del 7, trisomy 8, 11q23, other complex karyotypes

22
Q

How do you do cytogenetics?

A
  • Undergo tissue assay
  • Prepare 20 cells in metaphase
  • Pathologist looks at cells under microscope and tells you what’s going on
23
Q

How are most AML cases treated if 60 years or younger?

A
  • Induction chemotherapy with anthracycline (daunorubicin, mitoxantrone, idarubicin) plus cytosine arabinoside. “7 + 3” regimen.
  • If remission obtained (60-70% remission rate), then consolidation chemotherapy or transplantation
  • If no remission, then especially poor prognostic sign
  • –If remission induced with alternative regimen, then consider allergenic transplantation
24
Q

What is the “7 + 3” regimen?

A
  • 7 days of cytosine arabinoside (continuous infusion)
  • 3 days of 3 (idarubicin, mitoxantrone, daunorubicin)
  • They’re in the hospital for 3 weeks
25
Q

Who should receive consolidation chemotherapy and what is it?

A
  • High-dose cytosine arabinoside x 4 cycles
  • Good risk cytogenetics (8;21, inv16, 15;17)
  • Normal karyotype with NPM1+, Flt3-
  • Intermediate risk cytogenetics w/o matched sibling donor or unwilling/unable to have transplant in 1st CR
26
Q

What determines your eligibility for a stem cell transplant?

A

Poor risk cytogenetics

27
Q

Why is cord blood so good?

A
  • It is so simple and easy to do

- But it’s not good because you have such a limited supply (baby is not identified)

28
Q

When should you do allogenic stem cell transplantation?

A
  • Poor risk cytogenetics
  • Intermediate-risk cytogenetics with matched sibling donor
  • Extramedullary disease (chloroma)
  • 1st or 2nd relapse
  • Donor sources include siblings, children, parents, MUD-matched unknown donor, umbilical cord blood
29
Q

What is autologous stem cell transplantation used for?

A
  • No proven benefit over consolidation chemotherapy in 1st CR
  • Consider for patients w/o an allogenic donor
30
Q

What type of transplant is better?

A

Allogenic

31
Q

How are AML cases treated if older than 60 years?

A
  • USUALLY DON’T DO ALLOGENIC TRANSPLANTS
  • Induction chemotherapy with anthracycline (daunorubicin, mitoxantrone, idarubicin) plus cytosine arabinoside. “7+3” regimen.
  • If remission obtained (60% remission rate), then consolidation chemotherapy with reduced intensity cytosine arabinoside
  • Mylotarg (anti-CD33 moAb) coupled to calicheamicin) for relapsed disease
  • Consider observation and supportive care in lieu of induction chemotherapy
32
Q

Is GVHD (graft vs. host disease) curable?

A

NO!

33
Q

What are you thinking if patient has fatigue, malaise, fevers?

A

-Infection, Lyme’s, Tick-borne illness

34
Q

What are you thinking if patient has fatigue, malaise, fevers and nosebleed (epistaxis)?

A
  • Thrombocytopenia, problem with coagulation system (less common)
  • Tick borne illness can also present with thrombocytopenia
35
Q

What is normal range for WBC count?

A

In single digits

36
Q

What are normal platelets?

A

150-200 K

37
Q

If fibrinogen is under 100?

A

Patient is consuming their factors or they don’t have good liver function

38
Q

What is a common drug that can elevate WBCs?

A

Steroids - cause demargination of neutrophils from the vascular system!

39
Q

What can cause fever, fatigue, malaise and nosebleed? What does it look like on a blood smear?

A

M3 AML - acute promyelocytic leukemia

  • You’ll see heavily granulated promyelocytes!
  • Stack of AUER RODS seen in cells
  • Much mononuclear infiltrate is evident in slides!
40
Q

What should you remember about acute promyelocytic leukemia (M3)? (EXAM)

A
  • t(15;17) translocation

- If they relapse, they get arsenic trioxide

41
Q

What should you know about acute promyelocytic leukemia (M3)?

A
  • Most with t(15;17). Creates fusion gene, PML/RAR-alpha
  • Poor risk disease with t(11;17)
  • Induction therapy with ATRA plus anthracycline-based chemotherapy
  • Consolidation with 2 courses anthracycline-based chemotherapy
  • 2 years maintenance chemotherapy with ATRA, 6-MP, and methotrexate
  • Relapse
  • –Arsenic trioxide
42
Q

What commonly happens with APML - M3?

A
  • Auer rods
  • DIC a common presentation
  • –Coagulopathy
  • –Depressed fibrinogen
  • –Thrombocytopenia
  • –Fatal hemorrhage
43
Q

If a patient has M3 and DIC. . .

A

. . .start ATRA (all-trans retinoic acid) in

44
Q

What can you not ‘let the sun set on’ or miss?

A

AML M3

45
Q

What do you think when you hear 50 f, fatigue, headache, blurred vision?

A
  • Electrolyte balance
  • Dehydration
  • Needs glasses
46
Q

What does 1 gram of hemoglobin equal?

A

1 unit of blood

47
Q

What is seen in the blood smear of someone with M4 AML?

A

Hyperleukocytosis

  • Too big monocytes with cleft in nucleus
  • Lymphocytes are too large (much larger than red cells)
  • –Indicates = bone marrow failure
48
Q

What causes fatigue, headache and blurred vision in a patient with M4 AML?

A

Hyperleukocytosis
–Hyperviscosity
–Sludging in vasculature with ischemia and/or infarct
Leukopheresis to reduce WBC

49
Q

What happens with automated blood counters?

A
  • Can misdiagnose monocytosis - could actually be leukemia

- Cell counters can confuse blasts and monocytes

50
Q

What can happen with a blood transfusion?

A
  • Patient can have new blood type, the HLA of the donor

- This is called 100% donor chimerism - their cells even use the DNA of the donor

51
Q

What are two new treatment paradigms in AML?

A
  1. Flt-3 receptor tyrosine kinase inhibitors
    - Quizartinib
    - Effective (47% response rate ) in relapsed AML
    - May be effective “bridge to transplant” strategy
    - Studies underway to combine with conventional induction therapy
    - Notable side-effects include QTc prolongation
  2. CBF (core binding factor)
    - Dasatinib
    - C-kit overexertion in CBF+ AML

IHO Week 4 (25 decks)

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