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Blood & Lymph > Acute Leukemia - Simms > Flashcards

Acute Leukemia - Simms Flashcards

1
Q

List the 3 categories of WBC neoplastic proliferations

A
  1. lymphoid neoplasm
  2. myeloid neoplasm
  3. histiocytosis
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2
Q

______ block normal maturation, turn on pro-growth signaling pathways or protect cells from apoptosis.

A

Oncoproteins

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3
Q

Enhancement of self-renewal is a mutations property that allows activation of ______ → cell growth by enhancing MAPK.

A

tyrosine kinase which activates Ras

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4
Q

Proto-oncogenes are often activated in lymphoid genes by error during _______.

A

antigen receptor gene rearrangement/diversification

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5
Q

MC cause of proto-oncogene activation

A
  1. Germinal center B cells making an error during attempted class switching and somatic hypermutation
  2. V(D)J recombinase
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6
Q

V(D)J recombinase in precursor B/T cells modify Ig/T-cell receptor loci. They can accidentally _____ → proto-oncogene activation

A

join portions of other genes together

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7
Q

List 2 error made during somatic hypermutation and/or class switching

A
  1. MYC/Ig translocation → MYC
  2. BLC6 activation
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8
Q

How does BLC6 activation happen?

A

mistargeting by AID

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9
Q

How does MYC/Ig translocation occur?

A

AID translocated to transcriptionally active Ig locus

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10
Q

_____ are uncommon proliferative lesions of macrophages and dendritic cells

A

Histiocytosis

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11
Q

Lymphoid neoplasms include _____ (3) tumors

A
  1. B-cell
  2. T-cell
  3. NK cell
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12
Q

HIV leads to a risk of germinal B-cell lymphoma due to ____.

A

hyperplasia of germinal center

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13
Q

Chronic inflammation may lead to lymphoid neoplasms, almost always in the inflamed tissue. For example (2):

A
  1. H. pylori
  2. gastric B-cell lymphoma
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14
Q

T cells morphology of L2 (subtype of ALL) has grooves in the _____.

A

nuclei (highly irregular)

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15
Q

L3 (Burkitt type ALL) has _____ inside the cytoplasm.

A

vacuoles

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16
Q

Histochemistry of the ALL subtypes differentiates which 2 cell types?

A
  • myeloid cells
  • lymphoid cells (PAS +)
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17
Q

What is the main difference between Burkitt Leukemia & B-cell ALL?

A
  • Burkitt: B cell precursors
  • B-cell ALL: Mature B cells

(lends to prognosis)

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18
Q

Peak incidence for B-cell ALL is ______

A

3 y/o

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19
Q

How do you distinguish from T cell or B cell ALL?

A
  1. immunophenotyping
  2. cytogenetics
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20
Q

B-cell ALL is typically due to _____(2) mutations

A
  • t(12;21)→RUNX1 & ETV6 loss of fxn
  • t(9;22) → BCR-ABL fusion → poor prognosis
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21
Q

T cell ALL is categorized as _____

A

T cell (it can occur across the board; usually a dominance in “blasts”)

(no distinction that helps in terms of prognosis or tx)

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22
Q

TdT + is an important marker for ______.

A

lymphoid origin → ALL

(specific to lymphoblasts, negative for AML)

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23
Q

In both T cell and B cell ALL, there is a bone marrow failure which leads to accumulation of ______.

A

neoplastic (non-functioning) “blasts” in marrow → decreased hematopoiesis

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24
Q

Meningeal leukemia manifests as ______- type presentation; Mediastinal manifests as ______- type presentation.

A
  • CNS : HA, vision disruption, edema, sz
  • SOB, chest pain

(ultimately, CBC will give the dx)

25
Q

Leukemias start in _____ and spread to lymphoid organs. Lymphomas start in the _____ and spread to the bone marrow.

A
  • bone marrow
  • lymphoid organs
26
Q

Neoplastic B-cell lymphocyte proliferation originates in the_____ and spreads to ______.

A
  • lymph nodes
  • bone marrow

(if its just in the blood → CLL; just lymph nodes → small cell lymphoma)

27
Q

T-cell ALL prognosis

A

worse that B-cell

(getting better w/increase in tx technologies)

28
Q

> 35 y/o, WBC > 30k cell/L, absence of remission after 4 weeks of chemo = _____ prognosis of B-cell ALL

A

Poor (high-risk)

(very high risk = BCL/ABL)

29
Q

______ (histo finding) are found in AML.

30
Q

Lymphadenopathy are rare in _____, but usually a common first sign of _____.

A
  • AML: acute myeloid leukemia
  • ALL: acute lymphoblastic leukemia
31
Q

ALL metastasizes to the ____ (2)

A
  1. CNS
  2. TeSteS

(metaStaSizeS)

32
Q

AML (aka Acute myelogenous or Myeloblastic or Myeloid) is a disease of the _____.

A

elderly

(AML-M3 occurs in 15-40 y/o)

33
Q

In general, there are (3) types of myeloid disorders:

A
  1. myeloproliferative (too many)
  2. myelodysplastic (dysfunctioning)
  3. AML (arise from one of the above)
34
Q

Myeloproliferative/dysplastic disorders and Down Syndrome, Type I fibromatosis, and Fanconi Anemia are predisposing risk factors for ______.

A

AML

(radiation and smoking also)

35
Q

AML is a neoplastic proliferation of immature ______ in the bone marrow.

A

myeloid cells (myeloblasts)

36
Q

Which 4 acute myeloid leukemias account for 90% of cases?

A
  1. M1 - AML w/o differentiation
  2. M2 - AML w/maturation
  3. M3 - Acute PROmyelocytic Leukemia
  4. M4 - Acute MyeloMONOcytic Leukemia

(from least to most differentiated/mature)

37
Q

t (__;__) is the major translocation found in M1, M2, M3 AML

A

t(8;21) → CBFA2-ETO

38
Q

M1, M2, M3 AML are CD _____+

A
  • CD13
  • CD33

(3 types → 3, 3s in the CDs; more mature has CD11 or CD14)

39
Q

t (__;__) is the major translocation found in PML. The fusion gene that results stops myeloid maturation.

40
Q

Which of these cells is normal, which is PML-RARA fusion gene?

41
Q

myeloid peroxidase + is indicative of ____

42
Q

t(8;21)(q22;q22), t(15;17)(q22;q12) and inv(16)(p13q22) are indicative of a _____ prognosis for AML

A

good

(t(15;17) is APL)

43
Q

______ is indicative of a bad prognosis for AML

A

t(9;22)(q34;q11)

44
Q

Acute Promyelocytic Leukemia aka _____ (2)

A

aka APL or AML-M3

45
Q

APL (AML-M3) is typically seen in which age group (this sets it apart from the other types of AML)?

A

young adults

46
Q

What sets APL (AML-M3) apart from the other myeloid leukemias?

A

DIC: neoplastic cells are rich in pro-coagulant molecules within their cytoplasm, when they die → spills into blood

(risk of chemo for these pts)

47
Q

APL (AML-M3) is _____ negative (which is present in most other types of AML)

48
Q

Genetic mutations in APL

A
  • t(15;17) → PML-RARA fusion → activation of pre-mitotic receptor tyrosine kinase
  • t(11;17)
49
Q

APL is highly responsive to _____ therapy

A

ATRA-CR therapy (All-Trans Retinoic Acid)

50
Q

Wet purpura, petechiae, gingival hyperplasia and leukemia cutis (skin rash) are clinical features of ______

A

AML

(also fatigue, wt. loss, poor appetite, fever, severe infection)

51
Q

AML lab findings include _____ WBC, _____ Hb (normocytic; normochromic) and thrombocytopenia.

A
  • increased
  • decreased
52
Q

What is “mass effect”?

A
  1. bone pain (marrow expansion)
  2. lymphadenopathy
  3. hepatosplenomegaly

(ALL>AML)

53
Q

What is a mnemonic to remember the population affected and cause of T cell ALL?

A
  1. T-ALL
  2. Thymic lymphoma
  3. Teens (adolescent)

(3 T’s of T cell ALL)

54
Q

T cell ALL is due to a _____ gain-of-function mutation.

A

NOTCH1 → maturation arrest w/increased self renewal

55
Q

Morphology of ALL is lymphoblasts w/condensed nuclear chromatic, small nucleoli and scant agranular cytoplasm. What is the morphology of AML (4)?

A
  1. myeloblasts
  2. less condensed nuclear chromatin
  3. small nucleoli
  4. cytoplasm w/granules

(the exact opposite of ALL)

56
Q

hyper and hypo diploidy are only seen in _____.

A

B-cell ALL

57
Q

MC childhood cancer

58
Q

Plasma cell neoplasms are _____ tumors that arise in the bone marrow (lymphomas).

Blood & Lymph (29 decks)

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