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Acute Leukemia - Simms Flashcards

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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.

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

(ultimately, CBC will give the dx)

25
Leukemias start in _____ and spread to lymphoid organs. Lymphomas start in the _____ and spread to the bone marrow.
* bone marrow * lymphoid organs
26
Neoplastic B-cell lymphocyte proliferation originates in the\_\_\_\_\_ and spreads to \_\_\_\_\_\_.
* lymph nodes * bone marrow (if its just in the blood → CLL; just lymph nodes → small cell lymphoma)
27
T-cell ALL prognosis
worse that B-cell (getting better w/increase in tx technologies)
28
\> 35 y/o, WBC \> 30k cell/L, absence of remission after 4 weeks of chemo = _____ prognosis of B-cell ALL
Poor (high-risk) (very high risk = BCL/ABL)
29
\_\_\_\_\_\_ (histo finding) are found in AML.
Auer rods
30
Lymphadenopathy are rare in \_\_\_\_\_, but usually a common first sign of \_\_\_\_\_.
* AML: acute myeloid leukemia * ALL: acute lymphoblastic leukemia
31
ALL metastasizes to the ____ (2)
1. CN**S** 2. Te**S**teS (meta**S**ta**S**ize**S**)
32
AML (aka Acute myelogenous or Myeloblastic or Myeloid) is a disease of the \_\_\_\_\_.
elderly (AML-M3 occurs in 15-40 y/o)
33
In general, there are (3) types of myeloid disorders:
1. myeloproliferative (too many) 2. myelodysplastic (dysfunctioning) 3. AML (arise from one of the above)
34
Myeloproliferative/dysplastic disorders and Down Syndrome, Type I fibromatosis, and Fanconi Anemia are predisposing risk factors for \_\_\_\_\_\_.
AML (radiation and smoking also)
35
AML is a neoplastic proliferation of immature ______ in the bone marrow.
myeloid cells (myeloblasts)
36
Which 4 acute myeloid leukemias account for 90% of cases?
1. M1 - AML w/o differentiation 2. M2 - AML w/maturation 3. M3 - Acute **PRO**myelocytic Leukemia 4. M4 - Acute Myelo**MONO**cytic Leukemia (from least to most differentiated/mature)
37
t (\_\_;\_\_) is the major translocation found in M1, M2, M3 AML
t(8;21) → CBFA2-ETO
38
M1, M2, M3 AML are CD \_\_\_\_\_+
* CD1**3** * CD**33** (**3** types → **3**, **3**s in the CDs; more mature has CD11 or CD14)
39
t (\_\_;\_\_) is the major translocation found in PML. The fusion gene that results stops myeloid maturation.
t(15;17)
40
Which of these cells is normal, which is PML-RARA fusion gene?
41
myeloid peroxidase + is indicative of \_\_\_\_
AML
42
t(8;21)(q22;q22), t(15;17)(q22;q12) and inv(16)(p13q22) are indicative of a _____ prognosis for AML
good (t(15;17) is APL)
43
\_\_\_\_\_\_ is indicative of a bad prognosis for AML
t(9;22)(q34;q11)
44
Acute Promyelocytic Leukemia aka _____ (2)
aka APL or AML-M3
45
APL (AML-M3) is typically seen in which age group (this sets it apart from the other types of AML)?
young adults
46
What sets APL (AML-M3) apart from the other myeloid leukemias?
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
APL (AML-M3) is _____ negative (which is present in most other types of AML)
HLA-DR
48
Genetic mutations in APL
* t(15;17) → PML-RARA fusion → activation of pre-mitotic receptor tyrosine kinase * t(11;17)
49
APL is highly responsive to _____ therapy
ATRA-CR therapy (All-Trans Retinoic Acid)
50
Wet purpura, petechiae, gingival hyperplasia and leukemia cutis (skin rash) are clinical features of \_\_\_\_\_\_
AML (also fatigue, wt. loss, poor appetite, fever, severe infection)
51
AML lab findings include _____ WBC, _____ Hb (normocytic; normochromic) and thrombocytopenia.
* increased * decreased
52
What is “mass effect”?
1. bone pain (marrow expansion) 2. lymphadenopathy 3. hepatosplenomegaly (ALL\>AML)
53
What is a mnemonic to remember the population affected and cause of T cell ALL?
1. T-ALL 2. Thymic lymphoma 3. Teens (adolescent) (3 T's of T cell ALL)
54
T cell ALL is due to a _____ gain-of-function mutation.
NOTCH1 → maturation arrest w/increased self renewal
55
Morphology of ALL is lymphoblasts w/condensed nuclear chromatic, small nucleoli and scant agranular cytoplasm. What is the morphology of AML (4)?
1. myeloblasts 2. less condensed nuclear chromatin 3. small nucleoli 4. cytoplasm w/granules (the exact opposite of ALL)
56
hyper and hypo diploidy are only seen in \_\_\_\_\_.
B-cell ALL
57
MC childhood cancer
ALL
58
Plasma cell neoplasms are _____ tumors that arise in the bone marrow (lymphomas).
B-cell

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