malignancies Flashcards

1
Q

Auer rods (multiple)

A

AML (APL)

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2
Q

basophilic stippling

A

increased or defective RBC production

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3
Q

nRBC

A
bleedin/hemolysis
primary myelofibrosis (messed up BM architecture)
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4
Q

Howell-Jolly body

A

sign of asplenia (left over nuclear fragments not cleared)

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5
Q

ring sideroblasts

A

MDS: refractory anemia with ring sideroblasts

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6
Q

mononuclear Megs

A

MDS with del5q

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7
Q

smudge cells

A

CLL

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8
Q

what are forward scatter and side scatter proportional to on flow cytometry?

A

FS: size of cell
SS: granularity/segmentation of nuclei

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9
Q

what three commonly mutated molecules play a role in the epigenetics of acute leukemias?

A

Tet1/2: normally demethylate cytosines, deactivating mutation=no differentiation
WT-1: localizes Tet to target genes, deactivating mutation=no differentiation
IDH: makes alpha-kg which blocks Tet, gain of function mutation blocks Tet too much=no differentiation

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10
Q

what cytogenetics are associated with poor prognosis in AML? intermediate risk?

A
  • del or monosomy of chromosomes 5 and 7 (q)

- c-KIT mutation

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11
Q

APL: what mutation commonly drives proliferation?

A

FLT3, a receptor tyrosine kinase

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12
Q

what is the most common chromosomal abnormality in B-ALL in children? 2nd most common?

A

hyperploidy

TEL-AML

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13
Q

what is the most common chromosomal abnormality in adult B-ALL?

A

BCR-ABL

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14
Q

BCR-ABL promotes proliferation. what usually inhibits differentiation in ALL with BCR-ABL translocation?

A

mutated IKZF1 transcription factor

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15
Q

what is MLL and what does its translocation result in? what is commonly mutated with it?

A

MLL=histone methyl transferase, mutation=blocked differentiation
FLT3, tyrosine kinase–proliferation

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16
Q

what’s the translocation theme in T-ALL

A

oncogene to TCR on chromosome 14

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17
Q

what are 4common causes of leukocytosis beside infection or myeloproliferative disease?

A

smoking, obesity, corticosteroids, lithium

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18
Q

what is erythromelalgia and what is it seen in?

A

red, painful digits due to clogging of small vessels

-P vera and ET

19
Q

what cells are increased in the peripheral blood of AML? CML?

A

AML: blasts
CML: mature PMNs, bands, (meta)myelocytes, eosinophils, basophils, platelets

20
Q

what cells are increased in the BM of P vera?

A

erythroblasts, Megs, and granulocyte precursors

21
Q

what causes splenomegaly in P vera?

A

stagnation and congestions

-late, can cause hepatosplenomegaly due to extramedullary hematopoiesis after BM fibrosis occurs

22
Q

how might you treat P vera?

A
  • phlebotomy
  • aspirin to prevent platelet aggregation
  • hydroxyurea, IFN, or busulfan to prevent hematopoiesis
  • Jak inhibitor
23
Q

what kind of anemia may ET cause?

A

microcytic, hypochromic due to iron deficiency

24
Q

what condition is a strong indicator of ET?

A

splanchnic or portal vein HTN or thrombosis

25
Q

how might you treat ET?

A

NOT phlebotomy

  • hydroxyurea, IFN
  • anagrelide-specific to Megs
26
Q

what do azacytidine and decitabine do and what are they used for?

A

hypo-methylating agents to reprogram cells in MDS

27
Q

what is lenalidomide used for?

A

MDS with 5q-

MM: immunomodular (inhibits immune cells)

28
Q

what is ibrutinib and what is it used for?

A

BTK inhibitor

-relapses of B cell lymphomas

29
Q

which lymphomas are indolent?

A
  • follicular
  • CLL/SLL
  • mycoses fungoides
  • MALTomas
30
Q

which lymohomas are aggresive?

A
  • DLBL
  • mantle cell
  • peripheral T cell NOS
31
Q

which lymphomas are highly aggressive?

A

Burkitt’s and T cell lymphoblastic lymphoma

32
Q

CLL is a proliferation of which cells

A

memory B cells in marginal zone

33
Q

mantle cell lymphoma is a proliferation of which cells? which immunostains are used to diagnoseit?

A

B cells in mantle zone, not yet activated

-Ki-67 and cyclin D1

34
Q

what differentiates mantle cell lymphoma from follicular and CLL on a slide?

A
  • smaller lymphocytes than the centroblasts of follicular lymphoma
  • no proliferation centers as seen in activated B cells of CLL
35
Q

what is Burkitt’s lymphoma a proliferation of? what does it look like on slide?

A

memory B cells

  • cells very blue cytoplasm with cytoplasmic vacuoles and variation in size
  • starry-sky appearance from macrophages participating in high cell turnover
36
Q

what role does IL-6 play in which cancer?

A

MM

  • stimulates growth of plasma cells
  • high concentration = poor prognosis
37
Q

what two values define diagnosis of MM?

A

serum M protein > 3g/dL

BM plasma cells > 10%

38
Q

how does MM cause lytic bone disease?

A

produce DKK1 which stimulates RANKL and IL6 production by osteoblasts and stromal cells

  • osteoclast differentiation induced
  • osteoblasts inhibited
39
Q

what is lymphoplasmacytic lymphoma a proliferation of and what condition does it cause?

A

plasma cells
Waldenstrom’s macroglobulinemia: excess IgM production causes hyperviscosity of blood
-blurred vision, changed mental status, headache

40
Q

what does lymphoplasmacytic lymphoma do that MM doesn’t?

A

cause hepatosplenomegaly and lymphadenopathy

-overtakes BM and causes anemia

41
Q

what is follicular lymphoma a proliferation of?

A

centroblasts and centrocytes in germinal center

-larger with clumpier chromatin than small lymphocytes

42
Q

what chemo combo is commonly used in Hodgkin’s

A

ABVD: doxorubicin, bleomycin, vinblastine and dacarbazine

43
Q

are any cell lineages increased in aplastic anemia? what type of anemia is it?

A

lymphocytosis: longer lived

normochromic and normocytic with low reticulocytes