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Pathobiology of Neoplasia > Leukemia > Flashcards

Leukemia Flashcards

1
Q

Pathobiology of Leukemia

A
  • Cell arrest in early phase of maturation
    • Accumulation of immature cells (Blasts)
    • Abnormal proliferation of blasts
    • Crowding of marrow elements




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2
Q

Etiology of Leukemia

A

*Cause is unknown
-Related to genetic disorders
 -Down’s syndrome, Bloom’s syndrome, Fanconi’s sarcoma, Klinefelters syndrome
-55-78% of patients have ACQUIRED chromosome abnormalities
-XRT (atomic bomb survivors)
-Chemicals (Alkylators & antibiotics)
-Chemotherapy (20-25% of cause)
• -Etoposide & Topoisomerase II inhibitors

Viruses:
 Adult T-cell leukemia & HTLV-1 virus

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3
Q

Epidemiology of Leukemia

A

Most common type in adults is AML and CLL

Over 1/2 of cases are acute

Increasing incidence

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4
Q

Clinical Manifestations of Leukemia

A

Caused by:
• Increased proliferation of blasts in blood forming organs
• Infiltration of blasts into other organs
• Decrease in normal leukocytes, erythrocytes & thrombocytes
• displayed by Granulocytopenia, Anemia, Leukemic Infiltrates, Thrombocytopenia 

*Signs & symptoms usually present for

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5
Q

Diagnostic Tests for leukemia

A

Bone Marrow biopsy is standard
-AML is Myeloid line of cells (myelocytes)
-ALL is Lymphoid line of cells (lymphocytes)
-Usually Hypercellular
-Auer rods are diagnostic of AML

Cytogenetic studies
–2/3 of pt’s have chromosomal abnormalities 
prognostic indicators
Flow cytometry
-AML vs. ALL
-lymphoid & myeloid markers= biphenotypic

*Peripheral smear may show blasts


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6
Q

Classification of Leukemia

A

AML
-malignant clone of myeloid, monocytes, erythroid or megakaryocyte

M1 (Acute Myelocytic Leukemia)
-most common type

M3 (Acute Promyelocytic Leukemia)
• high risk of DIC; best response/prognosis at 95%

-M4 (Acute Myelomonocytic Leukemia)
-extra medullary infiltration 

M5 (Acute Monocytic Leukemia)
-extra medullary infiltration 

-M7 (Acute Megakaryocytic Leukemia)
◦ rare disease from platelet precursor line



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7
Q

Classification Systems for Leukemia

A 
FAB
	•	Morphology, cell stains and flow cytometry
	•	Myeloid M0-M7
	◦	MDS vs. AML threshold= 30% blasts
	◦	Lymphoid L1-L3
WHO
	•	uses prognostic factors
	◦	molecular markers
	◦	chromosome translocations
	◦	dysplasia present?
	◦	17 subclasses
	◦	MDS vs. AML threshold= 20% blasts



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8
Q

AML w/ characteristic genetic abnormalities

A

-chromosome 8 and 21 translocations
-chromosome 15 and 17 translocations
-chromosome 16 inversion
◦ Most favorable; no transplant in first remission

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9
Q

AML w/ multi lineage dysplasia


A

patients with MDS or MPD 


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10
Q

AML and MDS (therapy related)





A

prior treatment w/ chemo and/or XRT





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11
Q

AML; not otherwise categorized





A

other subtypes





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12
Q

Acute leukemia w/ ambiguous lineage


A

-both myeloid and lymphoid cells 
-or not distinguishable
-Mixed or biphenotypic 


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13
Q

AML Treatment

A 
Induction
-normally 7+3

Evaluation
-Day 14 BM Bx
-CR =
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14
Q

Classification of APL and treatment

A

Also called M3
Chromosome 15 and 17 translocation
Treated with Arsenic and Atra
Monitored by PML-RAR alpha

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15
Q

Description of ALL

A

Originates in thymus, lymph nodes and bone marrow
T-cell, B-cell, or NK cell
CNS disease common
Can be Philly positive (BCR-ABL testing)

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16
Q

ALL Presentation

A

Lymphadenopathy

Splenomegaly

17
Q

Induction therapy for ALL?

A

HyperCvad x8 treatments
A: Cytoxan, vincristine, doxorubicin, decadron
B: MTX, cytarabine, IT MTX
Also use IT Cytarabine

18
Q

Blinatumomab

A

TX of Relapse, refractory, Philly negative ALL
CD19 positive cells are attacked by cytotoxic T-cells
*CD19 is a specific B-cell marker

19
Q

Treatment of Philly + ALL

A

25% of ALL diagnosis
Need allo transplant
Tx with TKI: dasatinib, ponatinib

20
Q

How is MDS scored?

A

The IPSS

  • blast percentage
  • cytogenetics
  • # of cell types affected in circulating blood
  • Higher score=decreased survival rate (I.e. >2.5)
21
Q

Treatment for MDS

A 
Observation
Vidaza
Growth factors (procrit)
Revlimid
Decitabine 
Clinical trial 
HSCT w/ HLA identical donor
22
Q

Description of CML

A

95% of pts Philly +
Chromosome 9 and 22 translocation
BCR-ABL +

23
Q

S/S of CML

A 
LUQ pain
Early satiety 
Bone, joint pain
Abd fullness
*MANY ARE ASYMPTOMATIC
24
Q

Diagnosis of CML

A

BM BX for FISH and BCR-ABL

  • elevated WBC
  • Decreased Hgb
  • elevated platelets in chronic phase
25
Q

Treatment for CML

A

TKI’s

  • ponatinib
  • dasatinib
  • imatinib
26
Q

Description of CLL

A

Also called Small lymphocytic lymphoma
Accumulation of NORMAL appearing lymphocytes in marrow, spleen, liver and nodes
*RAI staging system

27
Q

Treatment of CLL

A

Fludarabine
Bendamustine
Ibrutinib (improves prognosis when used in conjunction)
Ofatumumab

28
Q

Hairy cell Leukemia

A

Chronic
Presents with pancytopenia and severe splenomegaly
Tx’d with cladrabine
Oral drugs for BRAF mutation

Pathobiology of Neoplasia (7 decks)

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