Unit III Flashcards
Congenital AML translocations (5)
- t(8,21)
- inv(16) or t(16;16)
- t(15;17)
- t91;22)
- 11q23
t-AML (2)
- alkylating reagent or radiation (whole/partial loss of 5/7)
- Topo II inhib (rearrangement of MLL) 11q23
NOS-AML (3)
- FLT3 (ITD)
- NPM1
- CEBPA
Markers for B-ALL (4)
- CD19
- 22
- 79a
- Lack CD20
3 B-ALL
- t(9;22)- p190
- MLL, 11q23
- t(12,21)
Markers for T-ALL (7)
- cd2
- 3
- 7
- 4/8 + or -
- 99
- 1a
CML
- t(9,22), p210
PV
JAK2 mutation (V617F), nearly all have this mutation
MPNs (4)
- CML- neutrophilia
- polycythemia vera-erythrocytosis
- Primary myelofibrosis- granu/megakaryocytic lineages
- Essential thrombocytopenia- thrombocytosis
Burkett’s positive (5)
GC B cell
- cd19
- 20
- 10
- BCL6
- c-myc
Burkett’s neg (4)
- BCL2
- CD5
- CD23
- TdT
Follicular lymphoma + (5)
- 19
- 20
- BCL-2
- 10
- BCL-6
Mantle cell lymphoma + (6)
- 19
- 20
- 5 ***
- BCL-1 **
- 10
- BCL-6
SLL/CLL + (3)
5
23
19
Signs/sympt of anemia (4)
fatigue, malaise, pallor, dyspnea
Signs/symptoms of thrombocytopenia (3)
bruising, petechial, hemorrhage
Signs/symptoms of neutropenia
fever, infections
The genetic perturbations that cause AML appear to occur at the level of the
pluripotential stem cell
one of committed progenitors
The genetic perturbations that cause ALL appear to occur at the level of the
lymphoid stem cell
WBC in ALL
increased, normal, or decreased
CML philias
neutrophils
sometime baso and platelets
OV philias
RBC
neutrophils and platelets
Thinking PV but no JAK2 mutation->
secondary erythrocytosis
Splenomegaly in ET
NOT COMMON
CD20
mantle cell B-cells and germinal center B-cells
CD3
T cells in paracortex
Smudge cell
CLL
CD38-, ZAP-70-, germline IGH@ V, pre-germinal center
in CLL
Favorable
Neg mantle cell lymphoma
CD23
T cell deficiencies infection (2)
candida albicans
pneumocystis jirovecci
(2) complement mediated damage Type II diseases
- myasthenia gravis
2. goodpasture