Pre-TBL independent study Flashcards
What is leukemia (generally speaking)
A neoplasm involving hematopoietic stem cells– can derive into leukemia involving any of the cells that arise from the main precursor, incl myeloid leukemia and lymphoid leukemia (from myeloid cells and lymphoid/lymphocytes!)
AML (Acute Myeloid Leukemia) vs CML
caused by BLOCK in differentiation process (called LEFT SHIFT) bc lots of immature blasts
-Chronic has overprolif of ALL lvls of cell maturation
AML
pop
cells
sx
mostly adults
periph cytopenias (cell deficiencies), eg decr plates/rbc/grans, lots of blasts
-malig clones of immature cells replace healthy marrow
-sx: anemia, fatigue, infections, bleeding (thrombocytopenia), fever etc, if invasive can be in skin/gums (thin tissue)
Four types of AML
- AML with recurrent genetic abnormalities (usu balanced translocations)
- AML with myelodysplasia-related changes
- Therapy-related myeloid neoplasms
- Idiopathic AML
Dx of AML
high # of blasts in periph blood smear (if no auer rods, >20%), hypercellularity
might have auer rods (red lines)
What do red lines inside cell confirm Dx of?
auer rods in AML!
AML prognosis? and why
only a quarter survive, bc AML reduces ability to fight off infxns
(some translocations indicate better px)
AML tx?
blood transfusions, antibios, bone marrow transplant, chemo
ALL (acute lymphoblastic leukemia/lymphoma)
pop
sx and diff from AML
mostly children
similar sx to AML but with HEPATOSPLENOMEGALY
2 types of AML based on lymphocytes?
-precursor B-cell ALL (B-ALL)
can have recurrent genetic abnormalities in chrom, or translocs
-T-ALL: also affects medistinal (THYMIC) involvement (obv)
BOTH affect bone marrow and periph blood
ALL dx?
many lymphocytes in periph blood smear
-IHC cytochem to dist bn lymphos and myeloblasts
(blasts should be >~20-25% of cells)
Tx of ALL
treatable in kids
adults with ALL worse than with AML
-early induction, consol, prolonged maint of tx use
-tx with intrathecal chemo/ brain/spine radiation bc ALL likes to hide in the spinal cord
ALL with favorable prognosis?
12;21 and hyperdiploid
ALL with poor px?
9;22, v;11q23, and hyPO diploid
between hyper and hypodiploid ALL, which has better px?
HYPERdiploid ALL!
MDS (MyeloDysplastic Syndrome)
Disorder where stem cells cannot properlY become mature cells, causing problems down the line incl cytopenias, ineff hematopoeisis, dysplasia in cell lines ,and incr risk of AML
What else besides AML does MDS increase risk for and why?
MDS increases risk for LEUKEMIA bc cells are unstable, usu bc of genetic abnormalities (soemtimes chemo)
MDS sx and pop
Incr risk for?
much older pts, >70
anemia, freq blood transfusions, otherwise asymptomatic (dont know they have it)
-Can dev AML, and infections/bleeding
-Dysplasia in marrow and periph smear
What does MDS periph blood smear show?
Decr plates/RBCs
Histo shows unusual WBCs with PSEUDO-PELGER HEUT CELLS (bilobed dumbell shaped nuclei)
What does MDS bone marrow show? (stain?)
HYPERcellularity
decr cell counts (blasts LESS than 20%)
Erytrhopoetic issues such as RC precursers, nucl irreg, IRON STAIN
issues with grans/megakars
Subtypes of MDS
- low risk (usu dont dev into AML), refractory anemia with unilineage dysplasia (RA) or with Ring sideroblasts (RARS), RAs are refactory to b12 or folate tx
- intermed risk: refractory anemia with multilin dysplasia or w.o ring sidereoblasts, or with excess blasts (more acronyms)
- high risk: RAEB-1 (RA with excess blasts 2)
clonal cytogenic abnormalities are observed in approx how much of MDS cases?
50%
(look for del(5q)/7q issues
Tx for MDS?
NONE (bone marrow ineffective bc older pts), colony stim factors $$$
Which MDS genome may have + clin course?
isolated del(5q)
What does imunophenotyping in hematopoeitic issues determine? What are 2 methods?
whether cell is B/T/myeloid and what lvl of maturation
(tells us cell type via staining)
Examples are: IHC and Flow cytometry
How IHC works
uses ab’s to detect certain prot in sample
Non-fluor, uses LM, catalyzes rxn to give colored product etc
How Flow cytometry works
Laser based
fluor ab’s attach to ag’s to count/sort/detect cells, ag/ab stained complex detected electronically in fluid, cells scanned for diff properties
Which is better: IHC or flow cytometry and why (and what is its disadv?)
FLOW CYTOMETRY!
improved sensitivity, more detail, buuut loss of cell structure
map cell pop on XY plane, in C shape, so top RIGHT quadrant is positive for both X and Y, whereas top LEFT is positive only for Y
What might pseudo-pelger-huet cells (bilobed nuclei) indicate?
MYELODYSPLASTIC SYNDROME (MDS)!
