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32 Cards in this Set

  • Front
  • Back
CML: Peripheral Blood Smear
CML - BM aspirate - Lots of meloid and very few erythroids – so ME ratio is quite elvated in CML
often seen in CLL
CLL - Lots of mature looking lymphocytes that all look the same – different from AML and ALL and CLL
CLL - Autoimmune hemolysis is very common – going to see shperocytes here – can see monocyte phagnocytising an RBC in the peripheral blood
CLL - Prolymphocytes in a patient previously diagnosed with CLL - a bad transforming event
Richters syndrome - CLL (left) and large cell NHL (right) in the same node of a single patient
Bone marrow involvement in CLL
Immunohistochemistry detects faint Bcl2 expression in a normal lymphoid follicle in the mantle area
CML - presentation
pretty nonspecific, but have Splenomegaly and Hepatomegaly
CML - pathophysiology
- Neoplastic transformation of a hematopoietic stem cell
- can self-renew and diff
- w/ ­inc prolif, and dec diff → accelerated phase and eventual blast crisis
CML - Common Laboratory Findings
- Neutrophilia with left shift
- Basophilia
- low LAP
- BM is Hypercellular, Dec fat, Inc ME ratio
CML - cytogenics
- conventional
- Philadelphia (Ph) chrom - t(9;22)
- bcr on 22 and abl on 9 make a fusion gene product on 22 - Brc/Abl
- FISH and PCR will find it but wont find other abnormalities
- conventional might not find it but will find other abnormalities
- Ras → MAPK, STAT1 and 5 and that causes inc prolif
- PI-3 kinase → AKT leads to inc survival
- adhesion defect
CML stages
- Chronic - Median 3-5 years
- Accelerated phase - 6–9 months, Increasing WBC, splenomegaly, increasingly unresponsive to therapy
- Blast crisis - Median survival 3–6 months, worsening constitutional symptoms, complications of cytopenias , extramedullary disease (skin, CNS, bone)
CML treatment
- Chemotherapy with hydroxyurea, busulfan - old
- IFN-a - bad SEs
- SCT - only curative therapy but high mortality
- Gleevec - Abl tyrosine kinase inhibitors
Gleevec resistance
- Amplification of Brc/Abl
- Mutations within the ABL kinase domain
- Drug efflux –
- Activation of downstream signaling pathways
Docs overcoming gleevec resistance
- Higher-dose Gleevec
- Second generation ABL kinase inhibitors (inhibit things downstream)
- Gleevec + novel therapies
Benign Neutropenia
- Left shift not as marked as CML
- Increased granulocytes but Normal basophil count
- will still see fat in BM
- molecular test normal
CLL - pathophys
accumulation of slowly dividing, mature B or (much more rarely) T cells in the peripheral blood, marrow, lymph nodes and spleen
CLL - lab findings
- Lymphocytosis greater than 5,000/µl3 - mature-appearing with numerous smudge cells
- BM has increased lymphocytes
CLL - assocated factors
- Autoimmune hemolytic anemia is common
- TRAP is negative in cytochemistry
CLL - Tranforming events
- Prolymphocytic leukemia is an uglier disease - poor prog
- Richter’s Syndrome - large cell NHL - Fever, abd. pain, wt. loss, adenopathy, HSM, anemia, thrombocytopenia
CLL - Flow cytometry
- Mature B-cell population (+CD19, 22 & k light chain)
- Monoclonal (light chain restricted, + for k only)
- Population expresses CD5 (normally a T-cell marker) & CD23
- Inhibits release of cyto c from mito which activate caspases which are are the effectors of apoptosis
- so it inhibits apoptosis
CLL - genetics
- overexpression of Bcl-2
- 13q deletion most common
- 17p realted to p35
- 11q, Tri12
CLL and p53 dysfunction
- 17p, point mutations of p53, ATM mutations (16%)
- ass w/ resistance to chemo and short survival
CLL - IgVH Gene Mutation Status
- if no mutation, very bad prognosis
- Zap-70 associated w/
CLL - treatment
- only if the patient is symptomatic
- Fludarabine
- Rituxan – binds to CD20 on B-cells
- Chlorambucil + prednisone
- Campath 1-H – targets CD52 on B and T cells - making them HIV
Benign Lymphocytoses
- associated w/ mono
- blood has Atypical lymphocytes
- Normal BM
– negative (TRAP)
- mixture of B and T w/ polyclonal B-cell
Atypical Lymphocytoses
- Flow cytometry - predominance of Ts and polyclonal Bs
- shows + k and l
- The negative cells are Ts
Hairy cell leukemia
- Abnormal cells that are TRAP positive
- Middle aged man
- Massive splenomegaly -> panyctopenia
- Mature B-cell population (19, 22 & k), monoclonal w/ k
- Population expresses CD11c, CD25 & CD103
- Treat w/ 2CDa, IFN-a, or deoxycoformycin