Week 4 Cancers Flashcards
Acute Myelogenous Leukemia
20%(WHO) of bone marrow is bone marrow myelobasts
M0
Undifferentiated myeloid leukemia
M1
Acute myeloid leukemia w/o differentiation
M2
Acute myeloid leukemia with differentiation
M3
Acute promyelocytic leukemia which can be readily cured t(15;17) commonly see auer rods
M4
acute myelomonocytic leukemia
M5
acute monocytic leukemia
M6
Acute erythroleukemia
M7
acute megakaryocytic leukemia
Favorable cytogenetics
t(8;21) t(16;16) t(15;17) and auer rods
Remission
less than 5% blasts after 14 days
Chronic Lymphocytic Leukemia
Disorder of B cells but CD5+(t cell antigen), CD20+ and TdT(lymphoblasts) negative “CD23+” , tx with patience. treat sx. infection is problem Adults only
Hairy Cell leukemia
Hairy cells, splenomegaly, no lymphadenopathy, pancytopenia. Is a chronic B cell proliferative disorder. often >40 Male. Chicken wire bone marrow. TRAP+ CD20+ CD5- Tx. chemo, good prognosis Adults only
Prolymphocytic Leukemia
prolymphocytes, splenomegaly w/o lymphadenopathy, rare and aggressive. very high wBC, Low Hgb and platelets. dark dense chromatin Adults only
Large granulated Lymphocyte leukemia
Large granulated lymphocytes. “T cell” leukemia. Neutropenia- suceptible to infections. Long survival. Adults only
Chronic Myeloid Leukemia
neutrophilic leukocytosis. basophillia, phildelphia chromosome t(9;22) bcr-abl tyrosine kinase, three phases. Slow onset, fever, fatigue, full abdomen, night sweats
tx. imatinib
CML Chronic phase
stable counts, easily controlled, half go on to accelerated phase, half go onto blast crisis.
CML Accelerated phase
unstable counts, blast crisis within 6-12 months
CML Blast crisis
-becomes acute leukemia, migh mortality, blasts over 20%. can get a lymphoid problem as well
Chronic myeloproliferative disorders
Chronic myeloid leukemia, Polycthemia vera, Essential thrombocytopenia, Myelofibrosis occur only in adults. Long clinical course, increased WBC with left shift, may evolve into acute leukemia
Polycythemia vera
High RBC (sludgy blood) can get infarcts downstream diferent from secondary polycythemia, thrombosis and hemorrhage, Jak-2 kinase mutation in mostly all. Dx. high red cell mass, normal O2 sats. can have splenomegaly, thrombocytosis, increased WBC, Leukocyte alkaline phosphatase, increased B12. Marrow full of eryth. precursors. tx. phlembotomy, myelosuppressive drugs. Death from thromb. or hemmor.
JAK-STAT pathway
Signal binds cytokine receptor which has JAK bound. JAK Phos. receptor, STAT binds P. JAK phosphorylates STAT, STATS dimerize and become transcription factors.