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Lecture

Leukemia summary.docx

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Department
Medicine
Course
MED1201
Professor
Dr Kingswell
Semester
Fall

Description
Acute and Chronic Leukemias ALL AML CLL CML General - most common leukemia Myeloid problem - most common adult Myeloid in children (4 – 7 years) leukemia characteristics problem (that  lymphocyte problem - over 95% B cell cases can lead to ALL (either B or T cell)! - men to women 2:1 or AML)! - median age 60 – 65 years Lymphocyte problem Signs/ - anemia, Same as ALL - 40% asymptomatic - B symptoms+ Symptoms thrombocytopenia, - Lymphadenopathy, fatigue, gout, neutropenia hepatomegaly, splenomegaly, - night sweats, fever, splenomegaly bone pain weight loss (B - B symptoms + infections symptoms) - bone pain - bone pain CBC - increased WBC Same as ALL (but - WBC elevated - WBC elevated, - decreased Hgb + differential shows - lack of antibodies (due platelets may or platelets increased myeloid to lack of functional B may not be lineage cells) cells) elevated Smear - Blasts: No cytoplasm, - Blasts: Large - mature-looking - all stages of big mauve nucleus, mauve nucleus with lymphocytes, smudge granulocytic prominent nucleoli cytoplasm + Auer cells (blasts) maturation from rods, cytoplasmic blast cells to granules neutrophils (basophils seen) - overall left shift Flow - pre-B cell: CD19, CD22, CD13, CD33, CD5, CD19, CD20, cytometry CD10 Myeloperoxidase CD23, light chain - T cell: CD7, CD3 restriction *similar to ALL Bone marrow - over 20% lymphoid - over 20% Most cells end up in - hypercellular biopsy blasts myeloblasts periphery – usually not bone marrow needed with granulocytic predominance Histochemical Periodic acid-schiff stain, Myeloperoxidase, * similar to ALL *flow cytometry staining Tdt sudan Black stain, indicative of combined esterase increased myeloid stain (granulocytes progenitors stain red, monocytes stain black) Treatment  Induction therapy  Supportive  - Gleevec or other (+CNS prophylaxis), therapy chemotherapy/treatment tyrosine kinase consolidation,  Chemotherapy: ONLY if symptomatic inhibitors maintenance therapies induction + (cytopenia, infections, tyrosine kinase inhibitor consolidation etc.) *same as ALL (if Phil+)  Bone marrow  bone marrow transplant transplant if eligible if needed Prognosis Children: > 80% 75% achieve - 8 years if enlarged - due to Gleevec, complete remission and remission with lymph nodes, 6 years if no need for bone finish 2 – 3 years, over induction therapy, enlarged liver/spleen, 2.5 marrow transplant 70% survival less than 30% cured years if anemia or (fairly good  Adults: 65- 85% thrombocytopenia prognosis) complete remission, less - IgVH mutations than 40% survival (very associated with better poor prognosis for Phil+) results Cytogenetics T(9;22) – poor prognostic - Favourable: 17p, 11q, 12q trisomy and T(9;22) – Phil+ t(8;21), t(15;17), 13q deletions
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