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Leukemias

Hematology

QuestionAnswer
Most commonly occurring leukemia CLL
CLL Mgmt Observation; chemo (fludarabine & cladribine. cyclophosphamide, Rituximab); BMT; tumor lysis prophylaxis (allopurinol, 300 mg/day, hydration, diuretics); radiation (vs bulky adenopathy); surgery (for diagnostic)
CLL prevalence Mainly disease of older people (>90% of cases >50yr); M:F = 2:1
Characterized by clonal proliferation and accumulation of mature-appearing B lymphocytes (95 % of cases) in blood and lymphoid tissue; clonal malignancy of B lymphs CLL
CLL S/S 25 % asymptomatic at dx; fatigue; drenching night sweats; lymphadenopathy (80%); wt loss; frequent/persistent infxn; skin infxn/shingles
CLL findings Anemia & thrombocytopenia; mature small lymphs & smudge cells; Hepatomegaly; Splenomegaly
RAI Staging System used for: CLL
CLL growth Tends to be slow growing and indolent
Lymphocytosis, WBCs >20,000/µL = hallmark of: CLL
RAI Stage 0 Inc WBC (leukocytosis blood & marrow); >150 mos survival
RAI Stage 1 Inc WBC & lymphadenopathy; >101 mos survival
RAI Stage 2 Inc WBC & Hepato/splenomegaly; >71 mos survival
RAI Stage 3 Inc WBC & Anemia (Hgb < 11g/dl); >19 mos survival
RAI Stage 4 Inc WBC & Thrombocytopenia; >19 mos survival
Blast crisis Acute phase, when blasts comprise >30% of BM cells. Pts with CML that evolves into acute phase have poor response to tx & die in this phase.
CML will likely transform to: Acute disease
Primarily disease of children ALL
What percentage of ALL patients are children (usually 3 -7 yo) 80%
Accounts for 10-20% of acute adult leukemia ALL
CML mgmt Tyrosine kinase inhibitors (Gleevec/imatinib; allogeneic SCT; Dasatinib, AMN107; interferon & hydroxyurea
3 phases of CML are defined by: blasts in marrow
Slowly progressing disease: too many WBCs made in BM (especially myeloid cells) = CML
CML prevalence Young to middle age adults (median 45-55 yo); CML accounts for 7-20% cases of leukemia
Philadelphia chromosome present in ??% of CML cases >95% of cases (t9:22 translocation of DNA)
_____ can trigger Philadelphia chromosome Exposure to radiation
CML Sx/Sx Fever (w/o infxn); bone pain; LUQ pain (enlarged spleen); night sweats; bleeding & bruising; petechiae; fatigue ; weakness
CML tx goal: Complete hemo & cytogenetic response; Five yr survival = 52-63% ; Median survival =6 yrs
Type of leukemia = immature, abnormal cells in BM (>20%) and blood (>10%) & in liver, spleen, lymph nodes Acute Leukemia
ALL prognosis 80% of children will be cured with chemo; 20-40% of adults will be cured
ALL & AML Sx/Sx Meningitis; fever (abrupt onset with children); petechiae; anorexia, gingival hypertrophy. DIC, retinal hemorrhages. Leukemia cutis (skin) in AML.
ALL & AML labs Pancytopenia; hyperleukocytosis; BM >20% blasts
AML: median age at onset: 65 yr (AML = 80% of all adult-onset acute leukemias)
AML: 5 year survival: 10-30%
Hyperleukocytosis Circulating blasts in peripheral blood (> 200,000/ mcl)
ALL mgmt Aggressive combo chemo [approx 2 yrs total (cytoxan, donorubicin, vincristine, prednisone)]; CNS prophylaxis (intrathecal chemo); BMT??
Chemo phases for ALL Induction phase (4-6 wks); Consolidation phase (several mos); Maintenance phase (2-3 yrs)
AML Etiology Possibly exposure to toxins (benzenes, radiation, chemotherapy)
AML findings Pancytopenia, circulating blasts, often WBC >200,000; BM >20% blasts; Auer Rods; high ESR; hepatosplenomegaly
AML mgmt Chemo; Induction & 3 consolidation treatments, in hospital. Induction (ARA-C with mitoxantrone, idarubicin, or daunorubicin). Post-induction: chemo vs SCT. Tumor lysis prophylaxis (allopurinol, 300 mg/day, hydration, diuretics)
Hairy Cell leukemia prevalence Median age of onset = mid 50s; M:F = 5:1; usually indolent, very responsive to tx
Hairy Cell leukemia presentation Fatigue, abd discomfort (markedly enlarged spleen); persistent infxn;
Hairy Cell leukemia tx 2-CDA (2-chlorodeoxyadenosine), oral for 5-7 days (watch for drop in CBC counts); 90% of pts complete remission
Disease treated w/tumor lysis Ppx AML &CLL & NHL
Hallmark of Hairy Cell leukemia Pancytopenia; “hairy” cells
Bulky lymphadenopathy seen in: CLL; NHL
Next-door disease HL
B-symptoms fever, wt loss, drenching night sweats (HL, NHL)
Drenching night sweats seen in: CLL, Hodgkins
Can affect T or B lymphocytes ALL
Pancytopenia seen in: ALL, AML, hairy cell
Lymphadenopathy seen in in 80% of patients with: CLL
Skin infection/shingles CLL
RAI staging is for CLL
Meningitis seen in: AML/ALL
Immunologic phenotypes include: Common; Early B lineage; T cell ALL
M0-M7 phenotypes (based on degree of differentiation & maturation of predominant cells) used to classify: AML
Co-expression of CD19, CD5 CLL
Hypogammaglobulinemia CLL
Anemia is seen in which leukemias MM, hairy cell (NOT seen in CML)
Isolated lymphocytosis CLL
Malignant proliferation of lymphoid stem cells in BM -> invade LNs, spleen, liver = ALL
Factors associated with worse prognosis in adults with ALL Age >60, Philadelphia chromosome-positive, long time to first remission, high WBC at time of dx
Binet Stage A = CLL: lymphocytosis with <3 LN groups, no anemia or thrombocytopenia
Binet Stage B = CLL: lymphocytosis with >3 LN groups
Binet Stage C = CLL: anemia / thrombocytopenia +/- LN groups
Caused by proliferation of abnormal myeloid cells that do not mature AML
AML may be preceded by: CML, P vera, idiopathic myelofibrosis, or MDS
Caused by proliferatin of myeloid cells that retain their capacity to differentiate CML
Philadelphia chromosome-negative CML is associated with: poor prognosis
Created by: Adam Barnard Adam Barnard