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