Oncology Flashcards
History and PE of acute leukemias
Rapid onset w/ si/sx of anemia (pallor, fatigue), thrombocytopenia (petechiae, purpura, bleeding), and bone pain (medullary expansion and periosteal involvement)
Hsm and swollen/bleeding gums
Blasts
immature blood cells
BM findings in acute leukemia
BM with 20-30% blasts
AML = myeloblasts
ALL = lymphoblasts
AML vs ALL blasts appearance
AML: large, uniform myeloblasts with round or kidney-shaped nuclei and prominent nucleoli
ALL: large, uniform lymphoblasts- large cells w/ high N:C ratio
Leukostasis
Occurs when WBC is very high
Blasts occlude the microcirculation -> pulmonary edema, CNS symptoms, ischemic injury, and DIC
Leukemoid reaction vs. CML
Both have increased WBC count, but leukemoid reaction has increased LAP
Leukemoid reaction: leukocytosis 2/2 infection/sepsis
Auer rods
Rods present in APL
APL treatment
all-trans retinoic acid
-ATRA therapy
APL associations
Increased incidence of DIC
Chromosomal translocation: q15,17
Treatment of acute leukemia
Patients should be well hydrated prior to therapy
High WBC = start allopurinol to prevent TLS
Chemotherapeutic agents; antibiotics, transfusions, and colony-stimulating factors are also used
BM transplantation may be required for those who do not achieve remission
Treatment of leukostasis
Hydroxyurea +/- leukopharesis to rapidly decrease the WBC
Ages of leukemia
0-20: ALL
20-40: AML
40-60: CML
60-80: CLL
CLL
Clonal proliferation of functionally incompetent lymphocytes
-accumulates in BM, blood, LN, spleen, liver
Involves well-differentiated B cells
Diagnosis of CLL
-cell markers
Biopsy is rarely required for diagnosis Clinical picture (fatigue, malaise, infection, LAD, splenomegaly) Flow cytometry: CD5, CD20, CD2 positive together (normally CD5 is T cell specific while CD20 and CD2 are B cell specific)
Peripheral smear: abundance of small, normal appearing lymphocytes and ruptured smudge cells on smear
-smudge cells 2/2 cover slip crushing fragile leukemic cells
Labs: granulocytopenia, anemia, thrombocytopenia 2/2 marrow infiltration
Abnormal leukemic function = hypogammaglobulinemia
Tx of CLL
Palliative treatment, often withheld until pts are symptomatic
-ie recurrent infection, anemia, thrombocytopenia, splenomegaly, LAD
Tx: chemo
Not curable, but long dz-free intervals can be achieved
CML
Clonal proliferation of myeloid progenitor cells -> leukocytosis with excess granulocytes and basophils
-sometimes increased erythrocytes and platelets also
CML = BCR-ABL translocation must be present (Philadelphia chromosome of q(9,22)
Sx of CML
Anemia, splenomegaly (LUQ pain and early satiety), hepatomegaly, constitutional symptoms
Disease phases of CML
Chronic: without treatment, usually anemia, splenomegaly, constitutional symptoms
Accelerated: transition to blast crisis -> increased peripheral and BM blood counts
-suspected when diff shows abrupt increase in basophils and thrombocytopenia
Blast crisis: resembles acute leukemia
Blast crisis
Occurs in CML
Increased basophils and thrombocytopenia
Resembles acute leukemia
Granulocytes in all stages of maturation
CML
Lab values in CML
Low LAP
High LDH, uric acid, and B12levels
Diagnosis of different leukemias
Acute: Circulating blasts in the peripheral blood, leukocytosis
CLL: Flow cytometry, lymphocytosis, granulocytopenia, anemia, thrombocytopenia, smudge cells
CML: luekocytosis (very high), granulocytes in all stages of maturation
Treatment of CML
Chronic: Imatinib, a non-receptor tyrosine kinase inhibitor
Blast crisis: same as for acute leukemia; can also involve dasatinib + stem cell transplantation