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52 Cards in this Set

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What is the peak age for acute lymphoblastic leukemia
peak age 3-4yr
p. 198
What is the most common neoplasm in children?
Actue lymphoblastic leukemia
p. 198
What are the signs and symptoms of acute lymphoblastic leukemia
sx: fever, fatigue
si: anemia, pallor, petechiae, infections
p. 198
What labs are used to diagnose acute lymphoblastic leukemia
Leukocytosis, blastsin pheripheral blood, decreased RBC count, decreased platelets, PAS+, CALLA+, TdT+, marrow bx shows increased blasts
p. 198
What cancer are increased blasts in bone marrow characteristic of?
acute lymphoblastic leukemia
p. 198
What cell markers are diagnostic of actue lymphoblastic leukemia?
PAS+, CALLA+, TdT+
p. 198
Describe the course of therapy in acute lymphoblastic leukemia
induction, condsolidation and maintenance (intrathecal chemotherapy during consolidation)
p. 198
What are the side effects of therapy given for acute leukoblastic leukemia? (3)
new cancers, incrased rate of sterility, growth defects
p. 198
What is the diagnosis given these markers: PAS+, CALLA+, TdT+?
acute lymphoblastic leukemia
p. 198
What is the most common leukemia in adults?
acute myelogenous leukemia
p. 198
Who gets acute myelogenous leukemia
adults
p. 198
How is actue myelogenous leukemia classified?
FAB system: M0-M7
p. 198
What are the signs and symptoms of acute myelogenous leukemia? (7)
fever, fatigue, pallor, petechiae, infections, splenomegaly, lymphadenopathy
p. 199
What leukemia is myeloperoxidase+, sudan black+, auer rods, throbocytopenia, peripheral blood & marrow bx shows myeloblasts
acute myelogenous leukemia
p. 199
What are 5 characteristic lab findings of actue myelogenous leukemia?
myeloperoxidase+
sudan black+
auer rods
throbocytopenia
peripheral blood & marrow bx shows myeloblasts
p. 199
What is the course of treatment for acute myelogenous leukemia?
induction and consolidation only
p. 199
What is the difference in treatment between actue lymoblastic leukemia and acute myelogenous leukemia?
actue lyphoblastic leukemia treatment has a maintenance phase
p. 199
M1: myeloblastic shows what 3 histologic features?
+ auer rods
+ sudan black
+ myeloperoxidase (MPO)
p. 198
M2: myeloblastic with differentiation shows what 3 histologic features?
++ auer rods
+ sudan black
+++ myeloperoxidase (MPO)
p. 198
What acute myelogenous leukemia subtype has prominent splenomegaly and + chloromas (green tumors made up of blasts)?
M2: myeloblastic with differention
p. 198
M3: promyelocytic shows what 3 histologic features?
+++ auer rods
increased granularity
+++ myeloperoxidase
p. 198
What leukemia has t(15:17) and what does it affect?
M3: Promyelocytic, affects retinoid acid receptor
p. 198
DIC is common in what leukemia
M3: promyelocytic (acute myelogenous leukemia)
p. 198
What drug is used to treat t(15:17)
ATRA - all trans retinoic acid is used to induce blast differentiation
p. 198
What subtype of acute myelogenous leukemia involves eosinophils?
M4: Myelomonocytic
p. 198
What subtype of actue myelogenous leukemia involves CNS and gingiva
M5: monocytic
p. 198
What condition often precedes M6: Erythroblastic subtype of acute myelogenous leukemia?
myelodysplasia
p. 198
What is the most common age for chronic myelogenous leukemia (CML)?
50's but can present at any age
What are 7 symptoms of CML?
fatigue
anorexia
abdominal discofort
early satiety
diaphoresis
arthritis
bone tenderness
What characterizes the peripheral blood smear
leukostatis (WBC >=10^5)
What are 7 clinical consequences of leukostatis (WBC >=10^5)?
dyspnea
dizziness
slurred speech
diplopia
confusion
retinal hemorrhage
pepilledema
p. 199
What are 4 lab findings of CML?
neutrophilia
thrombocytosis
Philadelphia chromosome
peripheral blood shows cells of all maturational states
p. 199
What treatment used in CML? What is it's target?
Gleevac, philadelphia chromosome product bcr-abl
p. 199
What is blast crisis in CML and what is it's outcome?
actue phase CML, leads to death in 3-4 mo, only BMT can prevent
p. 199
What is pathopnomonic of CML
Philadelphia chromosome
p. 199
What does the Philadelphia chromosome cause? Wha is the translocation?
constitutive tyrosine kinase activity, t(9:22) ->bcr-abl
promotes the cell cycle
p. 199
What is the level of leukocyte alkaline phosphatase in CML vs leukemoid reaction
CML: low
Leukemoid reaction: high
p. 199
What is the age distribution of chronic lymphocytic leukemia (CLL)?
increases with age
p. 200
What cell is proliferating in CLL?
95% are memory B-cel types (a flrom of blood borne lymphoma) expressing CD5 protein as a surface marker
p. 200
What are 3 signs of CLL
organomegaly
+/- anemia
later stages see throbocytopenia due to autoimmunity
p. 200
What are 3 lab findings of CLL
normal morphology lymphocytes of blood and marrow
monolonal antibodies (check to determine monoclonality)
autoimmune hemolysis (Coomb's +, increased indirect bilirubin, decreased haproglobin, spherocytosis)
p. 200
What are 4 causes of anemia in CLL
autoimmunity
splenomegaly
bone marrow infiltration
chemotherapy
p. 200
What causes death in CLL
infection
p. 200
What is the translocation in CLL and what is the result?
t(11:14), bcl1 next to heavy chain promoter
p. 200
What is the general presentation of T cell leukemias
erythematous rashes
p. 200
What type of leukemia is hairy cell leukemia
B cell type
p. 200
What are 3 findings that characterize hair cell leukemia
pancytopenia
erythema nodosum
hair cell morphology
p. 200
What is the treatment for hair cell leukemia
INF-alpha
splenectomy
p. 200
What are the most common ages for CML, CLL, AML, ALL
ALL: up to age 15
AML: 15-59
CML: 40-59
CLL: 60+
p. 200
What is HTLV and what dows it cause?
HTLV is human T cell leukemia virus
Causes leukemia and tropical spastic paraparesis
p. 200
Where is HTLV most common
Japan and Caribbean
p. 200
How is HTLV transmitted
Like HIV: placenta, body fluids & sex
p. 200