Wbc

Front 1

What is wrong in leukocyte adhesion disorder?

Back 1

Deficient selection of CD11a/CD18

Front 2

What's wrong in a phagocytosis defect

Back 2

ex. decreased opsonins in Bruton's agammaglobulinemia

Front 3

what's wrong in microbicidal defect?

Back 3

ex. deficiency of myeloperodixase

Front 4

What sort of pathogens will you find in a leukocyte function disorder?

Back 4

coagulase negitive staphylococcus, growth failure in children, frequent infections, lack of an inflammatory response, severe gingivitus

Front 5

What is typical of a leukamoid reaction?

Back 5

absolute leukocyte count great than 50k per microliter, can be from perforating appendicits (neutrophils), whooping cough (lymphocytes), cutaneous larva migrans (eosinophils)

Front 6

neutrophilic leukocytosis

Back 6

above 7,000 microliter from infection, or sterile inflammation with necrosis (MI), drugs (corticosteroids)

Front 7

Common leukemia newborn to 14

Back 7

ALL

Front 8

common leukemia 15-39 years

Back 8

AML

Front 9

common leukemia 40-60 years

Back 9

CML

Front 10

Common leukemia 60+years

Back 10

CLL

Front 11

Signs of acute leukemia

Back 11

arupt fever, bleeeding, fatigue, hepatosplenomegaly, lymphadenopathy, CNS involvement (esp ALL), skin (esp T cell), bone pain and tenderness

Front 12

Labs in ALL

Back 12

peripheral WBC less than 10k to more than 100K per microL, blasts more than 20%, normoto macrocytic anemia, thrombocytopenia

Front 13

Type of bone marrow in ALL

Back 13

more than 20% blasts, hypercellular

Front 14

Clinical findings in chronic leukemia

Back 14

hepatosplenomegaly and generalized lymphadenopathy; insiduous onset

Front 15

Lab findings in a chronic leukemia

Back 15

peripheral-blasts usually less than 10%, normocytoic to marcocyteic anemia thrombocytopenia in CLL (CML has thrombocytosis in 40% of cases)

Front 16

bone marrow in chronic leukemia

Back 16

hypercellular with less than 10% blasts

Front 17

Types of chronic myeloproliferative disorders

Back 17

polycythemia, vera, CML, myeloid metaplasia, Essential thrombocyotpenia

Front 18

General characteristics of myeloproliferative disorder

Back 18

splenomegaly, reactive marrow fibrosis, can transform to acute leukemia

Front 19

Lab signs for polycythemia vera

Back 19

increase Hb, Hct, and RBC count, low epo

(RBC count=RBC mass/plasma volume)

Front 20

relative polycythemia

Back 20

increased RBC count due to volume deplation, RBC mass should be normal as EPO, often after exercising

Front 21

Appropriate abosolute polycythemia

Back 21

due to hypoxic cause of EPO release (lung disease, congenital heart disease, Living at high alt) probably will have low O2 sat and normal plasma volume

Front 22

Clinical symptoms of p. vera

Back 22

ruddy face, pruritus after bathing, peptic ulcer disease (histamine release) thrombotic events (hyperviscous blood), gout, splenomegaly

Front 23

Risk factors for CML

Back 23

prior ionizing radiation and benzene

Front 24

Chromosomal abnormality and tx for CML

Back 24

Philadelphia chromosome; 9;22, imantinib (gleevac),

Front 25

how long to get a blast crisis for CML

Back 25

approx 5 years

Front 26

lab findings in CML

Back 26

peripheral WBC 5ok-100k/microL, myeloid in all stages, thrombocytosis n 40-50% of cases (thrombocytopenia in the others),

Front 27

Is leukocyte alkaline phosphate (LAP) ncreased with CML

Back 27

no, decreased. LAP is absent in neoblastic cells

Front 28

number of cells that have philidelphia chromosome in CML? Bcr-abl

Back 28

95% philidelphia, (philiedlphia can be present in other leukemias as well) and 100% with BCR-ABL fusion

Front 29

Clinical findings of myelofibrosis and myeoloid metaplasia

Back 29

peripheral WBC 10k microliters to 50k microliters, massive splenomegaly with portal hypertension, splenic infarcts with left sided pleural effusions

Front 30

Myelodysplastic syndrome lab findings

Back 30

severe pancytopenia, dimorphic RBC pop (both microcytic and macrocytic), ringed siderblasts in marrow (nucleated RBCs with excess iron)

Front 31

treatment fo AML?

Back 31

Induction: chemotherapy “7 + 3” cytarabine (ara-C; cytosine arabinoside) + daunorubicin (or idarubicin)
consolidation:High dose ara-C (aka Cytarabine) (HidAC)

fludarabine (used in minitransplant)

Front 32

chromosomal translocation in APL M3?

Back 32

t(15;17), treatment with transretinoic acid or ATRA (all trans retinoic acid)

Front 33

Smear finding in AML cells

Back 33

Auer rods in M1 (rare)-M4 (common)-splinter shaped to rod shaped in cytosol
auer rods ONLY in AML NOT CML

Front 34

clinical findings in AML

Back 34

DIC, gingival infiltration (esp M5),

Front 35

Most common subtype of ALL

Back 35

early pre-b cell (80%) of cases has CALLA, CD10, Tdt, and 90% complete remission

Front 36

Common places for ALL to metastasize

Back 36

CNS and testis -B cell types
anterior mediastinal masses-t cell types

Front 37

labs findings in ALL

Back 37

peripheral WBCs 10k to 100k per microL with over 20% lymphocytes, normocytic anemia

Front 38

what virus is associated with adult T cell leukemia?

Back 38

HTLV-1 human t cell leukemia virus

Front 39

treatments for ALL

Back 39

Daunorubicin, Prednisone, Vincristine, L-asparaginase

consolidation: High dose ara-C (aka Cytarabine) (HidAC)

HyperCVAD - Cyclophosphamide, Vincristine, Adriamycin (Doxorubicin), Dexamethasone then later, Methotrexate, Ara C - ALL

Front 40

bone marrow findings in ALL

Back 40

lytic bone lesions and marrow replaced by CD4 lymphocytes

Front 41

What is the most common leukemia overall?

Back 41

CLL

Front 42

pathogenesis of CLL?

Back 42

neoplastic disorder of virgin B cells

Front 43

clinical findings in CLL

Back 43

general lymphadenopathy, increased incidence of immune hemolytic anemia (both warm and cold)

Front 44

lab findings in CLL

Back 44

smudge cells on smear, less than 10% lymphoblasts, neutropenia, hypogammaglobulinemia

Front 45

stain for harry cell leukemia

Back 45

Positive trap stain