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29 Cards in this Set
- Front
- Back
most common leukopenia?
due to? leukopenia only commonly found in advanced HIV, following glucocorticoids, autoimmune dis., malnutrition, and viral infections? |
neutropenia; bacterial infection
lymphopenia |
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another name for neutropenia?
neutropenia due to suppression of myloid cells is often accompanied by (2)? |
agranulocytosis
anemia, thrombocytopenia (low WBC,RBC) |
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common cause of predictable agranulocytosis?
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drugs, alkylating agents and anti-metabolites
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two modes of leukopenia
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accellerated removal/ destruction
inadequate granulopoisis |
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four drugs that cause agranulocytosis
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chloramphenicol, sulfonamides, chlorpramazine, thiouracil
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most drug induced agranulocytosis mechanism?
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Ig-mediated cell lysis
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neutropenia with hypercellularity caused by which?
ineffective granulopoiesis excess destruct. of mat neutrophils destruction of granulo. precursers |
ineffective granulopoiesis
excess destruct. of mat neutrophils |
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neutropenia with hyporcellularity caused by which?
ineffective granulopoiesis excess destruct. of mat neutrophils destruction of granulo. precursers |
destruction of granulocyte precursers
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most serious infection giving rise to agranulocytosis have blood count of?
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less than 500/ mm3
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floowing myelosuprressive therapy treat w/ ? to elevate counts
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G-CSF
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three types of lymphoid neoplasms?
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B-cell (Burkitt's)
T-cell and NK Hodgkins |
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what is Lymphoma?
leukemia? |
cancer of lymph nodes/ thymus
cancer of the blood/ bone marrow |
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Neutrophils Like Making Everything Better.
state the % of each type of blood cells in peripheral smears. |
Neutrophils 60%
Like (lymphocytes) 30% Making (macrophages) 6% Everything (eosinophils) 3% Better (Basophils) 1% |
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whats happening in Acute myelogenous Leukemia?
myelodysplastic syndrome? |
immature progenitor cells are accumulating in the bone marrow
ineffective hematopoiesis / cytopenia |
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most lymphomas arise from germinal center B-cells ,why?
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inherent genome instability during recombination events
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etiologies of white cell neoplasia (5)?
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chromo translocation
inherited genetics viruses(EBV,HTLV1,KSHV) environmental (H. pylori) Iatrogenic (chemotherapy, drugs) |
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leukemias often present as/
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hematopoeitic suppression on CBC
hepato- splenomegaly |
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plasma cell neoplasmeas present as?
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bone destruction and fracture
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five broad categories of lymphoid neoplasms?
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immature precursor B-cell Lym.
mature precursor B-cell lym. immature precursor T-cell lym. mature T-cell and NK cell lym. Hodgkins lymphoma |
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how can you tell if a lymphocyte is from a neoplasia?
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the DNA will be identical instead of having a random generated antigen (gene splice)
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most common lymphoid neoplasia?
least? |
B-cell lymphomas
NK-cell lymphomas |
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how is hodgkins different than the other lymphoid neoplasms?
why does this matter? |
it tends not to become disseminated, rather it can be found restricted to one group of lymph nodes.
you can use this to guide treatment and make good guess at prognosis |
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what is ALL?
when do the two types present? |
neoplasia of pre-b or pre-t cells.
whites, boys>girls pre-b at age 4 pre-t in adolescence |
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markers on a pre B-cell ALL?
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TdT
CD22 CD10 CD19 (very early pre-B) no IgM ( early pre-B) |
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what is philadelphia chromosome?
signifies? |
t(9;22)
A.L.L. |
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common presenting factors in ALL and AML?
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abrupt stormy onset
depression of bone marrow (fatigue) bone pain/ tenderness splenomegaly/ hepatomegaly CNS signs ( headache, vomiting) |
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how treatable is ALL?
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90% complete remission
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ALL poor prognosis factors (4)?
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onset before 2
onset in adolescence blasts > 100,000 t(9;22) philadelphia chromo. |
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four good prognosis factors in ALL?
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aged 2 to 10
low white count early pre-B phenotype hyperploidy or t(12;21) |