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114 Cards in this Set
- Front
- Back
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abrupt onset, development halted at blast phase
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acute leukemia
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Sx evolve over mths to years, majority of leukocytes mature
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chronic leukemia
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do not go beyond blast in what phase
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acute
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high blast count
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= no control of leukemia
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increased production of lymphs does what
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decreases all other cells and vice versa
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what do the cells do in the chronic phase
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divide and multiply at an increased rate but still get mature
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facts about leukemia (3)
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- leukocytosis
- neoplastic proliferation of 1 cell type - unregulated prolif in bone marrow |
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how is leukemia classified
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according to stem cell line (lymphoid/ myeloid)
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neoplastic proliferation of one cell type
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leukemia
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rarely seen in peds
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chronic leukemia
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defect stem cells differentiating ino myeloid cells (monocytes, granulocytes, erythrocytes &plts)
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AML
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age typically effected with AML
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>40 with peak at 67 yrs
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what is the most common nonlymphacytic leukemia
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AML
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survival rate of AML
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5 yrs <65 yrs with 35%
after 65 it drops to 4% |
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what is AML r/t
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secondary cancer
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S&S of AML (5)
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- fever
-infection - weakness - fatigue - bleeding |
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what are the S&S of proliferation of leukemic cells in organs with AML (4)
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- pain from hepato/spleenomeg
- hyperplasia of gums - bone pain -expansion of marrow |
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what is usually the presenting factor that leads to dx of AML
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bone pain
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major causes of death with AML
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infection and bleeding
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what does prolonged neutropenia increase the risk of with AML
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fungal infections
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increases the risk of systemic infection
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neutrophils <100/mm
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what systems can be affected with bleeding from AML (3)
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-GI
-pulmonary -intracranial |
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aggressive, chemo for several wks
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induction therapy
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once recovered from induction this is the next step
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consolidation therapy
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destruction hematopoietic function bone marrow and replaced with donor stem cells
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BMT
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what is the purpose of Consolidation therapy
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to eliminate any remaining leukemia cells
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how long can the clean up phase last
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2-3yrs
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used with induction therapy (4)
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- cytarabine
-daunorubicin - mitoxantrone - indarubicin - |
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what happens with destruction of leukemia cells and normal cells
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pancytopenia
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high dose chemo to destroy abnormal cells
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induction
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abnormal function of clotting and bleeding.
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DIC
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what can DIC be an underlying sign of (6)
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- sepsis
- trauma - cancer -shock - toxins - allergic reaction |
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what triggers coag cascade with DIC
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inflammatory response
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what triggers the fibrinolytic system
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excessive clotting
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what does activation of fibrinolysis relases
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plasmin that breaks down fibrin to open microcirculation
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after breakdown of fibrin, what happens
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produces fibrin degradation product
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whats present with DIC (6)
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- low plt
- low fibrinogen levels - prolonged PT - pronlonged aPTT - prolonged thrombin time - elevated d-dimer |
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result of DIC
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compromised organ function and/or failure
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mortality % of DIC with ischemic thrombosis and frank hemorrhage
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80
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S&S OF DIC (7)
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- subtle, occult process, or massive
- petechia/purpura - spont bleeding gums/nose - thrombocytopenia - hemorrhage into SQ tissue/muscles/joints - ecchymosis - oozing from any puncture sites |
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tx for DIC (8)
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- tx underlying cause
- supportive care - improve oxygenation -replace fluids - correct electrolytes - vasopressor cyroprecipitate - FFP |
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what does FFP do for tx of DIC
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replaces coag factors
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what does cryoprecipitate replace with DIC
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-fibrinogen
- factors V and VII |
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malignant disease of most mature form a B lymphocyte-plasma cell
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multiple myeloma
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used for antibody production with MM
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immunoglobulins secreted by plasma cell
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what doe malignant plasma cells produce
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increased amt of specific immunoglobulin that is nonfunctional
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produce functional but in lesser amts
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nonmalignant
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can be detected in blood and urine
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monoclonal protein
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what does FFP do for tx of DIC
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replaces coag factors
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classic sx with MM esp in males
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bone pain
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what does cryoprecipitate replace with DIC
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-fibrinogen
- factors V and VII |
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tx for MM (3)
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-no cure
-chemo -radiation |
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what doe malignant plasma cells produce
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increased amt of specific immunoglobulin that is nonfunctional
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malignant disease of most mature form a B lymphocyte-plasma cell
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multiple myeloma
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produce functional but in lesser amts
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nonmalignant
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used for antibody production with MM
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immunoglobulins secreted by plasma cell
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can be detected in blood and urine
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monoclonal protein
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classic sx with MM esp in males
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bone pain
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tx for MM (3)
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-no cure
-chemo -radiation |
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classic sx with MM esp in males
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bone pain
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tx for MM (3)
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-no cure
-chemo -radiation |
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causes renal failure with DIC
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immunoglobulin moelcules damaging renal tubules
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causes hypercalcemia in DIC
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Ionized Ca lost from bone into serum
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heterogenous group cancers originating from neoplastic growth lymphoid tissue
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no hodgkins
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what is NHL thought to arise from
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single clone of lymphocyte (malignant B lymphs)
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what happens to lymphoid tissue
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infiltrated with malignant cells
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rare with NHL
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localized disease
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sites of infiltration with NHL
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-lymph nodes
- nonlymph tissue |
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age for NHL
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67 (increases with age)
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at increases risk for NHL (6)
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- immunodeficiencies
- autoimmune disorders - previous ca tx - organ transplant - viral infections - exposure to agent orange/pesticides/chemicals |
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S&S of NHL (5)
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- variable
- lymphadenopathy (most common) - 1/3 have B sx - tumors compress other structures - CNS involvement |
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Dx for NHL (4)
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- ct
-pet - bone marrow biopsy -csf analysis |
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what is staging of NHL based on
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- site of disease
- spread to other sites |
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not dx til later stage
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lymphadenopathy
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peak occurrence for hodgkin lymphoma
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early 20s and after 50
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where does HL originate from
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single node
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what is the marker for HL
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redd sternberg cells
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more common to see HL in whom (2)
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- pt receiving immunosuppressant tx
- veterans exposed to agent orange |
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how does HL spread
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continuously along lymphatic system
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why can it take multiple biopsies to identify reed sternberg cells
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bc tumors tend to be heterogenous
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which type of hodgkins is relatively rare
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HL
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often found in reed sternberg cells
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epstein barr virus
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S&S of HL (2)
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- painless enlarged nodes
-enlarged nodes on one side of neck(cervical supraclavicular, mediastinal) |
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infections that are common with HL
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herpes zoster
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% that present with B Sx in advanced stages
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40
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Dx for HL (6)
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- r/o other infectious causes
- lymph node biospy (reed-stern) -CXR - CT (chest,abd, pelvis) -bone marrow -cbc for anemia |
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what are organs vulnerable to with HL
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tumor cell invasion
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what can tumor size cause
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compression of structures depending on location
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long term risk for HL
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2ndary malignancy (lung and breast high, AML)
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tx for HL (3)
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- dependent on stage of disease
- ABVD (advance stage) - short course 2-4mths chemo followed by radiation (early stages) |
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what is ABVD
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- combination chemo for advanced stages of HL
- adriamycin (doxirubican) - blenoxane (bleomycin) - Velban ( vinblastine) - DTIC ( dacarbazine) |
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outcomes for HL
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highly cureable
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average onset for CLL
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72 yrs
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malignant clone of B lymphocytes. most mature cell.
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CLL
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what is rare with CLL
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T lymphocyte
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levels for leukocytosis with CLL
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>100,000
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although in CLL, the leukocytes are small and do not interfere with flow through microvasculature what happens?
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they get trapped in lymph nodes
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S&S of CLL (5)
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- enlarged nodes (sometimes painful)
- hepato/splenomegaly - anemia/thrombocytopenia (later stages) -may be asymptomatic ( until advanced stages) - B sx |
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how is CLL dx
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physical exam
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what are the S&S of B sx (3)
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- fever
- drenching sweats (esp night) - unintentional wt loss |
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In CLL what does leukocytosis cause in later stages
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- changes in erythrocyte and plts
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chemo tx for CLL (3)
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- fludara ( fludarabine)
- cytoxan ( clophoshamide) w/ antibody rituximab ( rituxan) |
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what can chemo tx for CLL result in
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70% 5 yr remission
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proliferation of immature lymphoid stem cells (lymphoblasts)
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ALL
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ALL % B lymphocytes
% T lymphocytes |
- 75% B lymphs
- 25% T lymphs |
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age for ALL
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uncommon after age 15
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remission rate for ALL
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85
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% of adults that have 5 yrs survival rate with ALL
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40
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S&S of ALL (4)
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- infiltration leukemic cells to other organs
- liver/spleen enlargement - bone pain - CNS involvement |
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what does production of immature lymphocytes impede with ALL
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production of normal myeloid cells (results in pancytopenia)
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helps to decrease CNS involvement with ALL
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- cranial irradiation
- intrathecal chemo |
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tx for ALL (5)
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- cranial irradiation
- intrathecal chemo - induction tx (corticosteroids and alkaloids) -BMT - consolidation (3yrs) |
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more likely to have this in ALL of adults due to decreased response without it
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BMT
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often used in conjunction of consolidation with ALL
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allogenic transplant
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