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Clinical Medicine

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Question
Answer
IDA (causes)   -chronic blood loss --> GI tract most common -Chronic NSAID/ASA use -Pregnancy -menstrual blood loss -low iron intake (women, children)  
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IDA (ssx)   -pallor, fatigue, DOE, tachycardia -*pica* -esophageal webs (plummer-vinson syndrome)  
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IDA (dx)   -hypochromic, microcytic anemia -elevated TIBC -low Fe, ferritin, and transferritin  
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IDA (tx)   -tx underlying cause -iron supplementation with ferrous sulfate x 6-12 months  
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Lead Poisoning (ssx)   -difficulty concentrating, fatigue, muscle weakness, paralytic ileus  
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Lead Poisoning (dx)   -mild microcytic anemia -basophilic stippling of RBC -elevated lead lvl  
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Lead Poisoning (tx)   -remove lead source -chelating agents if symptomatic or severe toxicity  
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Thalassemia   -inherited disorder of alpha or beta globulin synthesis -typically family hx -genetic counseling in sever forms  
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Thalassemia (dx)   -microcytic anemai that does not respond to iron therapy -normal iron and ferritin levels -confirm w/ hbg electrophoresis  
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alpha thal (dx)   -peripheral smear: target cells -Hgb H on electrophoresis  
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alpha thal (tx)   -Avoid iron -avoid oxidative drugs -folic acid supplements  
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beta thal major   -Cooley anemia -onset 4-6 months of age, seveer anemia, growth retardation, osteopenia, deformities, hepatosplenomegaly  
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beta thal minor   -moderate anemia  
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beta thal (dx)   -peripheral smear: basophilic stippling, target cells -microcytic  
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beta thal major (tx)   -transfusion with deferoxamine to prevent hemosiderosis  
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beta thal minor (tx)   -avoid iron -monitor  
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B12 deficiency   -vegans, pancreatic insufficiency, gastric bypass surgery, crohn's  
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B12 deficiency (exam)   -glossitis, pale icterus -neuro: stocking-glove paresthesias, loss of tast and vibratory sensation, ataxia  
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B12 deficiency (Dx)   -macrocytic anemia, poikilocytosis, anisocytosis -low retic count and serum B12 -high LDH and bilirubin  
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B12 deficiency (tx)   -high dose oral B12, nasal spray or IM  
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B12 deficiency (neuro ssx)   -will resolve if tx is initiated within 6 months of onset -if not corrected damage is irreversible  
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pernicious anemia   -autoimmune destruction of gastric parietal cells causing lack of intrinsic factor -most common cause of B12 deficiency  
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pernicious anemia (dx)   -macrocytic anemia -low serum B12 -shilling test positive  
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pernicious anemai (tx)   -lifelong IM B12 supplement  
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folic acid deficiency   -poor intake, EtOH abuse, pregnancy, bactrim, suflasalazine  
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folic acid deficiency (dx)   -macrocytic -hypersegmented PMNCs -folate level <150 ng/mL  
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folic acid deficiency (tx)   -folic acid 1 mg/day by mouth  
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hemolytic anemias (cuases)   -TTP, ITP, DIC -medication/transfusion reactions -sickle cell -G6PD deficiency -ifxns (malaria, parvo b19)  
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hemolytic anemias (exam)   -splenomegaly  
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hemolytic anemias (dx)   -elevated retic; falling hct -elevated indirect bilirubin -elevated LDH  
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sickle cell anemia   -autosomal recessive hemolytic anemia; african americans  
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sickle cell anemia (aggravators)   -sickling of RBCs increased by hypoxemia, high altitudes  
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sickle cell anemia (prognosis)   -life expectancy = 40-50 yrs  
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sickle cell anemia (ssx)   -painful crises, cholelithiasis, poor wound healing, priaprism, splenomegaly, AVN of femoral head  
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sickle cell anemia (dx)   -Hgb electrophoresis shows Hgb S in RBCs -sickled cells, target cells, howell-jolly bodies  
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sickle cell anemia (tx: symptomatic)   -analgesics, fluids, O2  
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sickle cell anemia (tx: crises)   -possible transfusion  
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sickle cell anemia (tx: asx)   -pneumococcal vaccine/folate supplements -genetic counseling  
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G6PD deficiency   -X linked recessive; mediterranean populations and african american males  
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G6PD deficiency (path)   -leads to episodic hemolysis or chonic hemolysis if severe  
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G6PD deficiency (risks)   -oxidative drugs; infxn -fava beans  
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G6PD deficiency (dx)   -bite cells, heinz bodies -G6PD low after hemolytic episode  
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G6PD deficiency (tx)   -most cases are self-limited -avoid oxidative meds (ASA, dapsone, sulfonamides, nitrofurantoin)  
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ACD (anemia of chronic dz)   -associated w/ kidney, liver, endocrine dz, or malignancy -renal dz leads to decreased EPO  
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ACD (dx)   -mild normochromic, normocytic anemia -normal cell morphology  
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ACD (tx)   -treat underlying dz and anemia will resolve -give EPO  
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aplastic anemia (ssx)   -weakness, bleeding, bacterial and fungal infections, purpura, petichiae, hepatosplenomagaly  
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aplastic anemia (causes)   -most common: T cell mediated autoimmune suppression -radiation, chemotherapy, medications, SLE  
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aplastic anemia (dx)   -pancytopenia w/ normocytic anemia -hypocellular marrow  
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aplastic anemia (tx: mild)   -supportive; EPO/transfusions  
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aplastic anemai (tx: severe)   -bone marrow transplant  
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polycythemia vera (primary)   -JAK 2 mutation -splenomegaly, normal O2 sat, increased red cell mass  
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polycythemia vera (secondary)   -chronic hypoxia, smoking, renal tumors -splenomegaly absent  
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polycythemia vera (who?)   -males>females -age>60  
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polycythemia vera (complications)   -bleeding (PUD/epistaxis), thrombosis, progression to leukemia  
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polycythemia vera (ssx)   -tinnitus, HA, dizziness, blurred vision, plethora -pruritis after bathing  
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polycythemia vera (dx)   -elevated Hct -leukocytosis, increased large/bizarre platelets -hypercellular bone marrow  
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polycythemia vera (tx)   -phlebotomy -hydroxyurea -low dose ASA  
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thrombocytopenia   -decrease in the number of platelets -most common cause of abnormal bleeding -associated w/ SLE and CLL  
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thrombocytopenia (ssx)   -gingival bleeding, epistaxis, menorrhagia, petichiae  
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thrombocytopenia (causal drugs)   -heparin, sulfonamides, thiazides, cimetidine  
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ITP   -autoimmune, IgG mediated  
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acute ITP (ssx)   -petechia, purpura, hemorrhagic bullae on skin  
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acute ITP (tx)   -most are self-limiting -steroids -splenectomy if severe  
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acute ITP (who?)   -children, following a viral infection  
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chronic ITP (who?)   -women>men; ages 20-50 yrs  
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chronic ITP (ssx)   -petechiae on skin and mucous membranes -associated w/ autoimmine conditions (SLE)  
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chronic ITP (tx)   -high dose steroids; IVIG; SCT -splenectomy -avoid ASA -platelet transfusion for severe bleeding  
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TTP (who?)   -women>men; age 20-50; previously healthy  
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TTP   -associated w/ HIV, pregnancy, estrogen, quinine, ticlopidine -rare but can be fatal  
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TTP (ssx)   -severe thrombocytopenia, anemia (schistocytes), elevated LDH, thrombosis -pallor, petechiae, purpura, pancreatitis, fever -neurologic signs that come and go  
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TTP (tx)   -emergent plasmapheresis (NO PLATELETS) -prednisone -antiplatelet agents  
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DIC   -SAS -occurs pts w/ sever systemic illnesses; sepsis, cancer, transfution reactions, trauma -high mortality (30-80%)  
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DIC (ssx)   -shock, hemorrhage from skin and mucous membranes, digital ischemia, gangrene  
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DIC (labs)   -coagulopathy: elevated D-dimer, prolonged PT  
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DIC (tx)   -urgently treat underlying cause -component blood transfusions -cyroprecipitate -+/- heparin  
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vW dz   -most common congenital coagulopathy -deficiency of facter VIII antigen and defective vWF  
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vW dz (gentics)   -autosomal dominant bleeding disorder  
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vW dz (ssx)   -bleeding of nasal passages, vagina, GI tract  
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vW dz (labs)   -prolonged bleeding time -decreased vWF  
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vW dz (tx)   -desmopressin acetate -factor VIII concentrates -avoid ASA and exogenous estrogen -pregnancy may exacerbate symptoms  
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hemophilia A   -most common hemophilia; factor VIII deficiancy -most severe bleeding disorder: 2nd most common congenital coagulopathy  
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hemophilia (genetics)   -x-linked recessive  
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hemophilia A (ssx)   -range from severe hemarthrosis, intracranial bleeding to milder prolonged post op bleeding  
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hemophilia A (labs)   -prolonged PTT -low factor VIII:C levels -normal vWF  
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hemophilia A (tx)   -heat treated factor VIII concentrates -mild dz can be treated w/ desopressin -avoid ASA  
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hemophilia B   -factor IX deficiency or Christmas dz -x-linked recessive; males  
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hemophilia B (tx)   -factor IX concentrates -FFP (fresh frozen plasma)  
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Vit K deficiency   -most common acquired coagulopathy  
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Vit K deficiency (causes)   -chronic liver dz (most common), dietary, meds  
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Vit K deficiency (ssx)   -post surgical pts; soft tissue bleeding  
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Vit K deficiency (labs)   -PT/PTT are prolonged -elevated LFTs -decreased Factors VII, IX, X, II (SNOT)  
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Vit K deficiency (tx)   -oral or IV vit K -treat acute bleeds with FFP  
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thrombotic disorders   -pts: >40, family history, recurrent thrombosis  
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aquired thrombotic disorders   -malignancy, estrogen use, immobilization, nephrotic syndrome, ulcerativ colitis, crohn's, heparin  
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congenital thrombotic disorders   -antithrombin III deficiency, factor V leiden, protein C&S deficiencies, lupus anticoagulant  
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thrombotic disorders (tx)   -anticoagulation w/ LMWH or coumadin -predinsone for lupus anticoagulant  
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hodgkin's dz (who?)   -men>women; ages 15-45  
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hodgkin's dz   -enlargement of lymphoid tissue, liver/spleen -associated w/ EBV  
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hodgkin's dz (ssx)   -painless LAD, fever, night sweats, pruritis, fatigue -pain w/ EtOH  
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hodgkin's dz (dx)   -ann arbor creteria -staging -staging tests: CT neck, chest, abdomen, pelvis, BM bx -*reed-sternberg cells*  
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hodgkin's dz (tx)   -combinations chemotherapy or radiation depending of stage at diagnosis -majority of pts are cured  
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non-hodgkin's lymphoma   -malignancy of lymphocytes (MC B lymphocytes) -age 20-40; more common with HIV/immune compromise  
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non-hodgkin's lymphoma (ssx)   -painless persistent LAD -abdominal fullness in Burkitt's lymphoma -spread to bone, bone marrow, GI, skin  
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non-hodgkin's lymphoma (labs)   -biopsy enlarged nodes -stage w/ CXR, CT abdomen and pelvis -BM bx  
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non-hodgkin's lymphoma (tx)   -radiation for single node -rituximab +/- chemotherapy -high grade: sct -spontaneous remission may occur  
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multiple myeloma   -malignancy of the plasma cells -more common in AA  
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multiple myeloma (ssx)   -osteolytic lesions, LAD, recurrent infections  
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multiple myeloma (labs)   -hypercalcemia -*rouleaux formation* of RBCs -monoclonal spike on electrophoresis (M spike on SPEP) -bence-jones proteins in urine  
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multiple myeloma (tx)   -dexamethason, doxorubicin, lenalidomide -bisphosphonates for osteoporosis  
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acute leukemia (ssx)   -epistaxis, gingival bleeding, gram-negatic bacterial infxns -anemai, DIC, elevated uric acid  
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acute leukemia (dx)   -pancytopenia w/ circulating blasts -elevated WBCs -confirm w/ BM bx  
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acute leukemia (tx)   -induction chemotherapy followed by consolidation therapy -allopurinol/diuretcs to prevent uric acid stones -sct  
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ALL   -most common childhood leukemia  
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ALL (ssx)   -rapid onset of fever, fatigue, joint pain, bone pain (sternum, femor), frank bleeding  
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ALL (cxr)   -mediastinal mass  
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ALL (labs)   -leukocytosis w/ lymphocytosis -philadelphia chromosome (poor prognosis)  
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ALL (tx)   - >50% cure rate for children undergoing chemotheraphy  
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AML (who?)   -adults: median onset of age 60 -MC acute leukemia  
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AML (ssx)   -gradual onset of fatigue, decreased appetite, weight loss, and dyspnea  
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AML (dx)   -*auer rods*  
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AML (tx)   -high remission rate in pts < 60  
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CLL (who?)   -MC of all leukemias -men>women -median age of onset 65 years  
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CLL   -malignancy of B lymphocytes, median survival 6 years  
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CLL (ssx)   -recurrent infections, LAD, Richter's syndrome  
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CLL (staging)   -Rai system  
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CLL (dx)   -lymphocytosis -peripheral smear: *smudge cells*  
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CLL (tx)   -palliative w/ advanced dz  
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CML   -myeloproliferative disorder seeen in middle aged adults  
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CML (ssx)   -gradual onset of weight loss, low grade fever, fatigue, sweating, splenomegaly, early satiety  
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CML (triphasic)   -progression from chronic to accelerated to acute phase (blast crisis/decreased survival  
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CML (dx)   -leukocytosis -*philadelphia chromosome* -bcr-abl gene identification -hypercellular bone marrow  
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CML (tx)   -imantinib mesylate(Gleevec), dasatinib, nilotinib -allogenic sct only curativ therapy (reserved for progressive disease)  
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