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56 Cards in this Set
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Iron Replacement Therapy
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PO: give as iron salts in ferrous form, continue tx for 3-6 mos after correction of initial anemia. Don't monitor iron stores
Parenteral: give a test does to make sure not allergic to dextran. Must monitor iron stores, possibility for toxicity. Fe2+ uses DMT1 to enter enterocytes, is stored in combo w/ ferritin. Ferroportin1 across basolateral membrane into circulation. Transported complexed w/ transferrin. Excess stored in enterocytes and macs in liver, spleen, and bm. Indications: blood loss (most common), incr demand, hookworm S/E: GI, n/v/d/constipation Tox: necrotizing gastroenteritis, lethargy, shock, dyspnea. May improve, then followed by acidosis, coma, death. Use chelators, NOT charcoal. Usually only seen in kids. |
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B12
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Indications: deficiency usually r/t malabsorption. Manifests as anemia, GI complaints, neuro s/sx
MOA: recycles folate via MS, also responsible for isomerization of MMA->succinly coA (heme synthesis) Cause of deficiency: Pernicious anemia, decr intake (vegans), fish tapeworm, EtOH abuse, dz of ileum Dx: Incr homocysteine and MMA levels. Mild/mod leukopenia and thrombocytopenia. May be secondary to autoimmune d/o. |
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Schilling test
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Give large dose of parenteral B12 to saturate receptors. Then give radiolabeled PO B12, if less than 7-10% in urine, have an absorption issue (being excreted in feces). Then give another dose assoc w/ intrinsic factor (to determine parietal cell dysfx).
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Folate
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Deficiency: decr intake, common in EtOH abuse, liver dz, pregnancy, hemolytic anemia. Drugs: methotrexate, trimethoprim, pyrimethamine.
Dx: incr. homocysteine, decr FH4. MUST exclude B12 def before starting tx |
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Hematopoietic growth factors
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Indications: hematologic dz, severe infection, CA chemo, BMT
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EPO
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Normal fx: made by kidneys in response to hypoxia, stimulates erythroid prolif and differentiation, can induce release of reticulocytes from BM. Signal through JAK/STAT pathways.
Indication: usually for patients w/ CKD, tx of anemia due to primary bm d/o. Best response in pts w/ endogenous EPO levels <100 U/L SE: htn, thrombotic complications |
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Megakaryocyte growth factors
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IL-11 (Oprelvekin-recombinant IL-11): stimul growth of multiple lymphoid and myeloid cells and primitive megak precursors. Incr peripheral plt and neutrophils
Indications: secondary prevention of thrombocytopenia in pts receiving chemo SE: fatigue, ha, dizziness, anemia, dyspnea, and transient atrial arrhythmias TPO: independently stim growth o primitive megak progenitors, stimulates mature megak, activates mature plt to respond to aggregation inducing stimuli. Still investigational. |
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Heparin
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MOA: Forms complex w/ antithrombin which then inhibits thrombin and Factors 9a and 10a via another complex formation. Acts as a cofactor for antithrombin-protease reaction w/o being consumed.
Preparations: LMW favored over UFH due to incr bioavailability, less freq dosing, and more predictable pharmacokinetics, and less need for monitoring. LMW fxs through inhibition of only 10a Indications: DVT, PE, anginia, MI C/I: hx of HIT, hypersens, hemophilia, ICH, htn, recent surgery of eye, brain, or spinal cord Tox: HIT, bleeding (reversed w/ Protamine), LMW-use caution in pts w/ renal insufficiency |
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Warfarin
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MOA: blocks gamma-carboxylation of glu residues in PT and factors 7, 9, and 10. Prevents reduction of Vit. K. Anticoag effects r/t partially inhibited synthesis and unaltered degradation of vit. k dependent clotting factors. Resulting anticoagulation dependent on degradation of the clotting factors in circulation.
Tox: crosses placenta, OD->bleeding Interactions: Barbs and vit K decr anticoag effects Reversal of bleeding: Vitamin K or recombinant Factor 7. Drug has long t1/2, may require more than one dose to fix bleeding. |
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Fibrinolytics (general)
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Indications: PE w/ hemodynamic instability, severe DVT, ascending thrombophlebitis, acute MI
Streptokinase: synth by bacteria, forms complex w/ plasminogen converting it to plasmin. Approved for peripheral arterial and venous thrombi Urokinase: synthesized by kidney, directly converts plasminogen to plasmin Anistreplase: purified human plasminogen + streptokinase that has been acylated to protect the enzymes active site |
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t-PA
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t-PA: preferentially activates plasminogen that is bound to fibrin, confines fibrinolysis to the thrombus
Reteplase: recombinant human t-PA, less specific than t-PA, lacks major fibrin binding domain, so less fibrin specific Tenecteplase: mutant t-PA with longer t1/2 |
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Anti-platelet drugs
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ASA: irreversibly binds and inhibits COX-I
Clopidogrel and ticlopidine: inhibits ADP binding to plts, thereby inhibiting plt activation and aggreg. Used to prevent thrombus formation Side effects: dyspepsia (more with ticlopidine) |
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gp 2b/3a receptor inhibitors
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Indications: Acute coronary syndrome (ACS)
MOA: blocks gp 2b/3a from binding w/ fibrinogen, fibronectin, and vWF Abciximab: monoclonal aby against receptor Eptifibatide: analog of carboxy terminal sequence of delta chain of fibrinogen. Competitively antagonizes fibrinogen binding to the receptor complex |
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Vitmin K
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Used as Ca chelator for factors 2, 7, 9, and 10
K1: found in food. Can be given as PO or IV supplement. Rapid infusion can cause dyspnea, confusion, chest and back pain, and death. Def. most often occurs in ICU pts K2: made by intestinal bacteria, variable absorption |
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Tx of bleeding d/o
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Desmopressin: incr Factor 8 activity, use for Hemophilia A or vWF dz.
Autoplex (FEIBA-Factor 8 inhibitor bypassing activity): Factor 9 concentrates that contain activated clotting factors, tx pts w/ inhibitors or aby to factor 8 or 9 Cryoprecipitate: plasma protein fraction from whole blood, tx deficiencies or qualitative abnormalities in fibrinogen, factor 8, or vWF Aminocaproic acid: inhibits fibrinolysis by inhibiting plasminogen activator. Given for hemophilia, bleeding, or re-bleeding prophylaxis in pts w/ intracranial aneurysm Aprotinin: Serine protease inhibitor that inhibits fibrinolysis by free plasmin. Us in pts undergoing CABG w/ are at high risk for blood lass. Reduces bleeding from many types of surgeries. Small risk of anaphylaxis. |
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Dimercaprol (BAL)
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Antidote against arsenic poisoning. Use w/ EDTA for acute Pb intox.
Admin: IM as 10% soln mixed w/ peanut oil. Readily absorbed, metabolized and excreted by kidney w/in 4-8 hrs S/E: htn, tachycardia, n/v, lacrimation, salivation, fever, pain at injection site |
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Succimer
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Water soluble analog of dimercaprol.
Tx: Arsenic and lead C/I: gastroenteritis MOA: binding to cysteine activates chelating moieties in vivo SE: GI upset, rashes |
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Edetate calcium disodium (EDTA)
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Tx: lead intoxication
MOA: chelates EXTRA-cellular ions, poor oral absorption (b/c polar) so must be given IV. PO admin may increase lead absorption in gut. Rapidly excreted from kidneys (delayed in pts w/ kidney dz) C/I: don't give to anuric pts SE: life threatening depletion of calcium can occur if not given w/ calcium disodium salt |
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Unithiol
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Analog of dimercaprol
Tx: Arsenic and lead Admin: PO or IV SE: low incidence, but must be given slow IV (too fast->vasodilation and hypotn) |
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Penicillamine
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MOA: derivative of pcn, resistant to metabolic degradation. Prevents copper accumulation, may incr excretion of lead
C/I: extreme caution in pcn allergy SE: hypersensitivity, nephrotoxicity, and pancytopenia w/ long-term usage |
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Deferoxamine
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MOA: Fe chelator, poorly absorbed when given PO, does not compete with biologically chelated iron
Admin: IV or IM (slowly) SE: minimal |
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Acute inorganic lead poisoning
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Initial therapy: IV EDTA or IM dimercaprol followed by EDTA w/ dimercaprol 4 hr later
After 5 days of tx: switch to PO succimer |
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Rho(D) Immune Globulin
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Plasma-derived IgG
Don't give to the baby. SE: not frequent |
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Hyperimmune globulin
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IGIV preps made from pools of donors w/ high titers of aby against specific toxins or viruses.
Results in PASSIVE immunity, reduces risk/severity of infection. Used for VZV, rabies, tetanus, and hep B |
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Tetracyclines
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MOA: Blocks A site on 30s subunit of bacterial ribosome.
SE: GI upset, photosensitivity, nephrotoxicity (except doxy), mito toxicity MOR: Multi-drug efflux pump, ribosomal protection protein, mutation of 30s, enzymatic inactivation of drug Indications: RMSF, Coxiella burnetii, E. chaffeensis |
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Chloramphenicol
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MOA: binds 50s, blocks transpeptidation, interferes w/ macrolides
SE: Anemia, thrombocytopenia, neutropenia, mito toxicity MOR: plasmid encoded acetyl transferase, lowered permeability, mutations Indications: meningitis and orientia tsutsugamushi |
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Chloroquine
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MOA: accumulates in food vacuole and inhibits formation of hemozoin. Free heme formed by parasite leads to lysis of parasite membrane and death.
SE: Cardiovascular effects, htn, CNS dysfx MOR: Decr accumulation, CRT gene (if positive, then resistant to chloroquine-acts as an efflux pump). Effective against erythrocytic stages of malaria |
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Mefloquine
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MOA: accumulates in food vacuole and inhibits formation of hemozoin. Free heme formed by parasite leads to lysis of parasite membrane and death. Effective against chloroqiune resistant strains. Used in malaria prophylaxis. Often used in adjunct to artesunate.
SE: CNS (ha, vivid dreams) |
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Artesunate
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MOA: release of ROS from endoperoxides that kill parasite. Heme cleaves endoperoxide which is an alkylater, then blocks ATPase. Gametocidal (ONLY one) and and erythrocidal. Effective against P. vivax and P. falciparum. CYP450 inducer.
MOR: assoc with high incidence of re-infection (effect abrogated when given in conjunction with mefloquine) Tox: teratogen, neurotoxic |
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Primaquine
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MOA: effective against hypnozoites and gametocytes. Generates ROS that block ETC of parasite.
Tox: anemia, cyanosis (by forming methgb), acute hemolysis in G6PD deficient patients. GI distress. Leukocytosis. May cause hypotn MOR: rare |
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Atovaquone
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MOA: interferes w/ ETC in mito of malaria. Given with proguanil. Effective against P. falciparum
SE: n/v/d/abd pain and rash MOR: mutations in cytochrome B and C1 genes. |
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Pyrimethamine-sulfadoxine
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MOA: Pyrimethamine inhibits plasmodial DHFR and TS. Sulfadoxine blocks DHFR synthesis from PABA.
SE: rash, decr hematopoiesis, low folate (tx w/ leucovorin). High doses lead to nephrotoxicity. MOR: mutations in DHFR and TS enzymes (both enzyme fx's controlled by single enzyme in Plasmodia). |
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Proguanil
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MOA: inhibits DHFR/TS. Active against erythrocytic and primary hepatic stages. Give with atovaquone.
SE: Diarrhea MOR: mutation in enzymes |
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Clindamycin
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MOA: Binds 50s, suppresses translocation of AA. Effective against babesia b/c contains a picoplast (non-photosynthetic ribosome that retains metabolic fx and has a 50s subunit). Use in conjunction w/ quinine against babesia.
SE: Hypoglycemia, postural hypotn, tinnitus, severe diarrhea (that can develop into pseuodmembranous colitis...overgrowth of C. dif) MOR: CRT gene (that acts as an efflux pump) |
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Azithromycin
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MOA: macrolide, binds 50s of babesia. Inhibits CYP450. Extensive tissue distribution and able to reach [high]. Use with Atovaquone against babesia.
SE: low toxicity |
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ALL
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Phase I: (1-4 weeks) vincristine, prednisone, daunorubicin, and asparaginase
Phase II: (5-8 weeks) cyclophosphamide, cytarabine, 6-mercaptopurine |
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Asparaginase
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Deprives leukemic cells of Asn by converting it to Asp. Leukemic cells can't synthesize Asn, so they die.
Asparaginase is a tetromer composed of two dimers |
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AML
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Usually tx w/ cytarabine.
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APL
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Tx w/ ATRA, plus daunorubicin or idarubicin. Arsenic trioxide for a second remision in relapsed pts after ATRA tx
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Cytarabine
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MOA: Inhibits DNA chain elongation.
MOR: Cytadine deaminase and dCMP deamninase as well as deficiency of deoxycytidine kinase (no phosphorylation to active form) Tox: GI, conjunctivitis, dermatitis, pulmonary edema |
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Idarubicin
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MOA: Topo II inhibitor, intercalates in DNA. Generates ROS.
Tox: cardiotoxicity. |
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Mitoxanthrone
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MOA: Topo II inhibitor, intercalates in DNA
Tox: less cardiotoxicity than Idarubicin because no free oxygen. |
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CLL
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Fludarabine, cyclophosphamide, rituximab, mixtoxantrone, alemtuzamab, and chlorambucil
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Fludarabine
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MOA: fluorinated purine analog, gets incorporated in DNA and RNA and stops DNA polymerase. Promotes apoptosis.
MOR: Resistant to deamination Cladribine is chlorinated version of fludarbine. |
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CML
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Gleevac (imatinib mesylate) in combo w/ hydroxyurea. Followed by allogenic stem cell transplantation
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Hydroxyurea
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MOA: inhibits ribonucleoside diphosphate reductase to block conversion of ribonucleotides to deoxyribonucleotides. Can't make DNA. Given PO, use in combo w/ gleeva
SE: GI distress, hematopoiesis suppression |
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Gleevac
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MOA: inhibitor of Bcr-Abl kinase (product of t(9;22) fusion gene) by binding at ATP site to inhibit kinase activity.
SE: n/v, edema, muscle cramps. NO myelosuppression. |
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Hairy Cell Leukemia (HCL)
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Cladribine (chlorinated purine analog) and pentostatin. Rituximab also shows promise. Possible splenectomy.
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Pentostatin
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MOA: inhibitor of adenosine deaminase, leads to buildup of adenosine. and deoxyadenosine nucleotides. Blocks DNA synthesis by inhibiting ribonucleotide reductase (by negative feedback)
SE: long lasting myelosuppresion, GI side effacts, rash |
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Hodgkin's dz
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MOPP (mechlorethamine, vincristine, procarbazine, and prednisone)
ABDV: doxorubicin, bleomycin, vinblastine, and decarbazine |
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Non-Hodgkin's Lymphoma
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Tx dependent on grade.
Single agent: chlorambucil, fludarabine, or rituximab. Combo tx for intermediate grade NHL is the CHOP+rituximab regimen: rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone. |
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Multiple myeloma
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Dexmethasone, thalidomide. DVd regime: vincristine, pegylated liposomal doxorubicin, dexamethasone.
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Thalidomide/Lenalomide
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MOA: G1 growth arrest and/or apoptosis by disrupting BCL2, blocks NF-kB signalling, inhibits production of IL-6.
SE: sedation, constipation, peripheral neuropathy MOR: none |
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Carmustine
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MOA: used against HL, NHL, MM. Degraded into two forms: the alkylating group (active moiety that leads to DNA damage) and the carbamoylated product (which binds proteins and leads to serious myelosupression).
Tox: myelosupression. |
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Rituximab
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MOA: chimeric aby against CD20 on B cells. Used to tx Non-hodgkin lymphoma. Given IV. Fab domain binds the CD20 while the Fc elicits an immune response. Causes apoptosis in lymphoma cells.
SE: skin rxns at site of injection (though not seen w/ humanized aby), neutropenia |
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Gemtuzumab ozogamicin
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MOA: aby against CD33 agn (present on leukemic myeloblasts in AML) used to deliver clicheamicin (a cytotoxic abx)
SE: toxicity occurs with first administration, treat with glucocorticoids. Hepatotoxicity and myelosuppression. |
