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IOS 6 Exam 3
Chemotherapy medication
| Question | Answer |
|---|---|
| Cisplatin | First platinum compound invented |
| Cisplatin SE | Renal Tubule necrosis- IV NS Before, dur, after, ototoxcity |
| Carboplatin | A platinum approved in 1989 for ovarian cancer |
| Oxaliplatin | A platinum that is the most effective inhibits DNA repair as well |
| Methotrexate MOA | Inhibits dihydrofolate reductase decrease tetrahydrofolate required for purine thus decreases DNA syn |
| Methotrexate-group | antimetabolite |
| Pemetrexed MOA | antimetabolite-inhibits dehydrofolate reductase and thymidylate and purine biosyn |
| 5-FU MOA | Converted to fluorodexyuridylate (F-dump) inhibiting thymidylate synthase |
| Capecitabine MOA | metabolized in liver, followed by cytidine deaminase, then thymidine phosphorylate to 5 -FU to covalently inactivate thymidylate synthase |
| Cyarabine MOA | Pro-drug activated to 5-mono-phosphate nucleotide (AraCMP) and inhibition of DNA polymerase and decrease chain elongation |
| Permetrexed Group | Antimetabolite |
| 5 FU group | Pyrimidine analog |
| Capecitabine group | Pyrimidine analog |
| Cytarabine group | Pyrimidine analog |
| Gemcitabine group | Pyrimidine analog |
| Gemcitabine MOA | Potent inhibitor of DNA enlogation and confluent against growing cells |
| 6-Mercaptopurine group | Purine |
| 6-Mercaptopurine MOA | Must activate to Inhibit conversion of inosine monophosphate to adenine and guanine nucleotides |
| Fludarabine Phosphate MOA | Converted to triphosphate and inhibits DNA polymerase, incorporated into DNA ans RNA |
| Hydroxyurea MOA | Inhibits ribonucleoside diphosphate reductase and enzyme that catalyzes coverstion to deoxyribonucleotide |
| Vinca Alkaloids MOA | block cells in mitosis |
| Vinca Alkaloids | Vinblastine, Vincristine, Vinorelbine |
| Paclitaxel, Docetaxel MOA | Promote microtubule formation leading to aberrant structures |
| Topoisomerase Inhibitors | Etoposide/Teniposide, Camptothecin, Topotecan,Irinotecan |
| Etoposide/ Teniposide MOA | Form a tertinary complex with TOPO II and DNA resulting in dsDNA break, S and G2 most sensitive |
| Camtothecin?Topotecan/Irinotecan MOA | Inhibit function of TOPO I by binding and stabalizing normally transient DNA-TOPO I |
| Dactinomycin, Doxorubicin, Mitoxantrone, Bleomycin group | Antibiotics |
| Dactinomycin MOA | Bind to dsDNA blockingtranscription of DNA by RNA polymerase |
| Doxorubicin MOA | Intercalate with DNA-TOPO II affecting DNA syntyhesis and forming a semiquinone radical that reacts with molecular O2 to produce ROS |
| Mitoxanatrone MOA | Cause DNA strand break via TOPO II, limited ROS, so less cardiotoxic |
| Bleomycin MOA | Oxidative damage of ssDNA and dsDNA, used with copper chelating peptides, A2, B2. Important role in combination therapy. |
| Alkylating Agents | Mechlorethamine, Carustine,Cyclophosphamide |
| Mechlorethamine MOA | Activates in alkaline or neutral pH, neutrophillic attack of unstable aziridine ring by electron donor, DNA damage |
| Carmustine MOA | Intrinisically reactive undergoes spontaneous degradation to for alkylating agent and carbamoylated intermediate with DNA |
| Cyclophosphamide MOA | Undergoes Phase 1 metabolism to activate forming 2 toxic metabolites Acrolyn and Phosphamide mustard (Active-anticancer) |
| Alkylating Agents-Resistance | Increased glutatione (Buthione sulfoximine) Cross-resistance, decreased permeation, increase activity of DNA repair enzymes, |
| Antimetabolite-Resistance (MTX) | Toxic against rapid growing normal cells of BM, GI, Liver, renal, increased or altered dihydrofolate reductase |
| Pyrimidine Resistance (5FU) | Amplification of thymidylate synthase, or altered thymidylate synthase that is not inhibited, Loss of enzyme activation, |
| VInca Alkaloids Resistance | MDR pumps, cross-resistance |
| Paclitaxel, Docetaxel Resistance | MDR pump, b-tubulin mutations |
| Etoposide/Teniposide | Amplification of MDR-1 gene that encode for P-gylcoprotein, mutation/decreased TOPOII, mutation of p53 (apoptosis) |
| Topotecan, Irotecan, Camptothecin Resistance | Alteration in drug metabolism, Alteration in TOPO I |
| Nitrogen mustards | Mechlorethamine, Chlorambucil, Cyclophosphamide |
| Nitrosourea | Carmustine |
| Alkyl Sufonate | Busulfan |
| Triaazene | Dacarbazine |
| Platinum compounds | Cisplatin, Carboplatin, Oxaliplatin |
| Intrinsically Reactive alkylating agents | Mechlorethamine, Chlorambucil, Cisplatin, Carboplatin, Oxaliplatin |
| Inactive alkylating agent | Cyclophosphamide |
| Methotrexate SE | oral sores(luecovorin), renal (pH>7-NaHCO3), BM, Hepatic, fibrosis |
| Cytarabine SE | Myelo-supression, GI , Hepatic obstruction |
| Capecitabine SE | Hand and Foot syndrome |
| Gemcitabine SE | myelosuppressive |
| 6-Mercaptopurine SE | Hyperuremia, BM supression, N/V, jaundice |
| Fludarabine SE | Muelosuppression, N/V, chills and fever |
| Paclitaxel SE | BM, hypersensitivity (Dexamethasone pre-chemo) , myalgias |
| Docetaxel SE | hypersensitivity (Dexamethasone x3 days) |
| Etoposide SE | Leukopenia, N/V, stomatitis, |
| Teniposide SE | Myelosuppression, N/V |
| Topotecan SE | Hematological tox, neutropenia, thrombocytopenia |
| Irinotecan SE | Delayed Diarrhea, myelosuppression |
| Dactinomycin SE | Anorexia, N/V, hematopoetic suppression |
| Doxorubicin | Cardiotoxic, , allopecia, Extravascular reactions |
| Mitoxantrone SE | Acute myelosuppression and cardiotoxcity |
| Bleomycin SE | Pulmonary SE |
| Acute N/V | Occurs w/in 24 hrs after chemo, usually 1-2 hrs after |
| Delayed N/V | Occurs > 24 hr after chemo peak in 48-72 hr |
| Anticipatory N/V | Learned or conditioned response |
| Breakthrouhgh N/V | Occurs despite preventative therapy |
| Risk for N/V | Age(young), women, non-drinker, prior chemo, motion sickness, pregnancy, anxiety N/V |
| Acute N/V treatment | Serotonin 5HT3 antagonist |
| Delayed N/V | Dexamethasone |
| Breakthrough N/V | Phenothiazines: Perchlorperazine, Promethazine |
| Acute -high moderate emetogenic | 5HT3+ corticosteroid-schedule |
| Low emetagoenic (2) | Dexamethasone or prochlorperazine, promethazine |
| Anticipatory N/V | Lorazepam |
| Agents that cause delayed N/V | Cisplatin, Carboplatin, cyclophosphamide, doxorubicin |
| Febrile Neutropenia | Fever>101, and ANC <500 |
| ANC | (WBC) (Seg+bands) Normal > 2000 |
| High Risks for Febrile Neutropenia | Comorbid illness (COPD, DM, Renal, CVD), Age >60, ECCOG>2, prior chemo, Bone marrow involvement, duration of neutropenia |
| Contra for Neupogen or Pegfilgrastim | Antibiotic and Fever |
| Primary Prevention-chemo | Risk FN 10-20%, patient conditions, comorbities |
| Neupogen MOA | Stimulate granulocytes to become neutrophils |
| Neulast MOA | Stimulates granulocytes to become neutrophils |
| Neupogen dosing | 5mcg/kg/dose 24 hours after chemo x 5 days |
| Sargramostim (Leukine) MOA | Stimulate macrocyte formation |
| Febrile Neutropenia Low risk: Treat | Oral Ciprofloxacin+Amoxicillin - clavulante |
| Febrile Neutropenia High Risk: Treat | Vancoymicin + Cefepine Quarentee (3-5 days) consider Colony stimulating factor-neupogen |
| Anemia Grade 3 | Stop transfusion |
| Risk of death w/o anemia treatment | 50% |
| Chemotherapy induced anemia | Type of disease, Malignancy, Stage of disease (metastatic higher) |
| Risk of anemia | Older, heavy pre-treated, myelosuppressive agents, Platinums, taxanes, anthracyclines, Alkylating agents, topoisomerase inhibitoes, weekly verse 3-4 wk |
| Eopetin-Anemia Dosing | Iron+ 40,000Sq week x4 then check(11-12) , 60,000 x4 |
| Darbeopetin-Anemia Dosing | Iron+ 200mcg Sq every 2 wk, check in 6 weeks, (11-12), 300mcg SQ 2 wk |
| Anemia-RBC response needed | 1g/dL |
| National Cancer Institute Scale | 1(mild) -5 (Severe) |
| Allopecia Risk High | Doxorubin,idarubin,eirubicin |
| Allopecia Low Risk | Tamoxifin, Fulvestrant, Anastrozole, LetrozoleLHRH, GnRH, Targeted agents |
| Bladder Toxcity | Cyclophosphamide and isofamide- acrolein bind renal tubes |
| Cyclophosphamide Bladder toxcity | Oral Hydration of 2-3 liters day, day before, night, morning |
| Isosfamide renal toxcity | IV hydration -prevention Mesna. |
| Cardiac Toxcity | Doxorubicin or Trazumab (reversible) |
| Acute cardiac toxcity | Onset hrs, no clinical intervention |
| Subacute cardiac toxcity | weeks or months later tachycardia, fatigue, progress to CHF |
| Late cardiac toxcity | late onset 5-20 years later, progressive damage |
| Doxorubicin cardio tox MOA | intercalating with DNA and TOPOII and semiquinone ROS |
| Prevention of cardiotoxcity | Dexrazoxane-iron chelator prevent formation of iron complexes-use in metastatic |
| Diarrhea-Grade 3 | > 7 stools, Hospitalizations |
| Diarrhea-Call PCP | > 3 loose stools |
| Diarrhea High Risk | Irinotecan, 5FU+ leucoforin, elderly female |
| Acute treatement | Atropine |
| Chronic | Loperamide 4mg, contact PCP,>3 stools |
| Gonadal Dysfunction HIgh Risk | Cyclophosphimide, Mechloethamine, Carmustine, Females near mentopause (avoid estrogen), Males, sterile but may return |
| Hypersensitivity Risk | Paclitaxel>> docetaxel, L-asparaginase (high), Carboplatin, Abarelix |
| Paclitaxil Hypersen Treatment | Dexamethasone or Benedryl |
| Docetaxel hyper treatment | Dexamethasone |
| Muscle Pain Risk | Paclitaxel, Aromase inhibitors |
| KIdney Damage Risk | Cisplatin, Methotrexate |
| Liver Damage Risk | Cytarabine, Flutamide |
| Ototoxcity Risk | Cisplatin |
| Oral Complications Risk | 5 -FH or methotrexate (w/o leucovorin) |
| Oral tissue regrow | Keratinocyte growth factor |
| Rash Risk-acniform | Cetuximab-sign drug is woeking |
| Hand-Foot risk | Capecitabine, 5 FU infisions, liposomal antracyclines |
| Reason for targeted cancer therapy | Hormone drives growth, Lack drug resistance |
| Advantage of Targeted therapy | Cytostatic-slow tumor growth |
| Antiestrogens | Tamoxifen, Tormifene, Fluvestrant(IM) |
| Aromatase inhibitors | Anastrozole, Letrozole, Exemestane |
| Antiandrogens | Bicalutamide, Nilutamide, Flutamide, |
| Leteininizing hormone-releaseing hormones | Leuprolide, Goserelin |
| Gonadotropin-releasing hormones | Abraelix |
| Monoclonal anabody types | Conjugated, unconjugated |
| Unconjugated monoclona antibodies | Rituximab, Trastuzumab, Cetuximab, Bevacizumab |
| Conjugated monoclonal antibodies | Ibritumomab, Tositumomab |
| Tyrosine Kinase Inhibitors | Erolotnib, Sorafenib, Imatniob, Imatniob(gleevec), Bortezomib |
| Tamoxifen MOA | Diffuse into cell and bind the estrogen receptor, dimerize and enter the nucleus prevent binding of transcription factors |
| Tamoxifen Dosing | 30mg PO 3-5 years |
| Anastrozole (aromatase inhibitor) MOA | Inhibit the conversion of androgen to estrogen (fat tissues) |
| Bicalutamide MOA (antiandrogen) | Inhibit the binding of testerone to the antrogen receptor and inhibits the antrogen receptor binding DNA |
| Leuopride or Goserelin MOA | Bind to the pitutary to stimulateand produce gonadatropins to initially increase then cause feedback inhibition (decrease) hormone release |
| Gonadotropin releasing hormone | Abarelix |
| Abaralix SE | Life threatening rxn |
| Antiestrogens SE | Fluid retention, thrombocytopenia, uterine cancer |
| Aromatase inhibitors SE | Asthenia, Arthralgias, Fatigue |
| Antiandrogens SE | Gynomastica, LFT increase, HTN |
| LH-RH SE | Gynomastica, decreased libido, impotence, Tumor flair |
| xi | chimeric |
| zu | humanized |
| mo | mouse |
| Rituximab | CD 20+ inhibitor |
| Rituximab SE | infusion Rxn=pre-treat |
| Trastuzumab MOA | HER2 epithelial growth factor receptor di-merization but prevent cell growth |
| Trastuzumab SE | Transfusion rxn,(No treat) , anemia, leukopenia, cardiotoxic, diarrhea |
| Cetuximab MOA | EGFR- prevents grow signaling pathway |
| Cetuximab SE | Infusion Rxn (pre-treat), acneform rxn, pulmonary |
| Bevacizumab MOA | VEGF antagonist- prevents angiogenesis |
| Bevacizumab SE | bleeding, HTN, thromboembolism, proteinurea |
| Ibritumomab MOA | conjugated to yttrium 90 localized radiation |
| Tositumomab MOA | Conjugated to iodine 131 localized radiation |
| EGFR inhibitors | Erlotnib, Gofitnib |
| Erlotnib MOA | Diffuse into cell and bind the EGFR receptor to prevent phosphorylation and activation of second messenger |
| Erlotnib SE | anemia, acneform rxn, LFT increase, pulmonrary |
| Multi kinase Inhibitor | Sorafenib |
| Sorafenib SE | anemia, hand and foot, HTN, rash DI-warfarin |
| Bcr-Abl inhibitor | Imatnib-Gleevec |
| Imatnib SE | diarrhea, fluid retention, muscle pain,N/V |
| Bortezomib MOA | ubiquitin/proteasome inhibitor prevent degradation of cyclin, oncogenes- cause apoptosis |
| Bortezomib SE | Anorexia, diarrhea, fatique, peripheral neuropathy, thrombocytopenia |
| CML treatment | Imatnib, hydroxyurea, busulfan, INF-y |
| CML prognosis | Age- 60's Chronic (4y), Accelerated (month-year), Blast (days-year) |
| CML-marker | Phil Chromosome (9-22) which causes increased activity in tyrosine kinase (increase WBC, PTL) |
| CLL treatment | 1. wait 2. Fludarabine (cyclophosphamide+ Rituximab) 3 Alemtuzumab 4 BM transplant |
| CLL prognosis | 10year |
| CLL etiology | Malignant B-cell line- FHx 2-3X risk age 50's |
| CLL risk stratification | Low=lymphocytosis Intermediat= Lymp +hepatomed or splenomeg, High= Lympocy +anemia |
| AML treat | Induction=cytarabine (7) + Daunorubin, Idarubin, Mitoxtrone (3) 2. Consolidation=cytarabine If M3= Retinoin 4. Salvage=Gemtuxumab, Asernic tiroxide or BM transplant |
| AML tumor lysis syndrome | 1. Allopurinol +hydration 2. NaHco3 3. Rasburicase |
| AML- Bleeding/anemia | Transfusion-irriated |
| AML-CNS toxcity monitor | Cytarabine |
| AML-Patho | Radiation, benzene, toluene, alkylating agents, cigarettes, HTLV-1 |
| AML-prognosis | M2-Great (retonic15:17) M3-great(8:21) and M4great (inv16) |
| ALL- Etilogy | Radiation, benzene, toluene, alkylating agents, cigarattes, HTLV-1 |
| ALL treatment | Induction- Prednisone + asparaginase 2. Consolidation Cytarabine or High MTX 3. Maintenance MTX + 6MP Salvage Clofarabine |
| ALL prognosis | L1 children(cure) L2,L3 adult poor |
| ALL Poor Prognosis | Age<1 and >9, L2, or L3, WBC, Delayed remission, cytogenic abnormalities |
| ALL-MOA | Primative lymphoid (pre-B-cell) which divide uncontrollable |
| AML-MOA | Myeloid progenitor cell dysfunction, decreased WBC, PTL |
| CLL- MOA | Dysfunctional B-cell or T-cell to produce maligant clones |
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