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IOS6 exam 3
Targeted Cancer Agents (O'Bryant)
| Question | Answer |
|---|---|
| 2 ways to inhibit hormone effect... | Block the hormone receptor or block synthesis of hormone |
| MOA of antiestrogens | Block estrogen receptor and thereby inhibit cell division that is normally promoted by estrogen. |
| Traditional antiestrogen agents... | Tamoxifen, Toremifene, Fulvestrant |
| Pharmacokinetics of tamoxifen & toremifine... | A: peak plasma in 3-6 hrs.; well absorbed D: highly protein bound M: CYP450 E: 75% feces; minimal urine Tamoxifen t1/2 7-14d; Toremifine t1/2 4-6d |
| Pharmacokinetics of fulvestrant | A: no oral absorption; IM inj. every month D: 99% protein bound M: CYP3A4 E: 90% feces; 1% renal t1/2 - 40 days |
| Indications for antiestrogen therapy... | Breast & endometrial cancer |
| AEs of antiestrogens... | Menopausal type AEs...hot flashes, fluid retention, nausea, HA, skin rash, thromboembolic events, endometrial hyperplasia |
| Good and Bad effects of antiestrogens... | Good: reduces breast cancer risk, lowers LDL, strengthens bones Bad: increase uterine cancer risk, increased blood clot risk |
| MOA of Aromatase inhibitors | Blocks aromatase and thus blocks the conversion of androgens into estrogens (blocks the effects of estrogen by decreasing the amount of estrogen production). |
| Aromatase inhibitors... | Competitive: Anastrozole & Letrozole Irreversible: Exemestane |
| Pharmacokinetics of anastrozole & letrozole... | A: oral; peak plasma 1 week D: Minimal protein binding M: CYP450 E: Anastrozole-feces>urine; Letrozole-urine t1/2 2 days |
| Pharmacokinetics of exemestane... | A: oral; peak plasma 1 week D: highly protein bound M: CYP450 E: feces > urine t1/2 24 hours |
| Indication for aromatase inhibitors... | Breast cancer |
| AEs for aromatase inhibitors | Fatigue, asthenia, hot flashes, nausea, HA, arthralgias, (less thrombolic risk) |
| MOA of antiandrogens... | Inhibit testosterone binding to androgen receptor thus inhibiting cell division that is normally induced by testosterone. |
| Antiandrogen agents... | Flutamide, Bicalutamide, Nilutamide |
| Pharmacokinetics of antiandrogens... | A: oral; peak plasma 1-2 hours D: moderate-major protein binding M: CYP450 E: urine > feces t1/2: flutamide 8-10hrs; bicalutamide 1 wk; nilutamide 41-49hrs. |
| Indication for antiandrogens... | Prostate cancer |
| AEs of antiandrogens | Hot flashes, gynecomastia, LFT abnormalities (could be fatal), diarrhea Flutamide: methemoglobinemia Bicalutamide: Fe-deficiency anemia, hematuria Nilutamide: disulfiram like reaction, visual problems, interstitial pneumonia |
| MOA of LHRH agonists... | Stimulates the pituitary gland to make LH. This stimulates androgen production so that you get secondary feedback to the pituitary to decrease production. You get acute tumor flare, but after 7 days you get decreased production. |
| LHRH agonists... | Leuprolide and Goserelin |
| Pharmacokinetics of LHRH agonists (leuprolide & goserelin)... | A: no oral absorption; 90% absorbed SC D: 30-50% protein bound; depot effect M: Hydrolysis of C-terminal amino acid E: urine t1/2: 3-5 hours |
| Indications for LHRH agonists... | Prostate cancer (primarily), may be used in breast cancer |
| AEs of LHRH agonists... | Hot flashes, decreased libido, impotence, gynecomastia, tumor flare (acute) |
| MOA of GnRH antagonists... | Directly competes with GnRH receptors in the pituitary, thus reducing androgen production. (produces no transient tumor flare) |
| GnRH antagonist agents... | Abarelix and Degarelix |
| Abarelix AEs... | life-threatening allergic reactions (monitor for 30 min; limits use), hot flashes, breast enlargement or pain, fatigue |
| Degarelix AEs... | Injection site reactions, hot flashes, weight gain, increase in transaminases (LFTs) |
| Monoclonal antibody identifiers: u, o, zu, xi | human, mouse, humanized, chimera |
| Monoclonal antibody target class identifiers: col, mel, mar, got, gov, pr(o), tum | colon, melanoma, mammary, testis, ovary, prostate, misc. |
| Two types of monoclonal antibodies... | Unconjugated (no drug or radioactive material attached) Conjugated (joined to chemotherapy drug, radioactive particle, or a toxin) |
| MOA of Rituximab... | mAB against CD20 on B-cells, which antagonizes the growth signaling pathway. May also mediate complement-dependent cell lysis. (stimulates immunologic response to tumor cells) |
| Pharmacokinetics of rituximab... | A: IV only D: peak/trough levels inversely proportional w/circulating CD20+ B cells E: Fc-receptor binding & phagocytosis t1/2: dose dependent (longer w/later infusions) |
| Indication for rituximab... | 1st line tx of patients w/low grade or follicular, CD20+ B-cell non-Hodgkin's lymphoma (primary). Relapsed or refractory low grade or follicular CD20+ B-cell lymphomas. |
| AEs of rituximab... | Potential infusion related side effects (pre-medicate w/benadryl & tylenol); tumor lysis syndrome |
| MOA of trastuzumab... | Binds to HER2 receptor and prevents the receptor from dimerizing and sending signal for tumor cell proliferation. Also targets tumor cell for destruction by the immune system (complement dependent cell lysis). |
| Indication for trastuzumab... | Breast cancer (adjuvant and metastatic) |
| AEs for trastuzumab... | Infusion related reactions (premeds not necessary), anemia, leukopenia, diarrhea, infection, cardiac dysfunction (watch for comorbidities) |
| Indication of response to trastuzumab (based on the amount of HER2 receptor present in the tissue)... | Immunohistochemistry (IHC): 3+ predictive of response, 2+ perform FISH, 0-1+ no indication FISH: + predictive of response, - in indication |
| MOA of cetuximab... | Bind to HER1 receptor and antagonizes growth signaling pathway. Also enhances chemotherapy-induced cytotoxicity. |
| Indication for cetuximab... | Colon cancer (alone or in combo w/irinotecan) Head & neck cancer (in combo w/radiation) |
| AEs for cetuximab... | Infusion related reactions (premedicate w/benadryl), acneform rash, malaise, diarrhea, hypomagnesemia, pulmonary toxicity (rare) |
| MOA of panitumumab... | Human mAB against HER1 that antagonizes growth signaling pathway |
| Indication for panitumumab... | Colon cancer (in metastatic patients w/disease progression on or following 5-FU, oxaliplatin, and irinotecan containing regimens) |
| AEs of panitumumab... | acneform rash, malaise, diarrhea, hypomagnesemia, pulmonary toxicity, (no infusion related reactions) |
| MOA of bevacizumab... | Humanized mAB to vascular endothelial growth factor (binds ligand, not receptor), which inhibits blood vessel formation. |
| Pharmacokinetics of bevacizumab | A: IV only D: SS in 100 days t1/2: 17-21 days w/min. CL by liver & kidneys |
| Indications of bevacizumab.. | Colon cancer (in combo w/5-FU) Lung cancer (in combo w/platinum compounds) Breast cancer (in combo w/paclitaxel) Dosing is dependent on type of cancer! |
| AEs of bevecizumab... | Infusion related reactions (no premeds), bleeding, thromboembolism, proteinuria, HTN, GI perforation |
| MOA of ibritumomab-yttrium-90 & tositumomab-iodine... | Conjugated murine mAB directed against CD20; delivers localized radiation to tumor cells. Indicated for lymphoma, and can produce prolonged hematological toxicity. |
| MOA of erlotinib & gefitinib | HER1 tyrosine kinase inhibitors |
| Pharmacokinetics of erlotinib & gefitinib | A: 60% oral absorption; increased w/food D: highly protein bound; SS 7-10 days M: CYP3A4 & CYP1A2 E: feces > urine t1/2: 36 hours |
| Indication for erlotinib & gefitinib | Erlotinib: lung and pancreatic cancer Gefitinib: lung cancer |
| AEs for erlotinib & gefitinib | Diarrhea, acneform rash, anoxrexia, fatigue, N/V, increased LFTs, pulmonary toxicity Interacts w/CYP3A4 inducers/inhibitors |
| MOA of lapatinib... | HER1 and HER2-TK inhibitor |
| Pharmacokinetics of lapatinib | A: variable; increased w/food D: highly protein bound; SS in 6-7 days M: CYP450 E: feces > urine t1/2: 24 hours |
| Indication of lapatinib | Breast cancer in combo w/capecitabine |
| AEs of lapatinib | diarrhea, acneform rash, N/V, fatigue, decreased EF & QTC prolongation, pulmonary toxicity Interacts w/CYP3A4 inducers/inhibitors |
| MOA of sorafenib | Multi-kinase inhibitor; RAF, KIT, VEGF, PDGF tyrosine kinase inhibitor |
| Indication of sorafenib | Renal cell cancer |
| AEs of sorafenib | rash, hand-foot reaction, HTN, bleeding Interacts w/CYP3A4 inducers/inhibitors |
| MOA of sunitinib | PDGF, VEGF, KIT, FLT3 tyrosine kinase inhibitor |
| Indication of sunitinib | Renal cell cancer & GI stromal tumor |
| AEs for sunitinib | GI effects, rash, hand-foot reaction, HTN, bleeding, fatigue, skin discoloration Interacts w/CYP3A4 inducer/inhibitors |
| Bcr-Abl inhibitors... | Imatinib, Dasatinib, Nilotinib Indicated for chronic myeloid leukemia |
| AEs of Bcr-Abl inhibitors | N/V, diarrhea, muscle cramps, fluid retention, neutropenia, thrombocytopenia, hepatotoxicity |
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