Antineoplastic Lectures 1-3
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| Cancer treatment involves interrupting cell division by the following methods: | show 🗑
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| show | a) monoclonal antibody b) tyrosine kinase inhibitor
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| show | ...metastasis has not occurred. Definitive local therapy should occur BEFORE surgery
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| show | 1) post surgery 2) Targeted to catch any remaining cancer cells around the excision site
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| show | Involves specific cell surface or intracellular targets
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| Systemic chemotherapy | show 🗑
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| show | a) increase dose and decrease time between intervals (intensity) b) decrease time between intervals
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| Treatment causes a loss of the WBC population. This is called... | show 🗑
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| show | WBC counts to return to regular count
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| Methods of monitoring improvement include: | show 🗑
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| show | Secondary malignancies, myelosuppression, N/V (treated with neurokinin or 5HT3 antagonists, e.g. odanestron), organ toxicity (heart, lung, kidney, CNS), alopecia (hair loss, balding), mucositis, diarrhea
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| Tumor Lysis Syndrome | show 🗑
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| Management of tumor lysis syndrome: What three things need to be done? | show 🗑
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| show | 1) hydration 2) acid/base correction 3) sodium bicarbonate
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| Tumor Lysis Syndrome management: What drug can prevent uric acid formation? | show 🗑
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| show | Ras-bur-i-case (Elitek)
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| show | Renal
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| This drug is for the treatment of gout and prevents uric acid formation by blocking xanthine oxidase | show 🗑
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| These drugs target mitotic spindles, which are only present during the mitotic M phase | show 🗑
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| show | Cell cycle non-specific
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| show | Cell cycle specific
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| Anti-cancer drugs work best in what kind of cell? Why? | show 🗑
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| Creating lesions in DNA flowchart | show 🗑
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| show | cytochromE C and "apoptosis activating factor", which activates a chain of caspases. AIF (apoptosis-inducing factor) is also released from the mitochondria and goes into the nucleus and binds to DNA, releasing free radicals to further damage the DNA
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| Nitrogen mustards. List prototype and other agents. | show 🗑
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| Alkyl sulfonates. List prototype | show 🗑
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| Nitrosoureas. List both prototypes | show 🗑
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| show | Thiotepa
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| show | Mitomycin C
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| show | Prototype: Cisplatin Other agents: carboplatin & oxaliplatin
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| Triazenes. List the prototype | show 🗑
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| Hydrazines. List the prototype. | show 🗑
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| show | Cyclophosphamide
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| show | Ifosfamide
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| show | Mechlorethamine
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| show | Busulfan
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| Clinical utilities: Astrocytoma, brain metastases, Hodgkin's, NHL, malignant glioma, medulloblastoma, multiple myeloma | show 🗑
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| show | Thiopeta
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| Clinical utilities: Pancreatic, breast, bladder, colorectal, gastric, H/N, lung, mesothelioma | show 🗑
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| show | Cisplatin
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| show | Carboplatin
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| show | Dacarbazine
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| Clinical utilities: HL, NHL, glioma, medulloblastoma, lung | show 🗑
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| show | Chlorethyl functional group
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| show | 1) Cyclophosphamide 2) Ifosfamide 3) Merchlorethamine 4)Melphalan 5) Chlorambucil
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| bis(chlorethyl)amine alkylating agents MOA | show 🗑
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| These groups are also modified by bis(chlorethyl)amine alkylating agents, but these modifications are not thought responsible for cytotoxic action | show 🗑
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| Cells in this stage are most susceptible to bis(chlorethyl)amine alkylating agents. | show 🗑
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| Resistance mechanisms to bis(chlorethyl)amine alkylating agents | show 🗑
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| These bis(chlorethyl)amine alkylating agents have a direct vesicant-action (blister forming) | show 🗑
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| show | bone marrow toxicity, GI, reproductive systems (oligospermia & amenorrhea), alopecia
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| A bis(chlorethyl)amine alkylating agent that is slightly different from the rest and has its own CNS toxicity | show 🗑
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| show | Cyclophosphamide, chlorambucil, melphalan. This causes fibrosis, progressive dyspnea, cyanosis, pulmonary insufficiency. These things can occur even after the drug is withdrawn.
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| Bis(chlorethyl)amine alkylating agent: more side effects | show 🗑
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| show | Acrolein. It is not anti-tumor, but it does cause renal toxicity.
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| Cyclophosphamide and ifosfamide can cause renal failure. Which tubules in the kidney are most greatly affected? The proximal or the distal? | show 🗑
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| Cyclophosphamide and ifosfamide release acrolein, which causes severe hemorrhagic cystitis ( blood in urine). What agent can be given prophylactically to prevent this toxicity? | show 🗑
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| show | Mesna remains in the intravascular fluid, is []ed in the bladder, and is less likely to be absorbed by tumor cells. It doesn't interfere with antitumor activity of ifosfamide or cyclophosphamide.
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| 2nd or 3rd line therapy because of AEs. Used for RA when DMARDS fail | show 🗑
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| show | Myelosuppression @ conventional doses, prolonged pancytopenia at high doses, pulmonary fibrosis, gastriintestinal mucosal damage, veno-occlusive dz of the liver (increased by CYP inhibitors). Longterm use-> impotence, sterility, amenorrhea, fetal toxicity
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| Rare side effects of busulfan | show 🗑
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| Nitrosoureas: list four | show 🗑
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| show | They can get into the BBB
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| show | Carmustine/BCNU and lomustine/CCNU
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| show | Carmustine. 2-chlorethyl isocyanate of carmustine inhibits DNA repair.
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| Carmustine/BCNU MOA (bifunctional MOA) | show 🗑
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| Cross resistance between carmustine/lomustine with other alkylating agents (like cyclophosphamide) is common or uncommon? | show 🗑
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| show | BCNU = parenteral CCNU = oral
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| show | BCNU/CCNU
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| show | N/V, acut injection site burning sensation, delayed phlebitis, pulmonary fibrosis and/or infiltrates (may be delayed by years), endocrine dysfunction with brain irradiation (HYPERprolactinemia and HYPOthyroidism), decrease T4, encephalopathy/seizures
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| show | Busulfan and BCNU
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