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Cancer treatment involves interrupting cell division by the following methods:
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If the drug name ends in a "mab" it is a --> If the drug name ends in a "nib" it is a -->
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Antineoplastics I-II
Antineoplastic Lectures 1-3
| Question | Answer |
|---|---|
| Cancer treatment involves interrupting cell division by the following methods: | 1) Interrupt formation of DNA and RNA with base analogs 2) Interrupt topology (3D winding) of DNA by distorting the helix or adding functional groups |
| If the drug name ends in a "mab" it is a --> If the drug name ends in a "nib" it is a --> | a) monoclonal antibody b) tyrosine kinase inhibitor |
| Local therapy with radiation or surgery effective when... | ...metastasis has not occurred. Definitive local therapy should occur BEFORE surgery |
| Systemic adjuvant or neoadjuvant chemotherapy is (pre/post) surgery and is targeted to... | 1) post surgery 2) Targeted to catch any remaining cancer cells around the excision site |
| Adjuvant biological therapy | Involves specific cell surface or intracellular targets |
| Systemic chemotherapy | •For disseminated disease (metastatic cancer that has extended into the bloodstream or lymph system) •Often only palliative |
| To increase: a)dose intensity b) dose density | a) increase dose and decrease time between intervals (intensity) b) decrease time between intervals |
| Treatment causes a loss of the WBC population. This is called... | myelosuppression. This leaves the pt susceptible to infection |
| Due to myelosuppression, there needs to be time between treatments to allow for... | WBC counts to return to regular count |
| Methods of monitoring improvement include: | X-ray, bone scan, CAT scan, MRI, decrease in tumor marker (ie. measuring levels of prostate specific antigen), normalization of organ function or neurologic status, "quality of life" improvement even if no increase in longevity |
| Methods of monitoring toxicity due to antineoplastic treatment include: | 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 |
| Tumor Lysis Syndrome | -Lysis of tumor releases purine nucleic acids, K+ and phosph -Renal elimination saturated --> hyperklemia, hyperphosphatemia, HYPOcalcemia, hyperuricemia -Uric acid-crystals formed |
| Management of tumor lysis syndrome: What three things need to be done? | 1) alkalinize the urine 2) Prevent uric acid formation 3) Degrade uric acid to water-soluble allantoin for elimination |
| Tumor Lysis Syndrome management: What three things can alkalinize the urine? | 1) hydration 2) acid/base correction 3) sodium bicarbonate |
| Tumor Lysis Syndrome management: What drug can prevent uric acid formation? | Allopurinol |
| Tumor Lysis Syndrome management: This drug is a recombinant urate oxidase and it degrades uric acid to water-soluble allantoin for elimination | Ras-bur-i-case (Elitek) |
| It is normal to give adjunct therapy to decrease what kind of toxicity? | Renal |
| This drug is for the treatment of gout and prevents uric acid formation by blocking xanthine oxidase | Allopurinol. An example of adjunct therapy. |
| These drugs target mitotic spindles, which are only present during the mitotic M phase | Vinca alkaloids |
| This term refers to when a drug can affect cells in any phase, even resting cells | Cell cycle non-specific |
| This term refers to when certain drugs’ targets only occur during certain phases of the cell cycle | Cell cycle specific |
| Anti-cancer drugs work best in what kind of cell? Why? | Proliferating cells because the cells have less time to repair themselves, and the decision for apoptosis has to be made so quickly. Abnormal proliferating cells tend to choose cell death over repair and continuing to cell division |
| Creating lesions in DNA flowchart | Activate apoptosis by initiating mitochondrial damage (either by free radical damage or by activation of sphingomyelinases and the production of ceramides that can have a direct action at mitochondria. |
| Damaged mitochondrai releases... | 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 |
| Nitrogen mustards. List prototype and other agents. | Prototype: Cyclophosphamide. Other agents: Ifosfamide, Mechlorethamine |
| Alkyl sulfonates. List prototype | Busulfan |
| Nitrosoureas. List both prototypes | BCNU, CCNU |
| Aziridines. List the prototype | Thiotepa |
| Antibiotics. List the prototype | Mitomycin C |
| Platinum drugs. List a prototype and two other agents. | Prototype: Cisplatin Other agents: carboplatin & oxaliplatin |
| Triazenes. List the prototype | Dacarbazine |
| Hydrazines. List the prototype. | Procarbazine |
| Clinical utilities: ALL, non-Hodgkin's, breast, cervix, ovary, testis, osteogenic | Cyclophosphamide |
| Clinical utilities: Testis, breast, cervix, lung, NHL, osteogenic, pancreatic | Ifosfamide |
| Clinical utilities: CLL, CML, Hodgkin's, NHL, lung | Mechlorethamine |
| Clinical utilities: CML | Busulfan |
| Clinical utilities: Astrocytoma, brain metastases, Hodgkin's, NHL, malignant glioma, medulloblastoma, multiple myeloma | BCNU, CCNU. These agents have the widest use for brain cancer. Can cross BBB |
| Clinical utilities: NHL, HL, breast, ovarian, bladder, soft tissue sarcoma | Thiopeta |
| Clinical utilities: Pancreatic, breast, bladder, colorectal, gastric, H/N, lung, mesothelioma | Mitomycin C |
| Clinical utilities: Ovarian, testis, bladder, breast, gastric, lung, glioma, melanoma, HL | Cisplatin |
| Clinical utilities: Ovarian, testis, H/N, NHL, breat, lung, neuroblastoma, ALL, AML | Carboplatin |
| Clinical utilities: HL, melanoma, neuroblastoma, soft tissue & osteogenic sarcoma | Dacarbazine |
| Clinical utilities: HL, NHL, glioma, medulloblastoma, lung | Procarbazine |
| What functional group is the most critical part of the drug? | Chlorethyl functional group |
| List 5 bis(chlorethyl)amine alkylating agents | 1) Cyclophosphamide 2) Ifosfamide 3) Merchlorethamine 4)Melphalan 5) Chlorambucil |
| bis(chlorethyl)amine alkylating agents MOA | Transfer an alkyl group to DNA. N7 guanine is much more accessible than the others. One chlorethyl group will be attached to one strand, and the second attaches elsewhere, leading to cross-linking of DNA strands --> prevents transcription |
| These groups are also modified by bis(chlorethyl)amine alkylating agents, but these modifications are not thought responsible for cytotoxic action | Sulfhydryl, amino, carboxyl, phosphate groups |
| Cells in this stage are most susceptible to bis(chlorethyl)amine alkylating agents. | late G1-S. (replicating cells). Leads to G2 block. |
| Resistance mechanisms to bis(chlorethyl)amine alkylating agents | 1) decreased drug uptake 2) Tumor cell repairs damaged DNA 3) increased metabolism of drug 4)o Tumor cell can supplement the function of the target protein with another protein, so the drug is rendered ineffective |
| These bis(chlorethyl)amine alkylating agents have a direct vesicant-action (blister forming) | Cyclophosphamide, melphalan, chlorambucil |
| Bis(chlorethyl)amine alkylating agents side effects (in addition to the direct vesicant-action agents) | bone marrow toxicity, GI, reproductive systems (oligospermia & amenorrhea), alopecia |
| A bis(chlorethyl)amine alkylating agent that is slightly different from the rest and has its own CNS toxicity | Ifosfamide. Can casue an altered mental status, coma, gen. seizures, cerebellar ataxia. |
| Many of the bis(chlorethyl)amine alkylating agents are deposited in the lungs, especially... | Cyclophosphamide, chlorambucil, melphalan. This causes fibrosis, progressive dyspnea, cyanosis, pulmonary insufficiency. These things can occur even after the drug is withdrawn. |
| Bis(chlorethyl)amine alkylating agent: more side effects | Carcinogenic (can cause leukemias and solid tumors). They are also teratogenic (1 in 6 chance of malformed infant). |
| Cyclophosphamide releases this agent, which is extremely nephrotoxic. ***** | Acrolein. It is not anti-tumor, but it does cause renal toxicity. |
| Cyclophosphamide and ifosfamide can cause renal failure. Which tubules in the kidney are most greatly affected? The proximal or the distal? | Proximal. There are difficulties in Ca2+ and Mg2+ reabsorption, glycosuria, and renal tubular acidosis |
| Cyclophosphamide and ifosfamide release acrolein, which causes severe hemorrhagic cystitis ( blood in urine). What agent can be given prophylactically to prevent this toxicity? | Mesna. It is a chemoprotectant, which differ from other rescue medications because they are administered prior to the chemotherapy to prevent toxicities. |
| Mesna: general info | 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. |
| 2nd or 3rd line therapy because of AEs. Used for RA when DMARDS fail | Cyclophosphamide |
| Aklyl sulfonates: Busulfan. Toxicities: name some | 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 |
| Rare side effects of busulfan | asthenia, HYPOtension, and a symdrome resembling Addison's dz (but w/o abnormalities of corticosteroid production, just muscle pain and weakness) |
| Nitrosoureas: list four | Carmustine = BCNU and Lomustine =CCNU |
| Distinguishing fact about BCNU (Carmustine) and CCNU (Lomustine) | They can get into the BBB |
| These two nitrosoureas are alkylators | Carmustine/BCNU and lomustine/CCNU |
| This nitrosourea's decomposition forms isocyanates | Carmustine. 2-chlorethyl isocyanate of carmustine inhibits DNA repair. |
| Carmustine/BCNU MOA (bifunctional MOA) | alkylation AND carbamoylation of amino acids in proteins |
| Cross resistance between carmustine/lomustine with other alkylating agents (like cyclophosphamide) is common or uncommon? | Uncommon |
| Administration routes of BCNU and CCNU | BCNU = parenteral CCNU = oral |
| Toxicities include bone marrow suppression, notably thrombocytopenia and leucopenia | BCNU/CCNU |
| Other toxicities seen with BCNU/CCNU | 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 |
| Specific hepatic toxicity seen with these two drugs | Busulfan and BCNU |
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Liza8986
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