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pharm
intro to antineoplastic pharmacology
| Question | Answer |
|---|---|
| Generally, this type of drug is used to treat neoplasia. it was historically used for metastatic cancer, but today can also be used in surgically resectable disease | cytotoxic agent |
| cytotoxic agents are important to be used today because they... | decrease post surgical recurrence of cancer later in life, and allows more (organ/function) sparing procedures. |
| true or false: the general rule for cancer chemotherapy is using drug combinations | true |
| When using drug combination therapy for chemo, it is important to understand these two properties of the drug: | drug resistance and cell kinetics. |
| general rules for drug combination regimes... | all drugs must be active as single agents, each drug should have a different mechanism of action and drug resistance, drugs should have nonoverlapping toxicities, each drug should be used at maximum dose and titrated to end organ toxicity |
| what are some reasons why cancer chemotherapy can fail? | patient status may limit therapy, growth fractions can be low, cancer cells may not be in a sensitive stage in cell cycle, cells not homogeneous, tumor perfusion not uniform, cancer spreads to different body compartments, can display drug resistance |
| what are some patient factors which determine his/her ability to tolerate chemotherapy | organ function, age prior to therapy, metabolic capacity of liver, kidney, ability to produce blood cells, ability of GI tract to recover. |
| generally speaking, patients with these characteristics will tolerate chemotherapy better | patients with asymptomatic illness, who are active, have good appetites, no weight loss |
| given to induce a remission. commonly used in the treatment of acute leukemias | induction |
| used after initial surgical or radiation therapy to minimize recurrence | adjuvant |
| given prior to surgery or radiation to reduce tumor burden | neoadjuvant |
| use dafter recurrence of refractory tumor following chemo | salvage |
| given concurrently with radiation to increase radiosensitivity | chemosensitive |
| given specifically to address symptom management without expecting to significantly reduce the cancer | palliative |
| treatment phases of leukemia | induction, intensification, maintenance |
| a complete disappearance of all clinical evidence of tumor | complete response |
| a greater than fifty percent decrease in the sum o fproduct of measured lesions; no simulataneous increase in the size of any leasion or the appearance of new lesions may occur; nonmeasurable leasions must remain stable or regress to be included | partial response |
| a steady state of response less than partial response, or progression less than progressive disease, lasting at least four weeks; no new lesions | stable disease |
| an unequivocal increased of at least half of the product of the measured lesion; new lesions also included | progressive disease |
| differences in anticancer vs. antimicrobial therapies | AM therapy uses low cont doseas, cancer chemo uses high intermittent doses, to cure cancer u need 100% cell kill, cancer cure is disappearance of any evidence of tumor for many years and high prob of normal life span, clinically complete remission. |
| do anticancer or antimicrobial drugs have a higher selective toxicity | antimicrobial because bacteria and human cells have many different structures. (cancer cells are more like normal cells) |
| T/F: selective toxicity to cancer cells is limited by considerable toxicity to normal cells. | true. this is partly because the patient is dosed with as much drug that they can tolerate. |
| this is one important target for anticancer drugs | mitotic activity. many chemo drugs also target apoptosis because DNA damage cannot be repaired. |
| this type of cell is most vulnerable to chemotherapy because it is progressing through the cell cycle | rapidly dividing |
| true/false slow growing cancers (colon and lung carcinoma) make chemotherapy difficult | true |
| what are tumor determinants in responsiveness to cancer chemotherapy | growth fraction, total tumor burden, cell cycle phase, drug resistance |
| what are some host determinants in responsiveness to cancer chemotherapy | general health status, immunocompetence, tumor site |
| what are simplistic determinants of tumor cell growth kinetics | cancer cell growth rate, tumor cell number, chemotherapy dose |
| what are some complex functions involved in the growth of a tumor mass | heterogeneous cell grwoth kinetics, cell death, development of cancer promoting growth properties |
| describe growth fraction | the fraction of tumor cells that are dividing |
| for this type of tumor, growth depends on nutrient availability and vasculariation; diffusion limited growth; center may be necrotic | solid tumor |
| will a tumor or mass with a large growth fraction have an increased or decreased drug susceptibility | increased |
| does tumor doubling time vary with tumor? | yes |
| describe the Gompertizian growth model | growth fraction of the tumor is not constant and peaks when the tumor is about one third of its maximum size. initial growth is first order with later growth being much slower. |
| what size tumors are least sensitive to chemotherapy? | large tumors |
| list some complications to effective treatment | number of dividing cells vs. resting cells change, biochemical character changes, number of cells that can metastasize change, by the time solid tumors are detected they contain many subclones of biochemically different cells, genetic instabiity |
| growth rate (decrease, increase?) as neoplasm size increase | decrease |
| how many cells are in a clinically detectable tumor (1cm big) | one billion cells |
| how many cells are contained in lethal tumors | one trillion |
| why are larger tumors harder to kill? | more difficult for drugs to penetrate, poor vascularization, slower growth, more metastasis occurring, more therapy time required, more toxicity. |
| describe the mitotoxicity hypothesis | tumors are most vulnerable to anticancer drugs while they are growing because they are metabolically active and rapidly replicating DNA. poisoning the cell during S phase can prevent it from entering M phase. |
| what are CCS drugs? | (cell cycle specific drugs)cells must be mitotically active for drug to produce its effects. the drug target is only available at a particular phase of the cell cycle. they are effective for high growth fraction malignancies. |
| what are CCNS drugs? | (cell cycle nonspecific drugs) drug effect may be enhanced but not dependent on mitotic activity. they are effective for both low growth fraction malignancies as well as high growth fraction malignancies. |
| what are the major mechanisms for drug resistance | decrease drug uptake, decrease drug activation, overexpression or mutation of drug target, increased rapair of drug damage to DNA, increased intracellular nucleophile concentrations of drug substances |
| what are some mechanisms of multidrug resistance. | efflux pumps, pgp: active transporter than can be upregulated in cancer cells, MRP: transporter that can pump drugs out of the cell. both MRP and pgp are part of the ABC. |
| list some multidrug resistance genes | pgp, MRP, |
| what is the therapeutic index for most chemotherapeutic agents? | 1 |
| what are some common side effects seen with many anticancer drugs | nausea, vomitting, stomatitis, mucositis, alopecia and myelosuppression (predisposition to infection) |
| describe some oral toxicities associated with chemotherapy | disruption of integrity of mucosal lining, oral ulcerations, dysphagia, gastritis, diarrhea, malabsorption, mucositis |
| how are most cytotoxic drugs mostly give? | via IV |
| chemotherapy induced tumors are especially a problem after therapy with what type of drug? | alkylating agents |
| what type of cancer cells are likely to be affected by anticancer therapy? | fast growing normal cells. (blood cells resulting in anemia, cells of GI, resulting in mouth ulcers, cells of repro sys, resulting in temporary infertility, hair loss, nausea/vomitting) |
| list some common targets of chemotherapeutic agents | purine synthesis, pyrimidine synthesis, DNA, RNA, proteins |
| what is the largest class of anticancer drugs? | alkylating agents. primary mechanism of antitumor action is alkylating DNA. the N7 position of guanine is the major site. |
| aklylating of DNA can cause this | excessive cross linking (where it's difficult for cancer cells to repair) and DNA strand breaks. |
| how do antimetabolites work in cancer therapy? | antimetabolites resemble cellular metabolites and interfere with DNA synthesis or the synthesis of DNA precursers. the general drug classes are antifolates and nucleoside analogs. |
| how do antibiotics work in cancer therapy | they bind to DNA and DNA associated proteins , inhibit RNA synthesis, some induce DNA strand breaks by free radical introduction or inhibition of topoisomerase |
| how do antimitotic agents work? | they disrupt chromosomal dynamics. and disrupt the cellular machinery necessary for DNA replication and mitotis. |
Created by:
aferdo01
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