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pharm final
cancer drugs
| Question | Answer |
|---|---|
| what is cancer | large group of diseases characterized by the uncontrolled cellular growth |
| define neoplasm | new growth of tissue that serves no physiological function |
| define tumor | clumping of neoplasmic cells |
| define malignant | cancerous |
| define benign | noncancerous |
| external factors causing cancer | chemicals, radiation, viruses, lifestyle |
| internal factors causing cacner | hormones, immune conditions, inherited mutations |
| how gene mutations cause cancer | disruption of RNA/DNA within normal cells; produce cells that differ in form, quality and function |
| 2 physiologic events that cause cancer | abnormal activation of genes that regulate cell growth; lack of tumor-suppressor gene |
| reproduce in response to need for tissue growth/repair | normal cells |
| stop reproduction when need is met | normal cells |
| apoptosis | normal cells |
| well differentiated in appearance and function | normal cells |
| have characteristic lifespan | normal cells |
| persistent proliferation (endless division) | neoplastic cells |
| decreased cellular differentiation | neoplastic cells |
| invasive growth | neoplastic cells |
| formation of metastases | neoplastic cells |
| neoplasms classification | hematologic malignancies, solid neoplasms |
| What neoplasm classification is liquid | hematologic malignancies |
| What tissues do hematologic malignancies invade | bone marrow and lymphoid tissue |
| 3 cancers that are hematologic malignancies | leukemias, lymphomas, multiple myeloma |
| leukemia | hematologic malignancies |
| lymphoma | hematologic malignancies |
| multiple myeloma | hematologic malignancies |
| carcinomas | solid neoplasms |
| what tissue do carcinomas affect | epithelial tissue |
| what tissue do sarcomas affect | connective tissue |
| sarcoma | solid neoplasm |
| define chemotherapy | use of medications to treat cancer rather than surgery/radiation |
| purpose of chemotherapy | kill, damage, or slow growth of cancer cells and prevent/treat adverse effects |
| problem with chemotherapy | kills normal cells also |
| Most chemotherapy regimens involve... | combination of drugs with differing cellular action |
| What is a major problem with chemotherapy drugs | drug resistance |
| adjuvant chemotherapy treatment strategy | short course of high-dose after radiation or surgery to destroy residual cell; prevent recurrence |
| neoadjuvant chemotherapy treatment strategies | prior to surgery, radiation to shrink tumor and improve outcome |
| palliative chemotherapy treatment strategies | control symptoms, comfort, improve quality of life if cure is not achieveable |
| salvage chemotherapy treatment strategies | potentially curative high dose for recurrence or treatment failure |
| induction chemotherapy treatment strategies | high-dose give to induce complete response or cure (1st part = early on) |
| consolidation chemotherapy treatment strategies | after remission, increase probability of cure or survival "moping things up" |
| intensification chemotherapy treatment strategies | after remission, high doses or different drug to improve chances of cure or remission "just in case" |
| maintenance treatment strategy | low dose in remission |
| What chemotherapy strategy occurs most often | combination chemotherapy |
| combination chemotherapy | suppress drug resistance, increase cancer kill, reduce injury to normal cells |
| delivery of chemotherapy | IV; intra-arterial; intrathecal; oral |
| what treatment would liquid cancer be given | more likely have chemo |
| what treatment would solid cancer be given | radiation |
| What to consider before giving antineoplastic drugs | age, functional status, nutritional status, blood count, kidney and liver function |
| What doses of antineoplastic drugs are usually most effective | high doses |
| antineoplastic drug doses are usually calculated according to.. | body surface area |
| Why would antineoplastic drugs be reduced? | for impairments that reduce the ability to eliminate medicaitons |
| 2 factors contributing to responsiveness to chemotherapy | cell cycle, growth fraction |
| another name for growth fraction | proliferating |
| What tissues are chemotherapeutic drugs more toxic to | tissues that have high growth fraction |
| What tissues in the body have high growth fractions | lining of intestine, hair, skin |
| Why is chemo not effective for solid tumors | low growth fraction |
| What cancers have high growth fractions and respond well to chemo | disseminated cancers |
| obstacles to successful chemotherapy | toxicity to normal cells; absence of truly early detection; solid tumors respond poorly; heterogeneity of tumor cells; drug resistance |
| why is toxicity to normal cells an obstacle to successful chemotherpy | cure requires 100% cell kill; not sure when to stop medicaitons = not sure when you get down to 1-cell tumor |
| Why is there an absence of truly early detection of cancer? | symptoms do not appear until tumors grow larger |
| Why are solid tumors poor responders to chemotherapy | low growth fraction; blood vessels carrying drugs can not reach tumor |
| 3 adjectives to describe cytotoxic antineoplastic medications | carcinogenic, mutagenic, teratogenic |
| Parenteral solutions of cytotoxic antineoplastics have what effect on the skin | irritating to skin/mucous membranes; |
| What should you avoid with cytotoxic antineoplasctics | direct contact with skin or respiratory tract |
| Will you administer cytotoxic antineoplastics as a student? | no; only monitor patients receiving antineoplastics |
| define vesicants | damage subcutaneous area by infiltration, causes "blisters" |
| 4 groups of cancer chemotherapy drugs | cell cycle specific and non-specific agents; biologic targeted therapies (cytotoxic); hormone inhibitors (noncytotoxic); medicaitons that reduce adverse effects of cytotoxic medications |
| What do cell cycle specific S phase antimetabolites minimic | purines, pyrimidines, and folates |
| What happens at the S phase of the cell cycle | where DNA synthesis occurs |
| cell cycle specific: S phase antimetabolite prototype | methotrexate (MTX) |
| What kind of antimetabolite is methotrexate (MTX) | folate antimetabolite |
| What does methotrexate do | works on RNA/DNA; need B12 to make RNA (folate) |
| What kind of antimetabolite is 5-fluouracil (5FU) | pyrimidine antagonist |
| What medication is the rescue for S phase antimetabolites | Leucovorin rescue (folic acid supply) |
| What does Leucovorin do? | rescues cells and goes back to normal (folic acid supply) |
| What do cell cycle specific: G2 phase medications do | inhibit cell division |
| What cancer drugs act where DNA synthesis occurs | cell cycle specific: S phase antimetabolites |
| What cancer drugs inhibit cell division | cell cycle specific: G2 phase |
| Cell cycle specific: G2 phase prototype | paclitaxel (Taxol) |
| paclitaxel (Taxol) | cell cycle specific: G2 phase |
| What cancer drugs work where spindles occur/cell division | cell cycle specific: M phase mitotic inhibitors |
| What do cell cycle specific: M phase drugs do? | interfere with mitotic spindles, causing metaphase arrest |
| Vincristine (Oncovin) | cell cycle specific: M phase mitotic inhibitor |
| vinblastine (Velban) | cell cycle specific: M phase mitotic inhibitor |
| Why are cell cycle specific: m phase mitotic inhibitors dose limiting | they are neurotoxic |
| symtpoms of neurotoxicity seen in cell cycle specific: m phase mitotic inhibitors | numbness, loss of reflexes, weakness |
| vinca alkaloids | cell cycle specific: m phase mitotic inhibitors from periwinkle flower |
| how do cell cycle nonspecific: alkylating agents work | attack cell in any cycle phase: transfer alkyl group to cell nucleotides - cannot replicate |
| adjective describing cell cycle nonspecific: alkylating agents | radiomimetic |
| define radiomimetic | mimic action of radiation on cells |
| what cancer drugs are radiomimetic | cell cycle nonspecific: alkylating agents |
| cell cycle nonspecific: alkylating agent prototype | cyclophosphamide (Cytoxin) |
| cyclophosphamide (Cytoxin) | cell cycle nonspecific: alkylating agent |
| What major role do cell cycle nonspecific: alkylating agents have in cancer treatment | hematologic: Hodgkin's myeloma, acute and chronic leukemia |
| drugs to treat Hodgkin's myeloma | cell cycle nonspecific: alkylating agents |
| drugs to treat acute and chronic leukemia | cell cycle nonspecific: alkylating agents |
| Why are cell cycle nonspecific: alkylating agents dose limiting | leukopenia |
| 2 adjectives descriging cell cycle nonspecific: nitrosoureas | alkalyting and cyctotoxic |
| distribution of cell cycle nonspecific: nitrosoureas | crosses blood-brain barrier |
| What cancers are cell cycle nonspecific: nitrosoureas used for | cancers of the CNS |
| cell cycle nonspecific: nitrosoureas prototype | carmustine (BCNU) |
| Kinetics of carmustine (BCNU) - cell cycle nonspecific: nitrosoureas | soft discs contain medications are placed in body and dissolve over time |
| physiologic effect of cell cycle nonspecific: nitrosoureas | delayed bone marrow suppression (6 weeks) |
| What cancers are cell cycle nonspecific: platinum compounds used for | testicular cancer |
| cell cycle nonspecific: platinum compounds prototype | cisplantin (Platinol-AZ) |
| cisplantin (Platinol-AZ) | cell cycle nonspecific: platinum compound |
| adjective of cell cycle nonspecific: platinum compounds | highly emetogenic; vomiting withing 1 hour |
| What medication is given before the administration of cell cycle nonspecific: platinum compounds | phenergan due to vomiting |
| What are cell cycle nonspecific: antitumor antibiotics derived from | various streptomyces |
| How do cell cycle nonspecific: antitumor antibiotics fight cancer | interfere with DNA directed RNA; prevent normal duplication and separation |
| "Red devil" | doxorubicin hcl (Adriamycin) |
| cell cycle nonspecific: antitumor antibiotic prototype | doxorubicin hcl (Adriamycin) |
| doxorubicin hcl (Adriamycin) | cell cycle nonspecific: antitumor antibiotic |
| 2 side effects from cell cycle nonspecific: antitumor antibiotics | cardiotoxicity; vesicants |
| How do cell nonspecific: hormones and hormone antagonists fight cancer | block or antagonize the naturally occurring substances that stimulate tumor growth |
| cell nonspecific: hormones and hormone antagonist prototype | Tomoxifen (Nolvadex) |
| Tomoxifen (Nolvadex) | cell nonspecific: hormones and hormone antagonist selective estrogen receptor |
| What medication is used with breast cancer | tomoxifen (Nolvadex) |
| gonadotropin-releasing hormone analogue | leuprolide (Lupron) |
| what medication is used with prostate cancer | leuprolide (Lupron) |
| What is a result of bone marrow suppression from cancer drug toxicities | decreased RBCs, neutropenia thrombocytopenia |
| illness occurring with decreased RBCs | anemia, fatigue |
| illness occurring with neutropenia | infection |
| illness occurring with thrombocytopenia | bleeding |
| Treatment of anemia from bone marrow suppression with cancer drugs | transfusion or epoetin |
| role of epogen in cancer treatment | recombinant human erythropoien that stimulates RBC production |
| Kinetics of epogen | subcutaneous 2-3 times per week |
| What must you use along with epogen to treat anemia from bone marrow suppression with cancer drugs | supplemental iron |
| Most serious complication of bone marrow suppression with cancer drugs | neutropenia |
| Onset of neutropenia after administration of cancer drugs | 10-14 days |
| How long does it take a patient to recover from neutropenia after administration of cancer drugs | 3-4 weeks |
| define nadir | when WBC are lowest in body = don't have defense against infection |
| When is nadir reached | 10-14 days after administration |
| Nursing implications during nadir period | monitor for fever, culture and sensitivity |
| teaching for nadir period | avoid direct contact with people; avoid salads |
| what is given during the nadir period | granulocyte colong-stimulating factor (GCSF-filgrastim) |
| reason for giving Neupogen | increase neutrophils during nadir |
| when is the most critical point during chemo administration | 2 weeks after given chemo |
| When can a second round of chemo be administered | not until WBC are at a safe level |
| oral side effects of chemo | teeth diminish; ulcers are in mouth |
| Thrombocytopenia is a disorder of what cell | platelets |
| Teaching with thrombocytopenia | soft tooth brush; avoid aspirin/anticoagulants; acetaminophen; caution with BP cuff |
| What is administered to patients with thrombocytopenia from cancer drugs | Neumega (platelet oprelevkin interleukin-11) |
| role of Neumega (platelet oprelevkin interleukin-11) | stimulate platelet production; response 5-7 days |
| digestive tract injuries from cancer medication | stomatitis; diarrhea; nausea; vomiting; premedicate with antiemetic |
| When is maximal hair loss seen with cancer medication administration | 1-2 months |
| when does alopecia begin with cancer medication administration | 7-10 days after receiving chemo |
| Do all chemotherapies cause alopecia | no |
| why do cancer patients do sperm banking/egg preservation | reproductive toxicity |
| Why would cancer patients need Allopurinol | hyperuricemia - uric acid in blood - breakdown of DNA - injury to kidneys - crystal formation |
| Why must chemo patients push fluids | flush uric acid out |
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