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Session 3 Pharm- 3

Pharm -3- Chemo Drugs

What is a solid tumor arising from epithelial cells Carcinoma
cancer originating from mesenchymal or connective tissue sarcoma
cancers that arise from cells of the hematopoietic system Leukemias, Lymphomas
This is a disease characterized by uncontrolled multiplication and spread of abnormal forms of the body's own cells cancer (aka malignant neoplasm, malignant tumor)
what are the two categories of genetic changes that are important to remember with regard to development of cancers activation of proto-oncogenes to oncogenes (proto oncogenes normally control cell division, apoptosis, and differentiation) or inactivation of tumor suppressor genes (normally suppress excessive cellular growth)
How are malignant tumors different from benign tumors since both show uncontrolled growth malignant tumor have a capacity for dedifferentiation and loss of function, ability to accumulate mutations, express invasiveness (express metalloprotease that break down extracellular matrix) ability to metastasize (spread from original location
What do malignant tumors secrete that allow them to break down extracellular matrix and invade surrounding tissue metalloprotease
Why is it important that malignant tumors are unresponsive to apoptotic signals this allows them to establish themselves in distant locations
What is meant by log kill (kill ratio) cytotoxic drugs only kill a constant fraction of malignant cells. If it kills 99.99% of cells and you have 10^11 cells you still have .01% of cells left or 10^7 equaling a 4 log kill. You still have a lot of cells to kill. Tx is aimed at a total kill
what are the different compartments of cells that tumor cells are classified as Compartment A- dividing cells continuously in the cell cycle; Compartment B- resting cells in G0 phase not dividing but could begin to; Compartment C- cells not able to divide but contribute to mass of tumor
What compartment classification of tumor cells doesn't present a treatment problem compartment C- they only contribute to mass of tumor and can't start to divide again
What compartment classification of tumor cells is actually susceptible to cytotoxic drugs Compartment A- made of continuously dividing cells that can get target by cytotoxic drugs
What compartment of classification of tumor cells presents a problem for tx Compartment B- cells are in G0 and not actively dividing they are not very susceptible to cytotoxic drugs and could enter compartment A and start actively dividing after tx
What is the S phase specific cytotoxic drug group Antimetabolites
What cytotoxic drug group is cell-cycle independent and can target drugs in G0 phase Alkylating Agents, antitumor antibiotics, nitrosoureas, dacarbazine, cisplatins
What cytotoxic drug group targets cells in M phase taxanes, Vinca alkaloids
What cytotoxic drug group targets cells in S-G2 phase Etoposide
What is the MOA of chemotherapeutic agents primarily prevents cell division- damages DNA inducing cells to undergo apoptosis. Chemotherapy harms cancerous cells and normal cells mostly a balance between which cells are most affected.
What are the two groups of chemotherapeutic agents cell-cycle specific (for hematologic malignancies and solid tumors w/ large growth fraction) and cell-cycle non specific (for solid tumors with low or high growth fraction)
What type of chemo agent will you use for hematologic malignancies cell-cycle specific
what broad type of chemo agent will you use for solid tumors with low or high growth fraction cell-cycle non specific
What are the cell cycle specific chemo agents antimetabolites, Taxanes, Vinca Alkaloids, Antitumor antibiotic Bleomycin, and the epipodophylllotoxins
What are the cell cycle nonspecific agents alkylating agents, Anthracyclines, Antitumor antibiotics (dactinomycin and mitomycin), camptothecin, and platinum analogs
What are the acute toxicity s/e of chemo agents N/V (affects cells of the GI tract), and bone marrow suppression resulting in alopecia, neutropenia, thrombocytopenia. These side effects are often reversible
What are the chronic s/e of chemo agents leukemia, cardiotoxicity (esp. anthracyclines), sterility, neuropathy, nephropathy. These side effects unlike acute are often not reversible
What are the alkylating agents Bis(chloroethyl)amines=Cyclophosphamide, mechlorethamine, Chlorambucil, Melphalan; Nitrosoureas= BCNU (carmustine), CCNU (lomustine), methyl-CCNU (semustine); Alkyl Sulfonate=Busulfan; Aziridines= triethylenemelamine, thiotepa,
what is the MOA of the alkylating agents transfer alkyl group to the DNA at N7 position of guanine resulting in cross linking within a DNA strand or between DNA strands. Causing miscoding, depurination and strand breakage when seen by checkpoint proteins apoptosis is initiated.
Are alkylating agents effective against non dividing cells yes but they are most effective against actively cycling cells
What is unique about the MOA of the nitrosoureas as alkylating agents they alkylate the 06 position of guanine and they have to undergo nonenzymatic conversion to active compound. Most importantly they are lipid soluble and can cross the blood brain barrier
If you patient has brain cancer what alkylating agent would you use to help combat their cancer Nitrosoureas BCNU and CCNU because they are lipid soluble and can cross the BBB
what may cause resistance to Alkylating agents and prevent their helping treat cancer in a pt pt has increased ability to repair DNA, Decreased permeability to agent to area where cancer is located, increased production of glutathione
what are the acute and delayed adverse effects of alkylating agents acute- neurotoxicity causing N/V; Delayed- leukopenia, thrombocytopenia, alopecia, sterility, carcinogenic, Busulfan can cause pulmonary fibrosis and hepatic toxicity
what is a major concern of using the alkylating agent Busulfan for treating cancers it has an adverse effect of causing pulmonary fibrosis and hepatic toxicity
what alkylating agent can be taken orally to combat NHL, ovarian and breast cancers and neuro blastoma Bis(chlorethyl)amines- such as cyclophosphamide, mechlorethamine, chlorambucil, melphalan
What is a concern with using cyclophosphamide to treat cancer it must be activated in liver it has a cytotoxic metabolite Acrolein that can cause hemorrhagic cystitis and mesna reacts with it to create an inactive compound. It also causes hepatic toxicity
What is the only alkylating agent that Bis(chorethyl)amines don't have a cross-resistance with nitrosoureas
what chemo agent form complexes with DNA causing intra and inter strand cross links resulting in cytotoxic effects but has nephrotoxicity, ototoxicity. Used for testicular, ovarian, bladder and lung cancers Cisplatin and other platinum analogs
What is the second generation platinum analog that has replaced cisplatin and why carboplatin- has less nephrotoxicity and GI toxicity. Myelosuppression is main dose limiting toxicity don't combine with drugs that have same dose limiting toxicity
What is the third generation platinum analog oxaliplatin
What is the MOA of the antimetabolites antimetabolites affect nucleotide and nucleic acid synthesis creating bottlenecks in the major enzyme pathways to creating these building blocks of DNA as a group antimetabolites don't cause acute toxicities
What is the MOA of methotrexate as a folic acid antagonist if binds the active site of DHFR and prevents the production of reduced folate. This interferes with the formation of DNA and RNA and key cellular proteins. Stops formation of thymidine by dUMP
Does methotrexate cross the BBB no but can be administered intrathecally to act on cells in sanctuary sites in the brain
What properties may cause a drug resistance to methotrexate decreased drug transport into the cell, increased synthesis of DHFR, DHFR with decreased affinity for MTX, decreased cellular retention of MTX
What are the adverse effects of methotrexate mucositis-diarrhea, Bone Marrow depression (leukopenia, thrombocytopenia). These effects can be prevented by rescue with leucovorin. Also has nephrotoxicity (keep patient well hydrated and generally not a problem)
What is the therapeutic use of methotrexate leukemias, lymphomas and breast cancer
what antimetabolite is used to tx acute lymphocytic leukemia 6-thiopurines- 6-mercaptopurine and 6-thioguanine
What is the moa of the 6-thiopurines they get converted to by HGPRT to active form and then inhibit enzymes required for purine synthesis blocking formation of DNA and RNA and leads to DNA and RNA using thiopurine
What are the toxicity problems with the 6-thiopurines cause myelosuppression, immunosuppression and hepatotoxicity
What causes a drug resistance to 6-thiopurines Resistance is common through decreased expression of HGPRT the enzyme needed to convert the 6-thiopurines into their active metabolite
What is the MOA of the antimetabolite 5-fluorouracil prodrug that undergoes a series of biotransformations to become fdUMP, this can prevent synthesis of thymidine. It can also be converted to FUTP which can get incorporated into RNA or can be incorporated into DNA as fdUTP
How do you have to give 5-fluorouracil IV because it will be broken down in the gut
what are the adverse effects of 5-fluorouracil Nausea, Diarrhea, mucositis, bone marrow depression, alopecia, hand foot syndromes
What is the therapeutic uses for 5-fluorouracil breast, ovarian head and neck cancers
why is leucovorin given with 5-fluorouracil (the fol-fox regimen) It helps potentiate the actions of 5-FU b stabilizing the ternary complex it forms with thymidylate preventing synthesis of thymidine
What is the MOA of gemcitabine an antimetabolite it get phosphorylated to become active then inhibits ribonucleotide reductase decreasing pool of nucleotides for DNA synthesis. DNA chain termination follows after it gets incorporated into the DNA.
What is the toxicity of Gemcitabine myelosuppression is the principle does limiting toxicity, also causes N/V and diarrhea
What cytotoxic agents shouldn't be combined because they both cause myelosuppression and that is their dose limiting toxicity Gemcitabine, Carboplatin, anthracyclines
What is the therapeutic use for Gemcitabine non small cell lung cancer, bladder cancer, non Hodgkins lymphoma
What is the MOA of the Vinca alkaloids vinblastine, vincristine, and vinorelbine inhibit tubulin polymerization by binding b-tubulin and prevents its interaction with a-tubulin preventing assembly of microtubules. Cell division gets stuck at metaphase because cell chromosomes can't separate leads to cell apoptosis
What can cause a drug resistance to Vinca alkaloids increased drug efflux, cross resistance with any drug that is substrate for transporters MDR, p-glycoprotein
What is the adverse effect of the Vinca alkaloids alopecia, local cellulitis, hyperuricemia (give allopurinol), hepatic elimination
What is the s/e of vinblastine a Vinca alkaloid painful ulceration if extravasation occurs, myelosuppression, least likely of them to cause neurotoxicity but causes GI problems
What are the s/e of vincristine Vinca alkaloid limited myelosuppression great to combine with those that are myelosuppressive. Neurotoxic effects (numbness tingling motor weakness, constipation) less GI effects, may cause SIADH
What are the s/e of vinorelbine a Vinca alkaloid myelosuppressive, granulocytopenia, low neurotoxicity may cause SIADH
What are the therapeutic uses of vinblastine Hodgkin, NHL, breast cancer, testicular
What are the therapeutic uses for vincristine ALL, Hodgkin, Leukemias, Wilms (cancer of the kidney)
What are the therapeutic uses for vinorelbine non-small cell lung cancer, breast cancer
What is the MOA of Taxanes (paclitaxel, docetaxel) binds to Beta-Actin to promote formation of microtubules causing atypical microtubule structures during M phase arrests mitosis leading to apoptosis
What can cause resistance to Taxanes P-glycoprotein, B-tubulin mutations
What are the adverse effects of taxanes myelosuppressive, cumulative neurotoxicity, mucositis, alopecia, hypersensitivity reaction (pretreat with corticosteroids and antihistamines) docetaxel causes fluid retention and edema
What are the therapeutic uses for paclitaxel broad range of solid tumors ovarian, breast, lung, head, neck
What are the therapeutic uses for docetaxel non-small cell lung cancer, head, neck, ovarian and bladder cancers
What is the MOA of the epipodophyllotoxins inhibit DNA topoisomerase II by forming ternary complex with topoisomerase, the DNA and the drug leading to strand breakage blocks cell division in late s-G2 phase
What are the adverse effects of epipodophyllotoxins dose reduction in renal dysfunction
What are the therapeutic uses for etoposide lung caner, Hodgkin, NHL
What are the therapeutic uses for teniposide ALL
What is the MOA of the anthracyclines (Doxorubicin, daunorubicin, idarubicin, epirubicin, Mitoxantrone) minor: inserts between base pair of DNA and RNA disrupting function; Major action is to inhibit topoisomerase II causing breaking of DNA strand
What are the adverse effects of using anthracyclines myelosuppression acute dose limiting toxicity, conversion to free radical can cause tissue damage causing cardiotoxicity, dose related N/V, damage due to extravasation,
What is the therapeutic use for the anthracycline doxorubicin Acute leukemias, lymphomas, solid tumors
What is the use for the anthracycline daunorubicin acute myeloid leukemia
what is the MOA of bleomycin one end binds DNA and the opposite end chelates Fe2+ oxidation of complex causes DNA fragmentation and stops cell cycle at G2
What are the adverse effects of bleomycin pulmonary fibrosis is the dose limiting toxicity, mucocutaneous reaction often involving palms of feet and hands. Low myelosuppression and alopecia
What are the therapeutic uses for bleomycin Hodgkin, testicular, head, neck, skin cancers
what is the MOA for dactinomycin (actinomycin D) intercalation, inhibition of topoisomerase II
What are the adverse effects of Dactinomycin (actinomycin D) N/V bone marrow depression
What are the therapeutic uses for dactinomycin pediatric tumors
what is the MOA for the hormonal agent Prednisone acts through glucocorticoid receptor to cause lymphocytopenia and decreases lymphoid mass it is metabolized in the liver to active form
What are the therapeutic uses for prednisone induces remission in ALL, treatment of Hodgkin's and NHL
What is the MOA for Tamoxifen competitive partial agonist inhibitor of estrogen. Lower affinity than estradiol at estrogen receptor must ablate endogenous estrogen
What are the s/e of tamoxifen menopausal symptoms
What are the therapeutic uses of tamoxifen breast cancer
what is the MOA of flutamide and bicalutamide antagonist at the androgen receptor
what are the s/e of flutamide and bicalutamide hot flashes and mild nausea
what is the therapeutic use for flutamide and bicalutamide prostate cancer
what is the MOA of gonadotropin releasing hormone agonists inhibits the release of testosterone to near castration levels
What are the adverse effects of gonadotropin releasing hormone agonists hot flashes, impotence, gynecomastia
What is the therapeutic use for gonadotropin releasing hormone agonists prostate cancer
what is the MOA of aromatase inhibitors (anastrozole, letrozole, exemestane) inhibit conversion of estrogen from androgen by aromatase
what are the adverse effects of aromatase inhibitors mild nausea, headache, fatigue, hot flushes, arthralgias
what are the therapeutic uses for aromatase inhibitors breast cancer
What is the MOA of monoclonal antibodies cytotoxicity based on antibody dependent lysis, complement dependent lysis, localize delivery of radiation, localize delivery of chemotherapy, inhibit angiogenesis
What is the class toxicity of using monoclonal antibodies cytokine release reaction that may be sever with fever chills and hypotension
What is he MOA of tyrosine kinase inhibitor imatinib inhibits platelet derived growth factor and intracellular kinase pathways
what adverse effects does tyrosine kinase inhibitor imatinib have N/D, GI pain, fatigue and headache
What is the therapeutic use for imatinib a tyrosine kinase inhibitor chronic myeloid leukemia
why is combining chemo agents helpful and what must you avoid by combining agents you can decrease likelihood of developing resistance and drugs can be used at full doses just don't combine drugs with same limiting toxicity
what are the bone marrow sparring agents cisplatin, bleomycin, vincristine
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