N203 CANCER AGENTS AND BIOLOGIC RESPONSE MODIFIERS
Upon completion of this class, the student will be able to:
1. Differentiate between cell-cycle specific and cell-cycle nonspecific drugs;
2. Identify general side effects and adverse reactions to chemotherapy agents;
3. State three ways the nurse can prevent absorption of chemotherapeutic agents;
4. Discuss the actions of the biologic response modifiers;
5. List adverse effects of interferons, colony-stimulating factors, and interleukin-2;
6. Describe the nursing process with safe administration of these agents.
I. Cancer
A. Influences on Cancer Development
1. environmental [chemicals, asbestos, radiation]
2. infective [viruses that cause tumors like Epstein Barr and Stomach ulcers, HPV, Herpes, Hep B and C]
3. diet [high fat]
4. genetic [BRCA 1 or BRCA 2 mutation]
“BRCA1 (breast cancer 1, early onset) is a human gene that belongs to a class of genes known as tumor suppressors, which maintains genomic integrity to prevent uncontrolled proliferation. The multifactorial BRCA1 protein product is involved in DNA damage repair, ubiquitination, transcriptional regulation as well as other functions. Variations in the gene have been implicated in a number of hereditary cancers, namely breast, ovarian and prostate. The BRCA1 gene is located on the long (q) arm of chromosome 17 at band 21….BRCA2 (Breast Cancer Type 2 susceptibility protein) is a human gene that is involved in the repair of chromosomal damage and belongs to a class of genes known as tumor suppressor genes. Tumor suppressor genes regulate the cycle of cell division by keeping cells from growing and dividing too rapidly or in an uncontrolled way. Although the structures of the BRCA1 and BRCA2 genes are very different, their functions appear to be similar. The proteins made by both genes are essential for repairing damaged DNA. The BRCA2 protein binds to and regulates the protein produced by the RAD51 gene to fix breaks in DNA. [wikipedia]”
B. Cancer causes: damage to DNA within cell; many mutations required
II. Cancer Drugs; ‘Chemotherapeutics’ aka ‘antineoplastics’
A. Cell-cycle Non Specific: don’t effect the cells during division: they are effective during the “G0” phase or resting phase between divisions…or they act at any time during the cell cycle.
B. Cell-cycle nonspecific: attack cancers when they are dividing, and during a specific phase of division.
C. Chemotherapy: most effective when able to kill cancer cells in all phases of cell cycle. Kills cancerous and normal cells.
1. systemic administration
2. used in conjunction with surgery and radiation
3. guided by protocols from research
4. length of treatment based on type and extent of malignancy, type of chemotherapy, expected side effects, and amount of time normal cells need to recover
5. combination therapy: combine drug types so that the cancer is attacked during all points of the cell cycle; so cycle specific and non-specific drugs are combined. This makes it likely that the effects are synergistic. This also avoids drug resistance by the tumors.
D. Adverse and side effects: hardest on quickly multiplying cells, esp. GI tract, vagina, and mucus membranes.
1. bone marrow suppression: resulting in low RBC, platelet, and WBC counts (anemia and neutropenia) Anemia: high BP, mental confusion/fatigue, high HR, high RR, and little peeing. Neutropenia: susceptible to infections. Thrombocytopenia: bruising, bleeding gums, etc.
2. GI disturbances: Anorexia, N/V, Diarrhea, Mucositis/Stomatitis. N/V caused by chemotherapies that trigger the CTZ, irritation to Gi, and radiation. Diarrhea caused by various effects and injury to the GI tract or infections. Mucositis is direct damage to the rapidly dividing tissues of the GI tract.
3. Alopecia: hair loss or thinning
4. Fatigue: due to stress, chemo, pain, infection, etc
5. Infertility: sometimes from severe radiation of the body—leaving sex cells useless.
E. Alkylating agent prototype: Cyclophosphamide (Cytoxan): Nitrogen Mustard
1. therapeutic uses: breast, lung, ovarian cancers; Hodgkin’s disease; leukemias; lymphomas
2. action: inhibits protein synthesis through interference with DNA replication
3. adverse effects: bone marrow depression [leukopenia, anemia, thrombocytopenia] cardiotoxicity, sterility, hepatotoxicity. Causes tissue necrosis if it infiltrates. Immunosuppresant.
F. Other types:
1. antimetabolites: disrupt metabolic processes and therefore enzyme synthesis. Treat head and neck, leukemia, breast, lung cancers, and non-hodgkin’s lymphoma. Need to give lots of “leukovorin calcium” to counteract effects on healthy cells.
2. antitumor antibiotics: certain antibiotics interfere with RNA and DNA production. Most of these are CCNS.
3. mitotic inhibitors: plant alkyloids that block division at the M cycle, so they are CCS. Made from periwinkle and yew. Periwinkle derivatives can be neurotoxic [they interfere w/ microtubules.] These can all cause common chemo adverse effects.
4. hormonal agents: corticosteroids [slow tumors and inflammation], androgens [testosterone to shink advanced breast cancers] and estrogen [slow the growth of hormone dependent tumors like prostatic and certain breast cancers,] antiestrogens [treats certain breast cancers,] antiandrogens [prostate cancer], etc.
5. liposomal chemotherapy: packages chemotherapeutic agents into synthetic fat globs called liposomes. The coating keeps the drug in the body longer and decreases side effects.
G. Nursing Process
Biologic Response Modifiers (BRMs)
A. Purpose: enhance body’s immune system. Immune proteins and chemicals produced w/ recombinant DNA tech and hybridoma tech [in which mice produce monoclonal antibodies.]
B. Interferons:
What I learned in micro: these are interesting because these are important in limiting virus replication, esp flu, hepatitis, herpes, colds, etc. We thought we could use them for all sorts of stuff, but they are deadly to the patient if over dosed/overused.
Interferons:
1. Use:
2: Action: has antiviral, antiproliferative, and immunomodulatory effects. Inhibits intracellular replication of viral DNA, tumor growth, and enhances natural killer cell activity.
2. Adverse effects: tachycardia, pallor, confusion, thrombocytopenia
C. Colony-stimulating Factors: These are ‘hematopoetic agents’ that manage/promote growth and differentiation of bone marrow stem cells—that create our RBCs, WBCs, etc. Therefore they do not attack tumors, but they do counteract those nasty chemo side effects, like prevent bone marrow suppression. That means greater doses of chemo can be given, aid in healing of suppressed marrow after chemo and transplant, promote immune cells to prevent infections.
1. Uses:
· decrease length of post-cancer treatment neutropenia
· permit delivery of higher doses of chemotherapy
· prevent severe thrombocytopenia with chemotherapy
2. Prototype: Filgrastim (Neupogen)
Action: increases neutrophils
Use: to prevent post-treatment infections
Life threatening Adverse effects: thrombocytopenia, MI
Adverse: Neutropenia, dyspnea, hematuria.
D. Epoeitin Alfa (Erythropoietin) (Procrit)
1. Action: stimulates RBC production in bone marrow
Life threatening adverse effects: CVA, MI
Adverse: Seizures, hyperkalemia, HTN
E. Nursing Process
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