PubMed HealthSearch

PubMed · 9201743

A comprehensive interdisciplinary chemotherapy teaching documentation flowsheet.

Abstract

PURPOSE/OBJECTIVES: To describe the development and implementation of one approach to standardize and document interdisciplinary chemotherapy education for patients and families. DATA SOURCES: Cancer center interdisciplinary team. Oncology Nursing Society standards of care, clinical experience, and published literature. DATA SYNTHESIS: Because chart reviews of patient records demonstrated inconsistent chemotherapy education, a comprehensive chemotherapy curriculum pain was designed as a template for patient education. A flowsheet was developed to document use of the patient curriculum as well as other chemotherapy-related education materials. Patient chemotherapy curriculum included information regarding cancer and its treatment, adverse effects, and self-care measures and material about psychosocial and spiritual care. CONCLUSIONS: A standardized approach dramatically improved chemotherapy-related patient education as well as interdisciplinary documentation of patient education. The curriculum and the flowsheet are interdisciplinary and consistent with the patient and family education standards required by the Joint Commission on Accreditation of Health Care Organizations. IMPLICATIONS FOR NURSING PRACTICE: The combination of a patient chemotherapy curriculum and a documentation flowsheet saves time and standardizes content. Patient information is comprehensive and consistent, yet open to individual interpretation. Use of the flowsheet also has increased interdisciplinary collaboration, and the standardized curriculum has decreased redundancy between providers because all members of the interdisciplinary team know what is required and what information has been taught by whom.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Steele, A K Carruth. 1997. A comprehensive interdisciplinary chemotherapy teaching documentation flowsheet.. https://pubmed.ncbi.nlm.nih.gov/9201743/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Deep generative neural network for accurate drug response imputation.

Drug response differs substantially in cancer patients due to inter- and intra-tumor heterogeneity. Particularly, transcriptome context, especially tumor microenvironment, has been shown playing a significant role in shaping the actual treatment outcome. In this study, we develop a deep variational autoencoder (VAE) model to compress thousands of genes into latent vectors in a low-dimensional space. We then demonstrate that these encoded vectors could accurately impute drug response, outperform standard signature-gene based approaches, and appropriately control the overfitting problem. We apply rigorous quality assessment and validation, including assessing the impact of cell line lineage, cross-validation, cross-panel evaluation, and application in independent clinical data sets, to warrant the accuracy of the imputed drug response in both cell lines and cancer samples. Specifically, the expression-regulated component (EReX) of the observed drug response achieves high correlation across panels. Using the well-trained models, we impute drug response of The Cancer Genome Atlas data and investigate the features and signatures associated with the imputed drug response, including cell line origins, somatic mutations and tumor mutation burdens, tumor microenvironment, and confounding factors. In summary, our deep learning method and the results are useful for the study of signatures and markers of drug response.

Antineoplastic Agents

Determination of doxorubicin and doxorubicinol in plasma of cancer patients by high-performance liquid chromatography.

A high-performance liquid chromatographic assay with fluorescence detection has been developed for the determination of doxorubicin and its metabolite doxorubicinol in plasma of cancer patients. Quantitative extraction was achieved by a single protein-precipitation step of 1-ml samples with 500 microl of acetone in the presence of 100 microl of zinc sulfate [70% (w/v) in water]. Doxorubicin and doxorubicinol were separated isocratically on a column packed with Inertsil ODS-80A material and a mobile phase composed of water:acetonitrile:tetrahydrofuran (76:24:0.5, v/v/v). The related compound daunorubicin was used as internal standard. The column effluent was monitored fluorimetrically at an excitation wavelength of 480 nm and an emission wavelength of 560 nm, with a band width of 40 nm. The calibration graphs of doxorubicin and doxorubicinol were linear over a range of 1.0 to 100 and 0.50 to 50. 0 ng/mL, respectively, with lower limits of quantitation of 1.0 and 0.50 ng/ml. Results obtained from a 4-day validation study demonstrated excellent accuracy (91.0-106%) and precision (0.90-10. 2%) across the calibration ranges for both compounds. The developed method has been applied extensively to a clinical study to examine the pharmacokinetics and metabolism of doxorubicin in patients cotreated with a potent inhibitor of MDR1 P-glycoprotein activity, GF120918.

Antineoplastic Agents

Induction of Bax protein and degradation of lamin A during p53-dependent apoptosis induced by chemotherapeutic agents in human cancer cell lines.

In this study, subcellular fractionation analysis was performed to investigate the intracellular localization of Bax protein. We demonstrated that Bax protein is localized primarily in the nuclear and heavy membrane fractions. The expression of Bax protein in the nuclear membrane was induced in wild-type p53 human cancer cells (COLO 205 and Hep G2) by a wide variety of cancer chemotherapeutic agents in order to scrutinize further the biologic function of the Bax protein in the nuclear membrane. We found that lamin A and poly-(ADP ribose) polymerase (PARP) protein degradation coincided when the Bax protein level was elevated in the nuclear membrane of cells affected by drug stimuli. By using anti-sense oligodeoxynucleotides specific to human Bax mRNA, we further demonstrated that inhibition of Bax expression could specifically block lamin A but not PARP cleavage in apoptotic cancer cells.

Antineoplastic Agents