Kaur S. Pharmacy Team - Including Faculty, Residents and Interns Integration - in an Outpatient Family Medicine Practice Model. Accepted for presentation at International Conference on Pharmacy and Pharmaceutical Sciences, Dubai UAE, April 2018.   

Abstract: This was a pilot program to incorporate clinical pharmacy services into Sutter Family Practice Residency Program that aims to provide sound pharmaceutical patient-centered care.  Sutter Family Practice is a primary care medical home (PCMH) model of care that provides comprehensive, coordinated, patient-focused care that is accessible and is actively engaged in quality and safety improvement activities according.  Incorporation of clinical pharmacy services aims to complement patient-focused care through consultation of pharmacotherapeutic medication selection and monitoring as well as aim to decrease the burden of medication-related adverse events that may contribute to the clinic’s quality and safety metrics.  This program is also intended to simultaneously enhance the education of family medicine residents and family medicine physicians. Description of the Activity: The practice includes integration of clinical pharmacist, pharmacy resident and Advanced Pharmacy Practice Experience (APPE) Intern to a Family Medicine Residency clinic responsibilities to provide evidence-based, patient centered medication therapy management in the ambulatory care setting for the provision of the quality of pharmaceutical care provided to patients.  Development of ambulatory care site included building a rapport with the family practice physicians and family practice residents of having integrated pharmacy team that can lead to improving quality of overall patient care. 

These were carried out by having a solid development of daily pharmacy practice operations which included the following pro-active activities conducted by the pharmacy team: 1) Pre clinic huddle with family medicine residents to review patients scheduled and screen all patients for potential pharmacotherapy needs. 2) Perform medication reconciliation particularly with patients of residents identified to be on 8 or more medications or patients with specific diagnosis such as diabetes mellitus, heart failure, diabetes mellitus, obstetric needs, hypertension, dyslipidemia, thyroid disorder, anxiety, depression, pain management, asthma, chronic obstructive pulmonary disease, etc. 3) Identify and assist in medication goals/therapeutic plan development, suggesting interchange, dose modification, and discontinuation where appropriate, drug-drug interactions. 4) Provide patient education with high risk, pain management, and diabetic patients. 5) Provide drug information service as a resource for care center/residency program: formats include mini-lecture, case studies as topic discussed with by family medicine residents. 6) Resource for registered nurse performing post discharge transition of care telephone calls as pertains to medication list.

Program Assessment/Improvement:

We currently do not employ a standardized systematic quality metric system to document pharmacy interventions however it is our goal to implement one starting January 2017.  We are currently utilizing a pharmacy intervention logbook that shows estimates the following interventions:


Fitzpatrick LR, Talbott G et al. al. Ex vivo effects of ROR-gamma T inhibitors on pro-inflammatory cytokine secretion from colonic strips of mice with DSS-induced colitis.  Accepted for presentation at Digestive Disease Week Annual Meeting, Washington DC, June 2018.

Abstract:  ROR gamma t (RORγt) inhibitors (e.g., GSK 805, VPR 254) have shown efficacy in murine models of colitis. To determine an optimal compound(s) for further in vivo testing, we utilized an ex vivo colonic strip model from mice with DSS-induced colitis. This colitis has been proposed by some investigators to involve IL-17, IL-21 and CCL20, which are under transcriptional control by RORγt. Therefore, we hypothesized that secretion of these cytokines by colonic strips would be attenuated by RORγt inhibitors. Methods: Five RORγt inhibitors were obtained from Visionary Pharmaceuticals (San Diego, CA). Dextran Sulfate Sodium (DSS) was given to male C57BL/6 mice (n = 16) in the drinking water (2% concentration), for a six-day period, to induce colitis. Control mice (n = 8) received water. The ex vivo effects of the RORγt inhibitors (0.05 to 5 μM concentration range) were tested in our 24 hour colonic culture system [Fitzpatrick et al., Inflammopharmacology, 2014]. We utilized ≈ 4 mm colonic strips (n = 4 to 10 per RORγt inhibitor group) from mice with DSS-induced colitis. Some colonic strips were stimulated with IL-1β (10 ng/ml) plus IL-23 (10 ng/ml) to induce enhanced cytokine secretion. The secretion of IL-17, IL-21 and CCL20 were determined in the cell culture media by ELISA. Results: Mice that were administered DSS showed clear evidence of colitis (enhanced disease activity indices and reduced colon lengths). Ex vivo treatment with VPR 254, VPR 425 and GSK 805 were most effective for inhibiting basal IL-17 secretion from colonic strips of mice with colitis. VPR 425 and GSK 805 most effectively attenuated basal (non-stimulated) secretion of IL-21 and CCL20. For dual cytokine stimulated IL-17 secretion, some IL-17 values (pg/ml) were: 112±35 (Vehicle), 87 ± 21 (VPR 254, 5μM), 64 ± 9 (VPR 425, 5 μM) and 45 ± 9 (GSK 805, 5 μM). The calculated IC50 value of VPR 425 for inhibiting stimulated IL-17 secretion was 0.13 μM, while for GSK 805 it is < 0.05 μM. Three compounds (VPR 254, VPR 425 and GSK 805) significantly attenuated (at certain concentrations) dual cytokine stimulated IL-21 secretion from colonic strips of mice with DSS-induced colitis. Overall, the most effective compounds were VPR 425 and GSK 805. Four compounds (VPR 426, VPR 254, VPR 425 and GSK 805) attenuated (to some degree) stimulated CCL20 chemokine secretion from colonic strips of mice with DSS-induced colitis. Chemokine secretion was reduced to the basal level by ex vivo treatment with VPR 425 (0.5 and 5 μM concentrations). Summary: Ex vivo treatment with structurally diverse RORγt inhibitors inhibited basal and stimulated pro-inflammatory cytokine secretion from colonic strips of mice with DSS-induced colitis. Conclusion: These data further contribute to the identification of optimal RORγt inhibitors, which can be used for follow-up in vivo testing in murine models of colitis.      


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