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1.
South Med J ; 114(5): 283-287, 2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33942112

RESUMO

OBJECTIVES: Goals of care discussions are a vital component of patient care, but Internal Medicine residents receive limited training in these skills. Existing curricula often require simulated patients or faculty development, limiting implementation in many residency programs. Thus, we developed and implemented a curriculum leveraging existing educational resources with the goal of improving resident attitudes and confidence in conducting goals of care discussions in training settings. METHODS: We developed cases and a detailed faculty guide for small-group discussion with three exercises to standardize the learner experience and minimize the need for faculty development. Exercises introduced established communication skill frameworks including SPIKES (setting, perception, invitation, knowledge, empathy, summary) and REMAP (reframe, emotion, map, align, propose a plan) for how to break bad news, respond to strong emotions, and conduct a goals of care discussion. Participants were 163 Internal Medicine postgraduate year 1, -2, and -3 residents at a large urban academic institution, where residency-wide curriculum is delivered in weekly half-day didactic sessions during the course of 5 weeks. Primary outcomes were resident self-reported confidence with goals of care communication skills. RESULTS: A total of 109 (response rate 67%) of residents reported improvement in overall confidence in goals of care discussion skills (3.6 ± 0.9 vs 4.1 ± 0.6, P < 0.001), responding to emotions (3.5 ± 0.9 vs 3.9 ± 0.6, P = 0.004), making care recommendations (3.5 ± 1.0 vs 3.9 ± 0.7, P < 0.001), and quickly conducting a code status discussion (3.6 ± 1.0 vs 4.0 ± 0.7, P < 0.001). Residents also expressed an increased desire for supervision and feedback to further develop these skills. CONCLUSIONS: This goals of care communication curriculum improves resident confidence and requires minimal resources. It may be ideal for programs that have limited access to simulated patients and/or faculty trained in communication skill simulation, but desire enhanced education on this important aspect of patient-doctor communication and high-quality patient care. Future studies measuring clinical outcomes and changes in learner behavior as a result of this intervention are needed. Ongoing observation and feedback on these skills will be important to solidify learning and sustain impact.


Assuntos
Comunicação , Medicina Interna/educação , Internato e Residência/métodos , Relações Médico-Paciente , Atitude do Pessoal de Saúde , Currículo , Emoções , Humanos , Planejamento de Assistência ao Paciente , Autoimagem
2.
J Neurosci ; 34(49): 16482-95, 2014 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-25471585

RESUMO

Frontotemporal dementia (FTD) is a neurodegenerative behavioral disorder that selectively affects the salience network, including the ventral striatum and insula. Tau mutations cause FTD, but how mutant tau impairs the salience network is unknown. Here, we address this question using a mouse model expressing the entire human tau gene with an FTD-associated mutation (V337M). Mutant, but not wild-type, human tau transgenic mice had aging-dependent repetitive and disinhibited behaviors, with synaptic deficits selectively in the ventral striatum and insula. There, mutant tau depleted PSD-95, resulting in smaller postsynaptic densities and impaired synaptic localization of NMDA receptors (NMDARs). In the ventral striatum, decreased NMDAR-mediated transmission reduced striatal neuron firing. Pharmacologically enhancing NMDAR function with the NMDAR co-agonist cycloserine reversed electrophysiological and behavioral deficits. These results indicate that NMDAR hypofunction critically contributes to FTD-associated behavioral and electrophysiological alterations and that this process can be therapeutically targeted by a Food and Drug Administration-approved drug.


Assuntos
Demência Frontotemporal/metabolismo , Demência Frontotemporal/fisiopatologia , Receptores de N-Metil-D-Aspartato/fisiologia , Proteínas tau/fisiologia , Potenciais de Ação/efeitos dos fármacos , Potenciais de Ação/fisiologia , Envelhecimento/psicologia , Animais , Comportamento Animal/efeitos dos fármacos , Comportamento Animal/fisiologia , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/fisiopatologia , Ciclosserina/farmacologia , Modelos Animais de Doenças , Proteína 4 Homóloga a Disks-Large , Agonistas de Aminoácidos Excitatórios/farmacologia , Agonistas de Aminoácidos Excitatórios/uso terapêutico , Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos , Potenciais Pós-Sinápticos Excitadores/fisiologia , Demência Frontotemporal/tratamento farmacológico , Guanilato Quinases/metabolismo , Humanos , Proteínas de Membrana/metabolismo , Camundongos , Camundongos Transgênicos , Mutação , Neurônios/fisiologia , Densidade Pós-Sináptica/genética , Densidade Pós-Sináptica/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Proteínas tau/genética
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