Mapping an undergraduate medical education curriculum against national and international palliative care reference learning objectives.

BACKGROUND: The teaching of palliative care competencies is an essential component of undergraduate medical education. There is significant variance in the palliative care content delivered in undergraduate medical curricula, revealing the utility of reference standards to guide curricular development and assessment. To evaluate our university's undergraduate palliative care teaching, we undertook a curriculum mapping exercise, comparing official learning objectives to the national Educating Future Physicians in Palliative and End-of-Life Care (EFPPEC) and the international Palliative Education Assessment Tool (PEAT) reference objectives. METHODS: Multiple assessors independently compared our university's UGME learning objectives with EFPPEC and PEAT reference objectives to determine the degree-of-coverage. Visual curriculum maps were created to depict in which part of the curriculum each objective is delivered and by which medical specialty. RESULTS: Of 122 EFPPEC objectives, 55 (45.1%) were covered fully, 42 (34.4%) were covered partially, and 25 (20.5%) were not covered by university objectives. Of 89 PEAT objectives, 40 (44.9%) were covered fully, 35 (39.3%) were covered partially, and 14 (15.7%) were not covered by university objectives. CONCLUSIONS: The majority of EFPPEC and PEAT reference objectives are fully or partially covered in our university's undergraduate medical curriculum. Our approach could serve as a guide for others who endeavour to review their universities' specialty-specific medical education against reference objectives. Future curriculum development should target the elimination of identified gaps and evaluate the attainment of palliative care competencies by medical learners.

Spatiotemporal distribution of spectrin breakdown products induced by anoxia in adult rat optic nerve in vitro.

Hypoxic/ischemic and traumatic injury to central nervous system myelinated axons is heavily dependent on accumulation of Ca ions in the axoplasm, itself promoted by Na influx from the extracellular space. Given the high density of nodal Na channels, we hypothesized that nodes of Ranvier might be particularly vulnerable to Ca overload and subsequent damage, as this is the expected locus of maximal Na influx. Adult rat optic nerves were exposed to in vitro anoxia and analyzed immunohistochemically for the presence of spectrin breakdown. Cleavage of spectrin became detectable between 15 and 30 mins of anoxia, and increased homogeneously along the lengths of fibers; localized breakdown was not observed at nodes of Ranvier at any time point analyzed. Spectrin breakdown was also found in glial processes surrounding axons. Confocal imaging of axoplasmic Ca also revealed a gradual and nonlocalized increase as anoxia progressed, without evidence of Ca 'hot-spots' anywhere along the axons at any time between 0 and 30 mins of anoxic exposure in vitro. Calculations of Ca diffusion rates indicated that even if Ca entered or was released focally in axons, this ion would diffuse rapidly into the internodes and likely produce diffuse injury by activating Ca-dependent proteases. Western blot analysis for voltage-gated Na channel protein revealed that key functional proteins such as these are also degraded by anoxia/ischemia. Thus, proteolysis of structural and functional proteins will conspire to irreversibly injure central axons and render them nonfunctional, eventually leading to transection, degradation, and Wallerian degeneration.