Clinical skills training in the third course of Medicine. Sequential evaluation of five cycles

Introducción: Existen pocos estudios que de forma selectiva valoren la docencia clínica de una determinada asignatura. En este artículo se presenta la experiencia en docencia clínica de la asignatura 'Semiología General y Propedéutica Clínica' en tercer curso del Grado de Medicina en la Facultad de Medicina de la Universitat de Barcelona. Materiales y métodos: Se han analizado los cursos 2011-2012, 2012-2013 y 2013-2014, representando un total de cinco 'cursos', ya que la asignatura es semestral y se imparte dos veces en cada curso académico. El período de docencia clínica de la asignatura es de siete semanas (28 días) y el número de alumnos oscila entre cuatro y ocho por cada una de las siete unidades/centros distintos. A su llegada se les informa de los objetivos de la estancia clínica y al final del período se les invita a cumplimentar una encuesta anónima y voluntaria en la que valoran distintos ítems. Resultados: Se han recogido 477 encuestas (95%). Se constató una muy buena valoración global del período de docencia clínica (mediana: 5; primer cuartil: 4, en escala de 1 a 5), sin variaciones significativas entre los distintos períodos evaluados (p = 0,658). Conclusiones: La docencia clínica en esta asignatura está muy bien valorada de forma global, sin detectar variaciones relevantes en los cinco cursos analizados

Clinical skills training in the third course of Medicine. Sequential evaluation of five cycles

Introducción: Existen pocos estudios que de forma selectiva valoren la docencia clínica de una determinada asignatura. En este artículo se presenta la experiencia en docencia clínica de la asignatura 'Semiología General y Propedéutica Clínica' en tercer curso del Grado de Medicina en la Facultad de Medicina de la Universitat de Barcelona. Materiales y métodos: Se han analizado los cursos 2011-2012, 2012-2013 y 2013-2014, representando un total de cinco 'cursos', ya que la asignatura es semestral y se imparte dos veces en cada curso académico. El período de docencia clínica de la asignatura es de siete semanas (28 días) y el número de alumnos oscila entre cuatro y ocho por cada una de las siete unidades/centros distintos. A su llegada se les informa de los objetivos de la estancia clínica y al final del período se les invita a cumplimentar una encuesta anónima y voluntaria en la que valoran distintos ítems. Resultados: Se han recogido 477 encuestas (95%). Se constató una muy buena valoración global del período de docencia clínica (mediana: 5; primer cuartil: 4, en escala de 1 a 5), sin variaciones significativas entre los distintos períodos evaluados (p = 0,658). Conclusiones: La docencia clínica en esta asignatura está muy bien valorada de forma global, sin detectar variaciones relevantes en los cinco cursos analizados

Platelet-activating factor causes ventilation-perfusion mismatch in humans

We hypothesized that platelet-activating factor (PAF), a potent inflammatory mediator, could induce gas exchange abnormalities in normal humans. To this end, the effect of aerosolized PAF (2 mg/ml solution; 24 micrograms) on ventilation-perfusion (VA/Q) relationships, hemodynamics, and resistance of the respiratory system was studied in 14 healthy, nonatopic, and nonsmoking individuals (23 +/- 1 [SEM]yr) before and at 2, 4, 6, 8, 15, and 45 min after inhalation, and compared to that of inhaled lyso-PAF in 10 other healthy individuals (24 +/- 2 yr). PAF induced, compared to lyso-PAF, immediate leukopenia (P < 0.001) followed by a rebound leukocytosis (P < 0.002), increased minute ventilation (P < 0.05) and resistance of the respiratory system (P < 0.01), and decreased systemic arterial pressure (P < 0.05). Similarly, compared to lyso-PAF, PaO2 showed a trend to fall (by 12.2 +/- 4.3 mmHg, mean +/- SEM maximum change from baseline), and arterial-alveolar O2 gradient increased (by 16.7 +/- 4.3 mmHg) (P < 0.02) after PAF, because of VA/Q mismatch: the dispersion of pulmonary blood flow and that of ventilation increased by 0.45 +/- 0.1 (P < 0.01) and 0.29 +/- 0.1 (P < 0.04), respectively. We conclude that in normal subjects, inhaled PAF results in considerable immediate VA/Q inequality and gas exchange impairment. These results reinforce the notion that PAF may play a major role as a mediator of inflammation in the human lung

Platelet-activating factor causes ventilation-perfusion mismatch in humans

We hypothesized that platelet-activating factor (PAF), a potent inflammatory mediator, could induce gas exchange abnormalities in normal humans. To this end, the effect of aerosolized PAF (2 mg/ml solution; 24 micrograms) on ventilation-perfusion (VA/Q) relationships, hemodynamics, and resistance of the respiratory system was studied in 14 healthy, nonatopic, and nonsmoking individuals (23 +/- 1 [SEM]yr) before and at 2, 4, 6, 8, 15, and 45 min after inhalation, and compared to that of inhaled lyso-PAF in 10 other healthy individuals (24 +/- 2 yr). PAF induced, compared to lyso-PAF, immediate leukopenia (P < 0.001) followed by a rebound leukocytosis (P < 0.002), increased minute ventilation (P < 0.05) and resistance of the respiratory system (P < 0.01), and decreased systemic arterial pressure (P < 0.05). Similarly, compared to lyso-PAF, PaO2 showed a trend to fall (by 12.2 +/- 4.3 mmHg, mean +/- SEM maximum change from baseline), and arterial-alveolar O2 gradient increased (by 16.7 +/- 4.3 mmHg) (P < 0.02) after PAF, because of VA/Q mismatch: the dispersion of pulmonary blood flow and that of ventilation increased by 0.45 +/- 0.1 (P < 0.01) and 0.29 +/- 0.1 (P < 0.04), respectively. We conclude that in normal subjects, inhaled PAF results in considerable immediate VA/Q inequality and gas exchange impairment. These results reinforce the notion that PAF may play a major role as a mediator of inflammation in the human lung

Immunoglobulin A and C reactive protein levels in ankylosing spondylitis

Correspondence: SIR, We read with interest the recent paper by Sanders et al on the correlation of immunoglobulin and C reactive protein (CRP) levels in 22 patients with ankylosing spondylitis (AS) and 20 patients with rheumatoid arthritis (RA).' The authors found that IgA serum levels, though raised in AS, do not correlate with CRP levels as they do in RA, suggesting that the mechanism of increase of IgA in the two diseases may be different. They conclude that production of IgA in AS is unrelated to the stimulation of acute phase reactants, reflecting a specific mucosal immune stimulation, possibly in the gut. Thus IgA may be a marker of the pathogenesis of AS

Effects of erythropoietin on muscle O2 transport during exercise in patients with chronic renal failure.

Erythropoietin (rHuEPO) has proven to be effective in the treatment of anemia of chronic renal failure (CRF). Despite improving the quality of life, peak oxygen uptake after rHuEPO therapy is not improved as much as the increase in hemoglobin concentration ([Hb)] would predict. We hypothesized that this discrepancy is due to failure of O2 transport rates to rise in a manner proportional to [Hb]. To test this, eight patients with CRF undergoing regular hemodialysis were studied pre- and post-rHuEPO ([Hb] = 7.5 +/- 1.0 vs. 12.5 +/- 1.0 g x dl-1) using a standard incremental cycle exercise protocol. A group of 12 healthy sedentary subjects of similar age and anthropometric characteristics served as controls. Arterial and femoral venous blood gas data were obtained and coupled with simultaneous measurements of femoral venous blood flow (Qleg) by thermodilution to obtain O2 delivery and oxygen uptake (VO2). Despite a 68% increase in [Hb], peak VO2 increased by only 33%. This could be explained largely by reduced peak leg blood flow, limiting the gain in O2 delivery to 37%. At peak VO2, after rHuEPO, O2 supply limitation of maximal VO2 was found to occur, permitting the calculation of a value for muscle O2 conductance from capillary to mitochondria (DO2). While DO2 was slightly improved after rHuEPO, it was only 67% of that of sedentary control subjects. This kept maximal oxygen extraction at only 70%. Two important conclusions can be reached from this study. First, the increase in [Hb] produced by rHuEPO is accompanied by a significant reduction in peak blood flow to exercising muscle, which limits the gain in oxygen transport. Second, even after restoration of [Hb], O2 conductance from the muscle capillary to the mitochondria remains considerably below normal