RESUMEN
BACKGROUND: Interprofessional education (IPE) is crucial in fostering effective collaboration and optimal team-based patient care, all of which improve patient care and outcomes. Appropriate interprofessional communication is especially important in geriatrics where patients are vulnerable to adverse effects across the care continuum. Transitions in geriatric care are complex, involving several disciplines and requiring careful coordination. As part of the University of Virginia's initiative on IPE, we developed and implemented an interprofessional geriatric education workshop for nursing and medical students with a focus on transitions in care. METHODS: A total of 254 students (144 medical students, 107 nursing students and 3 unknown) participated in a 90-min interactive, case-based workshop. Nursing and medical faculty facilitated the monthly workshops with small groups of medical and nursing students over 1 year. Self-perceived competencies in IPE skills and attitudes toward interprofessional teamwork were measured through post-workshop surveys. Data were analyzed using descriptive and nonparametric statistics, excluding the three unknown students. RESULTS: Over 90% of students were better able to describe the necessary interprofessional communication needed to develop a patient-centered care plan in transitioning patients between clinical sites. Four out of five students reported an enhanced appreciation of interprofessional teamwork. They were also able to identify legal, financial and social implications in transitions of care (75%). Nursing students consistently rated the workshop more highly than medical students across most domains (P < 0.05). CONCLUSIONS: Students improved and demonstrated their knowledge of interprofessional communication and teamwork skills required in transitions of geriatric care. Introducing these concepts in medical and nursing training may help in fostering effective interprofessional communication and collaboration.
Asunto(s)
Educación de Pregrado en Medicina/métodos , Bachillerato en Enfermería/métodos , Geriatría/educación , Actitud del Personal de Salud , Competencia Clínica/normas , Retroalimentación , Humanos , Relaciones Interprofesionales , Grupo de Atención al Paciente , Transferencia de Pacientes , Satisfacción Personal , Autoimagen , Estudiantes de Medicina/psicología , Estudiantes de Enfermería/psicología , VirginiaRESUMEN
Evaluating cough in the primary care setting can be very difficult and requires a thorough look through a long list of potential differential diagnoses. The most worrisome diagnosis is that of a lung malignancy. Primary care providers must assess each patient carefully in a logical, precise manner to determine a working diagnosis for acute versus chronic cough in smokers and nonsmokers. Early detection leads to a diagnosis of lung cancer at earlier stages and may offer the only possibility of cure. This article provides primary care providers with an overview of the most common causes of cough, an algorithm to assist with the diagnosis, and a brief overview of the staging, diagnostic workup, treatment, and management of lung cancer.
Asunto(s)
Tos/etiología , Neoplasias Pulmonares/diagnóstico , Enfermedad Aguda , Algoritmos , Carcinoma de Pulmón de Células no Pequeñas/diagnóstico , Carcinoma de Pulmón de Células no Pequeñas/mortalidad , Enfermedad Crónica , Tos/fisiopatología , Diagnóstico Diferencial , Humanos , Neoplasias Pulmonares/mortalidad , Enfermedades Respiratorias/diagnósticoRESUMEN
To evaluate our previous observation of renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied 13 conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 meq/day for 4 days). Five dogs were studied during combined acute hypoxemia (PaO2, 37 +/- 1 mm Hg) and hypercapnic acidosis (PaCO2, 59 +/- 1 mm Hg; pH 7.20 +/- 0.01). Each dog was studied during infusion of 1) the intrarenal vehicle (n = 5), 2) the intrarenal alpha 1-antagonist prazosin (0.2 micrograms.kg-1.min-1, n = 5), 3) intrarenal [Sar1,Ala8]angiotensin II (70 ng.kg-1.min-1, n = 5), and 4) intrarenal prazosin and [Sar1,Ala8]angiotensin II (n = 4). Immediate induction of combined hypoxemia and hypercapnic acidosis after control measurements during intrarenal vehicle infusion resulted in a decrease in effective renal plasma flow and glomerular filtration rate, increase in renal vascular resistance, and decrease in filtered sodium load in the first 20 minutes of the blood gas derangement. Intrarenal administration of [Sar1,Ala8]angiotensin II failed to reverse the effects of the combined blood gas derangement on renal function. In contrast, intrarenal prazosin administration either alone or in combination with [Sar1,Ala8]angiotensin II abrogated the increase in renal vascular resistance, decrease in glomerular filtration rate, and fall in filtered sodium load. These studies identify a major role for alpha 1-adrenoceptors in the renal vasoconstriction during combined hypoxemia and hypercapnic acidosis.
Asunto(s)
Angiotensina II/fisiología , Hipercapnia/fisiopatología , Hipoxia/fisiopatología , Riñón/metabolismo , Receptores Adrenérgicos alfa/fisiología , Circulación Renal , Acidosis/fisiopatología , Enfermedad Aguda , Antagonistas Adrenérgicos alfa/farmacología , Angiotensina II/sangre , Animales , Perros , Vehículos Farmacéuticos , Fenilefrina/farmacología , Prazosina/farmacología , Saralasina/farmacología , VasoconstricciónRESUMEN
In order to evaluate the role of the alpha-adrenergic system in the systemic and renal hemodynamic changes of the acute combined blood gas derangement, seven conscious mongrel dogs in careful sodium balance (80 mEq/day for 4 days) were evaluated. Each animal was evaluated during combined acute hypoxemia (PaO2 = 35 +/- 1 mm Hg) and hypercapnic acidosis (PaCO2 = 56 +/- 2 mm Hg; pH = 7.18 +/- 0.01) with (i) vehicle (D5W) alone and (ii) alpha 1-adrenergic blockade with prazosin, 0.1 mg/kg iv. Mean arterial pressure increased during the combined blood gas derangement with vehicle. In contrast, mean arterial pressure fell during combined acute hypoxemia and hypercapnic acidosis with alpha 1-adrenergic blockade. The mechanism for abrogation of the rise in mean arterial pressure during the combined blood gas derangement by alpha 1-adrenergic blockade appeared to be through attenuation of the rise in cardiac output rather than an exaggerated fall in total peripheral resistance. These observations suggest that the alpha-adrenergic system is important in circulatory homeostasis during the combined blood gas derangement.
Asunto(s)
Acidosis/fisiopatología , Sistema Cardiovascular/fisiopatología , Hipercapnia/complicaciones , Hipoxia/fisiopatología , Prazosina/farmacología , Receptores Adrenérgicos alfa/fisiología , Acidosis/etiología , Animales , Presión Sanguínea/efectos de los fármacos , Gasto Cardíaco/efectos de los fármacos , Presión Venosa Central/efectos de los fármacos , Perros , Tasa de Filtración Glomerular/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Receptores Adrenérgicos alfa/efectos de los fármacos , Circulación Renal/efectos de los fármacos , Renina/sangre , Volumen Sistólico/efectos de los fármacos , Resistencia Vascular/efectos de los fármacosRESUMEN
The role of the endothelium in hypoxic constriction of the intact pulmonary vascular bed has not been clearly elucidated. To test for a possible role for endothelium-derived relaxing factor(s) (EDRF) in the hypoxic pressor response, isolated, whole blood-perfused rat lungs from male Sprague-Dawley rats treated with meclofenamate were prepared. Three protocols were performed, including: (a) normal saline (control); (b) the putative EDRF inhibitors, eicosatetraynoic acid (ETYA, 1 X 10(-4) M) or nordihydroguaiaretic acid (NDGA, 1 X 10(-4) M) versus vehicle DMSO; and (c) the putative EDRF inhibitor hydroquinone (HQ, 1 X 10(-4) M) versus vehicle ethyl alcohol (ETOH). The pulmonary pressor response to angiotensin II (Ang II, 0.25 micrograms) injections alternated with 6-min periods of hypoxic ventilation (3% O2, 5% CO2) was measured before and after the administration of saline, inhibitors, or vehicles. The administration of the EDRF inhibitors ETYA, NDGA, and HQ resulted in a marked accentuation of the hypoxic pressor response that was not seen in the controls (P less than 0.05). In separate experiments, lungs precontracted with norepinephrine (1 X 10(-6) M) were pretreated with edrophonium (1 X 10(-4) M) and then observed for endothelium-dependent vasodilator responses to acetylcholine at increasing doses (1 X 10(-7)-1 X 10(-4) M). Administration of ETYA, NDGA, or HQ abrogated the observed vasodilatation to acetylcholine, which was not seen with vehicles alone (P less than 0.01). These studies suggest an important role for the endothelium in pulmonary vascular responsiveness to alveolar hypoxia through possible release of a relaxing factor(s) that attenuates the degree of pulmonary arterial constriction.
Asunto(s)
Factores Biológicos/antagonistas & inhibidores , Hipoxia/fisiopatología , Circulación Pulmonar , Vasoconstricción/efectos de los fármacos , Ácido 5,8,11,14-Eicosatetrainoico/farmacología , Animales , Hidroquinonas/farmacología , Masculino , Masoprocol/farmacología , Óxido Nítrico , Norepinefrina/farmacología , Perfusión , Ratas , Ratas EndogámicasRESUMEN
The role of endogenous opioids in systemic and renal circulatory changes during combined acute hypoxemia and hypercapnic acidosis was evaluated in seven conscious female mongrel dogs in rigid sodium balance. Animals were studied 2 wk apart in separate protocols of combined acute hypoxemia (arterial O2 tension = 33 +/- 1 mmHg) and hypercapnic acidosis (arterial CO2 tension = 56 +/- 1 mmHg, pH = 7.19 +/- 0.01) of 40 min duration during 1) naloxone, 5 mg/kg iv bolus followed by an intravenous infusion of 5 mg.kg-1.h-1, and 2) vehicle (5% dextrose in water) alone. Systemic circulatory changes during the combined acute blood-gas derangement including increased mean arterial pressure, heart rate, and cardiac output and decreased total peripheral resistance were comparable between naloxone and vehicle treatments. However, in striking contrast to the brief fall in renal hemodynamic function during combined acute hypoxemia and hypercapnic acidosis with vehicle, naloxone administration during the combined acute blood-gas derangement resulted in a sustained decrease in effective renal plasma flow, glomerular filtration rate, and filtered sodium load and enhanced rise in circulating norepinephrine and epinephrine. Changes in plasma renin activity were comparable between vehicle and naloxone protocols except that plasma renin activity increased from the first to the second 20-min periods of combined hypoxemia and hypercapnic acidosis with naloxone. These observations suggest that endogenous opioids may contribute to preservation of renal hemodynamic function during acute blood-gas derangements, possibly through attenuation of sympathetic nervous system and renin-angiotension activation.