Nurses' knowledge about palliative care in a critical care unit.

INTRODUCTION AND OBJECTIVE: Patients admitted to the Critical Care Unit (CCU) have a high mortality rate due to their complexity. Palliative care (PC) is a key aspect that can improve patient care. Because of the essential role of the nurse in providing this care, training, and including it in daily practice are needed. Our objective was to review the level of knowledge among the nurses in the CCU regarding PC and assess whether there is an association between each of the study variables. METHODOLOGY: We performed a descriptive observational cross-sectional study in the CCU of a tertiary level university hospital. The questionnaire Palliative Care Quiz for Nurses, previously validated and translated into Spanish, was used. This is a self-administered questionnaire consisting of 20 multiple-choice questions (True/False/Do not know-Do not answer) which evaluates three aspects of PC: philosophy, psychosocial and control of pain and other symptoms. In addition, sociodemographic data was collected. Descriptive and inferential statistics were used, a p < .05 was considered statistically significant in all cases. RESULTS: The questionnaire was administered to 68 nursers, with an average age of 34.98 ±â€¯12.12 years, and 13.00 ±â€¯11.75 years of professional experience. Twelve nurses have Master studies and 28 nurses have received training in PC. The percent of correct answers of the questionnaire was 56.98%. There were no statistically significant differences between the total average score and the variables studied. However, looking at each aspect on the scale, an association was found between PC training and control of pain and other symptoms (p = .033). CONCLUSION: Critical care nurses have a basic knowledge of PC, it being insufficient in the psychological sphere. Developing a training programme which identifies misconceptions and training deficits might improve the management of symptom control in palliative care patients, quality of care and its application.

Conocimientos de las enfermeras acerca de los cuidados paliativos en un área de críticos / Nurses’ knowledge about palliative care in a critical care unit

Introducción y objetivos: Los pacientes que ingresan en las áreas de críticos (AC) tienen alta tasa de morbi-mortalidad debido a su complejidad. Los cuidados paliativos (CP) se presentan como un componente clave y pueden ayudar a mejorar el cuidado del paciente. La enfermera es esencial para la administración de estos cuidados; para ello, es necesario tener formación y saber integrarlos en la práctica diaria. El objetivo fue examinar el nivel de conocimientos de las enfermeras del AC acerca de los CP, y evaluar si existe asociación entre cada una de las variables estudiadas. Metodología: Estudio observacional descriptivo transversal en el AC de un hospital universitario de nivel terciario. Se utilizó el cuestionario Palliative Care Quiz for Nurses, traducido y validado al español. Es un cuestionario auto-administrado que consta de 20 ítems de respuesta múltiple (verdadero/falso/no sabe-no contesta) que evalúa tres aspectos de los CP: filosofía, psicosocial, y control del dolor y otros síntomas. Además, se recogieron datos sociodemográficos. Se realizó estadística descriptiva e inferencial, considerándose estadísticamente significativo un valor de p<0,05 en todos los casos. Resultados: El cuestionario se administró a 68 enfermeras, con una edad media de 34,98±12,12 años, y 13,00±11,75 años de experiencia profesional. Doce enfermeras tenían formación de Máster y 28 enfermeras habían recibido formación en CP. El porcentaje de aciertos del cuestionario fue de 56,98%. No hubo diferencias estadísticamente significativas entre la puntuación media total y las variables estudiadas. Al analizar los aspectos de la escala, se encontró asociación entre la formación en paliativos y el control de síntomas (p=0,033). Conclusión: Las enfermeras del AC tienen un conocimiento básico sobre los CP, siendo el aspecto psicosocial del mismo insuficiente.(AU)

Introduction and objetive: Patients admitted to the Critical Care Unit (CCU) have a high mortality rate due to their complexity. Palliative care (PC) is a key aspect that can improve patient care. Because of the essential role of the nurse in providing this care, training, and including it in daily practice are needed. Our objective was to review the level of knowledge among the nurses in the CCU regarding PC and assess whether there is an association between each of the study variables. Methodology: We performed a descriptive observational cross-sectional study in the CCU of a tertiary level university hospital. The questionnaire Palliative Care Quiz for Nurses, previously validated and translated into Spanish, was used. This is a self-administered questionnaire consisting of 20 multiple-choice questions (True/False/Do not Know-Do not answer) which evaluates three aspects of PC: philosophy, psychosocial and control of pain and other symptoms. In addition, sociodemographic data was collected. Descriptive and inferential statistics were used, a p<.05 was considered statistically significant in all cases. Results: The questionnaire was administered to 68 nursers, with an average age of 34.98±12.12 years, and 13.00±11.75 years of professional experience. Twelve nurses have Master studies and 28 nurses have received training in PC. The percent of correct answers of the questionnaire was 56.98%. There were no statistically significant differences between the total average score and the variables studied. However, looking at each aspect on the scale, an association was found between PC training and control of pain and other symptoms (p=.033). Conclusion: Critical care nurses have a basic knowledge of PC, it being insufficient in the psychological sphere. Developing a training programme which identifies misconceptions and training deficits might improve the management of symptom control in palliative care patients, quality of care and its application.(AU)

Core elements to understand and improve coping with Parkinson's disease in patients and family carers: A focus group study.

AIMS: The aim of this study were: (1) To explore the meaning that coping with Parkinson's disease has for patients and family carers; (2) To suggest the components of an intervention focused on enhancing their coping with the disease. BACKGROUND: Adapting to Parkinson's disease involves going through many difficult changes; however, it may improve quality of life in patients and family carers. One of the key aspects for facilitating the psychosocial adjustment to Parkinson's disease is the strengthening of coping skills. DESIGN: A sequential explanatory mixed methods study was carried out. Findings from the qualitative phase are presented. METHODS: Data were collected in May 2014 through three focus groups: one of people with Parkinson's disease (n = 9), one of family carers (n = 7) and one of healthcare professionals (n = 5). All focus groups were digitally recorded and transcribed verbatim and content analysis was independently carried out by two researchers. FINDINGS: The participants coincided in highlighting that coping with Parkinson's disease helped the patient and the family carer in their search for balance; and it implied a transformation in their lives. To aid the process of coping with Parkinson's disease, a multifaceted intervention is proposed. CONCLUSION: Coping with Parkinson's disease is a complex process for both patients and family carers and it should therefore be considered a standard service in healthcare policies aimed at this group. The proposed intervention constitutes a nursing tool which has great potential to improve the quality of life in Parkinson's disease and in other long-term conditions.

[Key elements for patients and caregivers in the process of living with Parkinson's disease]. / Elementos clave en el proceso de convivencia con la enfermedad de Parkinson de pacientes y familiares cuidadores.

BACKGROUND: Parkinson's disease has a considerable impact on people's lives. It is necessary to identify the key elements that influence the process of living with Parkinson's disease so that health professionals can help patients and their relatives to live as well as possible with the changes and limitations produced by the disease. MATERIAL AND METHODS: A qualitative descriptive study was realized. This study corresponded to the first phase of a sequential, exploratory design (mixed method) that in turn included a quantitative phase. A multicentre project was carried out. Convenience sampling was applied to collect data, a semi-structured interview was realized individually with patients and carer-relatives and two questionnaires with patients: the Hoehn & Yahr scale and the PDNMS questionnaire. Content analysis of the interviews and a statistical description of the questionnaires were used. RESULTS: The sample was made up of 46 participants. Three key elements were identified in the process of living with Parkinson's disease: acceptance, adaptation and self-management. These elements conditioned the modes of living with Parkinson's disease: positive living, characterized by feelings of harmony, balance and naturalness; negative living characterized be feelings of frustration, loss of control and self-esteem. CONCLUSIONS: It is essential for health professionals to have a deep understanding of these elements, as well as of the factors that favor or hinder them. To the extent that research in this field progresses and effective interventions are identified, comprehensive patient care will be improved in consonance with the new directives for chronicity.

Changes in cytoskeletal gene expression linked to MPTP-treatment in Mice.

Parkinson's disease is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra and a marked reduction of dopamine (DA) levels in the striatum. Binding to its specific receptors, DA switches on a complex program of intracellular signaling that regulates gene expression. We evaluated the changes in striatal gene expression in a mouse model of Parkinson's disease, using differential display analysis. The mRNA for the cytoskeleton family proteins, radixin, cofilin and centractin/ARP-1, was abnormally expressed in the striatum of these MPTP-treated mice. Moreover, we also found that radixin mRNA and its protein levels are under DA control through specific D1-dopaminergic receptors in a dose- and time-dependent manner in the GT1-7 neural cell line. These findings suggest a role for DA for regulation of cytoskeletal proteins involved in the integrity and function of synapsis.

Comparative study of PrPc expression in rat, monkey, and cow gastrointestinal tract.

The gastrointestinal tract (GIT) appears to be the main site of entry for the pathological isoform of prions (PrP(sc)). To understand how the PrP(sc) internalization process occurs, it is important to characterize the cell types that express normal prion protein (PrP(c)) along the GIT. To do so, we studied the distribution of PrP(c) in the rat, monkey, and cow GIT. Using Western blot analysis, we found that PrP(c) is expressed in all digestive regions of the three species. Immunoreactivity for PrP(c) was found throughout the GIT in epithelial cells sharing the neuroendocrine (NE) phenotype. Immunostained cells appeared scattered throughout the epithelium of fundic and pyloric glands as well as in intestinal villi and crypts.

Characterization of PrPc-immunoreactive cells in monkey (Macaca fascicularis) gastrointestinal tract.

The gastrointestinal tract (GIT) is one of the most likely entry sites for the pathological isoform of prions (PrP(sc)). To understand how PrP(sc) crosses the digestive mucosa, it is crucial to characterize the cells expressing normal prion protein (PrP(c)). By means of double immunofluorescence applied to sections of the monkey GIT, we demonstrated that, in the stomach, PrP(c) immunostaining occurs in subsets of histamine, somatostatin (Som), ghrelin (Ghr), gastrin (G), and serotonin (5HT) cells. In the small and large bowels, PrP(c) cells were found in subpopulations of cells immunolabeled for 5HT, Som, G, and peptide YY (PYY).

Distribution of adrenomedullin and proadrenomedullin N-terminal 20 peptide immunoreactivity in the pituitary gland of the frog Rana perezi.

Adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) are two multifunctional peptides processed from a common precursor which have been described in numerous mammalian organs, including the pituitary gland. Previous studies have found AM immunoreactivity in neurohypophysis nerve fibers of amphibian pituitary. In the present study, immunocytochemical and Western blot analysis in the pituitary gland of the amphibian Rana perezi demonstrated in the adenohypophysis both AM and PAMP. AM-like immunoreactivity was found in a moderate number of endocrine cells of the pars distalis. In the neurohypophysis, AM was observed not only in nerve fibers of pars nervosa and axonal projections innervating the pars intermedia, but also in the outer zone of the median eminence. PAMP staining was observed in numerous endocrine cells scattered all over the pars distalis and in some cells of the pars tuberalis, but not in the neurohypophysis. In order to compare the quantity of AM and PAMP immunoreactivity between pars distalis of female and male specimens, an image analysis study was done. Significant differences for AM immunoreactivity (p<0.001) between sexes was found, the males showing higher immunostained area percentage. Differences of PAMP immunoreactivity were not significant (p=0.599). Western blot analysis detected bands presumably corresponding to precursor and/or intermediate species in the propeptide processing.

Distinguishing excitotoxic from apoptotic neurodegeneration in the developing rat brain.

Much confusion has arisen recently over the question of whether excitotoxic neuronal degeneration can be considered an apoptotic phenomenon. Here, we addressed this question by using ultrastructural methods and DNA fragmentation analysis to compare a prototypic apoptotic in vivo central nervous system cell death process (physiologic cell death in the developing rat brain) with several central nervous system cell death processes in the in vivo infant rat brain that are generally considered excitotoxic (degeneration of hypothalamic neurons after subcutaneous administration of glutamate and acute neurodegeneration induced by hypoxia/ischemia or by concussive head trauma). We found by ultrastructural analysis that glutamate induces neurodegenerative changes in the hypothalamus that are identical to acute changes induced in the infant rat brain by either hypoxia/ischemia or head trauma, and that these changes are fundamentally different both in type and sequence from those associated with physiologic cell death (apoptosis). In addition, we show by ultrastructural analysis that concussive head trauma induces both excitotoxic and apoptotic neurodegeneration, the excitotoxic degeneration being very acute and localized to the impact site, and the apoptotic degeneration being delayed and occurring in regions distant from the impact site. Thus, in the head trauma model, excitotoxic and apoptotic degeneration can be distinguished not only by ultrastructural criteria but by their temporal and spatial patterns of expression. Whereas ultrastructural analysis provided an unambiguous means of distinguishing between excitotoxic and apoptotic neurodegeneration in each example analysed in this study, DNA fragmentation analysis (TUNEL staining or gel electrophoresis) was of no value because these tests were positive for both processes.

Multifocal brain damage induced by phencyclidine is augmented by pilocarpine.

Phencyclidine and other antagonists of the N-methyl-D-aspartate subtype of glutamate receptor cause psychosis in humans. In low doses these agents induce a reversible neurotoxic reaction in the rat brain that is limited to the retrosplenial granular cortex. Some investigators have reported that phencyclidine at higher doses or by more prolonged treatment causes a more disseminated pattern of damage. However, it has not been clearly demonstrated whether the disseminated damage is reversible or irreversible and whether it is consistently reproducible, nor is it known how many and which neurons are at risk. In the present study we addressed these questions using several histological approaches (plastic-embedded thin sections for light microscopy and ultrathin plastic sections for electron microscopy, paraffin-embedded haematoxylin and eosin sections, 72 kDa heat shock protein immunocytochemistry and de Olmos silver impregnation) to study the lesions induced in rat brain by phencyclidine (alone or when augmented with pilocarpine). We found that phencyclidine can kill a relatively large number of neurons distributed over many cerebrocortical and limbic brain regions, but the multifocal pattern of damage occurred in only a small percentage of treated rats. The addition of a low dose of pilocarpine to phencyclidine caused the widespread pattern of damage to manifest on a much more consistent basis. Available evidence suggests that disinhibition of multiple converging excitatory pathways is the mechanism by which phencyclidine triggers widespread neuronal degeneration; however, the specific combination of excitatory inputs that contributes to the pathological process may differ from region to region.

Ultrastructural localization suggests that retinal and cortical inputs access different metabotropic glutamate receptors in the lateral geniculate nucleus.

Glutamate has an important neuromodulatory role in synaptic transmission through metabotropic glutamate receptors (mGluRs) linked to a variety of G-protein-coupled second messenger pathways. Activation of these receptors on relay cells in the lateral geniculate nucleus (LGN) with the agonist trans-(1S,3R)-1-amino-1, 3-cyclopentanedicarboxylic acid produces a membrane depolarization that inactivates the low-threshold Ca2+ spike, causing a transition from burst to tonic response mode. The excitatory effects of metabotropic receptor activation in the LGN appear to be produced through the receptors linked to phosphoinositide hydrolysis and apparently only through activation of the corticogeniculate pathway. Two mGluRs, mGluR1alpha (a splice variant of mGluR1) and mGluR5, are linked to the phosphoinositide system. We examined the localization of these receptors with affinity-purified, anti-peptide, polyclonal antibodies raised to the C-terminal region of each receptor protein. Under examination with the light microscope, we found that both types of receptors are present in the geniculate neuropil and in that of the overlying thalamic reticular nucleus, including the perigeniculate nucleus. We also examined the ultrastructural localization of immunolabel with the electron microscope, using a postembedding immunogold marker to identify terminals, dendrites, and somata that contain GABA. Label for the antibody directed against mGluR1alpha was primarily localized in the dendrites of relay cells, postsynaptic to various terminal types. Of these, terminal profiles normally associated with corticogeniculate inputs predominated, whereas retinal terminal profiles were scarce. Label for the antibody directed against mGluR5 label was prominent in inhibitory F2-terminal profiles associated with the retinal input to relay cells. In the perigeniculate nucleus, both mGluRs were localized to dendrites. The distribution of the two phosphoinositide-linked mGluRs in the LGN suggests very different functional roles for the two receptor types. We conclude from these data that mGluR1 appears to have a dominant role in corticogeniculate control of response mode through the feedback glutamatergic pathway from layer VI, whereas mGluR5 is positioned to affect retinogeniculate activation of relay cells through feed forward glomerular interactions.

Distribution of metabotropic glutamate receptor mGluR5 immunoreactivity in rat brain.

The receptor mGluR5 is a metabotropic glutamate receptor with messenger RNA abundantly present throughout cortex, hippocampus, and caudate/putamen that is also coupled to phosphatidyl inositide hydrolysis and calcium mobilization. In this study, the distribution of mGluR5 was examined in rat brain by immunocytochemistry. The antibody utilized is highly specific and does not cross react with the most closely related other metabotropic glutamate receptor, as determined by Western blot analysis of nonneuronal cells transfected with metabotropic receptor coding sequences. The receptor mGluR5 is widely expressed with the highest density in olfactory bulb, caudate/putamen, lateral septum, cortex, and hippocampus, as confirmed with both immunocytochemistry and Western blot analysis. Electron microscopic studies in hippocampus and cortex indicate that the labeling is mostly on membranes of dendritic spines and shafts. Light and electron microscopic evidence indicates that some mGluR5 immunoreactivity is located in presynaptic axon terminals, suggesting that mGluR5 may function as a presynaptic receptor.

NMDA antagonist neurotoxicity: mechanism and prevention.

Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, including phencyclidine (PCP) and ketamine, protect against brain damage in neurological disorders such as stroke. However, these agents have psychotomimetic properties in humans and morphologically damage neurons in the cerebral cortex of rats. It is now shown that the morphological damage can be prevented by certain anticholinergic drugs or by diazepam and barbiturates, which act at the gamma-aminobutyric acid (GABA) receptor-channel complex and are known to suppress the psychotomimetic symptoms caused by ketamine. Thus, it may be possible to prevent the unwanted side effects of NMDA antagonists, thereby enhancing their utility as neuroprotective drugs.

[Human diseases caused by free-living amoebae. II. Primary amebic ++ meningoencephalitis]. / Afecciones humans debidas a amebas de vida libre. II. La meningoencefalitis amebiana primaria.

This revision gives an overall view of the health problems caused by the amoebas of the Naegleria genus, which despite being free-life amoebas, can affect humans, almost always fatally, because they cause a syndrome known as primary amoebian meningoencephalitis, which affects people of all ages and physical condition, and especially those who have a prior history of contacts, even if not exclusive, with fresh waters especially sports-related contacts. Morphological data of the protozoon are given, as well as of the pathology of the illness and the epidemiology, diagnosis, and treatment, plus a table of cases successfully treated around the world to date.

[Human diseases caused by free-living amoebae. I. Acanthamoebiasis]. / Afecciones humanas debidas a amebas de vida libre. I. Acantamebiasis.

This summary offers an updated panorama of the problems caused in many countries, including our own, by free protozoan, Acanthamoeba class amoebas that in certain circumstances depend on either pathogenic potential or the immunological condition of the host and which produce significant disease syndromes. Presented here are the main morphological and ecological characteristics of these amoeba, a summarized study of their pathological characteristic, diagnostic and therapeutic data, as well as a synopsis of the majority of clinical cases diagnosed in the world to date.

Isolation of free-living amoebas from the intestinal contents of reptiles.

A total of 508 reptiles captured at Canary Islands (Spain) was examined for free-living amoebas. Two hundred seventy-three clones of amoebas were isolated by culture of gut contents, 157 of them belonging to the genus Acanthamoeba and 12 to the genus Naegleria.

[Isolation of free-living amoebas from samples of respiratory origin]. / Aislamiento de amebas de vida libre en muestras de origen respiratorio.

By seeding free-living amebas in isolation, a study was conducted on the contamination by these protozoa of nasal and pharyngeal mucus in 58 children from Madrid. Two positive cases were identified, leading to the isolation of 2 amoebic strains, identified as belonging to the genus Acanthamoeba. The pathogenic capacity of these amebas was tested in white mice, and one of the former was found to be extremely pathogenic for these mice. The potential hazard deriving from the presence of these pathogenic for these mice. The potential hazard deriving from the presence of these pathogenic protozoa among healthy populations is discussed.

Contrast-sensitivity functions of W-, X-, and Y-like relay cells in the lateral geniculate nucleus of bush baby, Galago crassicaudatus.

1. This paper represents a continuation of our effort to examine the relationship between the physiology of distinct classes of primate lateral geniculate nucleus (LGN) cells and spatial vision. The present study focuses on modeling the contrast-sensitivity functions (CSFs) of separate LGN cell classes, examining differences in the CSFs of different classes of LGN cells and comparing the results with behaviorally defined CSFs. 2. CSFs to drifting sinusoidal gratings were obtained from single LGN relay cells in the nocturnal primate, Galago crassicaudatus. The CSFs of 14 X-like, 27 Y-like, and 6 W-like cells with standard center-surround organization were well fit by a difference of Gaussians (DOG) model with small residual errors (mean error per data point +/- SEM = 0.008 +/- 0.002). The larger residual errors shown by a few of the Y-like cells were not due to nonlinearity of spatial summation. 3. The CSFs of eight cells that appeared to have nonstandard center-surround organization (primarily, a silent, suppressive surround) were also well fit by the DOG model. 4. The DOG curves that best fitted the data differed considerably between the three groups. As a group, X-like cells had a small center mechanism (Rc = 0.19 degrees) with high sensitivity (Kc = 76.53) and a small, sensitive surround (Rs = 0.71 degrees; Ks = 5.50). These parameters produced CSFs with high cutoff frequencies (Vcutoff = 2.5 c/deg) and low peak sensitivities (CSpk = 6.1) that occurred at 0.8 c/deg. 5. Y-like cells had a large center mechanism (Rc = 0.46 degrees) with low sensitivity (Kc = 21.16) and a large, insensitive surround (Rs = 2.38 degrees; Ks = 0.81). These parameters produced CSFs with lower cutoff frequencies (Vcutoff = 1.2 c/deg) and higher peak sensitivities (CSpk = 12.5) that occurred at 0.2 c/deg. 6. The few W-like cells that responded to gratings well enough to determine a CSF were quite variable. As a group they had a large center mechanism (Rc = 0.38 degrees) with intermediate sensitivity (Kc = 34.55) and a surround with intermediate size and sensitivity (Rs = 1.59 degrees; Ks = 1.59). These produced CSFs with intermediate cutoffs (Vcutoff = 1.6 c/deg) and low peak sensitivities (CSpk = 5.0) occurring at 0.4 c/deg.(ABSTRACT TRUNCATED AT 400 WORDS)