Burnout syndrome and depression in students of a Colombian medical school, 2018.

INTRODUCTION AND OBJECTIVES: Burnout syndrome (BS) has been evaluated in few populations of medical students, and its relationship with depression is even less studied. The objective was to determine the frequency of BS in medical students of the Universidad Pedagógica y Tecnológica de Colombia (UPTC), in Tunja, Colombia, as well as its association with depression and other social, economic, demographic, and academic factors. METHODS: An observational, analytical, cross-sectional study was carried out on 182 UPTC medical students during 2018. The Maslach Burnout Inventory-Student Survey (MBI-SS) was applied, with which 3 components were obtained to determine positive SB. This was crossed in the Stata 15 program for depression and other social, economic, demographic, and academic covariates with the Generalised Linear Model (GLM). RESULTS: Of 182 respondents, 51.4% were women. The median age was 21 years (20-23 years). 14% had BS, of which 48% had depression. In the multiple regression, BS was significantly associated with a higher frequency of depression (RPa = 5.54; IC95%, 2.36-13.02; P < 0.001) and the feeling of insufficient money (RPa = 4.37; IC95%, 1.95-9.83; P < 0.001), in contrast to a negative association with smoking (RPa = 0.13; IC95%, 0.06-0.30; P < 0.001) and being a woman (RPa = 0.32; IC95%, 0.12-0.82; P = 0.018). The age of onset of marijuana use was not significant. CONCLUSIONS: BS shows a high association with increased depression and a feeling that the money is not enough at the end of the month, but it showed a negative association with tobacco consumption and being a woman. Such students should be detected to provide them with adequate academic support.

Deficiencia de butirilcolinesterasa: Una revisión narrativa de la literatura / Butirilcholinesterase Deficiency: A Narrative Review of Literature

RESUMEN La butirilcolinesterasa es una enzima que metaboliza relajantes neuromusculares despolarizantes como la succinilcolina, fármaco de elección para procedimientos que requieran parálisis muscular a corto plazo como facilitar la intubación endotraqueal en pacientes sometidos a procedimientos de emergencia. La deficiencia de butirilcolinesterasa se define como la reducción cuantitativa de dicha enzima y su actividad para hidrolizar moléculas, constituyéndose en la principal causa de bloqueo neuromuscular prolongado tras la administración de relajantes neuromusculares como la succinilcolina. Es una condición patológica que puede ser de origen hereditario o adquirido; siendo más común la deficiencia enzimática de origen genético y de carácter autosómico recesivo, la cual se presenta aproximadamente en una de cada 3200 a 5000 personas en todo el mundo. Su manifestación clínica se caracteriza por relajación muscular persistente, la cual puede producir insuficiencia respiratoria aguda. El diagnóstico debe estar orientado a la identificación de sus características clínicas, la cuantificación serológica y el monitoreo neuromuscular. Debido a que no existe cura para esta deficiencia, el manejo debe estar orientado a realizar ventilación mecánica del paciente hasta que el medicamento empleado se metabolice por completo. Este artículo tiene como objetivo realizar una revisión del estado del arte, describiendo su epidemiología, etiología, fisiopatología, manifestaciones clínicas y actualidades en su diagnóstico y tratamiento.

ABSTRACT Butyrylcholinesterase is an enzyme that metabolizes depolarizing neuromuscular relaxants, such as succinylcholine, a chosen medication for procedures that require short-term muscular paralysis, to facilitate endotracheal intubation in patients undergoing emergency procedures, for example. Butyrylcholinesterase deficiency can be defined as a quantitative reduction of the enzyme and its activity to hydrolyze molecules, becoming the main cause of prolonged neuromuscular blockade after the administration of neuromuscular relaxants such as succinylcholine. It is a pathological condition that can be of either hereditary or acquired origin; being more common the enzymatic deficiency of genetic origin and of auto-somal recessive character, occurring in approximately one in 3,200 to 5,000 people worldwide. Its clinical manifestation is characterized by persistent muscle relaxation which can lead to acute respiratory failure. The diagnosis must be oriented to the identification of its clinical characteristics, serological quantification, and neuromuscular monitoring. Because a cure does not exist for this deficiency, management should be directed to mechanical ventilation of the patient, until the used drug is fully metabolized. This article aims to review the state of the art, describing its epidemiology, etiology, pathophysiology, clinical manifestations, and updates in its diagnosis and treatment.

Tay-Sachs disease / Enfermedad de Tay-Sachs

Abstract Introduction: Lysosomal storage disease is caused by the deficiency of a single hydrolase (lysosomal enzymes). GM2 gangliosidoses are autosomal recessive disorders caused by deficiency of β-hexosaminidase and Tay-Sachs disease (TSD) is one of its three forms. Objective: To perform a review of the state of the art on TSD and describe its definition, epidemiology, etiology, physiopathology, clinical manifestations, as well as advances regarding its diagnosis and treatment. Materials and methods: A literature search was carried out in PubMed using the MeSH terms "Tay-Sachs Disease". Results: after the initial search was conducted, 1 233 results were retrieved, of which 53 articles were finally selected. TSD is caused by the deficiency of the lysosomal enzyme β-hexosaminidase A (HexA), and is characterized by neurodevelopmental regression, hypotonia, hyperacusis and cherry-red spots in the macula. Research on molecular pathogenesis and the development of possible treatments has been limited, consequently there is no treatment established to date. Conclusion: TSD is an autosomal recessive neurodegenerative disorder. Death usually occurs before the age of five. More research and studies on this type of gangliosidosis are needed in order to find an adequate treatment.

Resumen Introducción. La deficiencia de una sola hidrolasa (enzimas lisosomales) da como resultado una enfermedad de almacenamiento lisosomal. Las gangliosidosis GM2 son trastornos autosómicos recesivos causados por la deficiencia de β-hexosaminidasa. La enfermedad de Tay-Sachs (TSD, por sus siglas en inglés) es una de las tres presentaciones de este tipo de gangliosidosis. Objetivo. Realizar una revisión del estado del arte de la TSD describiendo su definición, epidemiología, etiología, fisiopatología, manifestaciones clínicas y actualidades en su diagnóstico y tratamiento. Materiales y métodos. Se realizó una búsqueda bibliográfica en PubMed utilizando como único término MeSH "Tay-Sachs Disease". Resultados. Se encontraron 1 233 publicaciones y se seleccionaron 53 artículos. La TSD es originada por la deficiencia de la enzima lisosomal β-hexosaminidasa A (HexA) y se caracteriza por regresión del neurodesarrollo, hipotonía, hiperacusia y manchas maculares rojo cereza. La investigación de la patogenia molecular y el desarrollo de posibles tratamientos han sido limitados y en la actualidad no se cuenta con uno plenamente establecido. Conclusiones. La TSD es un trastorno neurodegenerativo autosómico recesivo y por lo general la muerte se produce antes de los 5 años de edad. Son necesarias más investigaciones y estudios sobre este tipo de gangliosidosis con el fin de encontrar un tratamiento adecuado.