RESUMEN
La Insuficiencia Adrenal (IA) es una patología ocasionada por la disminución en la secreción de hormonas esteroideas por parte de la corteza adrenal, caracterizada por el déficit predominante de glucocorticoides. Esta puede ser clasificada en primaria cuando el defecto subyace en la glándula adrenal, siendo la causa más frecuente la adrenalitis autoinmune; o secundaria, por alteración en la secreción de la corticotropina (ACTH) o de la hormona liberadora de ACTH (CRH), cuya causa más común es la suspensión brusca de los glucocorticoides posterior a su administración por un período prolongado. Tanto las formas primarias como secundarias de IA pueden presentarse de manera aguda o crónica. La mayoría de los síntomas de la deficiencia de cortisol son inespecíficos incluyendo debilidad, anorexia, náuseas, entre otros; los signos principales son pérdida de peso, hiperpigmentación, hipotensión, siendo más característicos de la IA primaria. Una vez que se sospecha la IA, se determinarán las concentraciones de cortisol, con un valor basal menor de 3 mg/dL y post-estímulo menor de 18 mg/dL como diagnósticos de esta entidad. La determinación de ACTH permite la distinción entre una IA primaria y secundaria. El tratamiento de la IA en la mayoría de los casos es simplemente sustitutivo del déficit de glucocorticoides, siendo la hidrocortisona el fármaco de elección. Debido a que ésta patología puede estar asociada con una significativa morbilidad y mortalidad en los sujetos que la padecen, surgió la iniciativa por parte de nuestro servicio de Endocrinología de sintetizar en este protocolo la información hasta ahora disponible, así como nuestra experiencia, con respecto al diagnóstico y manejo de esta enfermedad.
Adrenal Insufficiency (AI) is a pathology caused by a decreased secretion of steroid hormones by the adrenal cortex, characterized by a predominant deficiency of glucocorticoids. AI can be classified as primary, when the underlying defect is in the adrenal gland, being the adrenalitis autoimmune the most common cause, or secondary, due to alterations in the secretion of corticotropin-releasing hormone (CRH) or corticotropin (ACTH), which most common cause is the abrupt discontinuation of glucocorticoids after its administration for an extended period. Both primary and secondary forms of IA may occur in an acute or chronic manner. Most symptoms of cortisol deficiency are nonspecific, including weakness, anorexia, nausea, among others; the main signs are weight loss, hyperpigmentation and hypotension, being more characteristics of the primary AI. A concentration less than 3 µg/ dL of basal cortisol or less than 18 µg/dL of cortisol post-stimulus confirm the diagnosis of this entity. The ACTH determination allows the distinction between primary and secondary AI. The treatment in most cases is simply to replace the deficit of glucocorticoid, being hydrocortisone the drug of choice. Because this condition can be associated with significant morbidity and mortality, an initiative was taken by our Endocrinology Service to synthesize in this protocol the information so far available, as well as our experience, with respect to the diagnosis and management of this disease.
RESUMEN
Las úlceras del pie en los pacientes diabéticos constituyen un gran problema de salud pública que genera un alto costo para el paciente, sus familiares y los sistemas de salud. Son la principal causa de amputación no traumática de las extremidades inferiores. El pie diabético es considerado un síndrome clínico de origen multifactorial que incluye factores neuropáticos, angiopáticos e infecciosos que producen daño tisular y determinan el pronóstico de la extremidad. En la evaluación del pie diabético resulta clave el reconocimiento de la úlcera, presencia de infección, así como el estado vascular de la extremidad, de allí la importancia del uso de clasificaciones que estandaricen las diversas definiciones, permitan evaluar el curso clínico y los resultados de distintas terapias. El tratamiento del pie diabético debe enfocarse principalmente en los mecanismos patogénicos desencadenantes, ameritando atención multidisciplinaria para lograr el mejor pronóstico para el paciente. El objetivo principal es la implementación de terapia antibiótica que debe ir acompañado de debridamiento quirúrgico, así como, terapia coadyuvante ante la presencia de isquemia y dolor neuropático. En el presente artículo, basados en niveles de evidencia científica y en la práctica clínica de la Unidad de Endocrinología del IAHULA, se presenta el protocolo para el manejo del pie diabético que incluye sistemas de clasificación, evaluación clínica, paraclínica y tratamiento médico y quirúrgico.
Foot ulcers in diabetic patients are a major public health problem that generates a high cost to the patient, family and health systems. They are the main cause of non-traumatic amputation of lower limbs. The diabetic foot is considered a clinical syndrome of multifactorial origin, including neuropathic, angiopathic and infectious factors, producing tissue damage and determining the prognosis of the limb. In diabetic foot assessment, it is critical to identify the ulcer, the presence of infection and the vascular status of the limb. For that reason, it is important to use standard classifications with accepted definitions to evaluate the clinical course and the results of different therapies. The diabetic foot treatment should focus primarily on the triggering pathogenic mechanisms, requiering care multidisciplinary to achieve the best outcome for the patient. The main therapies are the initiation of antibiotics along with surgical debridement, and adjuvant therapy for the ischemia and neuropathic pain. In this paper, based on levels of scientific evidence and clinical practice in the Unit of Endocrinology, IAHULA, we present the protocol for the management of the diabetic foot, including classification systems, clinical, paraclinical evaluation and medical and surgical treatment.
RESUMEN
This paper reports the standardization of methods used for processing and embedding various vertebrate brains of different size in paraffin. Other technical details developed for avoiding frequent difficulties arising during laboratory routine are also reported. Some modifications of the Nissl and Klüver-Barrera staining methods are proposed. These modifications include: 1) a Nissl stain solution with a rapid and efficient action with easier differentiation; 2) the use of a cheap microwave oven for the Klüver-Barrera stain. These procedures have the advantage of permitting Nissl and Klüver-Barrera staining of nervous tissue in about five and fifteen minutes respectively. The proposed procedures have been tested in brains obtained from fish, amphibians, reptiles and mammals of different body sizes. They are the result of our long experience in preparing slides for comparative studies. Serial sections of excellent quality were regularly obtained in all the specimens studied. These standardized methods, being simple and quick, are recommended for routine use in neurobiological laboratories.
Asunto(s)
Animales , Sistema Nervioso Central , Coloración y Etiquetado/normas , Fijación del Tejido/normas , Adhesión del Tejido/normas , Vertebrados , Coloración y Etiquetado/métodos , Colorantes , Fijación del Tejido/métodos , Adhesión del Tejido/métodos , Microtomía , Manejo de EspecímenesRESUMEN
A new and peculiar morphological feature in acinar cells of the Harderian gland of the South American armadillo Chaetophractus villosus (Mammalia, Dasipodidae) is reported. The gland of adult males and females was studied at macroscopic, microscopic and electron microscopic levels. The gland is the largest structure in the bony orbit. It is located in its medial (nasal) and basal side. It shows a tubuloalveolar structure characterized by large alveoli with a single layer of columnar or cuboidal cells. Myoepithelial cells are located between the secretory ones and the basement membrane. The peculiar morphological feature consists of large intracellular membranous bodies located in the supranuclear cytoplasmic region. They are seen in every acinar cell of males and females. Their size is prominent being almost as large as the nucleus. Only one body is observed in each cell. The structure of the bodies displays an outstanding geometrical pattern which differs completely from other membranous structures described in other species.