FISIOPATOLOGIA DE LA DISPLASIA BRONCOPULMONAR PDF

Parte 1: Epidemiología, fisiopatología y clínica. Seguimiento neumológico de los niños con displasia broncopulmonar al alta de la Unidad de Cuidados. Epidemia de displasia broncopulmonar: incidencia y factores asociados en una cohorte de niños prematuros en Bogotá, Colombia. Juan G. Ruiz-Peláez1,2,3. Displasia Broncopulmonar. ES. eliana silva. Updated 6 September Transcript. Displasia Broncopulmonar Diagnostico general. Nesecidad de mantener.

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For each of the four samples of each case a degree of positive staining was assigned as follows: Morphometric analysis The formalin-fixed paraffin-embedded lung tissue samples were reexamined and classified into one of the three groups according to the histopathological and morphometric changes without considering the clinical data: The clinical profile of the study population is shown in Tables 23 and 4.

Displasia broncopulmonar fisiopatologia — Поиск по картинкам — [RED]

In the group “without” CLD, the length of time of oxygen therapy and the survival time mean 1. Activated Caspase 3 cleaves a variety of substrates, including DNA repair enzymes, cellular and nuclear structural proteins, endonucleases, broncopulmoonar many other cellular constituents, culminating in effective cell death 37 – Sherjon S, Smit Y. The staining was interpreted as follows: Anti-Capase 3 is a rabbit polyclonal antibody, clone 3CSP03, 1: However, the most important risk factor is the exposure to oxygen and mechanical ventilation 5.

Se compararon algunas medias de las variables cuantitativas mediante la prueba t.

There were no statistically significant differences in PTEN tissue immunoexpression between the “classic” CLD group and the group “without” CLD, compatible with data in literature indicating that “classic” CLD is more associated with inflammatory response than with the apoptosis processe Oxygen toxicity in mouse lung: The study was divided into three groups: Increased epithelial cell proliferation with chronic lung disease.

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It is important to bear in mind that we use only pathological criteria to define these three groups, without considering the clinical data. More or less the half of cases had a displaska early anemia and the independent factors associated with its appearance were the presence of a severe disease and to total volume of blood extracted.

The mechanisms involved in xe abnormal alveolar development are not yet well understood 6 – 8. The greater the number of cells expressing this protein in a particular tissue, the more likely the tissue would have a higher apoptotic index These findings may be associated with the ability of a pulmonary cell to proliferate in response to mechanical strain 3334knowing that the “classic” form was submitted to mechanical ventilation for more days than the group “without” CLD.

Enhancement and inhibition of apoptosis and cell proliferation play an important role in regulatory mechanisms involved in tissue remodeling 1. Anti-Caspase 8 is a rabbit polyclonal antibody, 1: Eficacia y costo del tratamiento con eritropoyetina.

On the other hand, the “classic” group had more time for cell differentiation, a process that is characteristic for this phase. The medical records were analyzed to collect the data related to the clinical events such as gender, gestational age, birth weight, Apgar score at the first e fifth minute, pregnancy hypertension event, gestational diabetes, chorioamnionitis, longer time with amniotic sac disruption, asphyxia, antibiotic therapy, surfactant therapy, necrotizing enterocolitis, bronchopneumonia, pulmonary hemorrhage, pulmonary hypertension, intracranial hemorrhage, sepsis, corrected age postpartum and time spent on mechanical ventilation and oxygen therapy.

Abstract Bronchopulmonary dysplasia chronic lung disease in infants constitutes a heterogeneous group of diseases with multifactorial etiology and pathogenesis.

Картинки: Displasia broncopulmonar fisiopatologia

TRADD was not submitted to morphometric analysis because most cases were negative for this protein. These mechanisms broncopulmnar to be part of the pathophysiology of BPD. X 2 4,33; gl 1; p 0, It is known to be multifactorial, with a genetic predisposition, prolonged use of oxygen at high concentrations, insufficient surfactant, exposure to mechanical ventilation leading to volutrauma, biotrauma and barotrauma and pre or postnatal infection as the main etiologic factors 8.

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Se analizaron los factores maternos, presencia de anemia cercana al nacimiento y antecedentes de gestorragias de la segunda mitad. FADD is an adaptor molecule that mediates cell apoptotic signals.

The data were analyzed using SPSS The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.

Fas is a protein that belongs to the subgroup of tumor necrosis factor receptor TNF-Rthis protein can trigger apoptosis. Recomendaciones para su tratamiento. The formalin-fixed paraffin-embedded lung tissue samples were reexamined and classified into one of the three groups according to the histopathological and morphometric changes without considering the clinical data: These findings were statistically significant and could indicate that the “new” form of the disease presents more cells susceptible to apoptosis than the group “without” CLD, consistent with the decreased alveolarization observed in this phase of the disease Figure and Table 5 6.

Decreased alveolarization in baboon survivors with bronchopulmonary dysplasia.

Apoptosis was involved in the pathophysiological of CLD. The process of lung tissue lesion appears to be related to an imbalance between inflammatory response, apoptosis and cell proliferation that affects alveolar formation and pulmonary vascular growth 2 – 4.