O manejo da cetoacidose em pacientes com Diabetes Mellitus : subsídios para a prática clínica de enfermagem

A cetoacidose diabética é uma condição aguda e grave que se desenvolve predominantemente em pacientes com Diabetes mellitus do tipo 1 e é induzida pela deficiência relativa ou absoluta de insulina. Ocorre comumente em associação a situações de estresse, que elevam os níveis dos hormônios contra-reguladores e constitui importante emergência clínica, que requer intervenções imediatas e efetivas. Assim, pretende-se, por meio deste artigo, com base na fisiopatologia e nas manifestações clínicas, fornecer subsídios para a prática clínica de enfermagem no manejo da cetoacidose diabética.

Essstörungen bei Adipositas und Diabetes mellitus [Eating disorders associated with obesity and diabetes].

Binge eating disorder is one of the most frequent comorbid mental disorders associated with overweight and obesity. Binge eating disorder patients often suffer from other mental disorders and longitudinal studies indicate a continuous weight gain during the long-term course. As in other eating disorders gender is a risk factor, but the proportion of male binge eating disorder patients is surprisingly high.In young women with type 1 diabetes the prevalence of subclinical types of bulimia nervosa is increased. In addition, insulin purging as a characteristic compensatory behavior in young diabetic women poses a considerable problem. In patients with type 1 diabetes, disturbed eating and eating disorders are characterized by insufficient metabolic control and early development of late diabetic sequelae. Patients with type 2 diabetes are often overweight or obese. Binge eating disorder does not occur more frequently in patients with type 2 diabetes compared to healthy persons. However, the comorbidity of binge eating disorder and diabetes type 2 is associated with weight gain and insulin resistance. Especially in young diabetic patients a screening procedure for disturbed eating or eating disorders seems to be necessary. Comorbid patients should be offered psychotherapy.

Representações sociais do pé diabético para pessoas com diabetes mellitus tipo 2

Trata-se de uma pesquisa qualitativa que objetivou compreender as representações sociais do pé diabético para pessoas com diabetes mellitus tipo 2. Foram realizadas entrevistas semi-estruturadas, com dez pessoas com diabetes mellitus que participavam de um grupo de convivência. Da análise de conteúdo emergiram duas categorias: a doença do pé com alterações percebidas e ameaças presentes e; o cuidado com os pés, com o cuidado como preocupação com o futuro e não cuidado como sentimento de culpa. Os resultados mostraram que movidos pelas representações de alterações e ameaças os sujeitos buscam no cuidado uma esperança de não desenvolver a doença do pé ou controlar a situação. Quando o não-cuidado ocorre, surge o sentimento de culpa por terem conhecimentos e não se cuidarem. As representações sociais contribuíram na busca da compreensão do modo como os sujeitos com diabetes mellitus constroem saberes que expressam sua identidade e guiam seus comportamentos, especialmente vinculado ao pé diabético.

A relação entre polifarmácia, complicações crônicas e depressão em portadores de Diabetes Mellitus Tipo 2

Os objetivos deste estudo foram: caracterizar a polifarmácia entre portadores de Diabetes Mellitus tipo2(DM2); e correlacionar polifarmácia e número de complicações do DM2 com indicadores de depressão (Inventário de Depressão de Beck[IDB] e cortisol urinário[CORT]). A amostra foi composta por 40 pacientes da Liga de Diabetes do HCFM-USP, avaliados quanto aos indicadores de depressão (CORT e IDB) e quanto à prática de polifarmácia e número de complicações do DM2. Os resultados mostraram que os medicamentos utilizados foram: antidiabéticos orais, insulinas, anti-hipertensivos, diuréticos, anti-lipêmicos e trombolíticos. No grupo estudado, 75% fizeram uso diário de 5 a 8 medicamentos, e 12,5% de 8 medicamentos/dia ou mais; todos fizeram no mínimo 3 tomadas diárias, 60% tinham entre 1 e 3 complicações do DM2, e 22,5% tinham 3 ou mais. A correlação entre os indicadores de depressão(IDB e CORT), o número de medicamentos e o número de complicações do DM2 não foi estatisticamente significante. No entanto, houve correlação positiva entre CORT e número de tomadas diárias de medicamentos (Spearman,r=0.319, p=0.019).

Validação de intervenções de enfermagem em pessoas com diabetes mellitus

Estudo descritivo e exploratório que objetivou validar as intervenções de enfermagem propostas pela Nursing Interventions Classification para os diagnósticos de enfermagem: Integridade da pele prejudicada, Conhecimento deficiente e Controle ineficaz do regime terapêutico predominantes em pessoas com diabetes. Participaram 21 enfermeiros especialistas em diabetes mellitus no Brasil, em 2007. As intervenções de enfermagem que obtiveram a maior média ponderada foram cuidado com lesões: drenagem fechada, precauções circulatórias para o diagnóstico de enfermagem Integridade da pele prejudicada, ensino: processo de doença, ensino: medicação prescrita para o Conhecimento deficiente e ensino: processo de doença e ensino: dieta prescrita para Controle ineficaz do regime terapêutico. Dentre as 1005 atividades de enfermagem, 51% foram validadas como muitíssimo características pelos especialistas. Acredita-se que outros estudos devam ser conduzidos para ampliar a validação das intervenções de enfermagem em pessoas com diabetes mellitus no Brasil, buscando evidências científicas para o cuidado dessa clientela.

No evidence for a causal link between uric acid and type 2 diabetes: a Mendelian randomisation approach.

AIMS/HYPOTHESIS: Epidemiological and experimental evidence suggests that uric acid has a role in the aetiology of type 2 diabetes. Using a Mendelian randomisation approach, we investigated whether there is evidence for a causal role of serum uric acid for development of type 2 diabetes. METHODS: We examined the associations of serum-uric-acid-raising alleles of eight common variants recently identified in genome-wide association studies and summarised this in a genetic score with type 2 diabetes in case-control studies including 7,504 diabetes patients and 8,560 non-diabetic controls. We compared the observed effect size to that expected based on: (1) the association between the genetic score and uric acid levels in non-diabetic controls; and (2) the meta-analysed uric acid level to diabetes association. RESULTS: The genetic score showed a linear association with uric acid levels, with a difference of 12.2 μmol/l (95% CI 9.3, 15.1) by score tertile. No significant associations were observed between the genetic score and potential confounders. No association was observed between the genetic score and type 2 diabetes with an OR of 0.99 (95% CI 0.94, 1.04) per score tertile, significantly different (p̴1;=̴1;0.046) from that expected (1.04 [95% CI 1.03, 1.05]) based on the observed uric acid difference by score tertile and the uric acid to diabetes association of 1.21 (95% CI 1.14, 1.29) per 60 μmol/l. CONCLUSIONS/INTERPRETATION: Our results do not support a causal role of serum uric acid for the development of type 2 diabetes and limit the expectation that uric-acid-lowering drugs will be effective in the prevention of type 2 diabetes.

Conhecimento de mulheres com diabetes mellitus sobre cuidados pré-concepcionais e riscos materno-fetais

Objetivou-se descrever o perfil reprodutivo de mulheres com diabetes mellitus (DM) e verificar o nível de conhecimento destas quanto aos riscos maternos e fetais e os cuidados pré-concepcionais. Estudo exploratório, que contou com a participação de 106 mulheres, realizado no Centro Integrado de Hipertensão e Diabetes, de março a julho de 2009. As variáveis reprodutivas foram: número de gestações, partos e abortos e planejamento da gravidez. Os dados foram coletados por meio de entrevista que seguiu um formulário pré-estabelecido. O perfil reprodutivo de mulheres com DM mostrou-se permeado de riscos e repercussões reprodutivas negativas à saúde materna e fetal. Das 106 (100%) mulheres estudadas, 44 (41,5%) apresentaram conhecimento moderado sobre os cuidados pré-concepcionais e 58 (54,7%) conhecimento limitado sobre os riscos maternos e fetais. Faz-se necessário oferecer informações às mulheres a fim de promover o conhecimento sobre os riscos maternos e fetais e os cuidados pré-concepcionais.

Glucagon-like peptide-1 protects beta-cells against apoptosis by increasing the activity of an IGF-2/IGF-1 receptor autocrine loop.

OBJECTIVE: The gluco-incretin hormones glucagon-like peptide (GLP)-1 and gastric inhibitory peptide (GIP) protect beta-cells against cytokine-induced apoptosis. Their action is initiated by binding to specific receptors that activate the cAMP signaling pathway, but the downstream events are not fully elucidated. Here we searched for mechanisms that may underlie this protective effect. RESEARCH DESIGN AND METHODS: We performed comparative transcriptomic analysis of islets from control and GipR(-/-);Glp-1-R(-/-) mice, which have increased sensitivity to cytokine-induced apoptosis. We found that IGF-1 receptor expression was markedly reduced in the mutant islets. Because the IGF-1 receptor signaling pathway is known for its antiapoptotic effect, we explored the relationship between gluco-incretin action, IGF-1 receptor expression and signaling, and apoptosis. RESULTS: We found that GLP-1 robustly stimulated IGF-1 receptor expression and Akt phosphorylation and that increased Akt phosphorylation was dependent on IGF-1 but not insulin receptor expression. We demonstrated that GLP-1-induced Akt phosphorylation required active secretion, indicating the presence of an autocrine activation mechanism; we showed that activation of IGF-1 receptor signaling was dependent on the secretion of IGF-2. We demonstrated, both in MIN6 cell line and primary beta-cells, that reducing IGF-1 receptor or IGF-2 expression or neutralizing secreted IGF-2 suppressed GLP-1-induced protection against apoptosis. CONCLUSIONS: An IGF-2/IGF-1 receptor autocrine loop operates in beta-cells. GLP-1 increases its activity by augmenting IGF-1 receptor expression and by stimulating secretion; this mechanism is required for GLP-1-induced protection against apoptosis. These findings may lead to novel ways of preventing beta-cell loss in the pathogenesis of diabetes.

Alcohol consumption and incidence of type 2 diabetes. Results from the CoLaus study.

BACKGROUND AND AIMS: Moderate alcohol consumption has been shown to decrease the risk of type 2 diabetes (T2DM), but whether this association is also valid for impaired fasting glucose (IFG) is less well known. We aimed at assessing the impact of alcohol consumption and of type of alcoholic beverage on the incidence of T2DM and T2DM + IFG. METHODS AND RESULTS: As many as 4765 participants (2613 women, mean age 51.7 ± 10.5 years) without T2DM at baseline and followed for an average of 5.5 years. The association between alcohol consumption, type of alcoholic beverage and outcomes was assessed after adjustment for a validated T2DM risk score. During follow-up 284 participants developed T2DM and 643 developed IFG. On bivariate analysis, alcohol consumption was positively associated with the risk of developing T2DM or T2DM + IFG. Moderate (14-27 units/week) alcohol consumption tended to be associated with a lower risk of T2DM, but no protective effect was found for T2DM + IFG. Multivariable-adjusted odds ratio (OR) and (95% confidence interval) for T2DM: 0.89 (0.65-1.22), 0.66 (0.42-1.03) and 1.63 (0.93-2.84) for 1-13, 14-27 and 28 + units/week, respectively (p for quadratic trend < 0.005). For T2DM + IFG, the corresponding ORs were 1.09 (0.90-1.32), 1.33 (1.02-1.74) and 1.54 (0.99-2.39), respectively, p for trend = 0.03. No specific effect of alcoholic beverage (wine, beer or spirits) was found for T2DM or for T2DM + IFG. CONCLUSION: Moderate alcohol consumption is associated with a reduced risk of developing T2DM, but not of developing T2DM + IFG. No specific effect of type of alcoholic beverage was found.

Therapy modifications in response to poorly controlled hypertension, dyslipidemia, and diabetes mellitus.

BACKGROUND: Poorly controlled cardiovascular risk factors are common. Evaluating whether physicians respond appropriately to poor risk factor control in patients may better reflect quality of care than measuring proportions of patients whose conditions are controlled. OBJECTIVES: To evaluate therapy modifications in response to poor control of hypertension, dyslipidemia, or diabetes in a large clinical population. DESIGN: Retrospective cohort study within an 18-month period in 2002 to 2003. SETTING: Kaiser Permanente of Northern California. PATIENTS: 253,238 adult members with poor control of 1 or more of these conditions. MEASUREMENTS: The authors assessed the proportion of patients with poor control who experienced a change in pharmacotherapy within 6 months, and they defined "appropriate care" as a therapy modification or return to control without therapy modification within 6 months. RESULTS: A total of 64% of patients experienced modifications in therapy for poorly controlled systolic blood pressure, 71% for poorly controlled diastolic blood pressure, 56% for poorly controlled low-density lipoprotein cholesterol level, and 66% for poorly controlled hemoglobin A1c level. Most frequent modifications were increases in number of drug classes (from 70% to 84%) and increased dosage (from 15% to 40%). An additional 7% to 11% of those with poorly controlled blood pressure, but only 3% to 4% of those with elevated low-density lipoprotein cholesterol level or hemoglobin A1c level, returned to control without therapy modification. Patients with more than 1 of the 3 conditions, higher baseline values, and target organ damage were more likely to receive "appropriate care." LIMITATIONS: Patient preferences and suboptimal adherence to therapy were not measured and may explain some failures to act. CONCLUSIONS: As an additional measure of the quality of care, measuring therapy modifications in response to poor control in a large population is feasible. Many patients with poorly controlled hypertension, dyslipidemia, or diabetes had their therapy modified and, thus, seemed to receive clinically "appropriate care" with this new quality measure.

Construction and validation of nursing diagnoses for individuals with diabetes in specialized care

OBJECTIVE To construct statements of nursing diagnoses related to nursing practice for individuals with diabetes in Specialized Care, on the basis of the Database of Nursing Practice Terms related to diabetes, in the International Classification for Nursing Practice (ICNP&#174;) and in the Theory of Basic Human Needs and to validate them with specialist nurses in the area. METHOD Methodological research, structured into sequential stages of construction, cross-mapping, validation and categorization of nursing diagnoses. RESULTS A list was indicated of 115 statements of diagnostic, including positive, negative and improvement statements; 59 nursing diagnoses present in and 56 nursing diagnoses absent from the ICNP&#174; Version 2011. 66 diagnoses with CVI ≥ 0.50 were validated, being categorized on the basis of human needs. CONCLUSION It was observed that the use of the ICNP&#174; 2011 favored the specifications of the concepts of professional practice in care with individuals with diabetes.

Interferon-gamma impacts at multiple points during the progression of autoimmune diabetes.

The role of interferon-gamma in autoimmune diabetes was assessed by breeding a null mutation of the interferon-gamma receptor alpha chain into the nonobese diabetic mouse strain, as well as into a simplified T cell receptor transgenic model of diabetes. In contrast to a previous report on abrogation of the interferon-gamma gene, mutation of the gene encoding its receptor led to drastic effects on disease in both mouse lines. Nonobese diabetic mice showed a marked inhibition of insulitis-both the kinetics and penetrance-and no signs of diabetes; the transgenic model exhibited near-normal insulitis, but this never evolved into diabetes, either spontaneously or after experimental provocation. This failure could not be explained by perturbations in the ratio of T helper cell phenotypes; rather, it reflected a defect in antigen-presenting cells or in the islet beta cell targets.