第45讲 兼症病学(各论部分) 第3章 第1节 急性胃粘膜病变

1　概　况1.1　定义　 AGML是指机体遭到严重疾病或严重创伤而处于应激状态 ,以及胃肠接触某些药物引起胃肠粘膜急性浅表性糜烂、急性溃疡的统称 ,视为严重疾病或严重创伤的继发症 (前者 ) ,或因病服用药物所致并发症 (后者 )。1.2　概念　因致本病症的原发病及发病机制较复杂 ,故命名也不很统一。文献中有把继发于颅脑病变称为库兴氏溃疡(Cushinq Syuleer)。Speranza等根据胃肠粘膜受损程度把仅粘膜受损的称之糜烂性出血性胃炎 ,把受损深达粘膜肌层以上的叫应激性溃疡。还有的称为表浅性溃疡、急性药物性溃疡、急性胃粘膜出血等。近几年…     

第45讲兼症病学(各论部分)第1章第2节肺心病高血糖症

1概述 1.1定义由于肺心病加重时使胰岛分泌胰岛素功能受到抑制,以及机体在应激状态下血糖升高.是并发症. 1.2概况肺心病加重期发生高血糖症约13%～17%.慢性肺心病常在慢支、慢阻肺等疾病基础上逐渐形成.晚期或加重期,心肺功能失代偿,易并发多系统器官功能衰竭(MSOF).该类除心肺功能异常外,部分有肝、肾功能不全及呼吸衰竭,加重期病情危重,患者常处于高度应激状态.     

第45讲兼症病学(各论部分)第4章第1节糖尿病肾病

1　概况1 1　定义　由ＤＭ的糖代谢异常引起的一系列代谢紊乱造成的肾小球硬化 ,临床上称为ＤＮ。糖尿病患者以肾小球高滤过开始 ,经微清蛋白尿和蛋白尿至终末期肾病 (ＥＳＲＤ)需数年至数10年。ＤＮ与ＤＭ有明确的因果关系 ,又因ＤＭ病情扩展而导致肾单位损伤 ,最终发生肾小球硬化称为糖尿病性肾病 ,为继发症。ＤＭ是泌尿系感染的高危因素 ,当肾脏感染后加速加重糖尿病对肾脏的损害。老病加新病 ,此时可视为并发症。糖尿病肾病病变包括感染性病变和血管性病变两大类 ,①感染性病变包括肾盂肾炎如肾乳头坏死。②肾小球硬化和肾动脉硬化 ,结…     

第45讲兼症病学(各论部分)第2章第2节心肌梗死后综合征

1 概况 1.1 定义 PMIS是指急性心肌梗死后数日至数周出现以心包炎、胸膜炎、肺炎等非特异性炎症为特征的一种综合征,并有反复发生的倾向,是继发症.     

第45讲 兼症病学(各论部分)

1 概述1．1 定义因COPD所致的PAH,是指平均肺动脉压(PAP)＞20mmHg(1mmHg=0.133kPa)。其发生、发展主要以继发症的模式演变,是发展成肺心病的重要环节。1．2 概况目前对PAH of COPD的发病率尚不清楚,估计至少占重症支气管炎、肺气肿的50%,占COPD尸检的10%~40%,占住院心衰的16%~38%。由此看来,COPD继发心血管病变比较常见。但对某一具体慢性肺疾病的发病率不清。可以肯定COPD占80%左右,少数为肺结核、矽肺、支气管扩张、肺纤维化等。PAH对ODPD的发生、发展、预后有显著影响。2 兼症模式     

第45讲 兼症病学(各论部分)

1 概 述1.1 定义 严重创伤造成的急性肺损伤后出现以肺部炎症和通透性增加而引起的,急性呼吸窘迫和难以纠正的进行性的低氧血症。其综合证不是一个独立的疾病,病因、诱因繁杂,但其发病机制、病理变化和临床过程基本相似,是复杂的兼症。1.2 概况 ARDS是目前认为较为科学的名称。该病从医学史上讲其名称很多,如:Me Nelesonn综合征、外伤后肺、输血后肺、休克肺、充血性肺不张、湿肺综合征、肺透明膜、急性肺微循环障碍性呼吸衰竭、特发性呼吸困难综合征、反射性肺不张、广泛性肺塌陷、进行性呼吸窘迫征、出血性肺综合征、进行性肺实变、肺微血管栓塞、呼吸机肺、体外循环肺、泵肺、移植肺、氧中毒肺、灌注后肺、创伤性湿肺、肺脂肪栓塞、苍白肺综合征等60多个名称。1967年Ashbaugh建议用成人呼吸窘迫综合征后被广     

第45讲 兼症病学(各论部分)

1 概述1．1 定义一般所说的肺性脑病(肺脑)是指在原发性肺功能不全的基础上出现呼吸减弱或节律不齐,通气和(或)换气障碍产生低血氧和高碳酸血症所引起的脑症状而言,即所谓的狭义肺脑。肺脑是复杂的兼症,是一综合征。1．2 概况肺脑是肺心病的严重并发症,是肺心病死亡的主要原因之一,在肺心病急性加重期其发生率15%~20%,而病死率近50%,其发病主要诱因是感染,特别是急性肺部感染。当肺心病患者出现神经精神症状时,必须仔细逐一排除脑动脉硬化、单纯性碱中毒、低渗、低血镁、低渗性所引起的脑症状,以及感染中毒性脑病、神经官能症等,才能确诊为肺脑。2 兼症模式     

Acute Respiratory Distress Syndrome (ARDS) after trauma: Improving incidence,but increasing mortality

PurposeAcute Respiratory Distress Syndrome (ARDS) is an infrequent, yet morbid inflammatory complication in injury victims. With the current project we sought to estimate trends in incidence, determine outcomes, and identify risk factors for ARDS and related mortality.Materials & methodsThe national Trauma Quality Improvement Program dataset (2010–2014) was queried. Demographics, injury characteristics and outcomes were compared between patients who developed ARDS and those who did not. Logistic regression models were fitted for the development of ARDS and mortality respectively, adjusting for relevant confounders.ResultsIn the studied 808,195 TQIP patients, incidence of ARDS decreased over the study years (3–1.1%, p < 0.001), but related mortality increased (18.–21%, p = 0.001). ARDS patients spent an additional 14.7 ± 10.3 days in the hospital, 9.7 ± 7.9 in the ICU, and 6.6 ± 9.4 on mechanical ventilation (all p < 0.001). Older age, male gender, African American race increased risk for ARDS. Age, male gender, lower GCS and higher ISS also increased mortality risk among ARDS patients. Several pre-existing comorbidities including chronic alcohol use, diabetes, smoking, and respiratory disease also increased risk.ConclusionAlthough the incidence of ARDS after trauma appears to be declining, mortality is on the rise.     

Intrinsic positive end-expiratory pressure in Acute Respiratory Distress Syndrome (ARDS) Network subjects

OBJECTIVE: We tested the hypothesis that subjects randomized to the 6 mL/kg predicted body weight tidal volume study group of the National Institutes of Health Acute Respiratory Distress Syndrome (ARDS) Network study had higher levels of intrinsic positive end-expiratory pressure (PEEP) than subjects randomized to the 12 mL/kg predicted body weight tidal volume study group. DESIGN: Secondary analysis of a subgroup from a randomized controlled trial. SETTING: Hospitals located in San Francisco, CA, and Seattle, WA. PATIENTS: Eighty-four patients enrolled in the ARDS Network tidal volume trial in San Francisco, CA, and Seattle, WA, with records of measurement of intrinsic PEEP. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Intrinsic PEEP was assessed a median of six times over the first 48 hrs of ARDS Network protocol ventilation in study subjects, with no significant difference in number of measurements between subjects randomized to the tidal volume protocol of 6 mL/kg compared with 12 mL/kg. We found that intrinsic PEEP was higher among subjects randomized to the 6 mL/kg protocol, with a median intrinsic PEEP of 1.3 cm H2O (interquartile range, 0-3.1 cm H2O), compared with a median intrinsic PEEP of 0.5 cm H2O (interquartile range, 0-1.5 cm H2O) among subjects randomized to 12 mL/kg (p = .029). There was no difference in total PEEP between the study groups. CONCLUSIONS: In a subgroup of ARDS Network subjects, intrinsic PEEP was statistically significantly higher in subjects randomized to the 6 mL/kg protocol than those in the 12 mL/kg study group. The amount of intrinsic PEEP was very low in both study groups, and difference of median intrinsic PEEP between the groups was <1 cm H2O. It is unlikely that the difference in intrinsic PEEP between the study groups was clinically important in the ARDS Network study of low tidal volume ventilation.     

胰岛素在急性呼吸窘迫综合症中的临床应用

目的:观察胰岛素在急性呼吸窘迫综合症中的抗炎作用,并探讨其机制.方法:将78名急性呼吸窘迫综合症的患者随机分成胰岛素治疗组(A组)和对照组(B组),对A组患者给予呼吸机辅助等常规治疗的同时持续性静脉输注胰岛素.使其血糖维持在4.0～8.0mmol/L;对B组患者常规使用呼吸机辅助及抗生素治疗,分别于入院当时(0 h)、入院后24 h、48 h、72 h留取外周静脉血标本,用放射免疫法测定血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-4(IL-4)浓度.结果:A组和B组TNF-α、IL-6浓度逐渐下降,IL-4浓度逐渐上升;与对照组比较有统计学意义.结论:胰岛素可降低促炎细胞因子浓度,同时升高抗炎细胞因子浓度,从而恢复细胞因子稳态.