肝性脑病演示教学.pptVIP

Hepatic Encephalopathy肝性脑病; 男性，56岁。因“发现HBsAg阳性25年，反复乏力、纳差、腹胀3年，加重伴神志淡漠2天”入院。 患者25年前起，体检时发现“乙肝两对半：HBsAg(+)，HBeAg(+)，HBcAg(+)”，当时肝功能正常，患者无不适，未作进一步诊治。3年前起，无明显诱因反复出现乏力、纳差、腹胀等不适，在外院以“乙肝肝硬化失代偿期”给予诊治（具体不详），病情一度好转后患者自行停药，病情反复，患者自服中成药治疗。3天前起，因酗酒并进食大量蛋白质后，患者出现腹胀加剧，伴有睡眠日夜颠倒，神志淡漠，无昏迷，为作进一步的诊治收入我院。起病以来，无呕血或排黑便，无身目黄染，无皮肤黏膜出血，无肝区疼痛不适，无消瘦，两便正常。 ; 既往有酗酒史20年，200g/天。余既往史，个人史，家族史不详或无特殊。 入院时体检：体温36.8℃，脉搏80次/分，呼吸16次/分，血压110/70mmHg。神志淡漠，计算力、理解力下降，扑翼样震颤阳性。全身皮肤巩膜无黄染，浅表淋巴结未触及肿大。心肺正常。腹软，呈蛙状腹，无压痛或反跳痛，无包块，肝脾肋下未触及，墨菲氏征（－）, 双肾区叩痛（－），移动性浊音（+），肠鸣音正常。双下肢无浮肿。 ;问题： 1 本病例完整诊断是什么? 2 进一步明确诊断还需做那些检查？ 3 如何治疗？;;Definition (2);Hepatic encephalopathy is a common complication in cirrhotic;Incidence/prevalence;Etiology ;HE---common precipitating factors;Clinical manifestation;Clinical manifestation;Clinical manifestation;Clinical manifestation;Clinical stages of HE;Clinical stages of HE;Laboratory and other tests;Diagnosis  differential diagnosis;Programme of diagnosis;Clues for the diagnosis of HE;Supportive proof for the Diagnosis;Diagnosis;Differential diagnosis;Pathogenesis;Postulated factors/mechanisms: Ammonnia neurotoxicity Synergistic neurotoxins Excitatory inhibitory neurotransmitters plasma amino acid imbalance hypothesis γ-Aminobutyric acid hypothesis;Ammonia neurotoxicity;Ammonia neurotoxicity;Treatment; Provision of Supportive Care Adequate supportive care is critical during all stages of HE and may involve other professionals in the provision of patient care. ; Reduction of Nitrogenous Load From the Gut Measures to reduce the nitrogenous load from the gut should be implemented.;TREATMENT OPTIONS --Treatment of HE is based on several, non–mutually exclusive options.;Patients with HE should avoid prolonged periods of dietary protein restriction and receive the maximum tolerable protein intake, aiming at 1.2 g of protein/kg/day (range 1–1.5).;Reduction in the Nitrogenous Load Arising From the Gut;Detoxification of toxic substances ;Drugs That Affect Neurotransmission Flumazenil a