济宁医学院病理学课件病毒性肝炎.pptVIP

坏死后性硬化：Thenodulesseenherearelargerthan3mmand,大结节硬化组织学和临床相关性差门脉高压portalhypertension肝功能衰竭hepaticfailure.Clinicalfeature门脉高压PortalhypertensionPortalhypertensionwillleadto:①脾肿大脾功能亢进②胃肠道淤血消化不良，腹泻③腹水有效血容量丧失大量白蛋白Enlargedspleen男性，58Y，肝炎病史21年HBsAg(+),肝硬化腹水7mAscites腹水形成机制静水压增高Increaseinhydrostaticpressureinthevenulesandsinusoids血清白蛋白低LowserumalbuminAtendencyofthekidneystoretainsodiumandwater（醛固酮和抗利尿激素）门体分流Porto-systemicshunting侧枝开放食管静脉曲张痔核hemorrhoids海蛇头caputmedusae不能解毒死于静脉曲张④侧枝循环开放内脏静脉血流经肝外的门V—腔V吻合支回流到上、下腔V门V胃冠状V食管下段-胃底V丛奇V上腔V肠系膜下V直肠V丛髂V下腔V脐旁V脐周V丛腹壁浅V上下腔V食管下段—胃底V丛曲张Thethin-walleddilatedveinsarepronetorupture,causingmassivehematemesiswhichcanbefatal.最重要上消化道大出血食管静脉曲张食管静脉曲张破裂Inflammationandhemorrhageisseenhereintheregionofarupturedvarixoftheesophagus.Consequencesof脾肿大腹水侧枝循环Caputmedusae①低蛋白血症Hypoalbuminaemia②出血③Ascites腹水④肝性脑病⑤激素灭活障碍肝功能衰竭Hepaticfailure亚急性黄色肝萎缩肝脏体积缩小，包膜皱缩，表面形成大小不等的结节结局：about50%mayrecovercompletelyotherscirrhosis临床：持续不退的GPT增高、黄疸及时治疗可停止进展—肝纤维化肝功衰竭、肾衰死亡转变成坏死后性肝硬变Clinicalfeatures食欲不振Appetiteloss疲劳乏力Feelingtired(fatigue)恶心呕吐Nauseaandvomiting浑身搔痒Itchingalloverthebody肝区痛Painovertheliver(ontherightside?oftheabdomen,underthelowerribcage)黄疸Jaundice尿颜色Urine?becomesdarkincolor(likecolaortea).粪便颜色Stools?arepaleincolorClinicalfeatures精神改变Mentaldisturbances(hepaticencephalopathy肝性脑病)易于出血Bleedingfromthenose,mouth,orrectumorbloodinthestool慢性肝损伤的终末改变不可逆弥漫分布affectstheentireliver纤维化和结节再生characterizedbyfibrosisandnodularregeneration特征：纤维化和结节再生肝硬化LivercirrhosisCIRRHOSISPORTAL-to-PORTAL(bridging)FIBROSISThe“normal”hexagonal“ARCHITECTURE”isreplacedbyNODULESBLINDMAN’sLIVERBl