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类型内科学-肝硬化-ppt课件.ppt

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    内科学 肝硬化 ppt 课件
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    1、ppt课件1肝硬化肝硬化 Cirrhosis ppt课件2 肝硬化是一种以肝组织弥漫性纤维化、假肝硬化是一种以肝组织弥漫性纤维化、假小叶和再生结节形成为特征的慢性肝病。是小叶和再生结节形成为特征的慢性肝病。是许多肝脏疾病晚期的共同病变。临床上有多许多肝脏疾病晚期的共同病变。临床上有多系统受累,以肝功能减损、门脉高压两大症系统受累,以肝功能减损、门脉高压两大症侯群为主要表现,晚期常出现上消化道出血,侯群为主要表现,晚期常出现上消化道出血,肝性脑病,继发感染等严重的并发症。肝性脑病,继发感染等严重的并发症。Cirrhosis is a pathological diagnosis.It is ch

    2、aracterized by widespread fibrosis with nodular regeneration.Its presence implies previous or continuing hepatic cell damage.ppt课件3ppt课件4ppt课件5*病病 因因 AetiologyAetiologyppt课件6l引起肝硬化的病因较多,同一病因可发展为引起肝硬化的病因较多,同一病因可发展为不同病理类型的肝硬化,而同一病理类型的不同病理类型的肝硬化,而同一病理类型的肝硬化亦可由不同病因引起。肝硬化亦可由不同病因引起。l常见的病因包括:常见的病因包括:病毒性肝炎病

    3、毒性肝炎(viral hepatitis)viral hepatitis)酒精性肝炎酒精性肝炎(alcoholic hepatitis)alcoholic hepatitis)胆汁郁积胆汁郁积(cholestasischolestasis)严重心力衰竭(严重心力衰竭(severe heart failure)severe heart failure)肝豆状核变性肝豆状核变性(hepatolenticular hepatolenticular disease)disease)-抗胰蛋白酶缺乏症(抗胰蛋白酶缺乏症(-antitrypsin antitrypsin deficiency)defici

    4、ency)。病病 因因 AetiologyAetiologyppt课件7一一、病毒性肝炎、病毒性肝炎(viral hepatitis)viral hepatitis)(肝炎后肝硬(肝炎后肝硬化)化)我国肝炎发病率达我国肝炎发病率达137/10万以上,仅乙肝病万以上,仅乙肝病毒携带者就有毒携带者就有1亿亿2千万人口。成人期感染千万人口。成人期感染HBV,10%左右演变为慢性肝炎,约左右演变为慢性肝炎,约3%发展为肝硬化。发展为肝硬化。丙肝的发病率远远低于乙肝,但感染丙肝的发病率远远低于乙肝,但感染HCV后约后约833%可演变为慢性肝炎,最后导致肝硬化。可演变为慢性肝炎,最后导致肝硬化。在我国可能

    5、演变为肝硬化的主要是乙肝,其在我国可能演变为肝硬化的主要是乙肝,其次是丙肝,或乙肝合并丁肝感染。而甲肝和戊肝次是丙肝,或乙肝合并丁肝感染。而甲肝和戊肝一般不发展为慢性肝炎和肝硬化。一般不发展为慢性肝炎和肝硬化。HBV感染感染免疫异常免疫异常肝细胞炎症、坏死、再生肝细胞炎症、坏死、再生纤维化纤维化假小叶假小叶病病 因因 AetiologyAetiologyppt课件8病病 因因 AetiologyAetiologyppt课件9lMan who drink over 80g of alcohol per day,or women who drink over 40g per day have a

    6、significant risk of developing cirrhosis.However,cirrhosis is not inevitable.Only 10-20%of chronic alcoholics develop cirrhosis even though they drink the same amount of alcohol over the same period as other alcoholics.ppt课件10 Risk factors for developing cirrhosis include genetics,gender(women devel

    7、op alcoholic hepatitis and cirrhosis younger,and after less intake,than men),nutrition(alcohol is better tolerated under optimal dietary conditions),and a synergistic effect with hepatotropic viruses*.ppt课件11病病 因因 AetiologyAetiologyppt课件12lPrimary biliary cirrhosis(PBC)is a chronic cholestatic liver

    8、 disease involving the interlobular and septal bile ducts.This disorder is characterized by progressive inflammatory destruction of these bile ducts with the development of portal and periportal inflammation,subsequent fibrosis,and eventually cirrhosis.Portal hypertension and the consequences of end

    9、-stage liver disease can lead to early death unless effective therapy or liver transplantation intervenes.ppt课件13四、循环障碍四、循环障碍(severe heart failure)severe heart failure)病病 因因 AetiologyAetiologyppt课件14五、工业毒物或药物五、工业毒物或药物病病 因因 AetiologyAetiologyppt课件15病病 因因 AetiologyAetiologyppt课件16七、营养障碍七、营养障碍病病 因因 Aet

    10、iologyAetiologyppt课件17病病 因因 AetiologyAetiology目目 录录ppt课件18 ppt课件19发病机理发病机理 Pathogenesis1234ppt课件20发病机理发病机理pathogenesisppt课件21发病机理发病机理 Pathogenesisppt课件22ppt课件23病病 理理Pathologyppt课件24 *ppt课件25ppt课件26病病 理理Pathologyppt课件27 1.1.小结节性肝硬化:最常见。结节小结节性肝硬化:最常见。结节D1cmD1cmMicronodular(portal cirrhosis)is characte

    11、rised by regular thick fibrotic bands joining the portal tracts to hepatic veins,and with small regenerative nodules.2.2.大结节性肝硬化:结节大结节性肝硬化:结节D1-3cmD1-3cmMacronodular(post-necrotic cirrhosis)is less common and is chracterised by course,irregular bands of fibrosis and loss of normal architecture and l

    12、arge regenerative nodules.It is believed usually to follow viral hepatitis with widespread necrosis.ppt课件28一、假小叶形成的病理基础 1肝细胞持续不断的坏死,肝小叶纤维支架塌陷破坏。2 再生的肝细胞不沿原支架排列,形成不规则的再生结节。3 汇管区、肝包膜下大量纤维结缔组织增生,形成纤维间隔,并向小叶内延伸,将残存的肝小叶重新分割,改建成假小叶,纤维收缩,肝脏变硬变小。ppt课件29假小叶的结构特征:假小叶的结构特征:由几个不完整的肝由几个不完整的肝小叶构成,内含多个中小叶构成,内含多个中央

    13、静脉或无中央静脉。央静脉或无中央静脉。肝细胞排列和血窦分布肝细胞排列和血窦分布不规则,假小叶内肝细不规则,假小叶内肝细胞变性坏死,脂肪浸润胞变性坏死,脂肪浸润,甚至坏死再生,汇管,甚至坏死再生,汇管区纤维结缔组织增生增区纤维结缔组织增生增宽,伴有炎症细胞浸润宽,伴有炎症细胞浸润及假胆管形成。及假胆管形成。病病 理理Pathologyppt课件30ppt课件31病病 理理Pathologyppt课件32 ppt课件33临床表现临床表现 Clinical presentationppt课件34lClinical presentationlThere may be no abnormal clini

    14、cal or biochemical features of liver disease.Later,features of hepatocellular failure,portal hypertension,or both may appear.ppt课件35临床表现临床表现 Clinical presentationppt课件36 临床表现临床表现 Clinical presentationppt课件37临床表现临床表现 Clinical presentationppt课件38 黄疸黄疸 约约505060%60%的病人出现黄疸,一般轻中的病人出现黄疸,一般轻中度,与肝细胞损害程度度,与肝

    15、细胞损害程度有关,黄疸进行性加重有关,黄疸进行性加重说明有肝细胞持续坏死,说明有肝细胞持续坏死,或有胆汁郁积,往往提或有胆汁郁积,往往提示预后不良。示预后不良。临床表现临床表现 Clinical presentationppt课件39临床表现临床表现 Clinical presentationppt课件40临床表现临床表现 Clinical presentation肝肝功功能能减减退退雌激素增多雌激素增多醛固酮增多醛固酮增多抗利尿激素增多抗利尿激素增多垂体性腺轴垂体性腺轴垂体肾上腺轴垂体肾上腺轴雄激素减少雄激素减少糖皮质激素减少糖皮质激素减少蜘蛛痣、肝掌蜘蛛痣、肝掌男男 性欲降低性欲降低,睾丸

    16、萎缩睾丸萎缩女女 月经失调月经失调,闭经闭经,不孕不孕少尿少尿,浮肿浮肿,腹水腹水水吸收增加水吸收增加色素沉着色素沉着钠重吸收增加钠重吸收增加ppt课件41 男性乳房发育男性乳房发育 肝掌肝掌(liver palms)临床表现临床表现 Clinical presentationppt课件42蜘蛛痣(spider nevi)蜘蛛痣沿上腔静脉引流的区域分布,乳头以上胸、颈、脸、上肢。由小动脉为中心,向四周呈辐射状的毛细血管组成,形似蜘蛛。蜘蛛痣的大小,多少以及肝掌与肝功有关,随着肝功改善,雌激素水平下降而减少、减轻。临床表现临床表现 Clinical presentationppt课件43临床表现

    17、临床表现Clinical presentationppt课件441、ppt课件45临床表现临床表现 Clinical presentationppt课件46lPortal vascular resistance is increased due to collagen deposition and fibrosis seen in liver cirrhosis and hence formation of varices in the gastro-oesophageal junction.In addition,sodium retention and vasoactive substan

    18、ces such as nitric oxide will increase plasma volume and splanchnic vasodilatation,respectively,and thus maintain portal hypertension.ppt课件471门门V胃冠状胃冠状V 胃底、胃底、食食管下段管下段V 奇奇V 上腔上腔V 常因食管粘膜炎症,进食粗糙,常因食管粘膜炎症,进食粗糙,刺激性食物,或腹内压突然增高而破刺激性食物,或腹内压突然增高而破裂出血,发生呕血,黑便,甚至休克裂出血,发生呕血,黑便,甚至休克等症状。等症状。2 门门V 附脐附脐V 脐周脐周V 丛丛

    19、胸腹壁胸腹壁V胸廓胸廓V上腔上腔V 腹壁浅腹壁浅V腹壁下腹壁下V下腔下腔V3 门门V 肠系膜下肠系膜下V 直肠上直肠上V 直肠直肠V丛丛 直肠中下直肠中下V 下腔下腔V*临床表现临床表现 Clinical presentationppt课件48ppt课件49临床表现临床表现 Clinical presentationppt课件50临床表现临床表现ppt课件51lSodium and water retention occur due to renin-angiotensin release secondary to arterial vasodilatation,caused by vasoa

    20、ctive substances such as nitric oxide.Portal hypertension per se causes fluid to accumulate in the peritoneal cavity due to increased hydrostatic pressure,hence further reduces intravascular volume and stimulates sodium and water retention via aldosterone.ppt课件52lAscites may be aggravated by low alb

    21、umin and thus a lowered oncotic pressure of the plasma as a result of reduced production by the liver.ppt课件53ppt课件54临床表现临床表现ppt课件55ppt课件56并发症并发症 Complicationsppt课件57并发症并发症 Complicationsppt课件58并发症并发症 Complications ppt课件59并发症并发症 Complicationsppt课件60并发症并发症 Complicationsppt课件61lThe renal abnormality is

    22、thought to be functional because transplanted kidneys from a donor patient with heptorenal syndrome to a recipient will result in a normal functioning kidney.However,extreme cases will cause tubular necrosis and renal damage.ppt课件62l是指严重肝病、肺血管扩张和低血氧血是指严重肝病、肺血管扩张和低血氧血症组成的三联征。症组成的三联征。l由于:肝硬化时血管活性物质增加,

    23、肺由于:肝硬化时血管活性物质增加,肺内毛细血管扩张,肺动静脉分流,造成内毛细血管扩张,肺动静脉分流,造成通气血流比例失调。通气血流比例失调。l表现:呼吸困难及低氧血症,肺血管扩表现:呼吸困难及低氧血症,肺血管扩张。张。l治疗:内科治疗无效,吸氧仅能暂改善治疗:内科治疗无效,吸氧仅能暂改善症状。症状。ppt课件63并发症并发症 Complicationsppt课件64并发症并发症 Complicationsppt课件65 ppt课件66实验及其他检查实验及其他检查 laboratory tests and investigationsppt课件67实验及其他检查实验及其他检查laboratory

    24、 tests and investigationsppt课件68lBiochemistry can be surprisingly normal but some abnormality will often be present with slightly raised transaminases and alkaline phosphatases.In severe cases,all live enzymes will be abnormal.Low sodium and albumin are also seen.lCoagulopathy is a very sensitive in

    25、dicator of liver dysfunction and is reflected in the prolonged prothrombin time.ppt课件69实验及其他检查实验及其他检查laboratory tests and investigationsppt课件70实验及其他检查实验及其他检查laboratory tests and investigationsppt课件71Ultrasound demonstrates fatty change,size,and fibrosis as well as hepatocellular carcinoma.实验及其他检查实验及

    26、其他检查laboratory tests and investigationsppt课件72实验及其他检查实验及其他检查laboratory tests and investigationsppt课件73ppt课件74诊诊 断断 DiagnosisDiagnosisppt课件75鉴别诊断鉴别诊断 Differential diagnosisppt课件76鉴别诊断鉴别诊断 Differential diagnosisppt课件77ppt课件78治治 疗疗 TreatmentTreatment*门静脉高压的手术治疗门静脉高压的手术治疗*并发症治疗并发症治疗*肝移植手术肝移植手术ppt课件79治治

    27、疗疗TreatmentTreatmentppt课件80治治 疗疗TreatmentTreatmentppt课件81治治 疗疗TreatmentTreatmentppt课件82治治 疗疗TreatmentTreatmentppt课件83Management of ascites in cirrhosislAscites is due to a combination o factors including portal hypertension,hypoalbuminaemia and secondary hyperaldosteronism.The patient is given a res

    28、tricted salt and water intake while on complete bed test.If weight loss does not occur,high coses of spironolactone and then a loop diuretic are given.Sodium-poor albumin infusions may be helpful in inducing diuresis.ppt课件84治治 疗疗TreatmentTreatmentppt课件85治治 疗疗TreatmentTreatmentppt课件86治治 疗疗TreatmentTr

    29、eatmentppt课件87治治 疗疗TreatmentTreatmentppt课件88治治 疗疗TreatmentTreatmentppt课件89治治 疗疗TreatmentTreatmentppt课件90治治 疗疗TreatmentTreatmentppt课件91治治 疗疗TreatmentTreatmentppt课件92治治 疗疗TreatmentTreatmentppt课件93lUrgent endoscopy is required,during which sclerosant is injected in or around the varices to cause inflam

    30、matory obliteration.Alternatively,elastic band ligation of the varices at endoscopy produces thrombotc obliteration.Repeat sclerotherapy or banding is usually needed to prevent further bleeds.ppt课件94治治 疗疗TreatmentTreatmentppt课件95治治 疗疗TreatmentTreatmentppt课件96治治 疗疗TreatmentTreatmentppt课件97项目项目治治 疗疗TreatmentTreatment

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