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Hepatic Cirrhosis

Hepatic Cirrhosis. Professor Wang Ji-yao Department of Internal Medicine Division of Gastroenterology, Zhongshan hospital , Fu Dan university. Cirrhosis---definition. chronic, progressed, diffuse hepatocellular injury fibrosis nodular regeneration Incidence: 17/100000/y

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Hepatic Cirrhosis

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  1. Hepatic Cirrhosis Professor Wang Ji-yao Department of Internal Medicine Division of Gastroenterology, Zhongshan hospital , Fu Dan university.

  2. Cirrhosis---definition chronic, progressed, diffusehepatocellular injuryfibrosis nodular regeneration Incidence: 17/100000/y Age: 20-50 yr.

  3. Hepatic cirrhosis Etiology Diffuse, chronic liver injury Formation of diffuse fibrous septa regenerative nodulesformation Hepato-cellular necrosis, collapse of hepatic lobules 》 Liver function Injury,Portal hypertension Complations: Upper GI Bleeding, Hepatic coma, infections, primary liver cancer, Functional renal failure

  4. Etiology of cirrhosis(I) 1.Chronic viral hepatitis (慢性病毒性肝炎): [HBV,HCV,HBV+HDV] 2. Long-term alcoholism(慢性酒精中毒) [80g/d, 10 yr.] 3. Prolonged cholestasis(长期胆汁郁积), intra-and extra-hepatic: [primary biliary cirrhosis, PBC] /[secondary biliary cirrhosis] 4. Drugs and toxins(药物和毒物) [toxic hepatitis---chronic active hepatitis---cirrhosis] 5. Nonalcoholic steatohepatitis (NASH)(非酒精性脂肪性肝炎)

  5. Etiology of cirrhosis(II) 6. Hepatic venous outflow obstruction(肝血液循环障碍) veno-occlusive disease, Budd-Chiari syndrome, constrictive pericarditis 7. Metabolic disorders(遗传代谢性疾病) hemochromatosis(血色病); Wilson‘s disease(肝豆状核变性); 8. Autoimmune hepatitis (AIH)(自身免疫性肝炎) 9. Schistosomiasis (血吸虫病) 10. Cryptogenic(隐原性) 11. Mixed: alcohol+virus , HBV+HCV, HBV+schistosomiasis

  6. Hepatic stellate cell activation

  7. Liver fibrosis accumulation of extracellular matrix in liver degradation of matrix proteins synthesis of matrix proteins Collagens type I and III constitute more than 95% of the total content of increased collagen in fibrotic liver

  8. Pathogenesis: chronic, progressed, diffuse • Hepatocyte injury leading to necrosis. • Chronic inflammation - (hepatitis). • Capillarization (肝窦毛细血管化) of the space of Disse is a key event. • Bridging fibrosis. • Regeneration of remaining hepatocytes proliferate as round nodules surrounded by fibrous septa. • Loss of vascular arrangement results in regenerating hepatocytes ineffective. • Cirrhosis may lead to liver failure, portal hypertension, or development of hepatocellular carcinoma

  9. Histopathologicclassification • micronodular uniformly small nodules (< 3 mm in diameter) and regular bands of connective tissue • macronodular nodules that vary in size (3 mm to 5 cm in diameter) • mixed macro and micronodular (incomplete septal cirrhosis) combines elements of micronodular and macronodular cirrhosis.

  10. Consequences of portal hypertension[I] 1.Splenomegaly (脾肿大) 2.Formation and open of portal-systemic collateral’s (门体侧支循环开放) --Esophageal/gastric varices(食管/胃静脉曲张)(short gastric/coronary veins) --Rectal collateral‘s(痔静脉丛)(Suphemorrhoidal/middle & inf. hemorrhoidal) --Caput medusae(水母头)(umbilical/epigastric) --abdominal wall varices (腹壁静脉曲张) --Portal system and left renal

  11. Consequences of portal hypertension[II] 3. Ascites (腹水) Theories of ascites formation • Underfilling theory (灌注不足假说） • Overflow theory (泛溢假说) • Arterial vasodilation theory (动脉扩张假说)

  12. Ascites • Sodium retention ---Renin angiotension aldosterone system(RAAS) ---sympathetic nerve system ,norepinephrine --- Intrarenal factors: Kallikrein-kinin system, Adenosine . • Water retention ---Antidiuretic hormone(ADH) ---Impaired renal synthesis of PGs (PGE2) • Renal vasoconstriction --- RAAS, AngiotensionII ---SNS ---ADH ---ET

  13. Endocrine system gynecomastia(男性乳房发育), telangiectases (毛细血管扩张症), spider nevi(蜘蛛痣), palmar erythema(肝掌) testicular atrophy(睾丸萎缩) menstrual irregularities (月经失调)

  14. Pulmonary manifestations Hepatic hydrothorax(肝性胸水) Hepatopulmonary syndrome (HPS, 肝肺综合征) HRS is characterized clinically by the triad of pulmonary vascular dilatation causing arterial hypoxemia in the setting of advanced liver disease.

  15. HRS(Hepatorenal syndrome, 肝肾综合征) Occurred in the setting of: ---chronic liver disease ---advanced hepatic failure ---portal hypertension  characterized by: ---impaired renal function ---marked abnormalities in arterial circulation ---activation of endogenous vasoactive system  Classified into 2 different types: ---Type I: Rapidly progressive ---Type II: Not rapidly progressive. Often results in mild renal insufficiency causing diuretic resistant ascites

  16. Mechanisms of HRS[II]

  17. Clinical features[I] Compensated cirrhosis (代偿期) Many people experience few symptoms at the onset of cirrhosis,symptoms are typically vague and nonspecific. ---Fatigue and loss of energy. ---Loss of appetite and nausea. ---Spider angiomas ---liver function is normal Decompensated cirrhosis (失代偿) Symptoms caused by loss of functioning liver cells --- System：fatigue, weakness, weight loss, malnutrition --- Digestive System:Loss of appetite, nausea, diarrhea.

  18. Clinical features[II] ---Tendency to hemorrhage(出血倾向) and anaemia(贫血): Due to reduced synthesis of coagulation factors (II,V,VII,IX,X), hypersplenism(脾亢), low platelet count, poor absorption，gastrointestinal bleeding. ---Hormonal abnormalities gynecomastia(男性乳房发育), telangiectases (毛细血管扩张症), spider nevi(蜘蛛痣), palmar erythema(肝掌) ---Jaundice(黄疸)

  19. Clinical features[III] Portal hypertension (门静脉高压) 1. Splenomegaly: anemia, leukopenia, thrombocytopenia due to hypersplenism 2. development and open of collateral vessels in portal hypertension a.Esophageal varices b. Rectal collateral's c. Caput medusae d. Abdominal wall varices e. Portal system and left renal 3. Ascites、hepatic hydrothorax

  20. Clinical features[IV] Palpation of liver firm, hard,irregular,enlargement rounded or sharp edge below the right lower ribs. The spleen is often palpable, and may be very large.

  21. The clinical manifestations found in cirrhosis 、

  22. Complications[I] • Upper gastrointestinal bleeding(上消化道出血): Hematemesis(呕血)/melena(黑粪). Esophageal/ gastric variceal bleeding (食管/胃静脉出血); portal hypertensive gastropathy (门脉高压性胃病); peptic ulcer(消化性溃疡)

  23. Infections: spontaneous bacterial peritonitis(自发性细菌性腹膜炎) (4-8%)：Fever, worsening jaundice or renal dysfunction, abdominal pain (occurring only in 50% of patients), and encephalopathy are the most common clinical findings in SBP. However, the patient is frequently asymptomatic. Because culture of ascites fluid is negative in a large number of patients with SBP, diagnosis should be based on the presence of >250 neutrophils/mm3.

  24. Complications[II] Hepatocellular carcinoma(肝细胞肝癌)  Hepatic encephalopathy(肝性 脑病) Asterixis(扑翼样振颤) Disoriented(定向障碍) Coma(昏迷)

  25. Complications[III] • Hepatorenal syndrome(HRS): Oliguria(少尿), azotemia(氮质血 症), hypotension(低血压),dilutional hyponatremia(稀释性低钠血症), low urinary sodium(低钠尿)

  26. Complications[IV] Electrolyte and acid-base imbalance(电介质酸硷平衡失调) hyponatremia, hypokalemia And hypochloremic alkalosis

  27. Laboratory findings[I] • Blood and urine routines • Liver function tests • ---to estimate the severity of liver dysfunction：ALT,AST,AKP,GGT, • serum total bilirubin, serum albumin, prothrombin time, globulin, cholesterol. • --- to differential diagnosis: • Alcoholic: AST/ALT>=2; • PBC: AKP,GGT>>ALT,AST • ---to refect hepatic fibrosis: PIIIP、HA、laminin • ---to quanlity liver function

  28. Immunology • Cellular immune, hormonal • immuneautoimmune liver disease: IgG,globulin ANA(+), SMA(+) • PBC: IgM, AMA(+) • Marker of virus • AFP

  29. Laboratory findings[II]  Ascites paracentesis: routine, culture, ADA, LDH, SAAG (serum ascites albumin gradient) (血清腹水白蛋白梯度) > 11g/L  Ultrasonography, CT scanning： biliary obstruction, liver masses, splenomegaly, ascites. Endoscopy: the number, appearance, and size of any esophageal/gastric varix, portal hypertensive gastropathy (PHG)

  30. Laboratory findings[III] Radionuclide: 99m TC-MIBI, H/L liver biopsy: to confirm the diagnosis  Laparoscopy  HVPG (hepatic vein pressure gradient)(肝静脉压力梯度) (wedged - free )hepatic venous pressure Normal: 5-6mmHg, >10mmHg: varices; >12mmHg:rupture

  31. Diagnosis [I]  Etiology of cirrhosis  Pathology of cirrhosis  Evaluating of liver function: Child-Pugh classification  Searching for complications

  32. Diagnosis[II] the history of disease contributes to identifying the cause of cirrhosis. history of viral hepatitis, blood transfusions, medication use, alcohol use, sexual practices should be carefully reviewed. signs and symptoms confirm to existence of portal hypertension and impared liver function. liver function tests: hypoalbuminemia,hyperbilirubinemia，the prolonged prothrombin time suggest hepatic decompensation. Imaging study: Ultrasound and CT readily identify the lesion, but have no characteristic findings.

  33. Diagnosis[III] Child-Pugh classification Scorea variable 1 2 3 Encephalopathy(degree) Nil Slight-Moderate Moderate-Severe Ascites(degree) Nil Slight Moderate-Severe Bilirubin(umol/L) <34 34-51 >51 Albumin(g/L) 35 28-34 <28 Prothrombin Index(%) >70 40-70 <40 Prothrombin Time(s) <14 15-17 >18 Prothrombin Time(INR)<1.3 1.3～1.5 >1.5 * PBC: SB(μmol/L) 17～68 68～170 >170 aScores are summed to determine Child’s class: class A=5-6 class B= 7-9 class C= 10-15

  34. Differential Diagnosis Other condition of hepatomegaly or splenomegaly ： chronic virus hepatitis,Gaucher’s disease, lymphomas and leukaemias, congestive splenomegaly Differebtial diagnosis of cirrhotic ascites and other types of ascites： malignant ascites, constrictive pericarditis, tuberculous peritonitis, et al. Portal hypertension:

  35. Treatment of cirrhosis[I] specific treatment for the underlying etiology of the liver disease antivirus therapy --viral hepatitis abstinence from alcohol--alcoholic Ursodeoxycholic acid(UDCA)(熊去氧胆酸)--PBC Penicillamine(青霉胺)—Wilson’s disease General Treatments: High calories (40 kcal/kg· d)、 adequate protein (1-1.5g/kg· d) 、vitamin、Herbal compounds.

  36. Treatment of Ascites a. Bed rest ,sodiumand water restriction. 1. Fluid intake: 800-1000ml/d (hyponatremia, serum sodium<130meq/L) 2. Dietary sodium intake：88mmol/d (2.0gNacl) Mild patients：rest on bed ，with dietary salt restriction, loss of ascites occurs in 10% to 15% of patients.

  37. Treatment of Ascites[II] b. Increasing renal sodium and water excretion: --Diuretics:urinary sodium /urinary potassium >1 Spironolactone(安体舒通) +furosemide(速尿) urinary sodium / urinary potassium <1 higher doses spironolactone，

  38. Treatment of Ascites(III) c. Large-volume paracentesisassociated with plasma volume expansion d. Ascites ultrafiltration and re-infusion e. Peritoneo-venous (LeVeen) shunts f.TIPS(transjugular intrahepatic porto-systemic stent)(经颈静脉门体分流术) g. Liver transplantation(肝移植)

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