THE FIRST AFFILIATED HOSPITAL OF JIANGXI MEDICAL COLLEGE ZHANG KUN HE （张焜和）

1. LIVER CIRRHOSIS THE FIRST AFFILIATED HOSPITAL OF JIANGXI MEDICAL COLLEGE ZHANG KUN HE （张焜和）

2. What is hepatocirrhosis • It is a kind of common,chronic,progressive and diffusing liver disease. • Its histological feature is nodular regeneration of liver cells, fibrosis and forming pseudo-lobule. • Contracture of fibrous tissue makes liver deform and sclerosis. • Manifestation: damage of liver cells and portal hypertension • Many serious complications occur in later period • It more occurs in males. Males:females=3.6~8:1 • It often occurs in forties(35~48)

3. ETIOLOGY

4. Etiologic classification • Viral hepatitis hepatocirrhosis • Alcoholic cirrhosis • Schistosomiasis hepatocirrhosis • Biliary cirrhosis • Metabolic hepatocirrhosis • Others

5. Viral hepatitis and livercirrhosis • The commonest factor of hepatocirrhosis in China • Infection of HBV, HCV or HBV+HDV • Superinfection of several kinds of virus causes it most easily. • Viral infection can result in chronic hepatitis, especially chronic active hepatitis • Chronic damage of liver develops into post-hepatitis cirrhosis in the end. • HAV and HEV only cause acute hepatitis.They can not result in hepatocirrhosis.

6. HBV

7. Chronic schistosomiasisand hepatocirrhosis • Schistosomiasis is still a common factor of hepatocirrhosis in epidemic-stricken area • Long-term or repeated infection of Japanese blood flukes • Mass eggs deposit in portal area • Mass fibrous tissues proliferate in portal area • Ultimately it develops into schistosomiasis hepatic fibrosis. • Portal hypertension is the major manifestation.Damage of liver is gentler

8. Chronic alcoholism and hepatocirrhosis • Liver is the unique organ where alcohol is metabolized • Long-term drinking(>10 years)and mass alcohol(>80g) may cause hepatocirrhosis • Metabolite(acetaldehyde) of alcohol can result in chronic lesion of liver • Alcoholic hepatitis and alcoholic fatty liver are caused and develop into alcoholic cirrhosis later

9. alcoholic cirrhosis

10. Cholestasis and hepatocirrhosis • Intrahepatic or extrahepatic bile duct obstruction lasts for a long time resulting in long-term depositing bile • Depositing bile damages liver and stimulates fibers proliferation which cause biliary cirrhosis at last • The cause of primary biliary cirrhosis is indistinct • Secondary biliary cirrhosis is caused by choleith blocking bile duct

11. primary biliary cirrhosis

12. Circulatory disorder and hepatocirrhosis • Liver chronic congestion→hypoxia → hepatocyte necrosis →fibrous tissue proliferation → cirrhosis of liver • Chronic congestive heart failure (constrictive pericarditis)→cardiac cirrhosis • Obstruction of hepatic veins or inferior vena cava → cirrhosis of liver

13. Toxicity hepatitis and cirrhosis of liver • Hepatotoxicity poison：tetrachloride, phosphorum, arsenic • Hepatotoxicity drug：isaphenin, methyl-DOPA、tetracycline • Chronic toxicity hepatitis→cirrhosis of liver

14. Metabolic disorders andcirrhosis of liver • Inherited diseases • Copper metabolic disorder: hepatolenticular degeneration→deposition of copper → fibers proliferation →cirrhosis of liver • Ferrum metabolic disorder：hemachromatosis →deposition of iron → cirrhosis of liver • a1-anti-trypsin deficiency syndrome • Galactosemia

15. Malnutrition and liver cirrhosis • Lose of nutrien and malabsorption:IBD • Long-term deficiency in food:malnutrition • Fatty degeneration of liver→necrosis →cirrhosis of liver

16. Hepatocirrhosis of unknown etiology • The etiology is difficult to define • Parts of them are of viral hepatitis

17. PATHOLOGY

18. Pathogenesis of hepatocirrhosis extensive necrosis of liver cells ↓ regenerated node ↓ pseudo-leaflet ↓ portal hypertension

19. Pathologic classification of hepatocirrhosis • Lesser tubercle cirrhosis：portal cirrhosis • Greater tubercle cirrhosis：necrotic cirrhosis • Mixed cirrhosis • Others

20. Lesser tubercle cirrhosis • Commonest，caused by chronic hepatitis • Smaller nodes: Ø0.3~0.5cm • The size of nodes is similar • Pseudo-lobules are also similar in size

21. Lesser tubercle cirrhosis

22. Greater tuberclecirrhosis • Caused by serious hepatic necrosis • Greater nodes : Ø1~3cm • Discrepancy in size • Broder fibrous spetum，and vary in width • Different size of pseudo-lobules

23. Greater tuberclecirrhosis

24. Mixed nodular cirrhosis greater tubercle + lesser tubercle

25. Unconspicuous regenerated nodular cirrhosis • Significant proliferation of fiber • Fibrous spetum extend into hepatic lobules, but not completely cut apart hepatic lobule • Fibrous tissues wrap many hepatic lobules and form multi-lobule nodes • Unconspicuous regeneration in nodes • Seeing in schistosomiasis hepatic fibrosis

26. Pathologic features of liver cirrhosis • Hepatomegaly early, evidently decreased in size later • Fibers increase and become hard, so called “sclerosis” • Nodular surface, so called “pineapple liver” • Section shows islanded, wrapped by gray fibrous tissues

27. Histologic features of liver cirrhosis • Consisted of several non-integrality hepatic lobules, containing 0~3 central veins • Consisted of regenerated nodes, irregular arrangement of cells • Degeneration, necrosis and regeneration of liver cells • Portal area significantly becomes broader because of proliferation of fibrous tissues and have infiltration of inflammatory cells and pseudo-bile duct

28. fibrous tissues

29. Pathologic features of other organs • Collateral circulation forming in esophagus, gastric fundus and abdominal wall varicosis • Splenomegaly: hyperemia, proliferation of splenic pulp, hyperplasia of fibers • Portal hypertension gastropathy: congestion, edema and erosion of gastric mucosa • Others

33. CLINIC PRESENTATION

34. Compensatory phase of liver function • Symptoms mild, no specificity • Digestive symptoms：anorexia, mild diarrhea • Systemic symptoms：characterized with fatigue • Signs：mild hepatomegaly, mildly hard quality, tenderness，mild~moderate splenomegaly • Liver function tests：basically normal or mildly abnormal

35. Decompensatory phase of liver function • Clinical presentations evident • Divided into two categories • Presentations of liver function disfunction • Presentations of portal hypertension • Presentations of complications

36. Systemic symptoms of subsidence of liver function • Malnutrition, weight loss • Bad spirit, fatigue • Facial features of liver disease, no politure, kraurotic skin • Jaundice, suggesting significant necrosis of liver cells • Irregular fever

37. Digestive symptoms • Poor appitite, nausea or epigastric distention after having food • Diarrhea, induced when intaking unhealthful or fatty food • Abdominal distention • serious distention when with a great quantity of ascites • Major causes of symptoms • Gastrointestinal congestion and edema, dysfunction of digestion and absorption • Dysbacteriosis of intestinal tract

38. Manifestations of the blood system • Hemorrhagic tendency：gingival bleeding, skin ecchymosis • Decreased synthesis of coagulation factors • Thrombocytopenia caused by hypersplenism • Increased capillary fragility • Anemia, with different degrees based on causes • Malnutrition caused by dysfunction of digestion and absorption • Hypersplenism • Blood loss: gastrointestinal bleeding

39. Endocrine disturbance • Decreased inactivation of estrogen • sexual disturbance • spider nevus, liver palm, capillary telangiectasia • Decreased inactivation of aldosterone：increased reabsorption of sodium, sodium retention • Decreased inactivation of antidiuretic hormone：increased reabsorption of water • Hypoadrenocorticism（feedback suppression）: skin pigmentation, especially on face

40. Splenomegaly • Mild~moderate splenomegaly • Spleen can temporarily shrink,even cannot be touched when upper digestive tract haemorrhages • Hypersplenia may exist when three series of blood cells decrease • Those with splenomegaly must exclude liver cirrhosis

41. Collateral circulation • When portal venous pressure exceeds 200mmH2O,collateral circulation is formed between portal vein and systemic vein • Varicosis of esophagus and gastric fundus • Varicosis of abdominal wall • Phlebectasia of hemorrhoid

44. Portal hypertension: ascites • The most significant presentation in decompensatory phase • See in more than 75% patients • Distention often prior to ascites • Frog belly • Part of patients with pleural fluid, mostly in right-sidedness • Caused by excessive accumulation of sodium and water

45. Causes of ascites • Portal hypertension • Hypoallbuminemia • Increased hepatic and possibly splanchnic lymph fluid formation • Secondary aldosteronism：increased reabsorption of sodium • Antidiuretic hormone increased：water reabsorption increased • Deficiency of effective circulating blood volume

46. Palpation of liver • Relatively hard quality • Sharp edge • Nodular or granular • No tenderness without hepatitis, but tenderness with active hepatitis

47. Cirrhosis type & presentations • Lesser tubercle liver cirrhosis • Greater tubercle liver cirrhosis • Schistosomiasis liver cirrhosis

49. COMPLICATIONS

50. Upper gastrointestinal hemorrhea • The commonest complication • Hematemesis and melena（tarry） • Often evoking hepatic encephalopathy and greatly increased ascites • Etiology • Esophageal and gastric varices • Erosive gastritis • Peptic ulcer disease