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Cirrhosis of the liver

Cirrhosis of the liver. Definition. Cirrhosis is a common chronic, progressive and diffusive liver disease, caused by one or several agents act repeatedly and persistently. Histologically, cirrhosis is an irreversible alteration of the liver architecture, consisting of

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Cirrhosis of the liver

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  1. Cirrhosis of the liver

  2. Definition Cirrhosis is a common chronic, progressive and diffusive liver disease, caused by one or several agents act repeatedly and persistently. Histologically, cirrhosis is an irreversible alteration of the liver architecture, consisting of hepatic fibrosis and areas of nodular regeneration

  3. Epidemiology Worldwide major heath problem Over 500,000 deaths per year Over 20% were latent 2 ~ 10% in postmortem examination Common and death leading disease in China

  4. Viral hepatitis Parasites (schistosomiasis) Alcoholic liver disease Cholestasis Hepatic-Venous outflow obstruction Toxicant and drugs Metabolic abnormality Malnutrition Cryptogenic cirrhosis Etiology and pathogenesis

  5. HBV HCV HBV + HDV HAV HEV Viral hepatitis

  6. Global prevalence:>300 million carriers 5% world population Varies widely High prevalence:8% ~ 15% Far East (southeast Asia China Philippines Indonesia) Middle East Africa parts of South America Intermediate prevalence: 2% ~ 7% Japan parts of south America parts of central Asia eastern and southern Europe Low prevalence:<2% US Canada northern Europe Australia Viral hepatitis (HBV)

  7. Viral hepatitis Elimination of viral infected hepatocytes is dependent on recognition of viral determinants in association with HLA proteins on the infected hepatocytes by cytotoxic T cells. HLA protein display is modulated by exposure to interferon and cytotoxic T cell, NK lytic processes. During chronic HBV infection, infected liver cells failed to induce IFN. Therefore, viral protein synthesis is not decreased, HLA protein display is not enhanced.

  8. Parasites (Schistosomiasis) Ova deposited in the portal zones Exciting a fibrous tissue reaction Co-existence of malaria and cirrhosis reflects malnutrition, viral hepatitis and toxic factors

  9. Alcoholic liver disease 1/3 cause of cirrhosis in Western country Most important factor: “threshold” dose: 600 Kg (men) 150~300 Kg (women) average daily consumption of alcohol > 40 ~ 80 g/D, over 10 ~ 15 years Liver: primary site of ethanol metabolism Ethanol can be oxidized by three enzymes systems ADH CYP2E1 catalase

  10. Alcoholic liver disease Mechanism Direct effect by ethanol, or its first metabolite (acetaldehyde redox shift oxidant stress) Cell-mediatedimmune Three histopathologic lesion: fatty liver, alcoholic hepatitis, cirrhosis

  11. Biliary cirrhosis Primary Biliary Cirrhosis: Progressive destruction of small and intrahepatic bile ducts Prevalence: 40~150 cases/million Women >90 of cases 50y Abnormal immunoregulation Associated with HLA phenotyeps

  12. Biliary cirrhosis Secondary biliary cirrhosis: Obstruction of the biliary tree, further divided into two groups intra-hepatic and extra-hepatic obstruction

  13. Hepatic-Venous outflow obstruction Veno-occlusive disease Budd-chiari syndrome Constrictive pericarditis Chronic congestive heart failure

  14. Toxicant and drugs Tetrachloride carbon （四氯化碳） - methyldopa （- 甲基多巴） Tetracycline （四环素） Phosphorus （磷） Arsenic（砷）

  15. Metabolic abnormality Iron storage disease (Hemochromatosis) Copper storage disease (Wilson’s disease)

  16. Malnutrition Chronic inflammatory bowel disease Prolonged lack of dietary proteins and vitamins

  17. Cryptogenic cirrhosis Etiology is unknown Viral infection are suscepted in some cases

  18. Pathology and classification Histopathological diagnosis: Excessive fibrous tissue Regenerating nodules Complete distortion of the normal relationship of hepatic venous outflow radicles and portal veins.

  19. Anatomical types of regenerating nodules Micronodular Macronodular Mixed cirrhosis

  20. Micronodular cirrhosis Features: Thick regular septa Regenerating small nodules (<3mm) Involvement of every lobule Alcoholism Malnutrition Biliary obstruction Hemochromatosis Venous outflow obstruction

  21. Macronodular cirrhosis Features: Septa Nodules of variable size (>3mm, even 1~ 3 cm) Normal lobules in the large nodules Two subtypes: postnecrotic posthepatitic

  22. Macronodular cirrhosis Postnecrotic type: Coarsely scarred liver Large nodules surrounded by broad fibrous septa Clumping togathered numerous portal trials Toxic cirrhosis Cryptogenic cirrhosis Multilobular cirrhosis

  23. Macronodular cirrhosis Posthepatitic type: Macronodules separated by slender fibrous strands Connect individual portal areas to each other Viral hepatitis Wilson’s disease

  24. Mixed cirrhosis Features: Presenting both micro- and macronodules From micronodules to macronodules Alcoholism Antitrypsin deficiency

  25. Some aspects of pathology The most useful morphologic classification: gross appearance of the liver The morphologic diagnosis of cirrhosis is more reliable than the histopathological diagnosis Schistosomiasis:incomplete septal cirrhosis coarse portal fibrosis Initially enlarged/subsequcetly shrinks

  26. Clinical manifestation Onset: Cryptical and slowly progressive Majority: 3~5 years or 10 years Minority: 3~6 months Stages: Compensated Decompensated

  27. Compensated stage Fatigue Loss of appetite Anorexia Abdominal discomfort Abdominal pain Hepatomegaly (slightly or moderately) Splenomegaly

  28. Decompensated stage Deterioration of liver function Feature of portal hypertention

  29. Deterioration of liver function General deterioration Deterioration of heath, anorexia, weight loss, weakness, fatigue, Flatulent dyspepsia, abdominal distress, swelling of legs or abdomen, mild fever, loss of libido and hemorrhage. Findings of physical examination Jaundice Dermatological and sexual signs Liver (enlarge or shrunken)

  30. Jaundice It always implies liver cell destruction exceeds the capacity for regeneration

  31. Dermatologic and sexual signs Skin pigmentation （皮肤色素沉着） Clubbing fingers （杵状指） Spider angioma （蜘蛛痣） Liver palms (palmar erythema) （肝掌） Purpura （紫癜） Spontaneous bruising （青肿）/epistaxes （鼻出血）

  32. Dermatologic and sexual signs Feminization （女性化）and hypogonadism （性腺 功能减退） Gynecomastia（男性乳房发育） testicular atrophy sparse body hair changes in hair distribution menstrual irregularities Mechanism: serum testosterone  estrogens 

  33. Liver Early stage Enlarged and palpable firm regular edge a fine to coarsely nodular surface Later stage Shrunk and impalpable

  34. Features of portal hypertension Portal-systemic collaterals Ascites Splenomegaly

  35. Anatomy and physiology of portal venous system Begins in the capillaries of the intestines Terminates in the hepatic sinusoids (肝窦） Formed by the confluence of the superior and inferior mesenteric veins （肠系膜上/下静脉）and splenic vein Liver receives 1500ml/min, 2/3 from portal vein Hepatic artery provides 50% oxygen The pressure within the sinusoids is low Lack of valves ***: Between the splanchnic venules （内脏小静脉）and the heart

  36. Portal-systemic collaterals Esophageal and gastric varices Dilation of the remnant of the umbilical vein （脐静脉） Dilation of abdominal veins Hemorrhoidial venous （痔静脉）collaterals

  37. Splenomegaly Slightly or moderatory enlarged Hypersplenism Leukopenia Thrombocytopenia Anemia

  38. Ascites Prominent feature of portal-hypertension 70% of patients are positive An early sign in presinusoidal portal hypertension relative late in intrahepatic portal hypertension Massive ascites: abdominal herniae (腹疝）

  39. Complications Upper gastrointestinal bleeding Hepatic encephalopathy Infection Hepatorenal syndrome Primary liver cancer Imbalance of electrolytes and acid-alkaline

  40. Upper gastrointestinal bleeding Major complication Incredible high mortality Source of bleeding: esophageal varices 60%~80% gastric varices 7% congestive gastropathy 5%~20% (paptic ulcer, acute erosive gastritis etc)

  41. Hepatic encephalopathy The most severe and deadly complications

  42. Infection Increased risk for bacterial infection pneumonia biliary infection E.coli infection and spontaneous bacterial peritonitis (SBP)

  43. SBP Pathogen of SBP:gram’s negative bacteria Features of SBP: fever, abdominal pain or tenderness decreased bowel sounds Suspected patients: sudden onset of HE or hypotension Diagnosis:elevated ascites fluid white blood cells positive ascitic fluid culture

  44. Hepatorenal syndrome Decreased renal function due to severe liver disease Histologically normal kidney Involved factors Sympathetic nervous system Renin-angiotensin-aldosterone Prostaglandins Endotoxemia Others ( vasopressin , leukotriene etc)

  45. Primary liver cancer Suspected signs Hepatomegaly within short time Persistent abdominal pain Enlarged liver with uneven surface or mass Bloody ascites Serum α-fetoprotein (α-FP) 70%

  46. Imbalance of electrolytes and acid-alkaline Hyponatraemia Hypokalaemia Metabolic alkalosis

  47. Laboratory and other tests Urine Serum Hematology Ultrasonograply Barium esophagogram Endoscopy Liver biopsy

  48. Diagnosis Patients with a history of viral hepatitis, prolonged alcohol overconsumption, schistosome infection, hemochromatosis Features of deterioration of liver function and portal hypertension Enlarged or shrunk liver with nodular surface Abnormal liver function tests Liver biopsy shows widespread fibrosis with nodular regeneration

  49. Complete diagnosis Etiology Morphology Hepatic function

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