1. LIVER CIRRHOSIS LIVER CIRRHOSIS

2. THE ANATOMY OF THE PORTAL VENOUS SYSTEM

3. LIVER CIRRHOSIS Diffuse disorganization of normal hepatic structure by regenerative nodules that are surrounded by fibrotic tissue.

4. NORMAL Metabolism – Carbohydrate, Fat & Protein Secretory – bile, Bile acids, salts & pigments Excretory – Bilirubin, drugs, toxins Synthesis – Albumin, coagulation factors Storage – Vitamins, carbohydrates etc. Detoxification – toxins, ammonia, etc. Liver Functions

5. Normal Liver - Microscopy

6. Micronodular Cirrhosis

7. Macronodular Cirrhosis

8. PATHOMORPHOLOGY

10. PATHOMORPHOLOGY

11. Liver Biopsy – Cirrhosis

12. LIVER CIRRHOSIS CLASSIFICATION (etiologic) Viral AlcoholicToxicAutoimmuneMetabolic Сongestive Biliary Cryptogenic

13. LIVER CIRRHOSIS CLASSIFICATION

16. CLASSIFICATION according to Child - Turcotte and Pugh Parameter Class A Compen sation (5-6 points) Class B Subcomp ensation (7-9 points) Class C Decompensa tion (10 and >points) Bilirubin, mcmol/l <3535-55>55 Albumine, g/l>3530-35<30 Prothrombin index60-80%40-59%<40% Ascitesabsenttreatableuntreatable Encephalopathyabsent 1-2 st. 3-4 st. Points: Points:123

17. LIVER CIRRHOSIS СOMPLICATIONS HEPATIC ENCEPHALOPATHY VARICEAL BLEEDING ASCITES HEPATORENAL SYNDROME PORTAL VEIN TROMBOSIS BACTERIALPERITONITISHEPATOCARCINOMA

18. LIVER CIRRHOSIS CLINICAL SYNDROMES Astenic syndrome Pain syndrome Dyspeptic syndrome Cholestatic syndrome Cholestatic syndrome Syndrome of jaundice Portal Hypertension

19. Spider naevus in liver cirrhosis in the ventral side of the left shoulder

20. Palmar erythema in liver cirrhosis

21. Gynaecomastia in liver cirrhosis

22. Xanthelasmas in biliary cirrhosis as a result of primary biliary cholangitis

23. Vein dilatation in the abdominal wall of a cirrhotic patient suffering from ascites and jaundice

24. ASCITES

25. Jaundice

26. Ascitis in Cirrhosis

27. Micronodular cirrhosis:

29. Alcoholic Hepatitis

30. Macronodular Cirrhosis

31. Liver Biopsy – Cirrhosis

32. Liver Biopsy – Cirrhosis:

33. Nutmeg Liver-Cardiac Sclerosis

34. Clinical Features Hepatocellular failure. –Malnutrition, low albumin & clotting factors, bleeding. –Hepatic encephalopathy. Portal hypertension. –Ascites, Portal systemic shunts, varices, splenomegaly.

35. Bleeding in Liver disease: vitamin K – in liver  gamma- carboxyglutamic acid – for coagulation factors II, VII, IX, and X. Liver disease  factor VII is the first to go  so the defect will appear initially in the extrinsic pathway, i.e., abnormal PT. When severe it affects both pathways.

36. Cirrhosis Clinical Features

37. Gynaecomastia in cirrhosis

38. Porta-systemic anastomosis: Prominent abdominal veins.

39. MRI Cirrhosis

40. Complications: Congestive splenomegaly. Bleeding varices. Hepatocellular failure. –Hepatic encephalitis / hepatic coma. Hepatocellular carcinoma.

41. Hepatocellular Carcinoma

43. LIVER CIRRHOSIS PLAN of INVESTIGATIONS Total blood count, Blood group and Rhesus factor ﻻ-globulins, Cholesterol, Biochemical analysis (Glucose, Bilirubin, ALT, AST, GGT, Alkaline phosphatase, Albumin, ﻻ-globulins, Cholesterol, Liver tests, Sodium, Potassium, Urea, Creatinine) Urinanalysis, Diastase of urine Coagulogram Viral Hepatitis (chain polimerase reaction, immunoenzyme analysis) Markers of Viral Hepatitis (chain polimerase reaction, immunoenzyme analysis)Immunogram ECG, Endoscopy, USD, CT, EEG Diagnostic paracentesis Needle liver biopsy

44. Diagnostic paracentesis.

45. Endoscopy reveals large, tortuous esophageal varices that have a characteristic bluish color

46. ESOPHAGEAL VARICES

47. Normal liver with portal vein (VP), inferior vena cava (VC) and right branch of the portal vein (RHA). Subcostal plane: 1 - left branch of VP; 2 - right branch of hepatic vein; 3 - cranial diaphragm

48. Liver cirrhosis with ascites (longitudinal section): the left lobe of liver is rounded and plump; intrahepatic vessels are reduced. Irregular and inhomogeneous structure. Clear undulatory limitation (arrow) on the underside due to nodular transformation. Wide hypoechoic fringe due to ascites

49. Post mortem specimen of cirrhotic liver and enlarged spleen Post mortem specimen of banded oesophageal varix

50. Monitoring of patients with ascites TREATMENT

51. LIVER CIRRHOSIS TREATMENT Diet №5 CORTICOSTEROID Prednisolone), ) CORTICOSTEROID THERAPY(Prednisolone), IMMUNOSUPPRESSIVE THERAPY(Azathioprine) HEPATOPROTECTORS DIURETICS (potassium sparing diuretic (Spironolactone 150-200 mg/day) +loop diuretic (Furosemid 20-80mg/day)) DEZINTOXICATION THERAPY VITAMIN VITAMIN THERAPY LACTULOSE (30 ml 3 times/day orally) DIGESTIVE ENZYMES CORRECTION OF ELECTROLYTE BALANCE DISTURBANCE SYMTOMATIC THERAPY LIVER TRANSPLANTATION

52. Liver transplantation Liver transplantation should be considered for most patients with end-stage liver disease or acute fulminant hepatic failure, and transplant units should be contacted early regarding referral.

53. LIVER CIRRHOSIS СOMPLICATIONS HEPATIC ENCEPHALOPATHY VARICEAL BLEEDING ASCITES HEPATORENAL SYNDROME PORTAL VEIN TROMBOSIS BACTERIAL PERITONITIS HEPATOCARCINOMA

55. Events precipitating hepatic encephalopathy in cirrhotic patients Electrolyte imbalance Electrolyte imbalanceDiureticsVomitingDiarrhoea Gastrointestinal bleeding Gastrointestinal bleeding Drugs Drugs Alcohol Alcohol Infection InfectionSpontaneous bacterial peritonitis UrinaryChest Constipation Constipation Dietary protein overload

56. Drugs that can cause hepatic encephalopathy BarbituratesAnalgesics Other sedatives

57. Treatment of hepatic encephalopathy Identify the precipitating factors Stop diuretics Check serum Na+, K+, and urea concentration Empty bowels of nitrogen containing content Control bleeding Protein­free diet Lactulose Neomycin (1 g four times a day by mouth for 1 week) Maintain energy, fluid, and electrolyte balance Increase dietary protein slowly with recovery

58. LIVER CIRRHOSIS СOMPLICATIONS HEPATIC ENCEPHALOPATHY VARICEAL BLEEDING ASCITES HEPATORENAL SYNDROME PORTAL VEIN TROMBOSIS BACTERIAL PERITONITIS HEPATOCARCINOMA

59. Characteristic findings associated with hepatorenal syndrome Ascites (but not necessarily jaundice) is usually present Hyponatraemia is usual Hepatic encephalopathy is commonly present Blood pressure is reduced compared with previous pressures recorded in patient Pronounced oliguria Low renal sodium concentration Urinary protein and casts are minimal or absent

60. Summary points Cirrhosis is the commonest cause of ascites (90%) Ninety per cent of cases can be managed by sodium restriction and diuretics Hepatic encephalopathy is most commonly precipitated by drugs or gastrointestinal haemorrhage Non­steroidal anti­inflammatory drugs should be avoided in cirrhotic patients as they can cause renal failure

61. Summary points Summary points PORTAL HYPERTENSION Normal portal vein pressure is 7 mmHg and pressure is usually above 12 mmHg when oesophageal varices develop. The majority of the oxygen supply of the liver comes from the portal vein, owing to its high flow compared to that in the hepatic artery. Portal hypertension has prehepatic, intrahepatic and post-hepatic causes. Patients with stable portal hypertension should be given beta-blockers. Treatment of ascites requires both dietary salt restriction and diuretics. Fluid restriction is only necessary if hyponatraemia develops.