1 / 73

Liver CIRRHOSIS

Liver CIRRHOSIS. Doç.Dr .Atakan Yeşil Yeditepe Unıversıty Department of Gastroenterology. Consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules leading to progressive loss of liver function.

jcuthbert
Download Presentation

Liver CIRRHOSIS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Liver CIRRHOSIS Doç.Dr.Atakan Yeşil Yeditepe UnıversıtyDepartment of Gastroenterology

  2. Consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules leading to progressive loss of liver function

  3. Hepatic fibrosis is a reversible wound healing response characterized by accumulution of extracelüler matrix made up collagen fibrils. • Cirrhosis is defined by global hepatic fibrosis and reduced hepatic synthetic function

  4. etiology • Alcohol • Chronic hepatitis B • Chronic hepatitis C • Other: Haemochromatosis Non-alcoholic fatty liver disease Primary biliary cirrhosis Sclerosing cholangitis Autoimmune hepatitis Cystic fibrosis...

  5. Pathology MICRONODULAR CIRRHOSIS • Uniform, small nodules up to 3 mm in diameter • Often caused by alcohol damage

  6. Pathology MACRONODULAR CIRRHOSIS • Large nodules • Often seen following hepatitis B infection

  7. Cirrhosis with complicatons of encephalopathy, ascites or variceal haemorrhage – DECOMPENSATED CIRRHOSIS • Cirrhosis without any of these complications – COMPENSATED CIRRHOSIS

  8. Manifestations of Liver Cirrhosis Fig. 42-5

  9. Clinical ManifestationsEarly Manifestations • Onset usually insidious • GI disturbances: • Anorexia • Dyspepsia • Flatulence • N-V, change in bowel habits

  10. Clinical ManifestationsEarly Manifestations • Abdominal pain • Fever • Lassitude • Weight loss • Enlarged liver or spleen

  11. Clinical ManifestationsLate Manifestations • Two causative mechanisms • Hepatocellular failure • Portal hypertension

  12. Clinical ManifestationsJaundice • Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

  13. Clinical ManifestationsJaundice • Intermittent jaundice is characteristic of biliary cirrhosis • Late stages of cirrhosis the patient will usually be jaundiced

  14. Clinical ManifestationsSkin • Spider angiomas (telangiectasia, spider nevi) • Palmar erythema

  15. Clinical ManifestationsEndocrine Disturbances • Steroid hormonesof the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

  16. Clinical ManifestationsEndocrine Disturbances • Alteration in hair distribution • Decreased amount of pubic hair • Axillary and pectoral alopecia

  17. Clinical ManifestationsHematologic Disorders • Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

  18. Clinical ManifestationsHematologic Disorders • Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

  19. Clinical ManifestationsPeripheral Neuropathy • Dietary deficiencies of thiamine, folic acid, and vitamin B12

  20. Complications • Portal hypertension and esophageal varices • Peripheral edema and ascites • Hepatic encephalopathy • Fetor hepaticus

  21. Complications of portal hypertension begin to devolop when portal pressure reahes values>=12 mmHG normal<7 mmHg

  22. ComplicationsPortal Hypertension • Characterized by: • Increased venous pressure in portal circulation • Splenomegaly • Esophageal varices • Systemic hypertension

  23. ComplicationsPortal Hypertension • Primary mechanism is the increased resistance to blood flow through the liver

  24. ComplicationsPortal HypertensionSplenomegaly • Back pressure caused by portal hypertension  chronic passive congestion as a result of increased pressure in the splenic vein

  25. ComplicationsPortal HypertensionEsophageal Varices • Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

  26. ComplicationsPortal HypertensionEsophageal Varices • Varices have fragile vessel walls which bleed easily

  27. ComplicationsPortal HypertensionInternal Hemorrhoids • Occurs because of the dilation of the mesenteric veins and rectal veins

  28. ComplicationsPortal HypertensionCaput Medusae • Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

  29. ComplicationsPeripheral Edema and Ascites • Ascites: - Intraperitoneal accumulation of watery fluid containing small amounts of protein

  30. ASCITES • Presence of fluid in the peritoneal cavity • Therapy: diuretics paracentesis

  31. ComplicationsPeripheral Edema and Ascites • Factors involved in the pathogenesis of ascites: • Hypoalbuminemia •  Levels of aldosterone •  Portal hypertension

  32. ComplicationsHepatic Encephalopathy • Liver damage causes blood to enter systemic circulation without liver detoxification

  33. ComplicationsHepatic Encephalopathy • Main pathogenic toxin is NH3 although other etiological factors have been identified • Frequently a terminal complication

  34. ComplicationsFetor Hepaticus • Musty, sweetish odor detected on the patient’s breath • From accumulation of digested by-products

  35. Development of Ascites Fig. 42-6

  36. Diagnostic Studies • Liver function tests • Liver biopsy • Liver scan • Liver ultrasound

  37. Diagnostic Studies • Esophagogastroduodenoscopy • Prothrombin time • Testing of stool for occult blood

  38. Collaborative Care • Rest • Avoidance of alcohol and anticoagulants • Management of ascites

  39. Collaborative Care • Prevention and management of esophageal variceal bleeding • Management of encephalopathy

  40. Collaborative CareAscites • High carbohydrate, low protein, low Na+ diet • Diuretics • Paracentesis

  41. SAAG: serum ascites albumin- ascitic ascites albumin • >1.1:portal hipertansiyon • <1.1 exculuda cirrosis and portal hypertension

  42. Ascitic total protein levels greater than 3.5 and asitic albumin levels greater than 2.5 suggest a cardiac cause

  43. Collaborative CareAscites • Peritoneovenous shunt • Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava

  44. Peritoneovenous Shunt Fig. 42-8

  45. Collaborative CareEsophageal Varices • Avoid alcohol, aspirin, and irritating foods • If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)

  46. Patients with cirrhosis should be screened for varices every year with UEG

  47. Collaborative CareEsophageal Varices • Endoscopic sclerotherapy or ligation • Balloon tamponade • Surgical shunting procedures (e.g., portacaval shunt, TIPS)

  48. Sengstaken-Blakemore Tube Fig. 42-9

  49. Portosystemic Shunts Fig. 42-11

More Related