Cirrhosis of the Liver

1. Cirrhosis of the Liver Dr Ibraheem bashayreh, RN, PhD

2. ANATOMY & PHYSIOLOGY LIVER • Weighing between 1,200 and 1,600 g, the liver is the largest glandular organ in the body. It is located in the right upper abdominal quadrant, under the right diaphragm. • The liver is divided into four lobes: left, right, caudate and quadrate. The lobes are further subdivided into smaller units known as lobules. • The liver contains several cell types including hepatocytes (ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that engulf bacteria). • Bile is continuously formed by hepatocytes (about 1L/day). Bile comprises water, electrolytes , lecithin,fatty acids, cholesterol, bilirubin and bile salts. • The Liver is surrounded by a tough fibroelastic capsule called Glisson’s capsule.

4. FUNCTIONS OF THE LIVER Regulating blood glucose level by making glycogen, which is stored in hepatocytes. Synthesizing blood glucose from amino acids of lactate through gluconeogenesis. Convertingammonia produced from gluconeogenetic by-products and bacteria to urea Synthesizing plasma proteins such as albumin, globulins, clotting factors, and lipoproteins. Breaking down fatty acids into ketone bodies Storing vitamins and trace metals Affecting drug metabolism and detoxification Secreting bile

6. Liver cirrhosis

7. Description • A chronic, progressive disease of the liver • Extensive parenchymal cell degeneration • Destruction of parenchymal cells

8. Description • Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis

9. Description • Normal lobular structure distorted by fibrotic connective tissue • Lobules are irregular in size and shape with impaired vascular flow • Insidious, prolonged course

10. Etiology and Pathophysiology • Cell necrosis occurs • Destroyed liver cells are replaced by scar tissue • Normal architecture becomes nodular

11. Etiology and Pathophysiology • Four types of cirrhosis: • Alcoholic (Laennec’s) cirrhosis • Postnecrotic cirrhosis • Biliary cirrhosis • Cardiac cirrhosis

12. Etiology and Pathophysiology • Alcoholic (Laennec’s) Cirrhosis • Associated with alcohol abuse • Preceded by a theoretically reversible fatty infiltration of the liver cells • Widespread scar formation

13. Etiology and Pathophysiology • Postnecrotic Cirrhosis • Complication of toxic or viral hepatitis • Accounts for 20% of the cases of cirrhosis • Broad bands of scar tissue form within the liver

14. Etiology and Pathophysiology • Biliary Cirrhosis • Associated with chronic biliary obstruction and infection • Accounts for 15% of all cases of cirrhosis

15. Etiology and Pathophysiology • Cardiac Cirrhosis • Results from longstanding severe right-sided heart failure

16. Manifestations of Liver Cirrhosis Fig. 42-5

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

18. Clinical ManifestationsEarly Manifestations • Abdominal pain • Fever • Lassitude (laziness) • Weight loss • Enlarged liver or spleen

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

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

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

23. Clinical ManifestationsSkin • Spider angiomas (telangiectasia, spider nevi) • Palmarerythema

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

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

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

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

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

29. Complications • Portal hypertension and esophageal varices • Peripheral edema and ascites • Hepatic encephalopathy • Fetor hepaticus: is bad breath with a 'dead mouse' or sweet faecal smell. ... It may be caused by severe hepatocellular damage

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

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

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

33. 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

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

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

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

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

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

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

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

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

43. Development of Ascites Fig. 42-6

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

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

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

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

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

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

50. Peritoneovenous Shunt Fig. 42-8