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Cirrhosis of the Liver

Cirrhosis of the Liver

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Cirrhosis of the Liver

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  1. Cirrhosis of the Liver

  2. Hepatic Cirrhosis • It is a chronic progressive disease characterized by: - replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver • Extensive parenchymal cell degeneration • Destruction of parenchymal cells

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

  4. Etiology and Pathophysiology A. Alcoholic or Laennec’s Cirrhosis • In which the scar tissue characteristically surrounds the portal areas • This is the most frequently caused by chronic alcoholism, common type of cirrhosis • Preceded by a theoretically reversible fatty infiltration of the liver cells

  5. B. Post necrotic cirrhosis • Complication of toxic or viral hepatitis • Accounts for 20% of the cases of cirrhosis • Broad bands of scar tissue form within the liver • Etiology and Pathophysiology

  6. C. Biliary Cirrhosis • In which scarring occurs in the liver around the bile ducts. • This type of cirrhosis usually results from chronic biliary obstruction and infection (cholangitis) • Accounts for 15% of all cases of cirrhosis • Etiology and Pathophysiology

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

  8. Diagnostic Finding 1. serum albumin • Decrease in level 2. liver enzymes • SGPT(ALT),SGOT(AST) increases 3.Serum bilirubin • Increases 4. Prothrombin time • prolong

  9. 5. Ultrasound scanning • Used to measure the difference in density of parenchymal cells and scar tissue. 6. CT-scan, MRI • It gives information about liver size, hepatic blood flow and obstruction 7. Liver biopsy 8.ABG • May reveal a ventilation-perfusion imbalance and hypoxia

  10. Manifestations of Liver Cirrhosis

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

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

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

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

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

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

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

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

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

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

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

  22. Steatorrhea • Fatty stool • The passage of abnormally increase amounts of fats in the feces (more than 5g/day) due to reduced absorption of fat by intestine • The feces are pale, smell offensive, look greasy

  23. Pruritus • Due to biliary obstruction leading to retention of bile salts. • Patients may develop vascular spider angiomas on the skin usually above the waistline • These are numerous small vessels resembling a spider’s leg

  24. Complications • Portal hypertension and esophageal varices • Peripheral edema and ascites • Hepatic encephalopathy • Hepato-renal Syndrome

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

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

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

  28. 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

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

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

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

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

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

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

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

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

  37. Hepatorenal syndrome • acute renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or severe alcoholic hepatitis) • characterized by: • Oliguria • benign urine sediment • very low rate of sodium excretion • progressive rise in the plasma creatinine concentration

  38. Hepatorenal Syndrome • Reduction in GFR often clinically masked • Prognosis is poor unless hepatic function improves • Nephrotoxic agents and overdiuresis can precipitate HRS

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

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