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 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 –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 Four types of cirrhosis: –Alcoholic (Laennec’s) cirrhosis –Postnecrotic cirrhosis –Biliary cirrhosis –Cardiac cirrhosis

4. 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 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 Etiology and Pathophysiology

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 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 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. D. Cardiac Cirrhosis –Results from longstanding severe right- sided heart failure 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 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 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 Manifestations Early Manifestations Onset usually insidious GI disturbances: –Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits Onset usually insidious GI disturbances: –Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits

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

13. Clinical Manifestations Late Manifestations Two causative mechanisms –Hepatocellular failure –Portal hypertension Two causative mechanisms –Hepatocellular failure –Portal hypertension

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

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

16. Clinical Manifestations Skin Spider angiomas (telangiectasia, spider nevi) Palmar erythema Spider angiomas (telangiectasia, spider nevi) Palmar erythema

17. Clinical Manifestations Endocrine Disturbances Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

18. Clinical Manifestations Endocrine Disturbances Alteration in hair distribution –Decreased amount of pubic hair –Axillary and pectoral alopecia Alteration in hair distribution –Decreased amount of pubic hair –Axillary and pectoral alopecia

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

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

21. Clinical Manifestations Peripheral Neuropathy Dietary deficiencies of thiamine, folic acid, and vitamin B 12

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 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 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 Portal hypertension and esophageal varices Peripheral edema and ascites Hepatic encephalopathy Hepato-renal Syndrome

25. Complications Portal Hypertension Characterized by: –Increased venous pressure in portal circulation –Splenomegaly –Esophageal varices –Systemic hypertension Characterized by: –Increased venous pressure in portal circulation –Splenomegaly –Esophageal varices –Systemic hypertension

27. Complications Portal Hypertension Primary mechanism is the increased resistance to blood flow through the liver

28. Complications Portal Hypertension Splenomegaly Back pressure caused by portal hypertension  chronic passive congestion as a result of increased pressure in the splenic vein

29. Complications Portal Hypertension Esophageal Varices Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

30. Complications Portal Hypertension Esophageal Varices Varices have fragile vessel walls which bleed easily

31. Complications Portal Hypertension Internal Hemorrhoids Occurs because of the dilation of the mesenteric veins and rectal veins

32. Complications Portal Hypertension Caput Medusae Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

33. Complications Peripheral Edema and Ascites Ascites: - - Intraperitoneal accumulation of watery fluid containing small amounts of protein Ascites: - - Intraperitoneal accumulation of watery fluid containing small amounts of protein

34. Complications Peripheral Edema and Ascites Factors involved in the pathogenesis of ascites: - -Hypoalbuminemia - -  Levels of aldosterone - -  Portal hypertension Factors involved in the pathogenesis of ascites: - -Hypoalbuminemia - -  Levels of aldosterone - -  Portal hypertension

35. Complications Hepatic Encephalopathy Liver damage causes blood to enter systemic circulation without liver detoxification

36. Complications Hepatic Encephalopathy Main pathogenic toxin is NH 3 although other etiological factors have been identified Frequently a terminal complication Main pathogenic toxin is NH 3 although other etiological factors have been identified Frequently a terminal complication

37. Complications Fetor Hepaticus Musty, sweetish odor detected on the patient’s breath From accumulation of digested by- products Musty, sweetish odor detected on the patient’s breath From accumulation of digested by- products

38. 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 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

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

40. Diagnostic Studies Liver function tests Liver biopsy Liver scan Liver ultrasound Liver function tests Liver biopsy Liver scan Liver ultrasound

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