1 / 50

CIRRHOSIS

CIRRHOSIS. Dr Ramadas nayak Professor & hod pathology. CIRRHOSIS. Definition: Cirrhosis is an end stage of any chronic liver disease. It is a diffuse process (entire liver is involved) characterized by fibrosis and

samaro
Download Presentation

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. CIRRHOSIS Dr Ramadas nayak Professor & hod pathology

  2. CIRRHOSIS • Definition: • Cirrhosis is an end stage of any chronic liver disease. • It is a diffuse process (entire liver is involved) • characterized by fibrosis and • conversion of normal architecture to structurally abnormal regenerating nodules of liver cells.

  3. CIRRHOSIS • Morphological Characteristics • The three main morphologic characteristics of cirrhosis are: • 1. Fibrosis • 2. Regenerating Nodules • 3. Loss of Architecture

  4. CIRRHOSIS • Morphological Characteristics • 1. Fibrosis • It is the characteristic feature of progressive liver damage. • The fibrous tissue form delicate bands or broad scars and link portal tracts with one another and portal tracts with terminal hepatic veins.

  5. CIRRHOSIS • Morphological Characteristics • 2. Regenerating Nodules • Liver cell damage is compensated by regeneration of hepatocytes. • These regenerating hepatocytes forms nodules and are surrounded by fibrosis. • Nodularity results from cycles of hepatocyte regeneration and scarring. • The regenerating liver cells does not maintain the normal architecture. • The size of nodules vary from very small (< 0.3 cm, micronodules) to large (several centimeters, macronodules).

  6. CIRRHOSIS • Morphological Characteristics • 3. Loss of Architecture • The hepatocyte injury and consequent fibrosis are diffuse processes, which occur in the entire liver. • This disrupts the architecture of the entire liver.

  7. CIRRHOSIS • Classification • Morphological Classification (Fig. 14.20) • Depending on the size of the regeneration nodules cirrhosis is classified • Micronodular Cirrhosis • Macronodular Cirrhosis • Mixed Cirrhosis

  8. CIRRHOSIS

  9. CIRRHOSIS • Classification • Morphological Classification • Micronodular Cirrhosis • It is characterized by regular and small nodules measuring less than 3 mm in diameter. • The fibrous tissue septa are usually thin and fibrous septa bridge portal tracts and central veins (portal-portal and/portal-central) resulting in a small nodule without central structures (e.g. alcoholic cirrhosis).

  10. CIRRHOSIS • Classification • Morphological Classification • Macronodular Cirrhosis • It is characterized by the presence of nodules of variable size, more irregular than in the micronodular cirrhosis and usually larger than 3 mm in diameter. • The fibrous tissue septa are broad and the nodules are more variable in composition and are often composed of multiple acini. • Micronodular cirrhosis can be converted into a macronodular form continued regeneration and expansion of existing nodules. • For example cirrhosis associated with chronic hepatitis. The macronodular cirrhosis has an increased risk of developing carcinoma of liver.

  11. CIRRHOSIS • Classification • Morphological Classification (Fig. 14.20) • Mixed Cirrhosis • It consists of both micronodules and some macronodules. • Depending on the activity, each of these forms may sub-classified as an active and inactive form.

  12. CIRRHOSIS

  13. CIRRHOSIS • Etiological Classification • This classification takes into consideration clinical, biochemical, immunological or biopsy features • Main causes of cirrhosis • Alcohol is one of the commonest causes • Viral hepatitis (HBV and HCV) • Non-alcoholic steatohepatitis (NASH) • Hemochromatosis • Autoimmune liver disease (autoimmune hepatitis and primary biliary cirrhosis) • Intrahepatic or extrahepatic biliary obstruction: Recurrent biliary obstruction (e.g. gallstones) • Metabolic disorders: Wilson’s disease • ‘Cryptogenic’ (hidden cause) or idiopathic • Drugs and toxins • Indian childhood cirrhosis.

  14. CIRRHOSIS • Pathogenesis • Four important processes are involved: • Death of liver cells with loss of architecture: • Fibrosis • Regenerating nodules • Vascular reorganization

  15. CIRRHOSIS • Pathogenesis • Four important processes are involved: • Death of liver cells with loss of architecture: • The pathogenesis of hepatocyte injury varies depending on the etiological agent.

  16. CIRRHOSIS • Pathogenesis • Fibrosis • It is mainly due to the activation of hepatic stellate cells, which are transformed into highly fibrogenic cells called myofibroblasts. • Regenerating nodules • The liver cell damage and fibrosis stimulate the surviving hepatocytes to regenerate and proliferate to form regenerating nodules • •Vascular reorganization: The parenchymal damage and fibrosis disrupt the vascular architecture of the liver

  17. Morphology • Loss of architecture • Fibrosis • Regenerating nodules

  18. CIRRHOSIS • Clinical Features • The clinical features of cirrhosis range widely: • Initial phase: It is termed as “compensated” cirrhosis, the patient may be asymptomatic. • Later phase: It is termed as “decompensated” cirrhosis, presents with complications of portal hypertension or liver dysfunction (or both).

  19. CIRRHOSIS • Clinical Features • Nonspecific clinical manifestations: Anorexia, weight loss, weakness, and in advanced disease, symptoms and signs of hepatic failure may develop. • Hepatic failure is usually precipitated by systemic infection or gastrointestinal hemorrhage.

  20. CIRRHOSISPortal Hypertension • Portal hypertension is defined as the elevation of the hepatic venous pressure above 7 mm Hg. • Causes of Portal Hypertension • The causes of portal hypertension can be divided into three categories: • Prehepatic causes: Obstructive thrombosis of the portal vein before it ramifies within the liver or massive splenomegaly with increased splenic vein blood flow. • Posthepatic causes: E.g. severe right-sided heart failure, constrictive pericarditis, and hepatic vein outflow obstruction. • Intrahepatic causes: E.g. cirrhosis (main cause), schistosomiasis, massive fatty change and diffuse fibrosing granulomatous disease (e.g. sarcoidosis).

  21. CIRRHOSIS • Pathogenesis of Portal Hypertension in Cirrhosis • It is produced by a combination of two simultaneously occurring processes: • 1. Increased intrahepatic resistance to blood flow through the liver: • 2. Increase in portal venous inflow (flow):

  22. CIRRHOSIS • Pathogenesis of Portal Hypertension in Cirrhosis • It is produced by a combination of two simultaneously occurring processes: • 1. Increased intrahepatic resistance to blood flow through the liver: • Deposition of fibrous tissue (scarring) • Fibrosis and compression by regenerative nodules (fixed component) increases the sinusoidal vascular resistance. • In the fibrous septa, anastomosis develop between the arterial and portal system. • These impose arterial pressures on the low pressure portal venous system and contribute to portal hypertension.

  23. CIRRHOSIS • Pathogenesis of Portal Hypertension in Cirrhosis • It is produced by a combination of two simultaneously occurring processes: • 2. Increase in portal venous inflow (flow): • It results from the hyperdynamic circulation/consequences of portal hypertension

  24. CIRRHOSIS • Consequences of Portal Hypertension • i. Ascites. • ii. Formation of portosystemic venous shunts. • iii. Congestive splenomegaly. • iv. Hepatic encephalopathy.

  25. CIRRHOSIS • Ascites • Ascites is defined as the accumulation of excess fluid in the peritoneal cavity. • The most common (85% of cases) cause of ascites is portal hypertension caused by cirrhosis. • Pathogenesis of Ascites in Cirrhosis • It is complex process and involves the following mechanisms: • Portal hypertension: It increases the hydrostatic pressure in portal vein. • Hypoalbuminemia: It is due to decreased synthetic function in a cirrhotic liver → reduces the plasma oncotic pressure. • Splanchnic vasodilation and hyperdynamic circulation. Percolation of hepatic lymph into the peritoneal cavity: In cirrhosis, hepatic lymphatic flow exceeds thoracic duct capacity. The excess lymph may percolate (pass through liver) into the peritoneal cavity and cause ascites.

  26. CIRRHOSIS

  27. CIRRHOSIS

  28. CIRRHOSIS • Portosystemic Shunts/Varices and Variceal Hemorrhage • Main Sites of Portosystemic Shunting/Bypasses • Main sites are • •Esophagogastric junction: These collaterals produce gastroesophageal varices. • •Veins around and within the rectum: It results in rectal varices (manifest as hemorrhoids). • •Retroperitoneum: Collaterals may form in the retroperitoneum, especially in females and communicate between the ovarian vessels and iliac veins. • •Umbilicus: Produce prominent collaterals around the umbilicus. They appear as dilated subcutaneous veins extending from the umbilicus toward the rib margins (caput medusae).

  29. CIRRHOSIS • Splenomegaly and Hypersplenism • Congestive splenomegaly. The spleen is enlarged and varies in size. • Massive splenomegaly may give rise to the syndrome of hypersplenism. • Hypersplenism is characterized by a decrease in the lifespan of all of the formed elements of the blood (pancytopenia). • Pancytopenia of hypersplenism is due to the prolonged transit time of blood through the hyperplastic spleen.

  30. CIRRHOSIS • Morphology • Gross: The spleen is firm and enlarged; up to 1000 g. • Cut surface is uniformly deep red. • Microscopy: The spleen shows dilated sinusoids with thickening of wall due to fibrous tissue. • Focal areas of hemorrhages may lead to the formation of fibrotic, iron-laden nodules. • These are known as Gamna-Gandy bodies.

  31. CIRRHOSIS • Endocrine Complications are Associated with Cirrhosis • It may be either due to the direct effects of alcohol abuse or hepatic dysfunction. • In Men • Hyperestrogenism • Chronic liver failure → reduced hepatic catabolism of estrogens + weak androgens are converted to estrogenic compounds in peripheral tissues → hyperestrogenism → leads to feminization. • The portosystemic shunts secondary to portal hypertension in cirrhosis allow these hormones to bypass the liver. • Feminization is characterized by gynecomastia, a female body habitus, and a female distribution of pubic hair. Hyperestrogenism also causes vascular manifestations, which include spider angiomas (upper trunk and face) and palmar erythema. • Hypogonadism • Chronic alcoholics also develop hypogonadism, which is manifested as testicular atrophy, impotence, and loss of libido. These are due to direct toxic action of alcohol.

  32. CIRRHOSIS • Endocrine Complications are Associated with Cirrhosis • In Women • They may show features of gonadal failure, presenting as oligomenorrhea, amenorrhea, infertility, ovarian atrophy, and loss of secondary sex characteristics. • These effects are due to direct toxic action of alcohol on gonads.

  33. THANK YOU

More Related