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CHRONIC LIVER DISEASE – CIRRHOSIS

By – Dr. T.VISHNU MURTHY
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Chronic active hepatitis is characterized pathologically by a normal labour architecture in which fibrous septaextend from enlarged tracts into parenchyma, disrupting the liver cell plates adjacent to the portal zones and separating off rosettes of parenchymal cells. Piecemeal necrosis of liver cells adjacent to the expanding portal zones, lymphocytes and plasma cells, and focal necrosis and inflammation with in liver lobules are present in varying degrees and reflect the “activity” of the lesion. Progressive destruction of the normal labour architecture with proliferation of fibroblasts in expanding portal areas and nodular regeneration of parenchymal cells may ultimately lead to cirrhosis in untreated patients.

LIVER CIRRHOSIS
ABOUT

The cirrhotic liver is one in which the normal labour archchitecture is destroyed by bonds of fibrous tissue which separate nodules of regenerated liver cells. Patients with cirrhosis usually present with symptoms that relate to the primary etiology, example; chronic active hepatitis or manifestations of excessive alcohol intake or with complications of cirrhosis (example:, ascites, bleeding from essophageal varices, or hepatic coma.) At the time of diagnosis major etiologic factors causing chronic liver disease may be evident, (example: documented hepatitis progressing to chronic active hepatitis, excessive alcohol intake or chronic biliary tract obstruction), but in many patients the etiology will never be determined.

Macroscopic and/ or microscopic examination of liver tissue is necessary to establish the diagnosis of cirrhosis; it was classified into six catogories.

  1. Posthepatitic and idiopathetic cirrhosis.
  2. Cirrhosis in the alcoholic.
  3. Metabolic cirrhosis (hemochromatosis disease)
  4. Biliary cirrhosis ( primary and secondary )
  5. Schistosomal fibrosis.
  6. Cardiac cirrhosis.
POSTHEPATITIC AND IDIOPATHETIC CIRRHOSIS

It has been shown by serial liver biopsy studies that active viral hepatitis or toxic hepatitis complicated by subacute hepatic necrosis or chronic active hepatitis may lead to a macro nodular cirrhosis. In many non alcoholic patients there is no history to suggest previous viral or toxic hepatitis. Idiopathic cirrhosis is sometimes associated with chronic ulcerative colitis, it has been suggested but not proved that chronic pericholangitis resulting from portal bacteraemia may cause cirrhosis. In these patients cirrhosis may be caused by immunologic destruction of parenchymal cells, an increased formation of immunoglobulin’s with hyper globulinemia may be stimulated by antigens released from necrotic cells, and may have no primary etiologic significance.

CIRRHOSIS IN THE ALCOHOLIC

The liver cirrhosis would explain why many persons with a chronic heavy intake of alcoholic do not develop liver disease; both genetic and dietary factors may be of importance. Some insight into the problem of liver disease in the alcoholic has been gained from experimental studies on the effect of alcohol ( ethanol ) on liver metabolism.

Liver function tests reveal conjugated hyper bilirubiremia elevated serum transaminase levels (50 to 300 UNITS ), variable increases alkaline phasphatase activity, and normal or depressed levels of albumin clotting factors. The serum cholesterol concentration may be increased, normal or depressed. Hypokalemia often results from increased urinary excretion of potassium. Hyperuricemia resulting from depressed urinary excretion of uric acid parallels lactic acidosis. Anaemia may be due to bleeding or hemolysis; acute severe hemolysis is sometimes associated with hyperlipemia (ZIEVE’S SYNDROME).

Cirrhosis in the alcoholic may present insidiously with anorexia, fatigue, and weakness,and a gradual onset of jaundice or coma, or symptoms of hepatic carcinoma. When the cirrhotic patient shows manifestations of often used in the absence of these complications the only stigmata of cirrhosis may be a firm, enlarged, non tender liver with or without splenomegaly, and the cutaneous manifestations of chronic liver disease.

BILIARY CIRRHOSIS

Primary biliary cirrhosis ( chronic suppuratives destructive cholangitis ) is a disease of unknown etiology. Chronic intrahepatic cholestasis is associated with progressive periportal fibrosis and chromic inflammation cirrhosis with nodular regeneration is a late pathologic finding. Although hypersensitivity reactions to drugs sometimes cause prolonged intrahepatic cholestasis , there is no evidence that acute intrahepatic cholestasis leads to primary biliary cirrhosis. It has been suggested that the primary lesion may be injury to small bile ducts , these are often absent in liver biopsy specimens taken early in the cause of this disease, but regenerate in the course of the disease, but regenerate in the cirrhotic liver. Patients with primary biliary cirrhosis may exhibit hypergammaglobulemia with circulating antibodies reactive against mitochondria (anti mitochondrial antibody ), but the significance immunologic phenomena has not been established.

In the secondary biliary cirrhosis, bile duct obstruction with or without infection causes periportal inflammation with progressive fibrosis, parenchymal cell destruction, and nodular regeneration.

CARDIAC CIRRHOSIS

Chronic congestive heart failure with valvular heart disease and tricuspid incompetence or constructive pericarditis may cause progressive fibrosis extending peripherally from centrilobular to portal areas .regeneration nodules are not prominent. Fat may accumulate in hypoxic cells.

The liver is usually firm, with tenderness and increase in size during more severe episodes of heart failure. Hepatic pulsation may be detected with tricuspid in sufficiency. The change in liver function are those of acute hepatic congestion, but hypoalbuminemia may be more severe when there is excessive enteric leakage of plasma protein. Although chronic congestive heart failure may raise the portal venous pressure, a portal – systemic collateral circulation, example : esophageal varices, does not develop in the absene of an increased pressure gradient between these systems.

TREATMENT

According to ancient treatment in Ayurvedic Research of the patient condition with the individual formula and by using of herbal medicine. ( www.nectarhealth.org ).