Cirrhotic liver

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

In domestic pigs, copper toxicosis results from eating diets containing 250 mg Cu/kg ration and is characterized by anemia, jaundice, elevated levels of Cu in serum and liver, and elevated serum AAT activity (USEPA 1980). Shortly before death, copper-poisoned pigs had white noses, poor balance, stomach histopathology, orange cirrhotic livers, anorexia, and anemia (Higgins 1981). 

A 34-year-old woman who had taken danazol 400 mg/ day for 13 years for hereditary angioedema developed a mass in the right hypochondrium. Her alcohol intake was under 20 g/day. She had a large heterogeneous hepatic tumor, a well-differentiated hepatocellullar carcinoma in a non-cirrhotic liver. 

The increased susceptibility to bleeding observed in patients with liver failure (raised INR) results from depressed fibrinogen levels and the reduced synthesis of clotting factors by the cirrhotic liver. In addition, the absorption of fat-soluble vitamin K is impaired in cholestasis and subsequently the synthesis of vitamin K-dependent clotting factors is reduced. 

Liver disease may be classified as cholestatic, hepatocellular or cirrhotic. Liver disease may be acute, with the history of onset of less than six months, or chronic, occurring over periods greater than six months. Viral infections and drug reactions are leading causes of acute liver disease in both adults and children. 

The use of hormonal contraceptives for eight years or more has led to a 4.4-fold increased risk of hepatocellular carcinoma [24]. Snch tumours develop in non-cirrhotic livers, and it has been found that they metastasise rarely and do not infiltrate [16]. There are limited data specifically on POCs. Results from a WHO study provided no evidence that use of DMPA altered the risk of developing liver cancer, but the power of the study to detect small alterations in risk was low [5]. 

In delayed-phase imaging, the signal increase in the liver parenchyma does not necessarily increase the conspicuity or detection of lesions because residual hepatocytes of a tumor of hepatocytic origin, such as hepatocellular carcinoma (HCC) and focal nodular hyperplasia, may influence the contrast enhancement. Gd-BOPTA is effective for use with delayed-phase MRI to detect metastases [130]. In cirrhosis, liver functioning is impaired and the number of normal hepatocytes is reduced. The entry of Gd-BOPTA into cirrhotic hepatocytes decreases, but the accumulation in the liver increases due to reduced biliary excretion [131]. As a consequence, contrast enhancement is reduced and the window of acquisition is widened. The contrast enhancement of a cirrhotic liver is therefore different from that observed in normal liver parenchyma. 

Yoo, H.J., Lee, J.M., Lee, M.W., et al. (2008) Hepatocellular carcinoma in cirrhotic liver double-contrast-enhanced, high-resolution 3. OT-MR imaging with pathologic correlation. Investigative Radiology, 43, 538-546. 

Liver damage from excessive ethanol consumption occurs in three stages. The first stage is the aforementioned development of fatty liver. In the second stage—alcoholic hepatitis—groups of cells die and inflammation results. This stage can itself be fatal. In stage three—cirrhosis—fibrous structure and scar tissue are produced around the dead cells. Cirrhosis impairs many of the liver s biochemical functions. The cirrhotic liver is unable to convert ammonia into urea, and blood levels of ammonia rise. Ammonia is toxic to the nervous system and can cause coma and death. Cirrhosis of the liver arises in about 25% of alcoholics, and about 75% of all cases of liver cirrhosis are the result of alcoholism. Viral hepatitis is a nonalcoholic cause of liver cirrhosis. 

Henriksen, J.H., Horn, T., Christoffersen, P. The blood-lymph barrier in the liver. A review based on morphological and functional concepts of normal and cirrhotic liver. Liver 1984 4 221—232... 

The size of the cirrhotic liver varies between hepatomegaly, normal finding and atrophy. The regular pro-... 

Detection of malignant tumours in end-stage cirrhotic livers efficacy of sonography as a screening technique. Amer. J. Roentgenol. 1992 159 727-733... 

M., Ishii, H. Enhanced expression of endothelin B receptor at protein and gene levels in human cirrhotic liver. J. Pathol. 2001 159 1353-1362... 

Kalayci, C., Johnson, P.J., Davies, S.E., Williams, R. Hepatitis B virus related hepatocellular carcinoma in the non-cirrhotic liver. X Hepatol. 1991 12 54-59... 

Terada, T., Nakamura, Y. Iron negative foci in siderotic macroregener-ative nodules in human cirrhotic liver. A marker of incipient neoplastic lesion. Arch. Path. Lab. Med. 1989 113 916-920... 

Mixed-nodular cirrhosis is considered to be a transitional form between micronodular and macronodular cirrhosis (V.J. Desmet et al., 1990). Due to variations in the regenerative capacity of the cirrhotic liver, 50% of... 

Causes The following causes are seen as being responsible for an acquired immune deficiency syndrome in liver cirrhosis (B.A. Runyon, 1995) (i.) hypofunction of the RES (a decrease in the filter or clearance function and phagocytosis capacity as well as reduced formation of immune modulators) (s. p. 65), (2.) reduction in hepatic synthesis of opsonins (s. p. 66), (3.) compromised function of leucocytes, (4.) impaired proliferation and activation of T lymphocytes, and (5.) increased mucosa permeability to bacteria. Both bacteria and bacterial lipopolysaccharides enter the organism in large numbers. They are responsible for increased serum levels of the cytokines (e. g. interleukins 1 and 6, TNF, y-interferon), and there is increased production of these substances together with their reduced breakdown in the cirrhotic liver. Cytokines are formed in the monocytes of blood and in the mononuclear cells of various organs (above all in ascites). 

Guslandi, M., Foppa, L., Soirghi, M., Pellegrini, A., Fanti, L., Titto-bello. A. Breakdown of mucosal defences in congestive gastropathy in cirrhotics. Liver 1992 12 303-305... 

Lafortune, M., Matricardi, L., Denys, A., Favret, M., Dery, R., Ponnier-Layrargues, G. Segment 4 (the quadrate lobe) a barometer of cirrhotic liver disease at US. Radiology 1998 206 157-160... 

Le Bail, B., Bernard, P.-H., Carles, J., Balabaud, C., Bioulac-Sage, R Prevalence of liver cell dysplasia and association with HCC in a series of 100 cirrhotic liver explants. X. Hepatol. 1997 27 835-842... 

Matsui, O., Kadoya, M., Kameyama, T., Yoshikawa, X, Aral, K., Gabata, T., Kakashima, T., Nakanuma, Y., Terada, T., Ida. M. Adenomatosis hyperplastic nodules in the cirrhotic liver differentiation from hepatocellular carcinoma with MR imaging. Radiology 1989 173 123-126... 

Winston, C.B., Schwartz, L.H., Fong, YJW., Blnmgart, L.H., Panicek, DJW. Hepatocellular carcinoma MR imaging findings in cirrhotic livers and noncirrhotic livers. Radiology 1999 210 75-79... 

Fig. 37.10 Fibrolamellar hepatocellular carcinoma as is usually seen in a non-cirrhotic liver...

Britto, M.R.C., Thomas, LA., Balaratnam, N., Griffiths, A.P., Duane, P.D. Hepatocellular carcinoma arising in non-cirrhotic liver in genetic haemochromatosis. Scand. J. Gastroenterol. 2000 35 889-893... 

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