Scarred liver

There have been reports on the transition from virus-induced acute liver failure to chronic hepatitis. As the final stage of fulminant viral hepatitis (also known as acute liver dystrophy or submassive hepatitic necrosis), a postdystrophic scarred liver ( potato liver ) can develop. (s. fig. 35.14) Cicatricial distortions with a continuing effect, regenerative processes, intrahepatic vascular disorders and hypoxia-related damage lead to the conclusion that a posthepatitic, postdystrophic scarred liver may well be a special form of cirrhosis. 

A scarred liver (H. Kalk, 1957) develops as a result of a large-scale loss of parenchyma, which is replaced by scar tissue without bulbiform metaplasia. Outside this scar. 

Localized transformation processes such as those observed in scarred liver (s. p. 405) are not considered to be cirrhosis. The loss of parenchyma in scarred liver is generally the result of reduced blood supply in the respective area. Deep-set scars create the picture of a funnel-shaped liver (s. p. 406). Similarly, pronounced liver fibrosis (s. p. 405) does not fulfil the criteria of cirrhosis, since the lobular architecture as well as the intrahepatic and intra-acinar vascular supply are uncompromised. While fibrosis constitutes a precirrhotic stage, it does not necessarily progress to cirrhosis itself Fibrosis can regress Thus, liver cirrhosis is characterized by the following five criteria ... 

Fig. 35.14 Postnecrotic scarred liver after severe viral hepatitis B. Atrophy of the left liver lobe with regenerations, broad cicatricial areas and scarred furrows (s. figs. 21.13 22.16 35.1 )...

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

Sinusoidal damage from cirrhosis is the most common cause of portal hypertension. The sinusoids are porous vessels within the liver that surround radiating rows of hepatocytes, the basic functional cells of the liver (Fig. 19-2). Progressive destruction of hepatocytes and an increase in fibroblasts and connective tissue surrounding the hepatocytes culminate in cirrhosis. Fibrosis and regenerative nodules of scar tissue... 

Progression of alcoholic liver disease moves through several distinct phases from development of fatty liver to the development of alcoholic hepatitis and cirrhosis. Fatty liver and alcoholic hepatitis may be reversible with cessation of alcohol intake, but cirrhosis itself is irreversible. Although the scarring of cirrhosis is permanent, maintaining abstinence from alcohol can still decrease complications and slow development to end-stage liver disease.22 Continuing to imbibe speeds the advancement of liver dysfunction and its complications. 

Primary biliary cirrhosis is characterized by progressive inflammatory destruction of the bile ducts. Immune-mediated inflammation of intrahepatic bile ducts results in remodeling and scarring, causing retention of bile within the liver and subsequent hepatocellular damage and cirrhosis. The number of patients affected with primary biliary cirrhosis is difficult to estimate because many people are asymptomatic and incidental diagnosis during routine health care visits is common. 

Figure 5. Detection of male MSC by Y-PCR. Y chromosome PCR at 24 h after MSC infusion from a male donor into female recipients with AKl. The only organ positive for Y chromosome DNA was the lung (lane 2). Kidney cortex and medulla as well as liver and spleen from 2 animals were negative (lanes 3-11). Lane designation A-female DNA B-male DNA 2 lung 3-kidney cortex 4-kidney medulla 5-liver 6-spleen 7-wound scar 8-lung 9-bone marrow 10-liver 11-spleen.

Whether liver regeneration will dominate over scar tissue formation depends on many factors, including the nature and the duration of the injury and the genetic background of the individual. It is still unclear at which point liver regeneration is no longer possible and fibroge-... 

As the process continues, the liver becomes less functional and a fibrosis process starts that can lead to cirrhosis or scarring of the liver. Continued drinking can result in death, but if the drinking stops, function of the liver can improve although the damage is irreversible. 

Alcohol is toxic to the liver, and prolonged use results in cirrhosis, a condition in which scar tissue replaces normal liver tissue, and impairs the ability of the liver to function. Ghronic use can also result in permanent damage to the GNS, partly due to a poor diet regimen and diminished intake of vitamin B1 (thiamine). 

Health consequences of chronic heroin abuse include scarred and collapsed veins, bacterial infections of the blood vessels and heart valves, boils, a variety of soft-tissue infections, kidney problems, and liver disease. Pneumonia, tuberculosis, and other lung diseases are also common among long-term users, which can be attributed to either poor nutrition and depressed respiratory function or both. Many of the additives heroin is cut with do not dissolve in the body and can block blood vessels, translating into higher risk of sudden death from stroke or heart attack. 

Ashbum LL, McQueeney AJ, Faulkner RR. 1948. Scarring and precirrhosis of the liver in chronic phosphorus poisoning of guinea pigs. Proc Soc Exp Biol Med 67 351-358. 

Toxic effects to the liver are studied under the topic of hepatotoxicity, and substances that are toxic to the liver are called hepatotoxins. Much is known about hepatotoxicity from the many cases of liver toxicity that are a manifestation of chronic alcoholism.6 Liver injury from excessive alcohol ingestion initially hampers the ability of the organ to remove lipids, resulting in their accumulation in the liver (fatty liver). The liver eventually loses its ability to perform its metabolic functions and accumulates scar tissue, a condition known as cirrhosis. Inability to synthesize clotting factors can cause fatal hemorrhage in the liver. 

Toxicity Ethylamine causes severe irritancy to exposed skin, eyes, and mucous membranes. Direct contact with the skin of experimental animals resulted in skin bums, scarring, and necrosis.37-39 The chemical also caused adverse effects and degenerative changes in heart, liver, lung, kidney, and associated injury to the endocrine system of animals.40... 

Figure 31-4. Hepatic stellate cell activation. Iron-induced injury to hepatocytes can activate Kupffer cells through the release of soluble growth factors that contribute to scarring of the liver through activation of hepatic stellate cells (HSQ. Reprinted with permission from Pietrangelo (1998). 1998, European Association for the Study of the Liver.

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