Cirrhosis Liver cirrhosis Liver cirrhosis
is a chronic inflammation of the liver that begins with degeneration and shrinkage of hepatocytes, formation of connective tissue septa and nodular areas of degeneration that leads to a serious disruption of the normal lobular architecture of the organ.
Cirrhosis can 'be the culmination of different diseases:
-can' be the final stage of post-hepatitis cirrhosis of the liver as it affects 10% of patients with hepatitis B inability 'to eliminate the virus liver.
vision, has been demonstrated by the existence and replication studies on molecular hybridization of biopsy specimens.
It 's not known, unfortunately,' cause of the persistence of the virus in these cases: it is known that the immune response involves the destruction of infected hepatocytes by activated lymphocytes and then the elimination of virus from the blood by specific antibodies, but these patients usually still high levels of HBsAg, HBcAb and of HBeAb, can 'be, however, Australia-negativity' and this is the rule in chronic hepatitis non A and B that they are becoming more and more 'frequent as in cases of post-transfusion hepatitis is now a non-A, not B.
happens in this case through the connective tissue proliferation in departing from the portal tracts and the spread of this industry within the lobules, resulting first "chipped" the edges and then fragmented by the formation of septa connective, the degenerative changes and necrosis of hepatocytes are relevant. In cases of acute hepatitis with massive necrosis occurs instead the formation of seven steps by the collapse of the parenchyma as in post-necrotic cirrhosis. With
mode 'similar diseases may progress to cirrhosis of the liver granulomatous and parasitic diseases such as schistosomiasis, which can' be the final stage of a fatty liver inherent in alcoholism or malnutrition.
And 'demonstrated a positive statistical correlation between alcohol and mortality consuno' for liver cirrhosis. And the risk increases with dose and with time in those who drink more 'than 160 grams of alcohol per day, the probability' of cirrhosis greatly increased.
L 'is ethyl alcohol metabolized to 90% from where it is transformed into fegto acetaldehyde by the action of an alcohol dehydrogenase
---------------- CH3CH2OH CH3CHO + NAD + NADH + H
Strong Notice of oxygen necessary for the reoxidation of NADH committed Krebs cycle by reducing the capacity 'to oxidize fatty acids which, esterified to triglycerides, are deposited as such in hepatocytes in fatty liver.
Fatty liver, manifested by hepatomegaly that is' sluggish liver, liver cells are filled with fat droplets that move the nucleus and cytoplasm to the periphery in common histological staining the fat is dissolved and hepatocytes as many as in the empty bladders microvesicular cirrhosis. The
cell necrosis is stimulating cell proliferation and deposition of collagen Kappfer that aggregate to form connective trabeculae these seven activities, which disrupt the lobular architecture, particularly the intrahepatic circulation.
The ability 'to regenerate the liver cells leads to the formation of regenerated liver nodules and also in a proliferation of nodules and bile' was interpreted in regenerative.
in end-stage liver shrinks, so it becomes hard and uneven surface texture: its section will 'detect small numbers of yellowish nodules surrounded by rings of dense connective tissue that annular cirrhosis of Morgagni-Laennec.
I believe, be universally accepted hypothesis that alcohol acts through a protein deficiency harmful to the liver, dyspepsia for atrophic gastritis of habitual alcoholics.
The dispute has arisen by analogy with other situations of hepatic steatosis due to nutritional although only a minority of these cases progress, in my opinion, in cirrhosis. In prolonged fasting
as in intestinal malabsorption and obesity '
It' obvious that additional protein deficiencies affecting popolazine of the world's poor, can accelerate the development of fatty liver disease alcoholic cirrhosis, and can 'be the final stage of proliferation with angiocholitis Connective pericolangitica spaces portals with the formation of connective tissue septa that extend to disrupt the hepatic lobules and achieve with their interconnecting bridges between areas of portal and centrilobular areas. Can 'be the final stage of un'emocromatosi in which iron accumulation damages the liver cells and stimulates proliferation connective. Can 'be the final stage of Wilson's disease in which the accumulation of damaged hepatocytes reme making in stages steatosis, necrosis leading to cirrhosis with large nodes.
Can 'be due to the absence of alpha-1-antitrypsin, and that' a glycoprotein acting antitriptica and antiplasmatica.
This is a rare autosomal recessive hereditary disease that manifests in childhood with liver cirrhosis and pulmonary emphysema.
Federico Cesareo
