الفهرس 
Liver cirrhosisOnly 14 pages are availabe for public view
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Abstract
The liver performs several vital functions: it processes and stores many of the nutrients absorbed from the intestine, it secretes bile into the intestine to help absorb nutrients, and it also makes some of the clotting factors needed to stop bleeding from a cut or an injury. In addition, the liver plays a very important part in removing toxic wastes from the body like alcohol and dietary toxins.
Cirrhosis of the liver is a long-term disease that represents the end stage of a chronic liver injury. It has many causes, including infectious and hereditary diseases and in some cases, the cause is unknown.
The liver plays a central role in whole body nitrogen metabolism so; liver failure and the resulting hepatocellular dysfunction will result in disturbed body nitrogen homeostasis. In liver failure, the diminished hepatic urea synthesis capacity and the intra- and/or extra hepatic shunting of portal blood into the systemic circulation are crucial. These characteristics lead to an alteration in interorgan ammonia trafficking, resulting in hyperammonemia.
Hepatic retinopathy is suggested to be caused by the high level of serum ammonia in patients with liver insufficiency and the primary pathological alterations are found in Müller cells.
In the retina, the detoxification of excess ammonia occurs predominantly in Müller cells, the main macroglial element in the retina, by the glutamate dehydrogenase (GS) and formation of glutamine from ammonia and glutamate.
As Müller cells play a wealth of crucial roles in retinal functioning, it has been suggested that alterations in Müller cells due to excess ammonia cause significant impairments of neuronal functions.
Retinal toxicity occurs during pegylated α-interferon and ribavirin therapy for chronic hepatitis C. In the majority of cases, fundoscopic changes are reversible during or after treatment, although in a small number of cases permanent changes to vision occur.
Clinically, the ophthalmic pathologies of cirrhosis involve vitamin A deficiency and night blindness since liver is the organ where vitamin A is deposited and cirrhosis of liver in itself is well known to cause malnutrition and malabsorption especially of fat soluble vitamins.
Patients suffering from cirrhosis with improved liver function after liver transplantation displayed significantly improved ERG parameters. This means that an improvement of retinal activity occurs in patients after liver transplantation, and that recovery of the cells involved in hepatic retinopathy, including the Müller cells, can be achieved.