Liver Cirrhosis
Cirrhosis of the liver is largely attributed to heavy alcohol use. To understand this disease process, the anatomy of the liver must first be processed. Blood flows from the abdomen and the spleen to the liver and then through it before reaching the heart. After the blood has passed through the liver, it flows into the hepatic vein. The liver receives blood from the hepatic artery. These blood vessels make up the portal system. The portal system is directly connected to the esophagus, stomach and small intestines with little to no back flow under normal conditions (Worman).
Bile, a product of the liver, is synthesized by hepatocytes (the predominant cell type in the liver). This is then secreted into the small bile ducts inside the liver. These ducts form a network that ultimately becomes the common bile duct which takes the bile to the small intestines. Bile helps in the metabolism of cholesterol, drugs and toxins, including alcohol. It also aides in the conversion process of proteins and fats into glucose (Worman).
Toxins, inflammation and other causes damage liver cells. Since the liver has the capability to regenerate itself, these damaged cells are then replaced with fibrous tissue which leads to scarring. The liver is then left firm and decreased blood flow occurs. This leads to the back up of blood in the portal circulation. The back up of blood leads to serious complications. Back up of blood into the spleen causes the spleen to enlarge and sequester blood cells, which then leads to a fall in the platelet count, and eventually, abnormal bleeding. The back up of blood into the stomach, esophagus, and rectum leads to gastric and esophageal varices, and hemorrhoids. These varices can rupture and cause death. Hypertension in the portal circulation can also lead to ascites when combined with other hormonal and metabolic abnormalities. Hepatocytes in cirrhosis decrease the amount of bilirubin secreted, leading to jaundice. The change in blood flow and the malabsorption of nutrients can lead to toxic effects on the brain, called hepatic encephalopathy (Worman).
The changes in the biochemical function of the liver can also lead to complications. Serum albumin falls, leading to an aggravation of ascites and edema. Men can suffer from gynecomastia as the metabolism of estrogen in the liver is decreased. Decreased clotting factors cause excessive bleeding and the metabolism of triglycerides, cholesterol, and sugar can lead to diabetes. Cirrhosis can also lead to immune system depression and kidney dysfunction and failure (Worman).
There are different types of cirrhosis depending on the cause. The first, and most common, is alcoholic cirrhosis. There are different stages of this process. The first is the fatty liver which is an excessive amount of fat accumulated in the liver. Continued alcohol use then leads to an acute inflammatory process in the liver that destroys individual liver cells and leads to scarring. This is called alcoholic hepatitis. The most advanced form of liver disease due to alcohol use is called alcoholic cirrhosis. This is characterized by extensive nonfunctioning scar tissue in the liver (McCance & Huether, 2006).
A second type of cirrhosis begins in the bile canaliculi and the bile ducts, leading to a back up of bile into the liver. This can be further separated into two subgroups; primary and secondary biliary cirrhosis. Primary biliary cirrhosis is an autoimmune disease in which the bile ducts in the liver are destroyed. This leads to portal inflammation and, later, fibrosis. Secondary biliary cirrhosis is caused by a prolonged obstruction of one or many of the bile ducts in the liver. This can be due to tumors, gallstones, or chronic pancreatitis. The chronic pressure in the bile duct leads to proliferation and inflammation of the portal ducts. Once bile spills into the surrounding hepatic tissue, the hepatic cells regenerate abnormally, developing into nodular cirrhosis (McCance & Huether, 2006).
Malnutrition in the alcoholic
Alcohol use can contribute to malnutrition in two ways. First of all, if the alcoholic is replacing nutrients with alcohol, the person will become malnourished. Secondly, even if a chronic alcoholic takes in enough nutrients, alcohol interferes with the absorption of many nutrients. It has been shown that alcoholics have deficiencies in certain vitamins, particularly thiamine, riboflavin, pyyridocine, ascorbic acid, and folic acid (Lieber, 2003 ). That is why often chronic alcoholics are given an intravenous solution containing thiamine, a multivitamin, and folic acid when they present to the hospital. As all vitamins are important to overall wellbeing, thiamine deficiency can lead to cerebral damage. Thiamine deficiency can lead to Wernicke’s encephalopathy, a neurologic disorder in which the patient suffers from acute confusion, nystagmus, paralysis of the oculomotor nerve, ataxia and polyneropathy. Often the patient doesn’t know he has these symptoms, or they are taken for symptoms of a head injury (Dawood, 2008).
Nutrition therapy in the chronic alcoholic is aimed at correcting electrolyte disturbances and shedding access fluid. Protein is essential as it can help to regenerate functional liver tissue. Sodium should be restricted to help reduce fluid retention. Foods should be soft, to avoid perforating an esophageal varice. Vitamins should be given to the patient in amounts almost twice that of what a healthy person should need. Lastly, and obviously, alcohol should be taken completely from the diet (Williams, 1999).
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