How Cirrhosis Happens Pathologically and Physiologically - Essay Example

Book Brennfleck Shannon, Joyce. Alcoholism Sourcebook (3rd ed). Detroit, MI: Omnigraphics Inc. Section 21.2 Cirrhosis Cirrhosis is a condition in which the liver slowly deteriorates and malfunctions due to chronic injury. Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver’s ability to: Control Infections Remove bacteria and toxins from the blood Process nutrients, hormones and drugs Make proteins that regulate blood clotting Produce bile to help absorb fats-including cholesterol and fat soluble vitamins A healthy liver is able to regenerate most of its own cells when they become damaged. With end-stage cirrhosis, the liver can no longer effectively replace damaged cells. A healthy liver is necessary for survival. Cirrhosis has various causes: In the United States, heavy alcohol consumption and chronic hepatitis C have been the most common causes of cirrhosis. Obesity is becoming a common cause of cirrhosis, either as the sole cause or in combination with alcohol, hepatitis C, or both. Many people with cirrhosis have more than one cause of liver damage. Cirrhosis is not caused by trauma to the liver or other acute, or short-term, causes of damage. Usually years of chronic injury are required to cause cirrhosis. 210 Symptoms of cirrhosis: Many people with cirrhosis have no symptoms in the early stages of the disease. However, as the disease progresses, a person may experience weakness, fatigue, loss of appetite, nausea, vomiting, weight loss, abdominal pain and bloating when fluid accumulates in the abdomen, itching, or spiderlike blood vessels on the skin. Figure 21.1. The Liver and Digestive System Diagnosis of cirrhosis: The diagnosis of cirrhosis is usually based on the presence of a risk factor for cirrhosis, such as alcohol use or obesity, and is confirmed by physical examination, blood tests, and imaging. The doctor will ask about the person’s medical history and symptoms and perform a thorough physical examination to observe for clinical signs of the disease. For example, on abdominal examination, the liver may feel hard or enlarged with signs of ascites. The doctor will order blood tests that may be helpful in evaluating the liver and increasing the suspicion of cirrhosis. 211 To view the liver for signs of enlargement, reduced blood flow, or ascites, the doctor may order a computerized tomography (CT) scan,tor may look at the liver directly by inserting a laparoscope into the abdomen. A laparoscope is an instrument with a camera that relays pictures to a computer screen. A liver biopsy can confirm the diagnosis of cirrhosis but is not always necessary. A biopsy is usually done if the result might have an impact on treatment. The biopsy is performed with a needle inserted between the ribs or into a vein in the neck. Precautions are taken to minimize discomfort. A tiny sample of liver tissue is examined with a microscope for scarring or other signs of cirrhosis. Sometimes a cause of liver damage other than cirrhosis is found during biopsy. Treatment of cirrhosis: Treatment for cirrhosis depends on the cause of the disease and whether complications are present. The goals of treatment are to slow the progression of scar tissue in the liver and prevent or treat the complications of the disease. Hospitalization may be necessary for cirrhosis with complications. Eating a nutritious diet and avoiding alcohol and other substances is advised. The health care team will also provide treatment for specific complications When is a liver transplant indicated for cirrhosis? A liver transplant is considered when complications cannot be controlled by treatment. Liver transplantation is a major operation in which the diseased liver is removed and replaced with a healthy one from an organ donor. A team of health professionals determines the risks and benefits of the procedure for each patient. Survival rates have improved over the past several years because of drugs that suppress the immune system and keep it from attacking and damaging the new liver. Generally, organs are given to people with the best chance of living the longest after a transplant. Article 1 Lee, Dennis. Cirrhosis (Cirrhosis of the liver). 2014. 13 May 2014. What is cirrhosis? Cirrhosis is a complication of many liver diseases characterized by abnormal structure and function of the liver. The diseases that lead to cirrhosis do so because they injure and kill liver cells, after which the inflammation and repair that is associated with the dying liver cells causes scar tissue to form. The liver cells that do not die multiply in an attempt to replace the cells that have died. This results in clusters of newly-formed liver cells (regenerative nodules) within the scar tissue. There are many causes of cirrhosis including chemicals (such as alcohol, fat, and certain medications), viruses, toxic metals (such as iron and copper that accumulate in the liver as a result of genetic diseases), and autoimmune liver disease in which the bodys immune system attacks the liver. Edema and ascites As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and water in the body. The excess salt and water first accumulates in the tissue beneath the skin of the ankles and legs because of the effect of gravity when standing or sitting. This accumulation of fluid is called edema or pitting edema. (Pitting edema refers to the fact that pressing a fingertip firmly against an ankle or leg with edema causes an indentation in the skin that persists for some time after release of the pressure. Actually, any type of pressure, such as from the elastic band of a sock, may be enough to cause pitting.) The swelling often is worse at the end of a day after standing or sitting and may lessen overnight as a result of the loss of the effects of gravity when lying down. As cirrhosis worsens and more salt and water are retained, fluid also may accumulate in the abdominal cavity between the abdominal wall and the abdominal organs. This accumulation of fluid (called ascites) causes swelling of the abdomen, abdominal discomfort, and increased weight. What are the common causes of cirrhosis? Alcohol is a very common cause of cirrhosis, particularly in the Western world. The development of cirrhosis depends upon the amount and regularity of alcohol intake. Chronic, high levels of alcohol consumption injure liver cells. Thirty percent of individuals who drink daily at least eight to sixteen ounces of hard liquor or the equivalent for fifteen or more years will develop cirrhosis. Alcohol causes a range of liver diseases; from simple and uncomplicated fatty liver (steatosis), to the more serious fatty liver with inflammation (steatohepatitis or alcoholic hepatitis), to cirrhosis.  Chronic viral hepatitis is a condition where hepatitis B or hepatitis C virus infects the liver for years. Most patients with viral hepatitis will not develop chronic hepatitis and cirrhosis. For example, the majority of patients infected with hepatitis A recover completely within weeks, without developing chronic infection. In contrast, some patients infected with hepatitis B virus and most patients infected with hepatitis C virus develop chronic hepatitis, which, in turn, causes progressive liver damage and leads to cirrhosis, and, sometimes, liver cancers.  Inherited (genetic) disorders that result in the accumulation of toxic substances in the liver, which leads to tissue damage and cirrhosis. Examples include the abnormal accumulation of iron (hemochromatosis) or copper (Wilsons disease). In hemochromatosis, patients inherit a tendency to absorb an excessive amount of iron from food. Over time, iron accumulation in different organs throughout the body causes cirrhosis, arthritis, heart muscle damage leading to heart failure, and testicular dysfunction causing loss of sexual drive. Treatment is aimed at preventing damage to organs by removing iron from the body through bloodletting (removing blood). In Wilson disease, there is an inherited abnormality in one of the proteins that controls copper in the body. Over time, copper accumulates in the liver, eyes, and brain. Cirrhosis, tremor, psychiatric disturbances and other neurological difficulties occur if the condition is not treated early. Treatment is with oral medication, which increases the amount of copper that is eliminated from the body in the urine.  Primary biliary cirrhosis (PBC) is a liver disease caused by an abnormality of the immune system that is found predominantly in women. The abnormal immunity in PBC causes chronic inflammation and destruction of the small bile ducts within the liver. The bile ducts are passages within the liver through which bile travels to the intestine. Bile is a fluid produced by the liver that contains substances required for digestion and absorption of fat in the intestine, as well as other compounds that are waste products, such as the pigment bilirubin. (Bilirubin is produced by the breakdown of hemoglobin from old red blood cells.). Along with the gallbladder, the bile ducts make up the biliary tract. In PBC, the destruction of the small bile ducts blocks the normal flow of bile into the intestine. As the inflammation continues to destroy more of the bile ducts, it also spreads to destroy nearby liver cells. As the destruction of the hepatocytes proceeds, scar tissue (fibrosis) forms and spreads throughout the areas of destruction. The combined effects of progressive inflammation, scarring, and the toxic effects of accumulating waste products culminates in cirrhosis.  Primary sclerosing cholangitis (PSC) is an uncommon disease frequently found in patients with Crohns disease and ulcerative colitis. In PSC, the large bile ducts outside of the liver become inflamed, narrowed, and obstructed. Obstruction to the flow of bile leads to infections of the bile ducts and jaundice, eventually causing cirrhosis. In some patients, injury to the bile ducts (usually as a result of surgery) also can cause obstruction and cirrhosis of the liver. Article 1 Ramadori, G, F Moriconi, I Malik and J Dudas. Physiology and pathophysiology of liver inflammation damage and repair. Journal of Physiology and Pharmacolog, 59.1 2008):107-117. The pictures are in the compressed file Article 1 Schuppan, Detlef, and Afdhal Nezam. Liver Cirrhosis. The Lancet, 371.9615(2008): 838-851. Detlef Schuppan, Nezam H Afdhal Cirrhosis is defi ned as the histological development of regenerative nodules surrounded by fi brous bands in response to chronic liver injury, which leads to portal hypertension and end-stage liver disease. Recent advances in the understanding of the natural history and pathophysiology of cirrhosis, and in treatment of its complications, have resulted in improved management, quality of life, and life expectancy of patients. Liver transplantation remains the only curative option for a selected group of patients, but pharmacological treatments that can halt progression to decompensated cirrhosis or even reverse cirrhosis are currently being developed. This Seminar focuses on the diagnosis, complications, and management of cirrhosis, and new clinical and scientifi c developments. Introduction Fibrosis describes encapsulation or replacement of injured tissue by a collagenous scar. Liver fi brosis results from the perpetuation of the normal wound-healing response, resulting in an abnormal continuation of fi brogenesis (connective tissue production and deposition). Fibrosis progresses at variable rates depending on the cause of liver disease, environmental factors, and host factors.1–3 Cirrhosis is an advanced stage of liver fi brosis that is accompanied by distortion of the hepatic vasculature. The resultant vascular distortion leads to shunting of the portal and arterial blood supply directly into the hepatic outfl ow (central veins), compromising exchange between hepatic sinusoids and the adjacent liver parenchyma—ie, hepatocytes. The hepatic sinusoids are lined by fenestrated endothelia that rest on a sheet of permeable connective tissue in the space of Disse, which also contains hepatic stellate cells and some mononuclear cells. The other side of the space of Disse is lined by hepatocytes that execute most of the known liver functions. In cirrhosis, the space of Disse is fi lled with scar tissue and endothelial fenestrations are lost, a process known as sinusoidal capillarisation.4 Histologically, cirrhosis is characterised by vascularised fi brotic septa that link portal tracts with each other and with central veins, resulting in hepatocyte islands surrounded by fi brotic septa and that are devoid of a central vein (fi gure 1). The major clinical consequences of cirrhosis are impaired hepatocyte (liver) function, an increased intrahepatic resistance (portal hypertension), and the development of hepatocellular carcinoma. The general circulatory abnormalities in cirrhosis (splanchnic vasodilation, vasoconstriction and hypoperfusion of kidneys, water and salt retention, increased cardiac output) are intimately linked to the hepatic vascular alterations and resulting portal hypertension. Cirrhosis and its associated vascular distortion are traditionally regarded as irreversible but recent data suggest that cirrhosis regression or even reversal is possible. Causes of cirrhosis Causes of cirrhosis can usually be identifi ed by the patient’s history combined with serological and histological investigation (table 1).9–17 Alcoholic liver disease and hepatitis C are the most common causes in developed countries, whereas hepatitis B is the prevailing cause in most parts of Asia and sub-Saharan Africa. After the identifi cation of hepatitis C virus in 1989 and of non-alcoholic steatohepatitis in obese patients with diabetes, the diagnosis of cirrhosis without an apparent cause (cryptogenic cirrhosis) is rarely made. The causes of cirrhosis can predict complications and direct treatment decisions. Knowledge of the cause also allows the discussion of preventive measures, for example, with family members of patients with alcoholic cirrhosis or chronic viral hepatitis, and cons ideration of (genetic) testing and preventive advice for relatives of patients with genetic diseases, such as haemochromatosis or Wilson’s disease. Epidemiological studies have identifi ed a number of factors that contribute to the risk of developing cirrhosis. Regular (moderate) alcohol consumption, age older than 50 years, and male gender are examples that increase cirrhosis risk18–20 in chronic hepatitis C infection, and older age, obesity, insulin resistance or type 2 diabetes, hypertension, and hyperlipidaemia (all features of the metabolic syndrome) in non-alcoholic steatohepatitis. Read More