Cirrhosis is a condition in which the liver does not function properly due to long-term damage. This damage is characterized by the replacement of normal liver tissue by scar tissue. Cirrhosis is most commonly caused by alcohol, hepatitis B, hepatitis C, and non-alcoholic fatty liver disease. Some causes of cirrhosis, such as hepatitis B, can be prevented by vaccination.
Treatment partly depends on the underlying cause, but the goal is often to prevent worsening and complications. 8 million people and resulted in 1. Of these, alcohol caused 348,000, hepatitis C caused 326,000, and hepatitis B caused 371,000. These signs and symptoms may be either a direct result of the failure of liver cells, or secondary to the resultant portal hypertension. There are also some manifestations whose causes are nonspecific but which may occur in cirrhosis. Likewise, the absence of any signs does not rule out the possibility of cirrhosis. The following features are as a direct consequence of liver cells not functioning. Palmar erythema is a reddening of palms at the thenar and hypothenar eminences also as a result of increased estrogen. This is different from increase in breast fat in overweight people.
Hypogonadism is associated with cirrhosis due to alcoholism or hemochromatosis. Liver size can be enlarged, normal, or shrunken in people with cirrhosis. This may be visible as an increase in abdominal girth. Fetor hepaticus is a musty breath odor resulting from increased dimethyl sulfide. The urine may also appear dark. Liver cirrhosis increases resistance to blood flow and leads to higher pressure in the portal venous system, resulting in portal hypertension.
When these blood vessels become enlarged, they are called varices and are more likely to rupture. Caput medusa are dilated periumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be shunted through the periumbilical veins and ultimately to the abdominal wall veins, manifesting as a pattern that may resemble the head of Medusa. There are some changes seen in cirrhosis whose causes are not clearly known. They may also be a sign of other non-liver related causes. It is not specific for cirrhosis.
Chronic proliferative periostitis of the long bones that can cause considerable pain. As the disease progresses, complications may develop. In some people, these may be the first signs of the disease. Bruising and bleeding resulting from decreased production of coagulation factors. Sensitivity to medication caused by decreased metabolism of the active compounds. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates.
In NASH, fat builds up in the liver and eventually causes scar tissue. Infection with the hepatitis C virus causes inflammation of the liver and a variable grade of damage to the organ. Over several decades, this inflammation and damage can lead to cirrhosis. The hepatitis B virus causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B and accelerates cirrhosis in co-infection. The bile ducts become damaged by an autoimmune process, leading to secondary liver damage.
Patients may be asymptomatic or have fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease. This disease is caused by an attack of the liver by lymphocytes, causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins. Usually presents with a family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, or cardiomyopathy, all due to signs of iron overload. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy and elevated 24-hour urine copper. May also have Kayser-Fleischer rings in the cornea and altered mental status. Indian childhood cirrhosis is a form of neonatal cholestasis characterized by deposition of copper in the liver.
Autosomal recessive disorder of decreased levels of the enzyme alpha 1—antitrypsin. Due to chronic right sided heart failure, which leads to liver congestion. If the cause is removed at this stage, the changes are fully reversible. The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma. This scar tissue blocks the portal flow of blood through the organ, raising the blood pressure and disturbing normal function. The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach.
Due to alcoholic marrow suppression, sepsis, lack of folate, platelet sequestering in the spleen as well as decreased thrombopoietin. However, normal aminotransferase levels do not preclude cirrhosis. 3 times the upper limit of normal. Typically much higher in chronic liver disease from alcohol. Levels normal when compensated but may elevate as cirrhosis progresses. Ultrasound is routinely used in the evaluation of cirrhosis.
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