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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.

Recent research shows the pivotal role of the stellate cell , a cell type that normally stores vitamin A , in the development of cirrhosis.

Damage to the hepatic parenchyma due to inflammation leads to activation of stellate cells, which increases fibrosis through production of myofibroblasts and obstructs hepatic blood flow.

Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors of matrix metalloproteinases , which prevents them from breaking down the fibrotic material in the extracellular matrix.

As this cascade of processes continues, fibrous tissue bands septa separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout.

Portal hypertension is responsible for the most severe complications of cirrhosis. The gold standard for diagnosis of cirrhosis is a liver biopsy , through a percutaneous , transjugular , laparoscopic , or fine-needle approach.

A biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk of complications from liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.

FibroTest is a biomarker for fibrosis that can be done instead of a biopsy. Ultrasound is routinely used in the evaluation of cirrhosis.

It may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas.

Other liver findings suggestive of cirrhosis in imaging are an enlarged caudate lobe , widening of the fissures and enlargement of the spleen.

Ultrasound may also screen for hepatocellular carcinoma, portal hypertension, and Budd-Chiari syndrome by assessing flow in the hepatic vein.

An increased portal vein pulsatility is an indicator of cirrhosis, but may also be caused by an increased right atrial pressure.

Cirrhosis is diagnosed with a variety of elastography techniques. Techniques used include transient elastography , acoustic radiation force impulse imaging , supersonic shear imaging and magnetic resonance elastography.

Compared to a biopsy, elastography can sample a much larger area and is painless. It shows a reasonable correlation with the severity of cirrhosis.

Liver cirrhosis as seen on a CT of the abdomen in transverse orientation. Gastroscopy endoscopic examination of the esophagus, stomach, and duodenum is performed in patients with established cirrhosis to exclude the possibility of esophageal varices.

If these are found, prophylactic local therapy may be applied sclerotherapy or banding and beta blocker treatment may be commenced. Rarely are diseases of the bile ducts, such as primary sclerosing cholangitis , causes of cirrhosis.

Macroscopically, the liver is initially enlarged, but with the progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and the color is often yellow if associated with steatosis.

Depending on the size of the nodules, there are three macroscopic types: Mixed cirrhosis consists of nodules of different sizes.

However, cirrhosis is defined by its pathological features on microscopy: The pattern of fibrosis seen can depend on the underlying insult that led to cirrhosis.

Fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: As cirrhosis can be caused by many different entities which injure the liver in different ways, cause-specific abnormalities may be seen.

For example, in chronic hepatitis B , there is infiltration of the liver parenchyma with lymphocytes. The severity of cirrhosis is commonly classified with the Child-Pugh score.

This scoring system uses bilirubin , albumin , INR , the presence and severity of ascites , and encephalopathy to classify patients into class A, B, or C.

Class A has a favourable prognosis, while class C is at high risk of death. This system was devised in by Child and Turcotte, and modified in by Pugh and others.

The hepatic venous pressure gradient, difference in venous pressure between afferent and efferent blood to the liver also determines the severity of cirrhosis, although it is hard to measure.

Key prevention strategies for cirrhosis are population-wide interventions to reduce alcohol intake through pricing strategies, public health campaigns, and personal counseling , programs to reduce the transmission of viral hepatitis, and screening of relatives of people with hereditary liver diseases.

Little is known about factors affecting cirrhosis risk and progression. Research has suggested that coffee consumption appears to help protect against cirrhosis.

Generally, liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process.

Close follow-up is often necessary. Antibiotics are prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose , decrease the risk of constipation; their role in preventing encephalopathy is limited.

Alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis.

Regardless of the underlying cause of cirrhosis, consumption of alcohol and paracetamol , as well as other potentially damaging substances, are discouraged.

Vaccination of susceptible patients should be considered for Hepatitis A and Hepatitis B. Treating the cause of cirrhosis prevents further damage; for example, giving oral antivirals such as entecavir and tenofovir in patients of cirrhosis due to Hepatitis B prevents progression of cirrhosis.

Similarly, control of weight and diabetes prevents deterioration in cirrhosis due to Non-alcoholic steatohepatitis. If complications cannot be controlled or when the liver ceases functioning, liver transplantation is necessary.

The survival rate depends largely on the severity of disease and other medical risk factors in the recipient.

Manifestations of decompensation in cirrhosis include gastrointestinal bleeding , hepatic encephalopathy HE , jaundice or ascites.

In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation , infection of any source , increased alcohol intake, medication , bleeding from esophageal varices or dehydration.

It may take the form of any of the complications of cirrhosis listed below. People with decompensated cirrhosis generally require admission to a hospital, with close monitoring of the fluid balance , mental status, and emphasis on adequate nutrition and medical treatment — often with diuretics , antibiotics , laxatives or enemas , thiamine and occasionally steroids , acetylcysteine and pentoxifylline.

Life expectancy without liver transplant is low, at most 3 years. Palliative care is specialized medical care that focuses on providing patients with relief from the symptoms, pain, and stress of a serious illness, such as cirrhosis.

Especially in the later stages, people with cirrhosis experience significant symptoms such as abdominal swelling, itching, leg edema, and chronic abdominal pain which would be amenable for treatment through palliative care.

Salt restriction is often necessary, as cirrhosis leads to accumulation of salt sodium retention. Diuretics may be necessary to suppress ascites.

Diuretic options for inpatient treatment include aldosterone antagonists spironolactone and loop diuretics. Aldosterone antagonists are preferred for people who can take oral medications and are not in need of an urgent volume reduction.

Loop diuretics can be added as additional therapy. If a rapid reduction of volume is required, paracentesis is the preferred option. This procedure requires the insertion of a plastic tube into the peritoneal cavity.

Human albumin solution is usually given to prevent complications from the rapid volume reduction. In addition to being more rapid than diuretics, 4—5 liters of paracentesis is more successful in comparison to diuretic therapy.

For portal hypertension, nonselective beta blockers such as propranolol or nadolol are commonly used to lower blood pressure over the portal system.

In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting TIPS is occasionally indicated to relieve pressure on the portal vein.

As this shunting can worsen hepatic encephalopathy, it is reserved for those patients at low risk of encephalopathy.

TIPS is generally regarded only as a bridge to liver transplantation or as a palliative measure. High-protein food increases the nitrogen balance , and would theoretically increase hepatic encephalopathy ; in the past, this was therefore eliminated as much as possible from the diet.

Recent studies show that this assumption was incorrect, and high-protein foods are even encouraged to maintain adequate nutrition.

People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis. This refers to changes in the mucosa of the stomach in people with portal hypertension, and is associated with cirrhosis severity.

Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize for example, worsening encephalopathy but no fever.

Hepatocellular carcinoma is a primary liver cancer that is more common in people with cirrhosis.

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