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An overview on Liver Cirrhosis

Cirrhosis is a condition that occurs due to chronic injury to the liver in which the liver slowly deteriorates and malfunctions [1]. In cirrhosis, the flow of blood through the liver is partially blocked as scar tissue replaces healthy liver tissue, preventing it from working as it should [1][2]. Scarring further impairs the liver’s ability to:

· control infections, remove bacteria and toxins from the blood [1]

· process nutrients, hormones, and drugs [1]

· make proteins that regulate blood clotting [1]

· produce bile to help absorb fats— including cholesterol—and fat-soluble vitamins [1]

· removes or neutralizes poisons from the blood [2]

· produces immune agents to control infection [2]

A healthy liver regenerates most of its own cells when they become damaged, however the liver can no longer effectively replace damaged cells when the liver reaches its end-stage of cirrhosis [1]. A healthy liver is necessary in keeping the body functioning properly, essentially in survival [2].

Furthermore, cirrhosis is not caused by trauma to the liver or other acute, or short-term, causes of damage [1]. Years of chronic injury are required to cause cirrhosis. The following are some of the major causes of liver cirrhosis [1]:

Alcoholic liver disease- Alcoholic cirrhosis usually develops after more than a decade of heavy drinking. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates [1][2].

Chronic hepatitis C- The hepatitis C virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis [2].

Chronic hepatitis B and D- similar to hepatitis C, the hepatitis B virus causes liver inflammation and injury that over several decades can lead to cirrhosis [2]. “Hepatitis D is another virus that infects the liver, but only in people who already have hepatitis B” [2].

Autoimmune hepatitis- This disease appears to be caused by the immune system attacking the liver and causing inflammation, damage, and eventually scarring and cirrhosis [1][2].

Inherited diseases- Alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, galactosemia, and glycogen storage diseases are among the inherited diseases that interfere with the way the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly [1][2].

Nonalcoholic steatohepatitis (NASH)- in NASH, fat builds up in the liver and eventually causes scar tissue. This appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications [1][2].

Blocked bile ducts- When the ducts that carry bile out of the liver are blocked, bile backs up and damages liver tissue. In babies, blocked bile ducts are most commonly caused by biliary atresia. In adults, the most common cause is primary biliary cirrhosis [1][2].

Drugs, toxins, and infections- Severe reactions to prescription drugs, prolonged exposure to environmental toxins, the parasitic infection schistosomiasis, and repeated bouts of heart failure with liver congestion can all lead to cirrhosis [1][2].

Many people with cirrhosis have no symptoms in the early stages of the disease [1]. However, as the disease progresses, a person may experience the following symptoms [1]:

· Weakness

· Fatigue

· Loss of appetite

· Nausea

· Vomiting

· Weight loss

· Abdominal pain and bloating when fluid accumulates in the abdomen

· Itching

· Spiderlike blood vessels on the skin

As liver function deteriorates, one or more complications may develop [1]. In some people, complications may be the first signs of the disease. The following are some of the complications of liver cirrhosis:

Edema and ascites- As liver damage progresses to an advanced stage [1]:

· fluid collects in the legs- edema,

· fluid collects in the abdomen- called ascites. Ascites can lead to bacterial peritonitis, a serious infection.

Bruising and bleeding- bruising and bleeding can occur easily when the liver slows or stops producing the proteins needed for blood clotting [1].

Portal hypertension- Normally, blood from the intestines and spleen is carried to the liver through the portal vein [1]. However, cirrhosis slows the normal flow of blood, which increases the pressure in the portal vein resulting in portal hypertension [1].

Esophageal varices and gastropathy- During portal hypertension, blood vessels may enlarge in the following two areas [1]:

· Enlarged blood vessels in the esophagus- called varices,

· Enlarged blood vessels in the stomach- called gastropathy.

Enlarged blood vessels are more likely to burst due to thin walls and increased pressure, which could cause serious bleeding requiring urgent medical attention [1].

Splenomegaly- “A low platelet count may be the first evidence of liver cirrhosis [1]. The reason behind this is that when portal hypertension occurs, the spleen frequently enlarges and holds white blood cells and platelets, reducing its numbers the blood” [1].

Jaundice- This is the yellowing of the skin, white areas of the eyes and darkening of the urine [1]. Jaundice occurs when the diseased liver does not remove enough bilirubin from the blood [1]. Bilirubin is the pigment that gives bile its reddish-yellow color.

Gallstones- “If cirrhosis prevents bile from flowing freely to and from the gallbladder, the bile hardens as gallstones” [1].

Sensitivity to medications- Cirrhosis slows the liver’s ability to filter medications from the blood [1]. The medications act longer than expected and build up in the body, hence increasing the persons sensitivity to the medication and their side effects [1].

Hepatic encephalopathy- A failing liver cannot remove toxins from the blood, and they eventually accumulate in the brain [1]. The build-up of toxins in the brain—called hepatic encephalopathy—can decrease mental function and cause coma [1]. Signs of decreased mental function include confusion, personality changes, memory loss, trouble concentrating, and a change in sleep habits [1].

“Cirrhosis is an extremely heterogeneous condition, extending from an early asymptomatic stage to an advanced disease with various complications, rather than a terminal stage of different chronic liver injuries” [3]. To distinguish the heterogeneous phases of cirrhosis a five-stage system is proposed [3]. Although not validated by prospective large studies, this classification is of clinical importance:

❖ Stage 1: fully compensated cirrhosis. No varices and ascites [3].

❖ Stage 2: compensated cirrhosis, presence of esophageal varice but absence of ascites. Potential transition to decompensation (stage 3 or 4) events [3].

❖ Stage 3: bleeding of the GI tract, related to portal hypertension (esophageal varices) [3].

❖ Stage 4: ascites, jaundice or encephalopathy present [3].

❖ Stage 5: more than one complication, usually refractory ascites, intermittent encephalopathy, acute kidney injury, and advanced liver dysfunction [3].

Stage 4 probably marks a critical threshold beyond which the chronic liver disease becomes a definite systemic disorder [3]. The development of infections is a very important point in stage 4 and stage 5 of cirrhosis. Mortality rate rises four-fold once the infections develops [3].

Liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications [2]. Treatment depends on the cause of cirrhosis and any complications a person is experiencing. For example:

· Cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Alcohol will only lead to more liver damage [2].

· 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 [2].

· Cirrhosis caused by Wilson disease, in which copper builds up in organs, is treated with medications to remove the copper [2].

Treatment will also include remedies for complications. For example:

· For ascites and edema- low-sodium diet or the use of diuretics, which are drugs that remove fluid from the body, are recommended [2]. Large amounts of ascitic fluid may be removed from the abdomen and checked for bacterial peritonitis [1]. Oral or intravenous (IV) antibiotics may be given to prevent infection [1]

· Protein intake is discouraged as it causes toxins to form in the digestive tract. Laxatives are often prescribed to help absorb the toxins and remove them from the intestines [2]. Additionally, Hepatic encephalopathy is treated by cleansing the bowel with lactulose—a laxative [1].

· Beta-blocker or nitrate may be prescribed for portal hypertension [1]. Beta-blockers can lower the pressure in the varices and reduce the risk of bleeding [1]

· On the other hand, Gastrointestinal bleeding will require an immediate upper endoscopy to look for esophageal varices [1]. If varices bleed, they may be injected with a clotting agent or a rubber-band ligation can be performed [2]. Rubber-band ligation uses a special device to compress the varices and stop the bleeding [2].

Malnutrition is common in people with cirrhosis, therefore a healthy diet is important in all stages of the disease. Health care providers recommend a meal plan that is well balanced [1]. When complications cannot be controlled or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary [2]. “About 80 to 90 percent of patients survive liver transplantation. Survival rates have improved over the past several years because of drugs such as cyclosporine and tacrolimus, which suppress the immune system and keep it from attacking and damaging the new liver” [2].


Reference:

1. Cirrhosis. U.S. Department of Health and Human Services. National Institute of Health. NIH Publication No. 09–1134. 2006

2. Cirrhosis of the Liver. Center of Integrated Healthcare. Information for Behavioural Health Providers in Primary Care. 1-5. 2013.

3. Irina Ivanova. Liver cirrhosis: New concepts. Research Gate. Medical University of Varna. Scripta Scientifica Medica, vol. 48, No. 2. 19-20. 2016.

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