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==Historical Perspective==
==Historical Perspective==
==Classification==


==Pathophysiology==
==Pathophysiology==
Alcoholic liver disease can vary in level of severity. Fatty liver occurs by the excess generation of [[NAD]] by enzymes [[aldehyde dehydrogenase]] and [[alcohol dehydrogenase]], leading to shunting of substrates into lipid biosynthesis. This can worsen into alcoholic hepatitis when [[inflammation]], [[necrosis]], and the generation of ROS occurs at the sites of fatty change. [[Cirrhosis]] is the final and irreversible stage of the progression of alcoholic liver disease, and is marked by fibrosis and disruption of liver architechture.
Alcoholic liver disease can vary in level of severity. Fatty liver occurs by the excess generation of [[NAD]] by enzymes [[aldehyde dehydrogenase]] and [[alcohol dehydrogenase]], leading to shunting of substrates into lipid biosynthesis. This can worsen into alcoholic hepatitis when [[inflammation]], [[necrosis]], and the generation of ROS occurs at the sites of fatty change. [[Cirrhosis]] is the final and irreversible stage of the progression of alcoholic liver disease, and is marked by fibrosis and disruption of liver architechture.
==Causes==


==Differentiating Alcoholic liver disease from other Diseases==
==Differentiating Alcoholic liver disease from other Diseases==
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{{reflist|2}}


[[Category:Pathology]]
 
[[Category:Gastroenterology]]
[[Category:Gastroenterology]]
[[Category:Hepatology]]
[[Category:Hepatology]]

Revision as of 16:05, 20 July 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2]

Overview

Alcoholic liver disease is the major cause of liver disease in Western countries, (in Asian countries, viral hepatitis is the major cause). It arises from the excessive ingestion of alcohol and can present as fatty liver, alcoholic hepatitis, and cirrhosis. Fatty liver and alcoholic hepatitis may be asymptomatic and reversible with abstinence from alcohol. Alcoholic hepatitis involves acute or chronic inflammation of liver parenchyma and is the most common precursor of cirrhosis in the United States.

Historical Perspective

Classification

Pathophysiology

Alcoholic liver disease can vary in level of severity. Fatty liver occurs by the excess generation of NAD by enzymes aldehyde dehydrogenase and alcohol dehydrogenase, leading to shunting of substrates into lipid biosynthesis. This can worsen into alcoholic hepatitis when inflammation, necrosis, and the generation of ROS occurs at the sites of fatty change. Cirrhosis is the final and irreversible stage of the progression of alcoholic liver disease, and is marked by fibrosis and disruption of liver architechture.

Causes

Differentiating Alcoholic liver disease from other Diseases

Alcoholic liver disease should be differentiated from other diseases that produce similar symptoms, and other types of liver diseases. It should also be differentiated from diseases of the gallbladder. Conditions that may present in a similar manner to alcoholic liver disease are; cholecystitis, cholelithiasis, drug toxicity, non-alcoholic fatty liver disease, and other forms of hepatitis (eg. viral, autoimmune).

Risk Factors

Risk factors for alcoholic liver disease include female gender, excessive alcohol use, malnutrition, and individual susceptibility towards liver injury due to the toxic effects of alcohol.

Screening

Natural History, Complications and Prognosis

Alcoholic liver disease progresses through three stages (steatosis, alcoholic hepatitis, and cirrhosis) with the continued use of alcohol. Serious complications begin to occur with the development of alcoholic hepatitis, when portal hypertension, coagulopathies, and intractable jaundice. Complications of cirrhosis include hepatic encephalopathy and hepatocellular carcinoma. Prognosis varies dependent on level of progression of illness, and whether treatment is given. Prognosis can be measured using laboratory values, and three prognostic scores: the MELD score, the Glasgow Alcoholic Hepatitis Score, and the ABIC score.

Diagnosis

Diagnostic Criteria

History and Symptoms

History should focus on the history of alcohol use by the patient, and the history of symptoms that may have developed. Pertinent symptoms that may be reported are; an increase in abdominal girth (due to ascites, loss of appetite, gynocomastia, skin changes, excessive thirst, fatigue, nausea, hematemesis, mental confusion, and jaundice.

Physical Examination

There are certain stigmata associated with alcoholic liver disease that one should look for on physical examination. These include; jaundice, gynecomastia, spider angiomata, bruising, hepatosplenomegaly, ascites, testicular atrophy, asterixis, and palmar erythema. A thorough neurologic and mental status exam should also be done to assess for signs of hepatic encephalopathy, or other neurologic deficits that may be caused by chronic alcohol use.

Laboratory Findings

Pertinent laboratory findings include elevated liver enzymes, with an AST to ALT ratio of about 2 to 1. An elevated level of gamma-glutamyl transferase is an indicator of excessive alcohol consumption. Other findings include; and increase serum bilirubin, increased alkaline phosphatase, a prolonged prothrombin time, decreased serum albumin, thrombocytopenia, leukocytosis, folate deficiency, and a macrocytic anemia.

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

References

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