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  • Fatty liver, also known as fatty liver disease, is a reversible condition wherein large vacuoles

  • of triglyceride fat accumulate in liver cells via the process of steatosis. Despite having

  • multiple causes, fatty liver can be considered a single disease that occurs worldwide in

  • those with excessive alcohol intake and the obese. The condition is also associated with

  • other diseases that influence fat metabolism. It is difficult to distinguish alcoholic FLD

  • from nonalcoholic FLD, and both show microvesicular and macrovesicular fatty changes at different

  • stages. Accumulation of fat may also be accompanied

  • by a progressive inflammation of the liver, called steatohepatitis. By considering the

  • contribution by alcohol, fatty liver may be termed alcoholic steatosis or nonalcoholic

  • fatty liver disease, and the more severe forms as alcoholic steatohepatitis and Non-alcoholic

  • steatohepatitis.

  • Causes Fatty liver is commonly associated with alcohol

  • or metabolic syndrome, but can also be due to any one of many causes:

  • Metabolic Abetalipoproteinemia, glycogen storage diseases,

  • Weber-Christian disease, acute fatty liver of pregnancy, lipodystrophy

  • Nutritional Malnutrition, total parenteral nutrition,

  • severe weight loss, refeeding syndrome, jejunoileal bypass, gastric bypass, jejunal diverticulosis

  • with bacterial overgrowth Drugs and toxins

  • Amiodarone, methotrexate, diltiazem, expired tetracycline, highly active antiretroviral

  • therapy, glucocorticoids, tamoxifen, environmental hepatotoxins

  • Alcoholic Alcoholism is one of the major cause of fatty

  • liver due to production of toxic metabolites like aldehydes during metabolism of alcohol

  • in the liver.This phenomenon most commonly occur with chronic alcoholism.

  • Other Inflammatory bowel disease, HIV, hepatitis

  • C, and alpha 1-antitrypsin deficiency Pathology

  • Fatty change represents the intracytoplasmatic accumulation of triglycerides. At the beginning,

  • the hepatocytes present small fat vacuoles around the nucleus. In this stage, liver cells

  • are filled with multiple fat droplets that do not displace the centrally located nucleus.

  • In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery

  • of the cell, giving characteristic signet ring appearance. These vesicles are well-delineated

  • and optically "empty" because fats dissolve during tissue processing. Large vacuoles may

  • coalesce and produce fatty cysts, which are irreversible lesions. Macrovesicular steatosis

  • is the most common form and is typically associated with alcohol, diabetes, obesity, and corticosteroids.

  • Acute fatty liver of pregnancy and Reye's syndrome are examples of severe liver disease

  • caused by microvesicular fatty change. The diagnosis of steatosis is made when fat in

  • the liver exceeds 5–10% by weight.

  • Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due

  • to imbalance in energy consumption and its combustion, resulting in lipid storage, or

  • can be a consequence of peripheral resistance to insulin, whereby the transport of fatty

  • acids from adipose tissue to the liver is increased. Impairment or inhibition of receptor

  • molecules that control the enzymes responsible for the oxidation and synthesis of fatty acids

  • appears to contribute to fat accumulation. In addition, alcoholism is known to damage

  • mitochondria and other cellular structures, further impairing cellular energy mechanism.

  • On the other hand, nonalcoholic FLD may begin as excess of unmetabolised energy in liver

  • cells. Hepatic steatosis is considered reversible and to some extent nonprogressive if the underlying

  • cause is reduced or removed.

  • Severe fatty liver is sometimes accompanied by inflammation, a situation referred to as

  • steatohepatitis. Progression to alcoholic steatohepatitis or Non-alcoholic steatohepatitis

  • depends on the persistence or severity of the inciting cause. Pathological lesions in

  • both conditions are similar. However, the extent of inflammatory response varies widely

  • and does not always correlate with degree of fat accumulation. Steatosis and onset of

  • steatohepatitis may represent successive stages in FLD progression.

  • Liver disease with extensive inflammation and a high degree of steatosis often progresses

  • to more severe forms of the disease. Hepatocyte ballooning and necrosis of varying degrees

  • are often present at this stage. Liver cell death and inflammatory responses lead to the

  • activation of stellate cells, which play a pivotal role in hepatic fibrosis. The extent

  • of fibrosis varies widely. Perisinusoidal fibrosis is most common, especially in adults,

  • and predominates in zone 3 around the terminal hepatic veins.

  • The progression to cirrhosis may be influenced by the amount of fat and degree of steatohepatitis

  • and by a variety of other sensitizing factors. In alcoholic FLD, the transition to cirrhosis

  • related to continued alcohol consumption is well-documented, but the process involved

  • in nonalcoholic FLD is less clear. Diagnosis

  • Most individuals are asymptomatic and are usually discovered incidentally because of

  • abnormal liver function tests or hepatomegaly noted in unrelated medical conditions. Elevated

  • liver biochemistry is found in 50% of patients with simple steatosis. The serum alanine transaminase

  • level usually is greater than the aspartate transaminase level in the nonalcoholic variant

  • and the opposite in alcoholic FLD. Imaging studies are often obtained during

  • the evaluation process. Ultrasonography reveals a "bright" liver with increased echogenicity.

  • Medical imaging can aid in diagnosis of fatty liver; fatty livers have lower density than

  • spleens on computed tomography, and fat appears bright in T1-weighted magnetic resonance images.

  • No medical imagery, however, is able to distinguish simple steatosis from advanced NASH. Histological

  • diagnosis by liver biopsy is sought when assessment of severity is indicated.

  • Treatment The treatment of fatty liver depends on its

  • cause, and, in general, treating the underlying cause will reverse the process of steatosis

  • if implemented at an early stage. Two known causes of fatty liver disease are an excess

  • consumption of alcohol and a prolonged diet containing foods with a high proportion of

  • calories coming from lipids. For the patients with non-alcoholic fatty liver disease with

  • pure steatosis and no evidence of inflammation, a gradual weight loss is often the only recommendation.

  • In more serious cases, medications that decrease insulin resistance, hyperlipidemia, and those

  • that induce weight loss have been shown to improve liver function.

  • Complication Up to 10% of cirrhotic alcoholic FLD patients

  • will develop hepatocellular carcinoma. The overall incidence of liver cancer in nonalcoholic

  • FLD has not yet been quantified, but the association is well-established.

  • Epidemiology The prevalence of FLD in the general population

  • ranges from 10% to 24% in various countries. However, the condition is observed in up to

  • 75% of obese people, 35% of whom progressing to NAFLD, despite no evidence of excessive

  • alcohol consumption. FLD is the most common cause of abnormal liver function tests in

  • the United States. "Fatty livers occur in 33% of European-Americans, 45% of Hispanic-Americans,

  • and 24% of African-Americans." See also

  • Steatosis Steatohepatitis

  • Alcoholic liver disease Non-alcoholic fatty liver disease

  • Metabolic syndrome Cirrhosis

  • Focal fatty liver References

  • External links American Association for the Study of Liver

  • Diseases American Liver Foundation

  • Fatty Liver Fatty Liver Disease, Canadian Liver Foundation

  • 00474 at CHORUS Photo at Atlas of Pathology

Fatty liver, also known as fatty liver disease, is a reversible condition wherein large vacuoles

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B2 中高級 美國腔

脂肪肝 (Fatty liver)

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    鍾佳芳 發佈於 2021 年 01 月 14 日
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