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ALCOHOLIC LIVER DISEASE

الداء الكبدي الكحولي ALCOHOLIC LIVER DISEASE
Ethanol is metabolized in the liver in two ways and the resulting increase in the ratio NADH / NAD. Oxidation and latency of the return variable causes an increase manufacturing fatty acids with lower hepatic oxidized, cumin oxidation and return the variable causes an increase manufacture of fatty acids with lower hepatic oxidized, both incidents would lead towards an accumulation of fatty acids in the liver and therefore fatty acid esterification to Glesiredat. Change in oxidation and return also weakens the metabolism of carbohydrates and proteins and is the cause of necrosis in the center of hepatic lobule Anbh where necrosis is considered a model for alcoholic injury. Alosat aldehyde is formed from the oxidation of ethanol and proteins affect the liver and can therefore be considered as a factor for incidence of liver.

The exact mechanism for the inflammation of the liver alcohol and cirrhosis alcohol is not known, but since that 10-20% only of people who consume alcohol excessively will develop cirrhosis of the liver, so it has been shown that the inheritance of a role in susceptibility Balchma, and the mechanism of immune has been brought up also .

 can enhance the toxic effects of alcohol from the products of metabolism of drugs (such as paracetamol) on the liver, also incites metabolic Almkroa by a Almkroa ethanol oxidation (MEOS)

Pathogenesis:
Alcohol can cause a wide spectrum of liver diseases ranging from infections to changes in fatty liver and hepatic cirrhosis.

1 - fatty change Fatty Changes:
Permanent result of alcohol metabolism in the liver to the formation of fat, particularly in Zone 3. These changes may be few if the amount of alcohol consumed is small, but larger quantities cause swelling of cells and fullness of guys (steatosis). I talk to hepatocellular injury, and these changes are irreversible when you stop alcohol consumption. Fatty degeneration may occur for reasons other than alcohol.
In some cases, collagen is located around the hepatic central veins (cirrhosis of the veins) Vtaatriqy to cirrhosis of the liver, even if it were not preceded by inflammation of the liver. Toxicity of the alcohol directly on the astrocytes, transforms into the cells of fibroblastic collagen-producing muscle.


2 - alcoholic hepatitis Alcoholic hepatitis
In this case changes occur in addition to fatty infiltration of the multi-core white cells and necrosis of liver cells, particularly in Zone 3. We find the contents of Sitoblasmih dense objects called Mallory Mallory bodies are sometimes seen within the liver cells in addition to the presence of giant mitochondria. Mallory's bodies are a manifestation indicative of liver injury, but not qualitatively, they might see in other liver diseases such as Wilson's disease and initial biliary cirrhosis.
Develop alcoholic hepatitis to cirrhosis if the consumption of alcohol.

3 - Alcoholic liver cirrhosis Alcoholic cirrhosis
Alcoholic cirrhosis usually have a small nodule of the style, but can also see a sample mixed with the conjugated fatty changes, we may find evidence of a former alcoholic hepatitis.


Clinical Features
In fatty liver:
In most cases there are no symptoms or signs. But may show some symptoms of digestive Allanoaah resulting from the general effects of alcohol on the gastrointestinal tract (nausea, vomiting, diarrhea).
Hepatomegaly may appear (may be severe at times) to accompany the demonstrations of other chronic liver disease.

Alcoholic hepatitis:
The clinical manifestations ranging between:
- Patient normally complain of mild symptoms and inflammation of the liver only pretending to liver biopsy with changes seen in the greasiness.
- Symptoms of mild to moderate severity of the disease is sometimes associated with mild jaundice

Tags: with all the signs seen in chronic liver disease.
Chemical analysis is useful in diagnosis, which depends mainly on the study of the liver and tissue biopsy.
- In the severe stage of the disease characterized by the occurrence of alcoholic cirrhosis.
Pretend to: jaundice, ascites, abdominal pain frequently in addition to the facilities to raise the caloric hepatic necrosis.

Clinical examination: we find severe jaundice, Hepatomegaly, sometimes splenomegaly, ascites and ankle edema in addition to signs of chronic liver disease.

Alcoholic cirrhosis:
Represents the final stage of liver disease caused by alcohol. However, the patient may be in good health and show mild symptoms. Clinical examination found signs of chronic liver disease.

Diagnosis is confirmed by liver biopsy. Disease usually manifests one of the complications of cirrhosis, has appeared in many cases the features of alcohol dependence as well as injuries to other devices such as multi-neuropathy polyneuropathy.


Surveys:
In fatty liver:
Note a rise in corpuscular volume MCV, which often refers to the excessive consumption of alcohol. Chemical analysis of the liver.
Show slight changes with the rise in the level of enzymes Alaminotransferraz (carriers of the Secretary) and serum gamma-glutamine is trans-peptidase Gamma-GT sensitive test to determine if the patient could still be using alcohol or stop eating.
In the event of severe fatty infiltration of the liver can show significant changes in the values ​​of all the chemical analysis of the liver.
Ultrasound or CT scan CT shows histological changes in liver lipid infiltration and the extent of it.
And can be used Alelastograve elastography as a way to estimate the degree of hepatic fibrosis.

Alcoholic hepatitis:
Surveys show leukocytosis with marked changes in the chemical analysis of the liver, where the high note:
• serum bilirubin.
• ALT and AST serum
• alkaline phosphatase.
• prothrombin time.
Is possible to see a decrease in the level of serum albumin, and rarely see excessive fat in the blood with the dissolution of blood (Zieve syndrome). Zieve's syndrome
The liver biopsy in case they are needed through the jugular vein for fear of bleeding disorders because of the high prothrombin time.

Cirrhosis of the liver:
The same surveys cirrhosis in general.


Measure and warning of the disease:
General measure:
Should be directed to the patient's abstinence from alcohol. Is treated delirium tremens (View the withdrawal) by diazepam diazepam
And thiamin thiamine should be given intravenously for the prevention of encephalopathy and Urnqh - Korsakov and provide the patient and giving him vitamins and high protein meal in addition to clinical comfort.
A meal containing protein are rarely identified due to encephalopathy. Patients should be directed to participate in programs to refrain from alcohol, and the patient's ability to refrain from alcohol depends on several factors, especially social and family factors

In fatty liver:
After excluding the patient's consumption of alcohol, the fat will disappear and chemical analysis will return to normal.

Alcoholic hepatitis:
In severe cases, requires the acceptance of patients in the hospital. Must be maintained on the patient's diet and provide vitamins may require enteral feeding. Balstroidat treatment improves outcome and, in more severe cases and followed the process according to the following sports: Discriminant function (DF).

DF prothrombin time above control = (4.6. In seconds) + bilirubin (mg dL
The situation would be severe if the value is greater than 32

Should prevent or treat sepsis immediately, and must use preventive medicine antifungal and start treating Alhabn and encephalopathy. The patient must refrain from alcohol for life, because alcohol would undoubtedly risk of cirrhosis of the liver. Warning of the disease is variable, and regardless of abstinence from alcohol, the liver disease is a progressive disease in many patients. The mortality rate in severe cases, at least 50%, but at higher time Albrootermben of the weakness of time and natural progression encephalopathy and renal failure, the mortality rate rises to 90%

Cirrhosis:
As mentioned previously, the consumption of alcohol will undoubtedly lead to cirrhosis of the liver, and to refrain from alcohol consumption will improve the promotion cirrhosis, where the survival rate for 5 years is estimated at 90%, and when abstinence from alcohol, but when the continuation of alcohol intake, this ratio drops to 60%.
When progression of the disease (ie, in the event of jaundice, ascites, dissolution of blood), the survival rate for 5 years reduced to 35%, as most deaths occur during the first year of cirrhosis.
Liver transplantation will lead to good survival rate, although the return of cirrhosis as a result of relapse are rare. Often, patients sign a contract with their doctor refers to abstaining from alcohol before and after the transplant.
The start to refrain from alcohol in order to test the improvement of liver to be mandatory, and should not be denied a liver transplant if the patient's condition continued to deteriorate, and follow-up is recommended especially for patients with regard to alcohol consumption.

HCC is one of the complications of cirrhosis especially in men.

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