Alcoholic Liver Disease

Introduction
Alcoholic liver disease is an inflammation of the liver cells from exposure to alcohol such as beer and or liquor.
Signs and Symptoms
Symptoms may not be present until the disease has progressed.
General Symptoms comprises of:

• Abdominal pain and tenderness
• Dry mouth and increased thirst
• Fatigue
• Jaundice
• Loss of appetite
• Nausea
• Swelling or fluid buildup in the legs (edema) and in the abdomen (ascites) when cirrhosis is present
• Weight loss
• Skin changes include:
• Abnormally dark or light skin
• Redness on feet or hands
• Small, red spider-like blood vessels on the skin
• Yellow color in the skin, mucus membranes, or eyes (jaundice)
• Abnormal bleeding
• Bloody, dark black, or tarry bowel movements (melena)
• Vomiting blood or material that looks like coffee grounds
• Brain and nervous system symptoms:
• Agitation (being stirred up, excited, or irritable)
• Changing mood
• Confusion (encephalopathy)
• Periods of decreased alertness or awareness
• Hallucinations
• Impaired short- or long-term memory
• Pain, numbness, or tingling in the arms or legs
• Problems paying attention or concentrating
• Poor judgment
• Slow, sluggish movements
• Other symptoms that can occur with this disease:
• Breast development in males
• Light-headedness or fainting, especially when rising to standing position
• Paleness

Etiology/Causes
Symptoms vary based on the severity of the disease. They are usually worse after a recent period of heavy drinking. Alcoholic liver disease usually presents itself after years of drinking excessively. The more extensively you use the substance and the more the dosage, you further increase the chances to develop the disease.
Alcohol may cause swelling and inflammation (hepatitis) in the liver. Over time, this can lead to scarring and then cirrhosis of the liver. Cirrhosis is the final phase of alcoholic liver disease.

Other important factors include:

• Genetics
• Not common to all heavy consumers
• A drunken state is not needed to develop this disease
• Females are likelier to acquire this disease
• People who consume excessively, on a regular basis fail to meet their nutritional needs. Inadequate nutrition can make liver disease worse.
• Acute alcoholic hepatitis may be caused by binge drinking (five drinks for men, four drinks for women). It may be life-threatening.

Occurrence
The prevalence of alcoholic liver disease (ALD) in a population is usually determined by measuring death rates from alcoholic cirrhosis (in which healthy liver tissue becomes increasingly replaced by scar tissue).
Mode of Transmission
Alcoholic Liver Disease, unlike the other forms of Liver Disease, is not viral, so it is not contagious. It can’t be transmitted from person to person trough blood or blood products.
The disease has been known to be achieved through these risk factors:
Quantity of alcohol taken: consumption of 60–80g per day (about 75–100 ml/day) for 20 years or more in men, or 20g/day (about 25 ml/day) for women significantly increases the risk of hepatitis and fibrosis by 7 to 47% 
Pattern of drinking: drinking outside of meal times increases up to 2.7 times the risk of alcoholic liver disease.
Gender: females are twice as susceptible to alcohol-related liver disease, and may develop alcoholic liver disease with shorter durations and doses of chronic consumption. The lesser amount of alcohol dehydrogenase secreted in the gut, higher proportion of body fat in women, and changes in fat absorption due to the with menstrual cycle may explain this phenomenon.
Hepatitis C infection: a concomitant hepatitis C infection significantly accelerates the process of liver injury.
Genetic factors: genetic factors predispose both to alcoholism and to alcoholic liver disease. Monozygotic twins are more likely to be alcoholics and to develop liver cirrhosis than dizygotic twins. Polymorphisms in the enzymes involved in the metabolism of alcohol, such as ADH, ALDH, CYP4502E1, mitochondrial dysfunction, and cytokine polymorphism may partly explain this genetic component. However, no specific polymorphisms have currently been firmly linked to alcoholic liver disease.
Iron overload (hemochromatosis)
Diet: malnutrition, particularly vitamin A and E deficiencies, can worsen alcohol-induced liver damage by preventing regeneration of hepatocytes. This is particularly a concern as alcoholics are usually malnourished because of a poor diet, anorexia, and encephalopathy.
Pathophysiology 

1. Fatty Change
Fatty change, or steatosis is the accumulation of fatty acids in liver cells. These can be seen as fatty globules under the microscope. Alcoholism causes development of large fatty globules (macro vesicular steatosis) throughout the liver and can begin to occur after a few days of heavy drinking. Alcohol is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, then further metabolized by aldehyde dehydrogenase (ALDH) into acetic acid, which is finally oxidized into carbon dioxide (CO2) and water ( H2O). This process generates NADH, and increases the NADPH/NADP+ ratio. A higher NADH concentration induces fatty acid synthesis while a decreased NAD level results in decreased fatty acid oxidation. Subsequently, the higher levels of fatty acids signal the liver cells to compound it to glycerol to form triglycerides. These triglycerides accumulate, resulting in fatty liver.
2. Alcoholic Hepatitis
Alcoholic hepatitis is characterized by the inflammation of hepatocytes. Between 10% and 35% of heavy drinkers develop alcoholic hepatitis (NIAAA, 1993). While development of hepatitis is not directly related to the dose of alcohol, some people seem more prone to this reaction than others[citation needed]. This is called alcoholic steato necrosis and the inflammation appears to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha, IL6 and IL8) are thought to be essential in the initiation and perpetuation of liver injury by inducing apoptosis and necrosis. One possible mechanism for the increased activity of TNF-α is the increased intestinal permeability due to liver disease. This facilitates the absorption of the gut-produced endotoxin into the portal circulation. The Kupffer cells of the liver then phagocytose endotoxin, stimulating the release of TNF-α. TNF-α then triggers apoptotic pathways through the activation of caspases, resulting in cell death.
3. Cirrhosis
Cirrhosis is a late stage of serious liver disease marked by inflammation (swelling), fibrosis (cellular hardening) and damaged membranes preventing detoxification of chemicals in the body, ending in scarring and necrosis (cell death). Between 10% to 20% of heavy drinkers will develop cirrhosis of the liver (NIAAA, 1993). Acetaldehyde may be responsible for alcohol-induced fibrosis by stimulating collagen deposition by hepatic stellate cells. The production of oxidants derived from NADPH oxi- dase and/or cytochrome P-450 2E1 and the formation of acetaldehyde-protein adducts damage the cell membrane.
Symptoms include jaundice (yellowing), liver enlargement, and pain and tenderness from the structural changes in damaged liver architecture. Without total abstinence from alcohol use, will eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension (high blood pressure in the portal vein due to the increased flow resistance through the damaged liver), coagulation disorders (due to impaired production of coagulation factors), ascites (heavy abdominal swelling due to build up of fluids in the tissues) and other complications, including hepatic encephalopathy and the hepatorenal syndrome.
Cirrhosis can also result from other causes than alcohol abuse, such as viral hepatitis and heavy exposure to toxins other than alcohol. The late stages of cirrhosis may look similar medically, regardless of cause. This phenomenon is termed the “final common pathway” for the disease.
Fatty change and alcoholic hepatitis with abstinence can be reversible. The later stages of fibrosis and cirrhosis tend to be irreversible, but can usually be contained with abstinence for long periods of time.
Diagnosis
There are many tests to assess alcoholic liver damage. Besides blood examination, doctors use ultrasound and a CT scan to assess liver damage. In some cases a liver biopsy is performed. This minor procedure is done under local anesthesia, and involves placing a small needle in the liver and obtaining a piece of tissue. The tissue is then sent to the laboratory to be examined under a microscope. The differential diagnoses for fatty liver non-alcoholic steatosis, drug-induced steatosis, include diabetes, obesity and starvation.
Treatment/Management

The first treatment of alcohol-induced liver disease is cessation of alcohol consumption. This is the only way to reverse liver damage or prevent liver injury from worsening. Without treatment, most patients with alcohol-induced liver damage will develop liver cirrhosis. Other treatment for alcoholic hepatitis include:
Nutrition
Doctors recommend a calorie-rich diet to help the liver in its regeneration process. Dietary fat must be reduced because fat interferes with alcohol metabolism. The diet is usually supplemented with vitamins and dietary minerals (including calcium and iron).[citation needed]
Many nutritionists recommend a diet high in protein, with frequent small meals eaten during the day, about 5–6 instead of the usual 3. Nutritionally, supporting the liver and supplementing with nutrients that enhance liver function is recommended. These include carnitine, which will help reverse fatty livers, and vitamin C, which is an antioxidant, aids in collagen synthesis, and increases the production of neurotransmitters such as norepinephrine and serotonin, as well as supplementing with the nutrients that have been depleted due to the alcohol consumption. Eliminating any food that may be manifesting as an intolerance and alkalizing the body is also important. There are some supplements that are recommended to help reduce cravings for alcohol, including choline, glutamine, and vitamin C. As research shows glucose increases the toxicity of centrilobular hepatotoxicants by inhibiting cell division and repair, it is suggested fatty acids are used by the liver instead of glucose as a fuel source to aid in repair; thus, it is recommended the patient consumes a diet high in protein and essential fatty acids, e.g. omega 3. Cessation of alcohol consumption and cigarette smoking, and increasing exercise are lifestyle recommendations to decrease the risk of liver disease caused by alcoholic stress.
Drugs
Abstinence from alcohol intake and nutritional modification form the backbone in the management of ALD. Symptom treatment can include: corticosteroids for severe cases, anticytokines (infliximab and pentoxifylline), propylthiouracil to modify metabolism and colchicine to inhibit hepatic fibrosis.
Antioxidants
It is widely believed that alcohol-induced liver damage occurs via generation of oxidants. Thus alternative health care practitioners routinely recommend natural antioxidant supplements like milk thistle. Currently, there exists no substantive clinical evidence to suggest that milk thistle or other antioxidant supplements are efficacious beyond placebo in treating liver disease caused by chronic alcohol consumption.
Nursing Intervention

1. Nursing Diagnosis: Acute Pain related to swelling of the liver is inflamed.

Expected outcomes :

• Showed signs of physical pain and pain behavior (do not wince in pain, cry intensity and location)

Nursing Interventions for Acute Pain - Nursing Care Plan for Hepatitis:

• Collaboration with patients, to determine the method can be used for pain intensity.
• Indicate the client's acceptance of the client's response to pain
  • Acknowledge the pain.
  • Listen attentively to the client about pain expression.
• Provide accurate information and explain the causes of pain, how long the pain will end, if known.
• Discuss with your doctor the use of analgesics that do not contain hepatotoxic effects.

2. Nursing Diagnosis : Ineffective Breathing Pattern related to intra-abdominal fluid collections, ascites decreased lung expansion and accumulation of secretions.

Expected outcomes :

• Adequate breathing pattern

Nursing Interventions for Ineffective Breathing Pattern - Nursing Care Plan for Hepatitis:

• Monitor the frequency, depth and respiratory effort
• Auscultation of breath sounds additional
• Give the semi-Fowler position
• Give a deep breath and coughing exercises effective
• Give oxygen as needed

3. Nursing Diagnosis: Imbalanced Nutrition Less Than Body Requirements related to failure to meet the metabolic needs of entry: anorexia, nausea / vomiting and disturbances of digestion absorption and metabolism: a decrease in peristalsis (visceral reflex), retained bile.

Expected outcomes :

• The patient will show behavioral changes in lifestyle to improve / maintain appropriate weight.
• Patients will show improvement with a goal weight and value-free laboratory signs of malnutrition.

Nursing Interventions Imbalanced Nutrition Less Than Body Requirements - Nursing Care Plan for Hepatitis

• Monitor the inclusion of diet / calories. Give a little meal in the frequency often, and offer the greatest breakfast.
• Provide oral care before meals.
• Encourage eating in an upright sitting position.
• Encourage intake of orange juice, beverage and candy carbonate heavy throughout the day.
• Consult an expert on diet, nutrition support teams to provide appropriate dietary needs of patients, with the input of fat and protein as tolerated.
• Keep an eye on blood glucose.
• Give extra food / nutrient total support when needed.