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Figure 1.
Notice the placement of the liver in the body, it fills the upper
right abdominal cavity.
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The liver is a complex
organ that is necessary for life. It
is the largest gland in the body and the second largest organ. The liver is about 1/50 of a person’s
weight. It fills the upper right
abdominal cavity and lies against the colon, right kidney and small
intestines. It is divisible into four
lobes containing liver cells and Kupffer’s cells (specialized cells in the
liver which filter bacteria and other small foreign proteins out of the
liver).
The liver receives almost all the blood flow from the digestive
tract; thus, when you drink alcohol which is absorbed directly into the
bloodstream, the liver is going to receive most of it and is going to have to
break it down and try to rid your body of this poison. The normal blood flow into the liveris
approximately 1.5 liters per minute.
Breaks down toxins absorbed from the
intestine or manufactured in the body and modifies them so they are no longer
harmful; then it excretes them into bile or blood.
Stores vitamins, especially fat-soluble
vitamins.
Synthesizes cholesterol, metabolizes or
stores sugars, and processes fats.
Assembles amino acids into various
proteins.
Controls blood fluidity and regulates
blood-clotting mechanisms.
Converts the products of protein
metabolism into urea for excretion by the kidneys, which will leave your body
as urine.
Stores minerals such as iron for red
blood cell production.
The connection between heavy alcohol
consumption and liver disease has been recognized for more than 200 years.
Because your liver is so large and has the
capacity to regenerate, people can function with only 10-20% of their liver;
the symptoms of liver disease will not be prevalent until you have progressed
substantially into the disease (see figure 1).
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Figure 1. Notice the difference between a healthy
liver and a liver with cirrhosis. |
Symptoms may remain latent until damage
is really detrimental!
The minimum dose of alcohol that must be consumed
for serious liver injury to become apparent in men is 5-6 standard drinks daily
for 20 years. For women, the minimum
dose is one-fourth to one-half that amount.
No more than one-half of heavy drinkers
develop alcoholic hepatitis and cirrhosis. Thus, other risk factors must play a role in the development of
alcohol-related liver complications.
Risk factors for alcoholic hepatitis and
cirrhosis are:
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Gender |
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Heredity |
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Diet |
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Co-occurring liver illness |
Three conditions of the liver are often associated with
alcohol abuse. Liver disease in
alcoholics usually progresses through the three conditions chronologically
starting with fatty liver and proceeding to alcoholic hepatitis which can
eventually lead to cirrhosis.
Fatty Liver: Fat deposits in the liver.
To some extent, fat deposits will happen in almost all heavy
drinkers. It can also happen in
non-alcoholics after just one incidence of drinking.
Symptoms: People with fatty liver
may have no symptoms and have just an abnormal enlargement of the liver that is
smooth and non-tender with minimal or no functional changes. However, alcoholics may have
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Abdominal pain
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Severe jaundice syndrome(a
yellow discoloration of the skin, mucus membranes, and white part around the
eyes caused by greater than normal amounts of bilirubin in the blood)
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Acute liver failure
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Ascites (abnormal accumulation
of fluid containing proteins and electrolytes and causing an abnormal swelling
in the abdomen)
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Coma
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Death.
Outcome: Chances of recovery are
better at this stage than with cirrhosis.
Damage is reversible and does not necessarily lead to more serious
damage.
Alcoholic Hepatitis: Widespread inflammation and destruction of
liver tissue. Patients may develop
fibrosis, where scar tissue begins to replace healthy liver tissue.
Symptoms: Fever, jaundice, and abdominal pain.
Outcome: May be fatal but also may
be reversed by abstaining from alcohol.
Frequency: Occurs in 50% of heavy
drinkers.
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Figure 2. Alcoholic liver:
Cut surface of gross autopsy specimen of liver showing unnatural paleness due
to a dense network of scar tissue (fibrosis, cirrhosis). Scarring has occurred
in response to chronic injury from alcohol abuse.
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Alcoholic cirrhosis: (see figure 2) Most advanced form of liver
disease, 15-30 percent of heavy drinkers.
Early Symptoms: General weakness, weight loss.
Later Symptoms: Loss of appetite, indigestion,
nausea, vomiting, abdominal swelling, and spider nevi (spidery red marks on
upper body arms and face). Causes
extensive fibrosis that stiffens blood vessels and distorts the internal
structure of the liver. Functions of
the liver may be impaired which may lead to malfunction of other organs such as
the brain and kidneys.
Outcome: Usually fatal due to
complications such as kidney failure, and hypertension (high blood pressure) in
the vein carrying blood to the liver.
This disease is usually fatal if chronic alcohol exposure continues;
however, if the patient quits drinking, their condition may become stable.
Frequency: Statistics from
different populations vary because of varying lifestyles; however, statistics
show that between 40-90% of the 26,000 annual deaths from cirrhosis are
alcohol-related.
The alcoholic will progress from fatty liver
to alcoholic hepatitis, to cirrhosis.
Sometimes heavy drinkers may develop alcoholic cirrhosis without first
developing alcoholic hepatitis, and it could also happen that an alcoholic may
have a sudden onset and rapid course of alcoholic hepatitis; then die before
cirrhosis develops.
Not all liver disease in alcoholics is caused by
alcohol. Also, alcohol induced liver
disease may be accompanied by other conditions not related to alcohol but which
can cause liver failure, such as nonalcoholic hepatitis and exposure to drugs
and occupational chemicals.
Furthermore, it is important to remember that fatty liver and alcoholic
hepatitis may be reversed if you stop drinking alcohol, and cirrhosis can be
stabilized if you stop drinking alcohol.
Most of alcohol that people drink is
metabolized in the liver. 
Alcohol dehydrogenase (ADH): This is the enzyme that converts alcohol to
acetaldehyde through a chemical process called oxidation.
The chemical, acetaldehyde, which is
generated, is more toxic than alcohol itself.
Aldehyde dehydrogenase converts acetaldehyde
to acetate, which can be used as fuel by the cell.
Acetate travels through the bloodstream to
other parts of the body where it can enter other metabolic cycles that produce
energy or useful molecules. The usual biological role of both ADH and ALDH is
to metabolize vitamin A.
Studies have shown that women, Asians, Native
Americans, and older people have less of the enzyme alcohol dehydrogenase; thus
they are not able to metabolize alcohol as efficiently as those who have more
of this enzyme possibly making them get drunk faster and experience liver
complications sooner.
In people who engage in heavier and more
chronic alcohol consumption, a second pathway is utilized with the enzyme
called microsomal ethanol-oxidizing system (MEOS).
MEOS helps get rid of toxic compound in the
body by using an enzyme called cytochrome P450 This enzyme converts alcohol to acetaldehyde.
Cytochrome P450 is thought to help eliminate
alcohol at high blood alcohol concentrations that prevail in heavy
drinkers.
Cytochrome P450 also generates reactive
oxygen radicals that damage cellular components.
Chronic alcohol consumption can
substantially increase iron levels in the body. In fact almost one third of alcoholics have excessive iron levels
in their livers much of which is free iron; thus these elevated levels may
damage liver.
Some acetaldehyde may combine with liver
proteins to form harmful compounds that can impair the function of various
cellular components and enzymes.
Also alcohol can combine with other molecules
in the cell to form potentially dangerous compounds such as fatty acid ethyl
esters and phosphatidylethanol.