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Chronic alcoholism is defined as the regular intake of a quantity of
alcohol that is enough to injure a person socially, psychologically,
or physically.
Although this
addiction is more common in men, the number of female alcoholics has
been rapidly increasing.
While there
are no firm rules for most people, a daily consumption of more than 40 g alcohol should probably be discouraged. Intake of 100 g or more a
day may be dangerous (10 g alcohol=one ounce).
The acute
effects of alcohol on the brain are familiar to most people, either
through personal experience or through the observation of acute
alcoholic intoxication.
Although the
mechanism of inebriation is not understood, alcohol, like other
anesthetic agents, acts as a central nervous system depressants.
It has been suggested that it may act by opening the chloride
channel of the neurons through an interaction with the receptor for gamma aminobutyric acid (GABA).
In the normal person, characteristic behavioral
changes can be detected at low alcohol concentrations (below 50mg/dl) are
usually associated with gross incoordination.
Above 300 mg/dl most most
people become comatose, and at levels above 400gm/dl death from
respiratory failure is common.
The situation
is somewhat different in chronic alcoholics, who develop central
nervous system tolerance to alcohol.
Such
individuals often easily tolerate blood alcohol levels of 100 to 200
mg/dl, and in fatal automobile accidents blood levels of 500 to 600
mg/dl or more have been found by medical examiners.
The mechanism
underlying tolerance has not been established for alcohol or any other
drug.
It has
been shown that chronic alcohol intake leads to adaptive changes in
neuronal membranes.
Acute alcohol
intoxication is hardly a benign condition.
About half of
all fatalities from motor vehicle accidents involve alcohol.
Alcoholism is
also a major contributor to fatal home accidents, death in fires, and
suicide.
Many of the
chronic diseases associated with alcoholism were, at one time,
attributed to malnutrition, and it is true that some alcoholics suffer
from nutritional deficiencies -for example, thiamine deficiency (Wernicke’s
encephalopathy) or folate deficiency (megaloblastic anemia).
However, most
alcoholics have an adequate diet, and the great majority of
alcohol-related disorders should be attributed to the toxic effects of
alcohol.
Mechanism of Alcohol-Induced
Tissue injury :
The mechanism by which alcohol injures any organ or tissue is not
understood.
In liver during the
oxidation of ethanol to acetaldehyde, NAD is reduced to NADH, thereby
greatly increasing the reducing power of the cell. However, although
certain metabolic abnormalities may be attributed to this change in the
NAD/NADH ratio, no tissue injury has been directly shown to be caused by
it.
Other organs that also exhibit alcohol-induced injury, such
as the heart and the pancreas, do not metabolize ethanol to any
appreciable extent.
Another proposed factor in tissue injury is
acetaldehyde, the highly toxic product of alcohol metabolism. In the
liver, acetaldehyde is rapidly converted by aldehyde dehydrogenase to
acetate, but measurable levels of acetaldehyde (usually < 50
micrometer) can be found in the liver. However, circulating levels of
acetaldehyde are extremely low, and it is difficult to attribute all of
the changes associated with alcoholism to this metabolite.
An effect of ethanol common to all cells,
regardless of their origin or location, is fluidization of cell membrane.
Like all anesthetics, ethanol
intercalates within the lipid bilayer and decreases the molecular order of
the phospholipids (a process known as fluidization). As an adaptive
response the composition of the membranes is changed, so that they become
resistant to this fluidizing effect of ethanol.
Such a mechanism may be important for central nervous system tolerance to
alcohol.
Complication of Chronic Alcoholism: click here
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