|The following changes are
noted in the major organs in alcoholics:
Cardiac Path Online
cardiomyopathy is associated with heavy consumption over an extended
period. An association between the ingestion of acute alcohol and
onset of cardiac arrhythmias was first reported in the early 70's.
Regular alcohol intake appears to increase blood pressure, leading to
arterial hypertension, which is a risk factor for other cardiovascular
and for sudden death.
also a higher risk of sudden cardiac death with alcohol abuse, which
increases with the amount ingested, regardless of the presence of previous
heart disease like ischemic heart disease or myocardial infarction.
consumption of large amounts of alcohol is associated with alcoholic
cardiomyopathy, a subtype of secondary dilated cardiomyopathy, known to be
associated with not only cardiac failure but also with atrial fibrillation
and other cardiac arrhythmia.
appears to be able to cause cardiac arrhythmias in healthy people either
following acute excessive alcohol ingestion, commonly known as "binge
drinking," or chronic ingestion.
Arrhythmia due to chronic drinking appears to be significantly associated
with consumption of >36 gm alcohol/day
Philip Ettinger described "Holiday
syndrome" for the
first time. This condition is characterized by cardiac arrhythmia in
healthy people without
heart disease. There is acute cardiac rhythm disturbance and atrial
fibrillation, after binge drinking. The name is derived from the fact that
episodes were initially observed more frequently after weekends or public
like Christmas or New Year's Eve. This disturbance
disappeared with subsequent abstinence, leaving no residual heart disease."
Holiday heart syndrome revisited after 34 years.
are many types of alcholic beverages like beer, wine, and distilled drinks
such as vodka and whisky. It is important to be aware if some of these
types of drink cause increased risk of
Beware of "holiday heart syndrome". Overdrinking may
cause your heart rhythm to go haywire.
encephalopathy and the Wernicke-Korsakoff syndrome are nutrition
deficiency disorders due to brain damage caused by a lack of thiamine
(vitamin B1). These disorders are often noted in
alcoholic patients. There
is mental confusion, ataxia, abnormal ocular motility, and polyneuropathy.
Severe impairment of
cognitive functions which is known as the "alcohol-associated dementia"
Thiamin is required for
energy production and proper functioning of neurons. Thiamin deficiency
can lead to damage or death of neurons.
Low levels of thiamine
damage more severely some vulnerable regions of the brain.
i) Thalamus (the major
relay station of the brain that serves many important functions) and
ii) Mammillary bodies,
which are part of the hypothalamus, located just below the thalamus. The
mammillary bodies receive many neural connections from the hippocampus,
which appears to be the primary part of the brain involved in the
formation of memories. Mammillary bodies neurons projects to the
thalamus, which in turn makes connections with the cerebral cortex,
where long-term memories are stored. These correlations may explain why
lesions involving the thalamus and the mammillary bodies can lead to
anterograde amnesia. Memories formed in the hippocampus cannot be stored
since connections within the cortex are disrupted.
Alcoholic cerebellar degeneration is differentiated from other forms of
acquired or familial cerebellar degeneration by the uniformity of its
manifestations. The cerebellar vermis shows shrinkage of the folia and widening of the sulci.
- Central pontine
myelinolysis is another change in the brain of alcoholics. It is caused by electrolytic imbalance, usually after electrolyte
therapy, after an alcoholic binge, or during withdrawal. The patient
present with progressive weakness of bulbar muscles causing dysphagia
and dysarthria. This is followed by inability to swallow. Quadriparesis
and coma eventually end in respiratory paralysis. Microscopic examination reveals foci of demyelination in pons.
The effect of alcohol on
the liver has been known for several thousand years, having been implied
in the Ayurveda,
the ancient medical text of India.
The liver involvement in
alcoholic liver disease classically ranges from alcoholic steatosis,
alcoholic hepatitis or steatohepatitis, alcoholic cirrhosis and even
Diagnosis of alcoholic
liver disease can be made in persons with excessive alcohol intake
(20-40 gm/day for men and 20 gm/day for women) and evidence of liver
The nature of the alcoholic beverage is largely irrelevant, only the total
daily dose of alcohol is relevant.
Pancreatic Pathology Online
is a major complication of
The risk of developing
pancreatitis increases with increasing doses of
alcohol exerts dose-related toxic effects on the
It has been suggested
that only few alcoholics develop the disease, indicating that an
additional trigger is needed to initiate clinically evident pancreatic
It is now well
alcohol is metabolized by the
both oxidative and non-oxidative metabolites.
Alcohol and its
metabolites produce changes in the acinar cells, which may promote
premature intracellular digestive enzyme activation predisposing the
gland to autodigestive injury.
cells are activated directly by
alcohol and its
metabolites and also by cytokines and growth factors released during
Acute and chronic
alcohol ingestion causes a variety of pathological changes in the
including gross morphological lesions and functional changes.
Reflux esophagitis may be particularly painful.
Peptic ulcers are also more
common in the alcoholic.
Violent retching may lead to tears at the
esophageal-gastric junction (Mallory-Weiss syndrome). In serious cases
there is severe bleeding.
Chronic consumption of
a significant increase in the risk for squamous carcinoma of the
Alcohol consumption is a
risk factor for osteoporosis based on the frequent finding of a low
formation rate, and increased fracture incidence in alcoholics. Alcohol
also has been shown to reduce
in healthy humans.
is extremely common in alcoholics and is often due to general
debility and nutritional deficiency.
Clinically, even well-nourished alcoholics usually show some weakness,
particularly of the proximal muscles.
A wide range of changes in skeletal
muscle is seen in chronic alcoholics, varying from mild alterations in
muscle fibers evident only by electron microscopy to a severe,
debilitating chronic myopathy, with degeneration of muscle fibers and
On rare occasions, acute alcoholic rhabdomyolysis, acute
necrosis of muscle fibers and release of myoglobin to the circulation is
seen. This sudden event can be fatal, because of renal failure secondary
anemia secondary to a deficiency of folic acid can occur in
nutritional deficiency of folic acid is the most important factor. Absorption of folate
in the small intestine may be decreased in alcoholics.
alcohol intoxication can cause an increase in
red blood cell volume.
alcoholic cirrhosis the spleen is often enlarged by portal hypertension. In such cases hypersplenism often causes hemolytic anemia.
Acute transient thrombocytopenia is
common after acute alcohol intoxication and may result in bleeding.
Alcohol also interferes with the aggregation of platelets, which may
contribute to bleeding.
increases risk of
cancer of oral cavity and pharynx,
colorectum, liver, larynx and female breast.
There is also evidence
drinking is associated with some other cancers such as pancreas
and prostate cancer
As a doctor today I prescribe
B1) rich food:
Prevent Beriberi, Wernicke’s Encephalopathy, and Korsakoff’s Psychosis