Alcohol

V Sem
KMC IC
 ACUTE ETHANOL
INTOXICATION
• An increased reaction time,
• diminished fine motor control,
• impulsivity,
• and impaired judgment become evident when the
concentration of ethanol in the blood is 20 to 30
mg/dl.
• More than 50% of persons are grossly intoxicated
by a concentration of 150 mg/dl.
• In fatal cases, the average concentration is about
400 mg/dl.
• In the United States, most states set the ethanol
level defined as intoxication at 80 mg/dl.
• There is increasing evidence that lowering the
limit to 50 to 80 mg/dl can reduce motor vehicle
injuries and fatalities significantly.
• While alcohol can be measured in saliva, urine,
sweat, and blood, measurement of levels in
 Treatment of acute alcohol
intoxication
• The treatment of acute alcohol
intoxication is based on the severity of
respiratory and CNS depression.
• Acute alcohol intoxication can be a
medical emergency,
• Patients who are comatose and who
exhibit evidence of respiratory depression
• Should be intubated to protect the airway
and to provide ventilatory assistance.
• The stomach may be lavaged, but care
must be taken to prevent pulmonary
aspiration of the return flow.
• Since ethanol is freely miscible with water,
• Acute alcohol intoxication is not always
associated with coma, and careful
observation is the primary treatment.
• Usual care involves observing the patient in
the emergency room for 4 to 6 hours while
the patient metabolizes the ingested
ethanol.
• Blood alcohol levels will be reduced at a
rate of about 15 mg/dl per hour.
• During this period, some individuals may
display extremely violent behavior.
• Sedatives and antipsychotic agents have
been employed to quiet such patients.
• Great care must be taken, however, when
using sedatives to treat patients who have
ingested an excessive amount of another
CNS depressant, i.e., ethanol, because of
synergistic effects.
• The use of alcohol to treat patients in
alcohol withdrawal or obstetrical
patients with premature contractions
is no longer recommended.
• Some medical centers continue to
use alcohol to prevent or reduce the
risk of alcohol withdrawal in
postoperative patients,
• but administering a combination of a
benzodiazepine with haloperidol or
clonidine may be more appropriate.
 Methanol Poisoning
• Added to rectified spirit to render it
unfit for drinking
• No pharmacological relevence
• Highly toxic
 Treatment consists of
• Keep patient in quiet,dark room:protect
eyes from light---even 15ml of methanol has
caused blindness
• Gastric Lavage with sodium bicarbonate to
combat acidosis,
• hemodialysis, and the
• Pot Chloride is needed only when
hypokalemia occurs
• administration of ethanol,
• Slows formate production by competing
with methanol
• For metabolism by alcohol dehydrogenase.
• Fomipezole – inhibits Alcohol Dh
• Folate therapy-Ca leucovorin reduces blood
formate levels
 CLINICAL USES OF
ETHANOL
• Dehydrated alcohol may be injected in close
proximity to nerves or sympathetic ganglia
-to relieve the long-lasting pain related to
trigeminal neuralgia, inoperable carcinoma, and
other conditions.
• Epidural, subarachnoid, and lumbar paravertebral
injections of ethanol also have been employed for
inoperable pain.
• For example, lumbar paravertebral injections of
ethanol may destroy sympathetic ganglia
• and thereby produce vasodilation, relieve pain,
and
• promote healing of lesions in patients with
• Systemically administered ethanol is
confined to the treatment of
poisoning by methyl alcohol and
ethylene glycol.
• The ingestion results in
• formation of methanol's metabolites,
formaldehyde and formic acid .
• Formic acid causes nerve damage;
its effects on the retina and optic
nerve can cause blindness.
 PHARMACOTHERAPY OF
ALCOHOLISM
• Currently, three drugs are approved
in the United States for treatment of
alcoholism: disulfiram (ANTABUSE),
naltrexone (REVIA), and
acamprosate.
• The goal of these medications is to
assist the patient in maintaining
abstinence.

Naltrexone
approved by the FDA for treatment of
alcoholism in 1994.
• opioid-receptor antagonist
• has higher oral bioavailability and a
longer duration of action.
• Animal research and clinical
experience suggested that
• blocks activation by alcohol of
dopaminergic pathways in the brain
that are thought to be critical to
reward.

Reduces the urge to drink and

increasing control when a "slip"
occurs.
• not a "cure”.
• It typically is administered after
detoxification and given at a dose of
50 mg/day for several months.
Adherence to the regimen is
 Side effect of naltrexone
• Nausea,
which is more common in women than
in men
subsides if the patients abstain from
alcohol
When given in excessive doses,
naltrexone can cause liver damage.
It is contraindicated in patients with
liver failure or acute hepatitis
 Disulfiram
(tetraethylthiuram disulfide;
ANTABUSE)
• Similar responses to alcohol
ingestion are produced by various
congeners of disulfiram, namely,
• cyanamide,
• the fungus Coprinus atramentarius,
• the hypoglycemic sulfonylureas,
metronidazole,
• certain cephalosporins,
• and animal charcoal.
• It inhibits ALDH activity
• causes the blood acetaldehyde
concentration to rise to 5 to 10 times
• when ethanol is given to an
individual not pretreated with
disulfiram.
• oxidation of ethanol by ADH
produces Acetaldehyde,
• does not accumulate in the body
because it is further oxidized almost
as soon as it is formed primarily by
ALDH
• Following the administration of
disulfiram,
• both cytosolic and mitochondrial
forms of ALDH are irreversibly
inactivated to varying degrees,
• Concentration of acetaldehyde rises.
• It is unlikely that disulfiram itself &
• several active metabolites of the
drug, especially
diethylthiomethylcarbamate,
• behave as suicide-substrate
inhibitors of ALDH
• The ingestion of alcohol by
individuals previously treated with
disulfiram
• Gives rise to marked signs and
symptoms of acetaldehyde
poisoning.
• Within 5 to 10 minutes,
• the face feels hot and soon
afterward becomes flushed and
scarlet in appearance.
• As the vasodilation spreads over the
whole body,
• Respiratory difficulties,
• nausea,
• copious vomiting,
• sweating, thirst,
• chest pain,
• considerable hypotension,
• orthostatic syncope,
• marked uneasiness,
• weakness,
• vertigo,
• blurred vision, and confusion are
• The drug never should be
administered until the patient has
abstained from alcohol for at least 12
hours.
• In the initial phase of treatment, a
maximal daily dose of 500 mg is
given for 1 to 2 weeks.
• Maintenance dosage then ranges
from 125 to 500 mg daily depending
on tolerance to side effects.
• Sensitization to alcohol may last as
long as 14 days after the last
ingestion of disulfiram because of the
• Patients must learn to avoid
disguised forms of alcohol,
• as in sauces,
• fermented vinegar,
• cough syrups,
• and even after-shave lotions and
back rubs.
 Side Effects
• Rashes ,Metallic taste
• Nervousness,malaise,abdominal pain
• It inhibits a number of enzymes
including Alcohol Dehydrogenase and
Dopamine Beta Hydroxylase
• Thus shall prolong the t half of many
drugs
• Disulfiram like reaction---
Metronidazole
 Acamprosate

• Weak NMDA receptor antagonist with

modest GABAA receptor antagonistic
activity
• Used in conjugation with Motivational
therapy
• Reduces relapse of drinking behaviour
• Efficacy comparable to naltrexone