The document discusses acute alcohol intoxication, including its definition, contributing factors such as body weight and absorption rates, and metabolism pathways in the liver. It outlines the clinical symptoms which range in severity and may include slurred speech and respiratory depression, highlighting that treatment focuses on supportive care to manage these symptoms. Key interventions include maintaining airway and circulation, correcting hypoglycemia, and administering thiamine to prevent neurological complications.

1. PHARMACOTHERAPY OF ACUTE
ALCOHOL INTOXICATION
BY- HIMANSHU MAURYA
ROLL NO. 33
MBBS-2022

2. CONTENTS
 Introduction
 Factors affecting intoxication risk
 Alcohol metabolism
 Pathophysiology
 Clinical features
 Treatment

3. INTRODUCTION
Acute alcohol intoxication occurs when someone drinks
too much alcohol in a short amount of time.
It makes them act and feel different than ususal.
Signs of intoxication typical of CNS depression are
observed in most people after 2-3 drinks with the most
prominent effect seen at time of peak blood alcohol
concentration, about 30-60 min following consumption
on an empty stomach.

4. FACTORS AFFECTING INTOXICATION RISK
 Body weight and composition
 Rate of absorption from GIT
 On average, the ingestion of 3 standard drink on an empty
stomach results in a maximum blood conc. Of 67-92mg/dl
in men.
 Concentrations of alcohol in blood will be higher in women
because on average women are smaller than men, have
less body water per unit of weight into which alcohol can
distribute, and less gastric Alcohol dehydrogenase activity
than men.

5. ALCOHOL METABOLISM
 Ethanol is metabolized via several pathways, each of which can
contribute to toxicity.
 The primary hepatic pathway generates acetaldehyde and reduced
nicotinamide adenine dinucleotide (NAD)
 Ethanol is metabolized first in the liver to acetaldehyde; this process
occurs in the hepatocyte cytosol via a reaction catalyzed by the
enzyme alcohol dehydrogenase (ADH)
 The acetaldehyde that is generated is subsequently metabolized to
acetate, a process that occurs in the mitochondria and is catalyzed
by a different enzyme, acetaldehyde dehydrogenase (ALDH)

6. PATHOPHYSIOLOGY
 Ethanol (CH 3 CH 2 OH) is a water-soluble alcohol that
rapidly crosses cell membranes.
 Absorption of ethanol occurs via the gastrointestinal
system, primarily in the stomach (70 percent) and
duodenum (25 percent), with a small amount absorbed by
the remaining intestine .
 When the stomach is empty, peak blood ethanol levels are
reached between 30 and 90 minutes after ingestion.

7. CLINICAL FEATURES
Signs and symptoms of acute ethanol intoxication vary with severity
and can include
 Slurred speech
 Incoordination
 Unsteady gait
 Hypotension
 Hypoglycemia
 Anterograde dementia
 Memory impairment
 Nystagmus
 Stupor or coma
 Respiratory depression

8. TREATMENT
It is a medical emergency. The treatment for acute alcohol intoxication
is primarly supportive. The main aim of therapy is to prevent severe
respiratory depression and aspiration of vomitus.
Maintain:-
 Airway
 Breathing
 Circulation
 Fluid and Electrolyte balance
 Gastric lavage if come within 2 hours
 Correction of hypoglycemia by glucose infusion till alcohol is
metabolised

9.  Patient presenting with coma secondary to ethanol
intoxication should receive atleast 100mg of parenteral
thiamine to prevent or treat wernicke’s
encephalopathy(presence of neurological symptoms
caused by biochemical lesions of the central nervous
system after exhaustion of vitamin-B1 reserves) along
with dextrose

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