Ethanol

 Alcoholism is a complex disorder with genetic

and environmental determinants.
 Ethanol is absorbed from the upper GIT and
distributed in the body water.
 The majority is oxidized, primarily in the liver;
breath contains 0.05% of blood.
 It follows zero order kinetics (220mmol/hr).
Ethanol metabolism

 The Alcohol
Dehydrogenase
(ADH) pathway in
the cytosol.
 The Microsomal
Ethanol Oxidizing
System (MEOS)
located in the smooth
endoplasmic
reticulum.
 Ethanol
Alcohol Dehydrogenase Pathway in Liver
 The major pathway of alcohol metabolism converts
alcohol into acetaldehyde and leads to generation of
NADH.
 The rate of ethanol oxidation is determined by the
capacity to re-oxidize NADH.
 If the ability of the liver to maintain redox
homeostasis is overwhelmed, then a number of
metabolic disturbances arise including lactic acidosis,
↑uric acid and abnormalities of lipid metabolism.
Ethanol
 Ethanol

MEOS (Cytochrome P 450):

 Its role in ethanol metabolism is very less, when
blood ethanol concentrations are low (<100mg%).
 Chronic alcohol is associated with an induction of
the MEOS system; can account for up to 10% of
ethanol oxidation
 Ethanol

Mechanism of action: Ethanol

 Ethanol enhances the action of GABA through
GABA-A receptor
 It also inhibits NMDA receptor
 Ethanol potentiates the action of BZD and
barbiturates and can result in fatal CNS depression.
 Ethanol

Central nervous system effects :

 Ethanol inhibits the release of ADH from pituitary
and produce diuresis.
 It produces vasodilatation and hypothermia.
 Thiamine deficiency occurs due to poor diet and
decreased absorption leading to nerve
demyelination.
 Ethanol

Toxicity of Ethanol:
 Acetaldehyde acts as a poison by inhibiting oxidative
phosphorylation.
 Lactic acidosis.
 Hypoglycemia.
 All redox reactions are perturbed
 Death can occur when the blood alcohol levels is
>400-500mg/dl.
Ethanol

BAC
 Ethanol

Withdrawal syndrome of alcohol

 Tremors, hallucinations, seizures, insomnia,
hyperthermia, nausea/vomiting
Delirium tremens or withdrawal syndrome is
treated by chlordiazepoxide or diazepam.
Illustration of the craniofacial features associated with
fetal alcohol syndrome.

Malformation of skeletal, cardiovascular, renogenital system

 Ethanol
Disulfiram :
 Acts by inhibiting aldehyde dehydrogenase and thus
acetaldehyde is accumulated.
 It should not administered with alcohol.
 It results in flushing, headache, tachycardia,
vomiting, confusion and convulsions.
 Naltrexone helps to abstain from alcoholism by
decreasing craving and relapse.
FOMIPEZOLE
Ethanol

Disulfiram
 Ethanol

Drugs used to treat alcohol dependence

 To render alcohol unpleasant Disulfiram
 To reduce alcohol craving Naltrexone &
Acamprosate
 Ethanol

Drugs causing disulfiram like effect:

 Metronidazole
 Cefotetan
 Cefoperazone
 Chlorpropamide
 Methanol

 Methyl alcohol ‘Wood alcohol’ is widely used

in the industrial production of organic
solvents (windshield washing products).
 The most characteristic feature of methanol
poisoning is a delayed visual disturbance.
 Methanol

The treatment of methanol poisoning includes –

1. Suppression of metabolism by alcohol
dehydrogenase – Ethanol and Fomipezole
Fomipezole (antizol) is an alcohol
dehydrogenase inhibitor, approved for the
treatment of methanol and ethylene glycol
poisoning.
2. Methanol concentration in excess of 50 mg/dl is
an absolute indication for hemodialysis.
 Ethylene glycol

 Ethylene glycol is widely used as an automotive

antifreeze, engine coolants and hydraulic brake
fluids. .
 Ethylene glycol is toxic, and its ingestion should be
considered a medical emergency.

Fomipezole

Ca Oxalate stones
Renal failure