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Pharmacology of Alcohols

Alcohols are manufactured by fermentation of sugar. Important alcoholic beverages are malted liquids like beer and wines.



Ethyl alcohol,

Methyl alcohol,

Propyl alcohol


Ethylene glycol,

propylene glycol



Poly hydroxy



Ethanol / ethyl alcohol 


History dates back 8000 years. Before 19th century, alcohols (beers, wines) were the main beverages. Use of water intake was associated with disease. If is one of the most commonly abused drug. Almost 80% in west is used, 10-15% is abused.

Alcoholism is when people take alcohol for recreation

Abuse is when person depends on alcohol for physiological and physical purposes.

Alcoholism is due:

  1. Genetic factors
  2. Environmental factors

Alcohol Breath test

Used to identify a person during driving. In UK 80 mg/100 ml of blood is recognized as drunk.

Industrial solvent

Also an important industrial solvent.


·       Small water soluble molecule, rapidly absorbed from GIT. Presence of food delays absorption.

·         Tmax     — 30 min

·         Vd  – 0.5  –  0.7 l/kg –crosses all biological membranes

·         Metabolized in liver. Oxidation  occurs 90 %, 10% is excreted through urine and lungs, so forms the basis of alcohol breath test.

·         Zero order kinetics –  in normal individual 7 – 10 g/hr. alcohol is metabolized.

Metabolic pathways 
1.      Alcohol  dehydrogenase pathway

When up to 100 mg / dl, after that NAD is saturated, and second pathway comes into play.

2.      Microsomal  ethanol  oxidizing system (MEOS)


Mechanism of action

There is no exact mechanism. It involves many organs/systems.

1.  Proteins

Acts through proteins which participate in signaling pathway.

2.  Receptors –GABA/ NMDA/ glutamate

3.  Ion channels

4.  Neurotransmitters –serotonin, histamines and noradrenaline

5.  Enzymes –Na K ATPase, phosphotidyl inositol

6.  Cellular organelles –mitochondria

7.  Oxidative stress –liver is most commonly involved, leading to hepatitis

 Depending on dose and no. of times consumed. In hepatitis, chances of liver failure are increased.

 Acute ethanol consumption

1.      CNS

In low doses:

  1. Relief from anxiety
  2. Feeling of euphoria

Increased dose:

a.       Sedation

b.      Ataxia

c.       Instability

d.      Difficulty in motor functions 

e.       stupor 

f.       coma  

g.       death

2.      CVS

Decreases cardiac contractility

3.  Smooth muscle

Relaxing effect.

a.      Blood vessels

vasodilatation    vasomotor center  /  direct effect  

b.      Uterus

                       Relaxation of uterine smooth muscles.

Clinical uses of alcohol
1. As antiseptic

2. Rubifacient and counter irritant for sprains and joint pain

3. Rub into skin to prevent bedsores

4. As astringent

5. Alcohol sponges to reduce body temperature

6. Intractable neuralgias around the nerve cause permanent loss of transmission

7. Appetite stimulant

8. Reflex stimulation in fainting and hysteria

9. To treat methanol poisoning

Chronic alcoholism

Mechanism of Action

 Formation of radicals.

Tissue damage

1.      Direct injury to mitochondria

2.      Metabolic products

3.      Organ effects

a.      Liver/ GIT

I.                    Fatty liver – hepatitis  –  cirrhosis  –  failure. Treatment is liver transplant

II.                 Acinar cells of pancreas are damaged so leads to chronic pancreatitis

III.               Gastritis

IV.              Chronic use leads to malnutrition –due to diarrhea and faulty absorption

b.      Nervous system

I.Tolerance – changes in CNS/ metabolism

Extra alcohol is required to produce same effects.

II.  Dependence – physical/ psychological

III.Withdrawal syndrome – delirium, tremens, may cause confusion, ataxia, weight gain, stupor, seizures and death.

IV.  Neurotoxicity and parasthesias due to involvement of lower limb nerves.

V.  Degenerative changes – peripheral / central nerves, dementia and demyelinating changes

VI. Wernicke – korsakoff syndrome– due to deficiency of thiamine. Paralysis of extra ocular muscles occurs, leading to confused state, ataxia, coma and death.

c.       CVS

I.                 Cardiomyopathy / heart failure

      II.                Arrhythmias

     III.               Hypertension

     IV.               Coronary heart disease

d.      Blood

I.                    Directly effects bone marrow leading to anemia / indirect nutritional effects

          II.            Hemolytic syndrome

e.       Endocrine system and electrolyte balance

               I.            Gynecomastia

             II.            Testicular atrophy

          III.            Edema, effusion, ascities

          IV.            Hypoglycemia

            V.            K+ derangement – secondary aldosteronism

f.     Immune system

               I.            Lungs – inhibited immunity leading to lung infections

             II.            Liver/pancreas – hyperactive, cytokines are produced which damage liver and pancreas.

g.   Increased cancer risk

I.                    Mouth,

II.                 pharynx,

III.               larynx,

IV.              esophagus,

V.                 liver,

VI.              breast

h.      Fetal alcohol syndrome

I.                     IUGR / mental retardation

      II.            Microcephaly / poor coordination

     III.                Underdeveloped midfacial region

     IV.            Heart and joint defects

 Drug interactions

Pharmacokinetic – enzyme inducer

Acute alcoholism – enzyme inhibitor

Pharmacodynamics – additive effect with:

  1. Tranquilizers
  2. Sedatives/hypnotics
  3. Anti-epileptics
  4. Anti-histamines

If alcohol is consumed with these drugs, toxicity is increased.

1.      Acute  alcoholic  intoxication

Respiratory / CVS depression

Dehydration / hypoglycemia / ketosis


a)      ABC

b)      Gastric lavage

c)      IV fluids + electrolytes

d)      Glucose

e)      Thiamine

Alcohol withdrawal syndrome

a)      Prevention of seizure/ delirium/ arrhythmias

b)      Electrolyte balance

c)      Thiamine

2. Chronic alcoholism

a.       Detoxification

b.      Substitution by sedatives/hypnotics (long acting benzodiazepines) used as substitute to alcohol.

c.       Tapering gradually

      d.  Psychosocial therapy

      e.  Aversion therapy – drugs to:

I.                    Stop craving

II.                 Avoid relapse

Drugs used for aversion therapy are:

1.      Naltrexone

Opioid receptor antagonist,

50 mg OD


2.   Acamprosate

Weak NMDA – receptor antagonist

GABA receptor activator

333 mg TDS

GIT/ renal toxicity

3.   Disulfiram

Aldehyde dehydrogenase inhibitor

Person taking alcohol has adverse effects including (only for those who themselves want to stop):

a.       Flushing

b.      sweating

c.       vomiting

d.      Headache

e.       hypotension

f.       confusion

Metronidazole/ cefotetan/ trimethoprim

4.   Other drugs

Topiramate – epilepsy

Ondansetron – 5- HT3 receptor antagonist

Methanol / methyl alcohol

Used as solvent

Accidental poisoning

May lead to:

       a.       Respiratory / CVS depression

b.      Seizure

c.       coma


a.       Ethanol t/m

      b.  Hemodialysis

      c.  Folic acid / alkalization of urine

     d.  Fomepizole – alcohol dehydrogenase inhibitor / orphan drug –used for rare diseases, not made by pharma companies as there is no profit.

Ethylene glycol

Heat exchanger / antifreeze formulation

Converted to aldehyde / oxalate


Excitation  – depression

Oxalate in renal tubules damages nephrons

Treatment same as methanol poisoning

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