introduction, uses, manifacturing, mechanisam of action, pharmacological action, pharmacokinetic, disulfiram

1. Presented by
Miss. Ashvini Vijay Govande
Assistant Professor
Kandhar College of Pharmacy, Kandhar
PHARMACOLOGY OF ALCOHOL

2. Content
 Introduction
 Uses of alcohol
 How alcohol Manufactured
 Mechanism of action
 Pharmacological action
 Pharmacokinetics

3. Introduction
 Alcohol is a chemical name for a group of compound that
contain a hydroxyl group (-OH) bonds to carbon atom.
 The alcohol consumed by human is ethyl alcohol or ethanol.
 Structural formula is C2H5OH / C2H6O.
 It is clear colourless liquid rapidly absorbed from git tract and
distributed throughout the body.

4. Uses of alcohol
 As antiseptic
 As astringent
 Bactericidal and antifungal activity
 Topical disinfectant
 Appetite stimulator
 Rubifacient and counter irritant for sprains and joint pain
 Alcohol sponges reduce body temperature
 Reflex stimulation in fainthing and hysteria
 To treat methanol posioning
 Solvent and preservative in pharmaceutical preparation
 Primary ingredient in alcoholic beverages

5. How alcohol Manufactured
 It is manufactured by fermentation process.
 Fermentation is a biochemical process through which yeast
converts sugar to alcohol.
 C6H12O6 2(CH3-CH2-OH) + 2CO2

6. Mechanism of action
 It affects a large number of membrane protein that
participate in signalling pathway including neurotransmitter
receptor , enzyme and ion channel.
 Alcohol mainly affects on CNS
 It affects on neurotransmission by glutamate and gamma
aminobutyric acid (GABA) the main excitatory and
inhibitory neurotransmitter in CNS.

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Fig- a Fig-b

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 Actions of the brain’s glutamate system (Fig-a). In the
presence of alcohol, the activity of the N-methyl-Daspartate
receptors (NMDARs) and α-amino-3-hydroxy-5-methyl-
isoxazole-4-proprionic acid receptors (AMPARs), is
inhibited, reducing cation entry into the cell. As a result, the
activity of the neuron is reduced and no or fewer nerve
signals are generated.
 Actions of the brain’s γ-aminobutyric acid (GABA)
system(Fig-b). In the presence of ethanol, GABA activity is
enhanced, resulting in greater Cl influx into the
postsynaptic neuron and, consequently, greater inhibition of
the neuron.

9. Pharmacological action
1) CNS-
 At small doses- Alcohol causes sedation, relief of anxiety
 At moderate doses- Inhibit attention and information
processing skill as well as motor skills
 At higher doses - slurred speech, ataxia, impaired
judgement and disinhibited behaviour (intoxication or
drunkenness)
 Chronic drinker- who are tolerant to effect of alcohol,
required higher conc. for their effect and causes marked
intoxication/coma

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2) CVS-
 At small doses- Cutaneous vasodilation, flushing
 At moderate doses- Tachycardia and mild rise in BP
 At large doses- Vasodilatation due to direct vascular smooth
muscle dilation and vasomotor centre depression
3) Body temp. –
 Feeling of warmth due to cutaneous blood flow is increased

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4) Smooth muscle-
 Ethanol is a vasodilator
 It produces vasodilation effect by two mechanisam-
i) Depression of vasomotor center
ii) Direct smooth muscle relaxation caused by its
metabolite, acetaldehyde
 It also relaxes uterus so it was used intravenously for the
suppression of premature labor before the availability of
more effective and safer uterine relaxant.

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5) Liver-
 Liver diseases is most common cmplications of alcohol
abuse
 Alcohol induces liver damage due to production of its
metabolite acetaldehyde
 This acetaldehyde radialy reacts with proteins, lipids and
other comp. leads to impaired in mitochondrial function.
 Chronic alcoholics increases fat accumulation in liver
severe liver damage and cirrhosis

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6) GIT-
 Dilute alcohol at low doses- stimulate GI secretion
 Higher doses- inhibit GI secretion
 Long term ingestion of high conc.- Esophageal varices and
bleeding, erosive gastritis, diarrhea and malabsorption of
neutrients and vitamins.
 Increases risk of tumors in the GI system as well as in other
tissues including lungs and breast.
7) Sex-
 Decreases sexual performance

14. Pharmacokinetic
 Absorption-
 Absorbed from GIT (rapidly absorbe from small intestine
and colon but slowly absorbed from stomach)
 The maximum blood conc. Is reached within 30 min.
 Can be absorbed from lungs
 Can be absorbed from skin

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 Distribution-
 Uniformly distributed throughout the tissue and body fluid
 The volume of distribution of ethanol is approximate total
body water (0.5-0.7L/kg)
 Rapidly crosses placenta for the exposure to fetus
 It cross BBB rapidly

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 Excretion-
 Through lungs and urine
 Metabolism-
 About 90% alcohol is metabolised in liver
 The metabolite product of alcohol is acetaldehyde

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Fig. Metabolism of alcohol

18. Drug-Drug interaction
 Alcohol enhance the hepatotoxic effect of acetaminophen
and gastric irritating effects of NSAIDs, thus increasing the
risk for development of gastritis and upper GI bleeding.
 Alcohol enhances the sedation effect of antihistamines and
produces significant CNS depression.
 Chronic alcoholics interfere with metabolism of certain
drugs due to enhanced levels of liver enzyme.

19. Disulfiram
 It is a carbamate derivative used as an alcohol deterrent.
 It is nontoxic sub. when administered alone but when
ingested after administration of alcohol it immediately alter
the metabolism of alcohol.
 Disulfiram inhibit oxidation of acetaldehyde so blood
acetaldehyde conc. are increased and causes an unpleasent
reaction of facial flushing, systemic vasodilatation,
respiratory difficulty, nausea, hypotension and other
symptoms.
 It act by inhibiting aldehyde dehydrogenase (ALDH).

20. Thank you