Alcohol abuse

ALCOHOL ABUSE
DR AMIT GUPTA MD PSYCHIATRY
Gupta Hospital, Power house road, Bathinda

HISTORY OF ALCOHOL
 Discovery of late Stone age jugs suggest
that intentionally fermented beverages
existed at least as early as the Neolithic
period (cir. 10,000 BC)
 Babylonians regularly used both beer and
wine as offerings to their gods. Around 1750
BC, the famous Code of Hammurabi devoted
attention to alcohol. Although it was not a
crime, the Babylonians were critical of
drunkenness.
1/24/2017Dr Amit Gupta MD Psychiatry
2

HISTORY
OF
ALCOHOL
.
 Alcoholic beverages were consumed
in INDUS VALLEY CIVILIZATION
 These beverages were in use
between 3000 BC - 2000
 The Hindu Ayurvedic texts describe
both the beneficent uses of
alcoholic beverages and the
consequences of intoxication and
alcoholic diseases.
 Most of the peoples in India and
China, have continued, throughout,
to ferment a portion of their crops
and nourish themselves with the
alcoholic product.
3

.
4
The ancient Egyptians
made at least 17 types
of beer and at least 24
varieties of wine.
The earliest evidence of
alcohol in what is now China
are jars from Jaihu which
date to about 7000 BC.

WHAT IS ALCOHOL ?
 Ethyl alcohol - for which the more
scientific name is ethanol - is the
substance that we find in beverages.
 Formed through fermentation of a
variety of products including grain
such as corn, potato mashes, fruit
juices, and beet and cane sugar
molasses
5

Alcohol abuse is associated with many
accidents, fights, driving offenses and
unprotected sex.
It is responsible in the world for 1.8
million deaths and results in disability in
58.3 million people. About 40 percent of
these have alcohol related neuropsychiatric
disorders.
Alcohol consumption is estimated to
cause from 20% to 50% of cirrhosis of
the liver, epilepsy, poisonings, road
traffic accidents, violence and several
types of cancer.

Kerala led the states in terms of
consumption followed by Maharashtra &
Punjab.
Over 11% of the population in India
indulged in heavy or binge-drinking.
The global figure stood at 16%
A global study has found that alcohol consumption
in India has risen by 55 % over a period of 20 yrs.
More worryingly, the young are getting initiated to
alcohol much earlier, while more women are
indulging in hazardous and binge drinking
One Indian dies every 96 minutes due to alcohol
consumption- The Indian Express

8

Punjab has consumed liquor worth Rs
35,000 cr in last decade: RTI reply
The Tribune Chandigarh, March 15
The Punjab Cabinet today approved the Excise
Policy for the year 2016-17 by implementing which
the state government expects to collect Rs 5,440
crore as against Rs 5,040 crore in current year, an
increase of about Rs 400 crore
9

Making of ‘Ghar di shrab”
Home made liquor in rural
Punjab
10

World map showing alcohol per capita consumption
Worldwide consumption
The report stated that 38.3% of the global
population consumed alcohol. On an average, an
individual over 15 years of age consumed 6.2 liters of
alcohol annually.
11

INTRODUCTION
The term First used by
Magnus Huss, a Swedish
Public Health Authority, in
1849, the word Alcoholism
was quickly adopted by many
other languages, with only minor
variation.
12

RECOGNIZING THE STAGES OF ALCOHOLISM:
THE JELLINEK CURVE
E. Morton Jellinek—was a biostatistician,
physiologist, and an alcoholism
researcher- the man whose research
provided the foundations for the Curve.
Jellinek coined the expression “the
disease concept of Alcoholism” and
significantly accelerated the movement
towards the medicalization of
drunkenness and alcohol habituation.
13

JELLINEK’S1960 BOOK IDENTIFIED FIVE TYPES OF
ALCOHOLISM
 .
14
Alpha alcoholism: the earliest stage, purely psychological continual dependence
of alcohol to relieve bodily or emotional pain. "problem drinker", drinking
creates social & personal problems. These people can stop if they want to;
thus, argued Jellinek, they have not lost control, do not have a "disease".
Beta alcoholism: polyneuropathy, or cirrhosis liver without physical or
psychological dependence. heavy drinkers that drink a lot, almost daily. Do not
have physical addiction or withdrawal symptoms. This group do not have a
"disease".
Gamma alcoholism: acquired tissue tolerance, physical
dependence, and loss of control. alcoholic, who is out of control,
by Jellinek's classification, has a "disease".
Delta alcoholism: as in Gamma alcoholism, but with inability to
abstain, instead of loss of control.
Epsilon alcoholism: the most advanced stage of the disease,
manifesting as dipsomania, or periodic alcoholism.

JELLINEK CURVE’S BEST PURPOSE MAY BE AS A WAY FOR PEOPLE TO
UNDERSTAND THEIR OWN STRUGGLES WITH ADDICTION AND NOT AS A
DIAGNOSTIC TOOL. “IT’S A LEARNING TOOL. IT’S A VISUAL AND IT’S A WAY THAT
PEOPLE CAN KIND OF NORMALIZE (IN THE SENSE OF) ‘THIS IS WHAT HAPPENS TO
SOME PEOPLE.'” Contentment in Soberiety,
Increasing tolerance
Emotional stability, Self care
Stable friends , Economic stability
15
Progressi
ve phase
Crucial
Phase
Chronic
Phase
Rehabilitation
Phase
Recovery
Phase
Defeat admitted
Obsessive drinking
Relief drinking
tolerance
Efforts to control fail
Family &friends avoided
Neglect’s food
Tremors, physical problems
Guilt
Blackouts
Stops drinking
New hope
Right thinking

ALCOHOL ABUSE
 Alcohol abuse is defined as repetitive problems
with alcohol in any one of four life areas
 social
 interpersonal
 Legal
 Occupational
 repeated use in hazardous situations such as
driving while intoxicated in an individual who is
not alcohol dependent.
16
Alcohol Use Disorder DSM-5 312.9 (F91.9)
According to the DSM-5, the symptoms of alcohol use
disorder include a combination of craving, physical
dependence, an increasing tolerance for alcohol and
loss of control. .

ETIOLOGICAL FACTORS: BIOLOGICAL :
Genetic vulnerability -most replicated Association and
linkage studies
 genes encoding proteins involved in
alcohol metabolism (ADH1B*2 & ADH1C*2
alleles) chromosome 4q
 and in the rewarding circuits, including
dopamine (dopamine D2 receptor, DRD2
gene) allele A1 at the DRD2 locus on
chromosome 11 & dopamine transporter gene
DAT1) and
 GABA neurotransmitter biological pathways,
17

.
 single nucleotide polymorphism in the
hTAS2R16 gene (codes for a bitter receptor)
located on the 7q chromosomal region, is
associated with less sensitivity to bitter-taste
 Findings consistent with previous
investigations of the relationship between
taste perception and alcohol dependence.
 Another candidate gene in the 7q locus is
the CHRM2 gene. It codes for a
Cholinergic muscarinic 2 receptor and
shows significant association with alcohol
18

CANDIDATE GENES ALCOHOL METABOLISM
 alcohol dehydrogenase (ADH) gene
 The chromosome 4q region surrounding the (ADH) gene
was linked in a genome-wide scan with a phenotype
associated with alcohol dependence .
 . ADH1B*2 and ADH1C*2 alleles, and confer an
increase in alcohol degradation rate
 ADH1B*2 is common among Asians , is associated
with a diminution in alcohol consumption
• ADH1C*2 has protective effects on liver cirrhosis
and alcohol chronic pancreatitis , an is also
associated with a lower rate in alcohol dependence
among Asians.
19

ETIOLOGICAL FACTORS: PSYCHOLOGICAL
 Curiosity
 Early initiation of alcohol & tobacco
 Poor impulse control
 Low self-esteem & Poor stress management skills
 Childhood trauma / loss & Psychological distress
20

ETIOLOGICAL FACTORS: SOCIAL FACTORS
 Peer pressure . Modeling . Ease of availability
 Religious reasons . Poor social / familial support
 Rapid urbanization
21

PHYSIOLOGY
22
mouth and
esophagus (in
small amounts)
stomach and
large bowel (in
modest
amounts)
proximal
portion of the
small intestine
(the major site).
Absorption Rate of absorption is
increased
Carbonated
beverages
 Absence of
proteins, fats,
or
carbohydrates
 Dilution of
ethanol (20%
by volume).

NEUROTRANSMITERS-ALCOHOL
.
• Disinhibition
• Sedation
• Loss of
balance
• Hypertension
• Memory
disruption
• Sedation
• Euphoria
• Mood
elevation
.
• GABA
• Epinephrine
• L Glutamic acid
• Serotonin
• Dopamine
.
• Anxiety
• Insomnia
• Seizures
• Hypertension
• Tachycardia
• Delirium
• Seizures
• Insomnia
• Mood
disorder
• Dysphoria
23
Intoxication Withdrawal

AA
Alcohol Physiology
 CNS depressant : acting at several sites in
Brain
Enhances GABA activity
Stimulates serotonin receptor- pleasure &
nausea.
Stimulates dopamine & opioid receptors *
euphoria & reinforcement.
 Provide energy ( empty calories) no
nutritional value.
 Is a toxin to multiple organs.
24

BEHAVIORAL EFFECTS
Effects of Blood Alcohol Levels in the Absence
of Tolerance
Blood Level,
g/dL
Usual Effect
0.02 Decreased inhibitions, a slight feeling of
intoxication
0.08 Decrease in complex cognitive functions
and motor performance
0.20 Obvious slurred speech, motor
incoordination, irritability, and poor
judgment
0.30 Light coma and depressed vital signs
0.40 Death
25

.
26

COMPLICATIONS :CENTRAL NERVOUS
SYSTEM:
Blackout(35%)
Disturbed sleep
Impaired judgment &
coordination.
Hangover syndrome
Head injury &
fractures
27
With chronic use
Delirium tremens
Seizures (Rumfits )
Alcoholic hallucinosis
Delusional disorder
Alcoholic dementia
Sexual dysfunction

.
 Peripheral neuropathy(10%)
 Cerebellar degeneration or atrophy(1%)
 Wernicke's (ophthalmoparesis, ataxia, and
encephalopathy)
 Korsakoff's (retrograde and anterograde
amnesia) syndromes
28
1 in 500
alcoholics
Complications :Central Nervous System:

COMPLICATIONS OF ALCOHOL DEPENDENCE:
II. Social Complications:
 Accidents
 Marital disharmony
 Divorce
 Occupational problems
 Criminality
 Financial difficulties
29

.
Jessica Lal murder case Model and celebrity barmaid
Jessica Lal was shot dead for refusing to serve
alcohol to Union minister Venod Sharma’s son Manu
Sharma at Delhi, in April 1999.
30
2002 Hit & Run case. Salman khan was
drunk and driving that night
The Real Reason Why Women Were
Molested In Bangalore On New Year’s
Eve"Everyone was drunk and pushing
each other, people behaved indecently.
How Alcoholism Scars India
By Kristen McGuiness 05/01/13
Amid alarming reports of soaring
sexual assault rates, The Fix reports
from India on the extent to which
alcohol is to blame.

Alcohol abuse is associated
with significantly higher
rates of marital dispute &
divorce
31
In India about 40% of work accidents
have been attributed to alcohol use.
The economic consequences of
alcohol consumption can be severe,
particularly for the poor. Apart from
money spent on drinks, heavy drinkers
may suffer other economic problems
such as lower wages and lost
employment opportunities &
increased medical and legal
expenses.

COMPLICATIONS - ACUTE INTOXICATION
blood alcohol levels between 100 and 200
mg/dl
Symptoms of intoxication includes
disinhibition of sexual or aggressive
impulses, mood lability, impaired
judgement, social or occupational
functioning, slurred speech, incoordination,
unsteady gait, nystagmus & flushed face.
.
32

COMPLICATIONS - ALCOHOL WITHDRAWAL
signs and symptoms of AW typically appear between 6
and 48 hours after heavy alcohol consumption
decreases.
Initial symptoms may include headache, tremor,
sweating, agitation, anxiety and nausea and
vomiting, heightened sensitivity to light & sound,
disorientation, insomnia
These initial symptoms of AW intensify and then
diminish over 24 to 48 hours.
Severe Alcohol Withdrawal syndrome characterized
by one of the following 3 disturbances;
delirium tremens, alcoholic seizures ,alcoholic
hallucinosis.
33

.
34
Alcohol simultaneously enhances inhibitory tone (via
modulation of GABA activity) and inhibits excitatory
tone (via modulation of excitatory amino acid activity).
Constant presence of ethanol preserves
homeostasis.
Abrupt cessation unmasks the adaptive responses to
chronic ethanol use resulting in overactivity of the
central nervous system.
The symptoms of AW
reflect overactivity of
the
autonomic nervous
system.

1. DELIRIUM TREMENS:
most severe alcoholwithdrawal syndrome. It occurs usuallywithin 2 – 4 days
of complete or significant abstinence from heavy alcohol drinking in 5%
of patients. Thisis with the characteristicof
 Severe agitation,tremor, disorientation,
 visualhallucinations,
 tachycardia, hypertension,
 fever, sweating, insomnia,
 dehydration andelectrolyte imbalance.
Delirium tremens is a medical emergency with ~10% mortality if not
treated
35

2. Alcoholic Seizures (“rum fits”):
Generalized tonic clonic seizures occur in
about 10% of alcohol dependence patients.
Usually 12 – 48 hours after a heavy bout of
drinking. Multiple seizures 2 – 6 at one time,
are more common
36
3. Alcoholic hallucinosis:
This is characterized by the presence of
hallucinations during abstinence, following
regular alcohol intake.
These hallucinations persist after the
withdrawal syndrome is over, and classically
occur in clear consciousness

PT’S USUALLY COME IN COMPLAINING OF WITHDRAWAL
SYMPTOMS
37
exclude other causes of presentation
“What is it that has brought you in to the clinic today?”
Any other substances of misuse ?
Depression/ Suicidality ?
Reasons why drinking was exacerbated ?
Age of starting drinking ?
Last drink?
How often they drink (try to take a day history) ?
Try to quantify alcohol use to grams/SD
symptoms of dependence? (withdrawal /tolerance)
CAGE questionnaire
Taking an alcohol history

.
 Social Situation ? Effects on daily living ? Occupation ?
Relationships ?
 Diet – adequate intake? / type of food (balanced?) / eating pattern
 Alcohol related crime? Living situation?
 Previous attempts at abstinence:
 “Have you ever tried to stop drinking before? Why?“
 “Why do you think unsuccessful?“
 If not already revealed, assess desire to stop drinking
38
General medical history / previous surgery
Alcohol-use specific -Liver disease / peptic ulcers /pancreatitis
/ischaemic heart disease/ injuries?”
Drug history- Prescribed / OTC / Recreational
Allergies
Family history -Focus on history of alcohol/drug dependence /mental
illness
Assess risk to self / & risk to others:

can relieve patient’s discomfort and
forestall cumulative effects that might
worsen future withdrawals.
39
• mild to moderate
symptoms can be treated
successfully on an
outpatient basis
Hospital
admission
provides the
safest setting
for the
treatment
Severe AW requires pharmacological intervention
Appropriate treatment of (AW)

TREATING WITHDRAWAL
Physical
examination &
history
Lab
evaluation
treatment
40
CBC, LFT’S, KFT’S, Sr
Amylase, glucose , Sr
electrolytes
Chest Xray, USG Abdomen
Brain Imaging, ( MRI &
EEG)
Out
patient
Indoor
search for evidence of liver
/pancreatic disease , gastrointestinal
bleeding, portal HT , cardiac
arrhythmia, anemia , malnutrition
& infection

 History of severe withdrawal symptoms
 History of alcohol withdrawal seizures or
delirium tremens
 Multiple past detoxifications
 Concomitant medical or psychiatric illness
 Recent high levels of alcohol consumption
 Lack of reliable support network
 Pregnancy
41
Relative Indications for Inpatient Alcohol
Detoxification

Providing a quiet environment,
reduced lighting,
Physical restraints temporarily to protect
agitated patients from injuring themselves
and to protect staff
Careful monitoring & supportive care.
fluids (p/o or IV fluids if dehydrated).
Correction of electrolyte imbalance
Parenteral Thiamine 100 mg daily
Restrict access to addicting substances
42
Liaison
with other
specialists
as required
General principles of treating AW

• American Psychiatric Association Task Force
1989; Institute of Medicine 1990; Anton and
Becker 1995; Moskowitz et al. 1983
BZ’s are considered
medications of choice
to treat
• These assessments have employed a
standard AW scale like (CIWA-Ar)
BZ administration
based on the severity
of symptoms.
• (Moskowitz et al. 1983).
No single BZ appears
to be superior
43
Recent clinical reviews have stressed the value of short-
acting BZ’s, such as oxazepam (Serax®) and lorazepam
(Ativan®) (Gallant 1989).
More than 150 medications have been investigated for AW,
clinicians disagree on the optimum medications & prescribing
schedules.

.
Treatment goal Adequate
level of Sedation
cardiac monitoring and oximetry
and resuscitative equipment
should be available
44
Examples of Medication Regimens DT
Diazepam
5 mg IV (2.5
mg/min).
repeat the
dose in 5 to
10 minutes
third and
fourth
doses
every 5 to
10 minutes
20 mg for
the fifth and
subsequent
doses
Lorazepam
1 to 4 mg IV or IM
every 5 to 15 minutes
1 to 4 mg every 30 to
60 mins , until calm,
then every hour as
needed to maintain
light somnolence
5 to 20 mg
every hour
as needed to
maintain light
somnolence
Haloperidol
0.5 to 5mg IV or
IM every 30 to 60
minutes as
needed for
severe agitation.
.

.
 .
Adrenergic Medications. ( Propranolol) No evidence ,
however, that these medications block delirium or
seizures. Most reviewers have concluded that
adrenergic medications are of value largely as
adjuncts to BZ’s in the management of AW. may be
useful in outpatient settings
Antiseizure Medications. In Europe, carbamazepine and
valproic acid and others) have been used successfully to treat
AW Advantages- decrease seizures, non sedating, non habit
forming, treat mood ,anxiety & agitation
Antipsychotics such as haloperidol have been used to treat DT’s. Lesser
sedation and hypotension & provide behavioral control. Increase susceptibility to
seizures, restlessness, agitation, and abnormal movements.
Baclofen -GABA receptor agonist is able to suppress AWS Addolorato et al. (2003)
also reported the ability of 75 mg/day baclofen (25 mg t.i.d.) to stop delirium
tremens, the most severe complication of AWS.

RELAPSE PREVENTION
Aversion therapy agentslike disulfiram,
Anti-cravingagents: Acamprosate,Naltrexone, Baclofen ,
Topiramate, Fluoxetineetc.
Behaviourtherapy (The mostcommonlyusedtherapy is
aversion therapy)
Psychotherapy, Group therapy
Psychosocialrehabilitation
46

MEDICATIONS FOR RELAPSE PREVENTION - 11/24/2017Dr Amit Gupta MD Psychiatry
47
Drug Dosage MOA Benifit Remarks
NALTREXONE 50–150 MG/D
ORALLY,
BLOCKING OPIOID
RECEPTORS,
DECREASE ACTIVITY IN
THE DOPAMINE-RICH
VENTRAL TEGMENTAL
REWARD SYSTEM
SHORTEN
SUBSEQUENT
RELAPSES
G ALLELE OF
THE AII8G
POLYMORPHIS
M
Contraindicated
in liver disease,
comorbid Opiate
dependence
ACAMPROSATE
2 G/D
DIVIDED
INTO THREE
ORAL DOSES
INHIBITS NMDA
RECEPTORS
DECREASING
MILD
SYMPTOMS
OF
PROTRACTED
Withdrawal.
DISULFIRAM 250 MG/D.
PRODUCES VOMITING AND
AUTONOMIC NERVOUS
SYSTEM INSTABILITY IN
THE PRESENCE OF
ALCOHOL AS A RESULT OF
RAPIDLY RISING BLOOD
LEVELS OF THE FIRST
METABOLITE OF ALCOHOL,
ACETALDEHYDE
AVERSION
THERAPY
CAN BE
DANGEROUS
WITH HEART
DISEASE,
STROKE,
DIABETES
MELLITUS, OR
HYPERTENSION

MEDICATIONS FOR RELAPSE PREVENTION- 11
48
Drug Dosage MOA Benifit Remarks
Baclofen
10–20
MG/three
times
/day
ORALLY,
GABA-b receptor agonist
Blocks dopamine release in
central reward areas (ventral
straitum & prefrontal cortex)
DECREASING
SYMPTOMS
OF Withdrawal
Decrease
cravings
Can be used in
liver disease
Topiramate
escalating
dose of
25 to
300
mg/day
dual action facilitate
GABAA-mediated inhibitory
impulses, antagonize
AMPA and kainate
glutamate receptors, -
suppress ethanol-induced
nucleus accumbens dopamine
(DA) release, thereby inhibiting
the reinforcing effects of alcohol
decrease
alcohol
reinforceme
ntreduced
craving
adverse events
are paresthesia
(transient),
anorexia,
difficulty with
memory/
concentration,
and taste
perversion
Ondansterone 16mg
/day
5-HT3 antagonist
that exerts its
effects through
cortico-mesolimbic
DECREASING
SYMPTOMS
OF WIthdrawal
Mild adverse
effects

Thank you
49

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