This document provides information on alcohol use and alcohol use disorder. It defines alcohol and describes its absorption, metabolism, and effects on the brain and other body systems. It also discusses alcohol dependence, different types of alcoholism, acute intoxication, withdrawal syndrome, and various neuropsychiatric complications of chronic alcohol use such as Wernicke's encephalopathy, Korsakoff's psychosis, and Marchiafava-Bignami disease.

1. ALCOHOL USED
DISORDER
Presentee: Priyanka Singh (28)
(2008 batch) Sheeba Ali (30)
Md. Bilal Kaleem (33)
Md. Zahid (35)
Chairperson: Dr. Santosh Kumar,
A. P., Psychiatry, RMCH.

2. ALCOHOL
 The term alcohol refers to a
large group of organic
molecules that have a hydroxyl
group (-OH) attached to a
saturated carbon atom.

3.  Ethyl alcohol ,also called ethanol,
is the common form of alcohol,
sometimes referred to as beverage
alcohol, ethyl alcohol used for
drinking.

4.  A single drink is usually
considered to contain about 12 g
of ethanol, which is the content of
12 ounces of beer, one 4-ounces
glass of nonfortified wine, or 1-1.5
ounces of an 80 proof (40%
ethanol) liquor (eg-whiskey)

5. ABSORPTION
 About 10% of consumed
alcohol is absorbed from the
stomach, the remainder from
the small intestine.

6.  Peak blood conc. of alcohol is
reached in 30 to 90 min & usually
in 45 to 60 min, depending on
whether the alcohol taken on an
empty stomach or with food.
 Body has protective devices
against inundation by alcohol.

7.  For ex-- if the conc. of alcohol in the
stomach becomes too much high,
mucus is secreted, & the pyloric
valve closes.
 These action slow the absorption &
the keep alcohol from passing in to
the small intestine.

8.  Once alcohol is absorbed in to the
blood stream, it is distributed to all
body tissue. because alcohol is
uniformly dissolve in body’s water.

9. METABOLISM
 About 90% of absorbed alcohol is
metabolized through oxidation in the
liver, the remaining 10% is excreted
unchanged by kidney & lungs.
 Alcohol is metabolized by 2 enz:-
alcohol dehydrogenase (ADH) &
aldehyde dehydrogenase .

10. ALCOHOL
ADH
ACETALDEHYDE
ALDEHYDEDEHYDROGENASE
ACETIC ACID

11. EFFECTS OF
ALCOHOL

12. EFFECTS ON THEBRAIN
BEHAVIORAL EFFECTS:-
 As the net result of molecular
activities, alcohol functions as a
depressant much as do the
barbiturates & BDZ’S, with which
alcohol has some cross tolerance
& cross-dependence.

13.  At the level of 0.05% alcohol in the
blood ,thought, judgment, &
restraint are loosened &
sometimes disrupted.
 At a conc. of 0.1% voluntary motor
actions usually become
perceptibly clumsy.

14.  In most state legal intoxication
range from 0.1to 0.15% blood
alcohol level.
 At 0.2% function of entire motor
area of the brain is measurably
depressed & parts of brain control
emotional behavior are also
affected.

15.  At 0.3% , a person is commonly
confused or may become
stuporous.
 At 0.4-0.5%, the person falls into a
coma.

16.  At higher levels, the primitive
centers of brain that control
breathing & heart rate are affected &
death cause secondary to direct
respiratory depression or aspiration
of vomitus.

17. SLEEP EFFECTS
 although alcohol consume in the
evening usually the ease of
falling asleep ( sleep latency),
alcohol also has an adverse effect
on sleep architecture.

18.  Specifically, alcohol use is
associated with a in rapid eye
movement sleep & deep sleep
& more sleep fragmentation
,with more & longer episode of
awakening.

19. OTHERPSYCHOLOGICALEFFECTS
LIVER:-
major adverse effect relate
to alcohol effects are liver
damage.

20.  Alcohol use, even as short as week-long
episodes of increased drinking, can
result in an accumulation of fats &
proteins, which produce the appearance
of fatty liver.
 Alcohol use, however, is associated with
the development of alcohol hepatitis &
hepatic cirrhosis.

21. GIT
 long term heavy drinking is
associated with developing
esophagitis, gastritis,
achlorhydria, & gastric ulcer.

22.  Development of esophageal varices
can accompany particularly heavy
alcohol abuse.
 Disorder of small intestine occasionally
occur, & pancreatitis, pancreatic
insufficiency, pancreatic cancer are
also associated with heavy alcohol
used.

23. Other bodily systems
 significant intake of alcohol also
associated with blood pressure,
dysregulation of lipoprotein &
triglyceride metabolism, & risk
for MI & CVS diseases.

24.  Evidence indicate that alcohol intake
adversely affect the heamatopoetic
system & can the incidence of
cancer, particularly head, neck,
esophageal, stomach, hepatic, colonic,
lung cancer.
 Acute intoxication may also associated
with hypoglycemia.

25. ALCOHOLDEPENDENCE
 Alcohol dependence was
previously known as alcoholism.
 This term like addiction has been
dropped due to its derogatory
meaning.

26.  According to jellinek, there are five ‘species’
of alcohol dependence on the basis of
pattern of use:-
 Alpha alcoholism:-
 Excessive & inappropriate drinking to
relieve physical &/or emotional pain.
 No loss of control.
 Ability to abstain present.

27.  Beta alcoholism:--
 Excessive & inappropriate drinking.
 No dependence.
 Gamma alcoholism:--
 Also called malignant alcoholism
 Progressive coarse.
 Physical dependence with tolerance.
 Psychological dependence, with ability to
control drinking.

28.  Delta alcoholism:-
 Inability to abstain.
 Tolerance.
 Withdrawal symptoms.
 Epsilon alcoholism:-
 Dipsomania (compulsive-drinking)
 spree-drinking.

29.  Alcohol dependence is more common in
young males & has an onset in late
second or early 3rd decade.
 The course is usually insidious.
 If the onset occurs in late in life,
especially after 40 years of age, an
underlying mood disorder should be
looked for.

30.  There are 6 criteria to diagnosed
dependence:-
1. Sense of compulsion.
2. Difficulty in controlling substance taking.
3. A physiological withdrawal state.
4. Evidence of tolerance.
5. Progressive neglect of alternative
pleasures.
6. Persisting with substance use despite clear
evidence overtly harmful consequences.

31. ACUTEINTOXICATION
 After a brief period of excitation, there
is a generalized depression with
alcohol use.
 With increasing intoxication, there is
reaction time, slowed thinking,
distractibility & poor mental control.

32.  Later dysarthria, ataxia & incoordination
occur.
 There is progressive loss of self control
with frank disinhibited behavior.
 Duration of intoxication depends on the
amount & the rapidity of ingestion of
alcohol.

33. BODY FLUID ALCOHOL
LEVELS
BEHAVIORAL CORRELATES
25-100 mg % Excitement
80 mg % Legal limit for driving (in UK)
100-200 mg% Serious intoxication, slurred
speech, incoordination,
nystagmus
200-300 mg % Dangerous
300-350 mg % Hypothermia, dysarthria, cold
sweats
350-400 mg % Coma, respiratory depression
>450 mg % Death may occur

34. WITHDRAWALSYNDROME
 The most common withdrawal
syndrome is a hangover on the next
morning.
 Mild tremor, nausea, vomiting,
weakness, irritability, insomnia &
anxiety are the other common
withdrawal symptoms.

35.  sometimes., the withdrawal syndrome may
be more severe, characterized by one of the
3 disturbances:-
 Delirium tremens
 Alcoholic seizures
 Alcoholic hallucinosis.

36. DELIRIUMTREMENS
 It is the most severe alcoholic
withdrawal syndrome .
 It occur usually with in 2-4 days of
complete or significant abstinence from
heavy alcohol drinking in about 5 % of
pt., as compared to acute
tremulousness which occur in about
34% of pt.

37.  The course is short with recovery
occurring with in 3-7 days.
 This is an acute organic brain syndrome
(delirium) with the characteristic
features of :-
 Clouding of consciousness with
disorientation in time & place.

38.  Poor attention span & distractibility.
 Visual hallucinations & illusions which
are often vivid & very frightening.
 Marked autonomic disturbances
tachycardia, fever , sweating,
hypertension, & pupillary dilatation.

39.  Psychomotor agitation & ataxia.
 Dehydration with electrolyte
imbalance.
 Death, if occurs, is often due to
cardiovascular collapse, infection,
hyperthermia or self inflicted injury.

40. ALCOHOLICSEIZURES(RUMFITS)
 Generalized tonic clonic seizures
occur in about 10% of alcohol
dependence pt. usually 12-48 hrs
after a heavy bout of drinking.

41.  Multiple seizures (2-6 at 1 time) are
more common than single seizure.
 Some times status epilepticus may be
precipitated.
 In about 30% of cases delirium tremens
follows.

42. ALCOHOLICHALLUCINOSIS
 It is characterized by presence of
hallucination (usually auditory)
during partial or complete
abstinence, following regular
alcohol intake.
 It occurs in about 2% of pt.

43.  These hallucinations persist after the
withdrawal syndrome is over, &
classically occur in clear
consciousness.
 Usually recovery occur with in 1 month
& the duration is very rarely more than
6 months.

44. NEUROPSYCHIATRIC
COMPLICATIONS OF
CHRONICALCOHOLUSE

45. WERNICKE’SENCEPHALOPATHY
 It is an acute reaction to a severe
deficiency of thiamin, the
commonest cause being chronic
alcohol use.
 characteristically, the onset occurs
after a period of persistent
vomiting.

46.  The Important clinical signs are:-
 Ocular signs:-coarse nystagmus,
ophthalamoplegia, with bilateral external
rectus paralysis occur early. in addition,
pupillary irregularities, retinal
hemorrhage & papilloedema can occur,
causing an impairment of vision.

47.  Higher mental function disturbances:-
disorientation, confusion, recent
memory disturbances, poor attention
span & distractibility are quite
common.
 Other early symptoms are ataxia.
 Peripheral neuropathy & serious
malnutrition are often coexistent.

48. KORSAKOFF’SPSYCHOSIS
 It often follows wernicke’s
encephalopathy, these are together
referred to as wernicke-korsakoff’s
syndrome.
 Clinically, korsakoff’s psychosis
presents as an organic amnestic
syndrome, chracterized by gross
memory disturbances with
confabulation.
 insight is often impaired.

49. MARCHIAFAVA-BIGNAMI DISEASE
 This is a rare disorder characterized by
disorientation, epilepsy, ataxia,
dysarthria, hallucinations, spastic limb
paralysis, & deterioration of
personality.

50.  There is a widespread demyelination of
corpus callosum, optic tracts &
cerebellar peduncles.
 The cause is probably an alcohol-
related nutritional deficiency.

51. THANK
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