This document summarizes alcohol dependence syndrome. It discusses the prevalence of alcohol use disorders globally and their health impacts. It profiles the substances in different alcoholic beverages and how alcohol is absorbed, metabolized, and affects the brain and body. The document outlines classifications of alcoholism, disorders related to alcohol use and intoxication, withdrawal, and dependence. It describes the effects of long-term heavy alcohol use on multiple organ systems like the liver, heart, and pancreas.

1. ALCOHOL DEPENDENCE
SYNDROME
Dani Paul
M. Sc (N) II yr
College of Nursing, CMC, Vellore.

2. INTRODUCTION
• Alcohol has been a part of human life
• Record of Harappan civilizations has storage and various use of wine and
alcoholic beverage
• 9% prevalence in India
• Alcohol use disorders have accounted for 1.4% of the global burden.
• Alcohol consumption cause 3.2% deaths and 4% disability adjusted life
years lost
• World 3rd largest risk factor for disease and disability

3. PROFILE OF SUBSTANCE
• Natural substance formed by fermenting sugar with spores
• Alcoholic beverage is known scientifically as ethyl alcohol
• Chemical formula C2H2OH
• Classified as food, because it contains calories; however has no nutritional value
• Different alcoholic beverage are produced by using different sources of sugar.
• Distilled beverage are derived by concentration of alcohol through a process called
distillation

4. • Alcohol content varies by type of beverage-
– Beer 3-6% alcohol
– Wine 10-20% alcohol
– Distilled beverage 40-50% alcohol
• 12 ounce of beer/3 – 5 ounce of wine/cocktail with 1ounce of whiskey= 0.5 ounce
alcohol
• All contain same effect on body
• Alcohol exerts a depressant effect on CNS, resulting behavioral and mood changes
• Effect of alcohol on CNS are proportional to alcohol concentration in the blood

5. • According to Drunk Driving law, blood alcohol content of 0.03% in 100ml blood is the
legal limit
• Body burns alcohol at the rate of 0.5ounce /hour or 15mg/dl/hr
• Alcohol is thought to have a more profound effect when an individual is emotionally
stressed or fatigued

6. CLASSES OF PSYCHOACTIVE SUBSTANCE
• Alcohol
• Amphetamines and related
substances
• Caffeine
• Cannabis
• Cocaine
• Hallucinogens
• Inhalants
• Nicotine
• Opioids
• Phencyclidine and related
substances
• Sedative, hypnotics or
anxiolytics

7. HISTORICAL ASPECTS
• Alcohol use traced back to Neolithic age.
• Beer and wine are known to have been used around 6400BC
• The term “alcoholism” was coined by the Swede Magnus Huss (1849) to
describe “those disease manifestations which without any direct
connection with organic changes of the nervous system take on a chronic
form in persons who, over long periods, have partaken of large quantities
of brandy”

8. • Physicians in America (Rush, 1785), and Britain (Trotter, 1804) made
graphic descriptions.
• Jellinek (1946) described the evolution of drinking behaviour, recognized
the heterogeneity of the condition, and described five species of
alcoholism.
• In 1955, the World Health Organization made the distinction between
the physical and psychological basis of alcohol-seeking behaviour.
• “One drink led to one drunk”.

9. 5 SPECIES OF ALCOHOL
a. Alpha: purely psychological continued dependence without loss of
control or inability to abstain.
b. Beta: physical complications without physical or psychological
dependence.
c. Gamma: acquired tissue tolerance, adaptive cell metabolism,
physical dependence and loss of control.
d. Delta: shares the first three features of gamma, but inability to
abstain replaces loss of control.
e. Epsilon: dipsomania or periodic alcoholism.

10. Classification of alcoholism
I. Type 1 alcoholism (milieu
limited)
• Age of onset over 25 years
• No criminality or treatment for
alcohol problems in the
biological parents
• Loss of control (or
psychological dependence)
• Guilt and fear about
dependence
• Harm avoidance
• Reward dependence
II. Type 2 alcoholism (male
limited)
• Teenage age of onset (under 25
years)
• Alcohol abuse, criminality and
treatment are extensive in the
biological father
• Inability to abstain
• Aggressive behaviour
• Novelty-seeking personality
traits

11. Classification based on amount
consumed
• Binge drinking: Over twice the daily guidelines in one day (8 units
for men, 6 units for women).
• Low to moderate: Weekly,
drinking up to 14 units for
women and 21 units for men.
• Heavy to moderate: Weekly, drinking 14–35 units for women and
21–50 units for men.
• Very heavy drinking: Weekly consumption of 35 units or more for
women, and 50 units or more for men.
• Chronic: Sustained drinking, which is causing or is likely to cause
harm.

12. Terms
discussion

13. ETIOLOGY
• Many factors affect decision to drink, like social, religious,
psychological factors and genetic factors contribute.
• 60% genetic and 40% environment influence in contributing
to alcoholism
1. Psychological theories
2. Psychodynamic theories
3. Behavioural theories
4. Socio-cultural theories
5. Childhood history
6. Genetic factors
• Family and adoption studies
• Twin studies
• Molecular genetics-linkage and association

14. CHARACTERS
• Hydroxyl group (OH)
• Ethyl alcohol/ethanol 1st form of alcohol
• Referred as beverage alcohol
• Chemical formula CH3-CH2-OH

15. • Character:
– Taste and flavor depends on preparation
– For marketing, congeners may confer different psychoactive
substance
– A single drink has 12 gm of ethanol
– Single drink can increase blood alcohol of 68 kg man by 15 to
20mg/dl, which an average man can metabolize in 1 hour
– Possible beneficial effects are highly controversial, based on
epidemiological data.

16. ABSORPTION
• 10% absorbed in stomach, rest in small intestine
• Peak blood concentration is reached in 30-90mts (depends on
empty stomach consumption)
• Rapid drinking reduce the time to peak concentration, slower
drinking increases it
•Body has protective device against inundation of alcohol (vomiting)

17. •This action slows the absorption and keeps alcohol from passing into
small intestine, where there are no significant restraints to absorption.
•Thus a large amount of alcohol can remain in stomach for hours
unabsorbed.
•Once absorbed it is distributed to all body tissues, because alcohol is
uniformly distributed dissolved in body’s water. Body part with high
water proportion receive high concentration of alcohol
•Intoxicating effect are greater when blood alcohol concentration is rising,
than when falling (Mellanby effect)
•Rate of absorption bears directly on the intoxication response

18. METABOLISM
• 90% of alcohol is metabolized through oxidation in liver, remaining 10%
excreted by kidney and lungs
• Oxidation of liver Is constant and independent of body’s energy
requirements
• Body can metabolize alcohol at 15mg/dl/hr.
• In average person who consumes large amount of alcohol, upregulation
of necessary enzymes results in rapid alcohol metabolism.

19. • Alcohol is metabolized by 2 enzymes alcohol dehydrogenase (ADH) and
Aldehyde dehydrogenase (ALDH)
• ADH -> alcohol->acetaldehyde (toxic); ALDH catalyzes conversion of
acetaldehyde into acetate.
• ALDH is inhibited by Disulfiram (antabuse)
• Women are more intoxicated than men with same amount of alcohol

20. PATTERNS OF USE
Jellinek (1952) - 4 phases:
1. The Pre-alcoholic phase (parent to child)
2. The Early Alcoholic phase (black outs following a period of
drinking)
3. The Crucial phase (lost control and physiological
dependence is evident)
4. The Chronic phase (emotional and physical disintegration)

21. • Chart

22. The Six stages of drunkenness
1. THE JOVIAL PHASE: frontal lobe affected.
2. THE SLURRING PHASE: parietal lobe affected.
3. THE CAN’T-SEE-PROPERLY PHASE: occipital lobe involved.
4. THE FALLING-DOWN PHASE: cerebellum involved.
5. THE DOWN-AND-OUT PHASE: midbrain involved.
6. IN THE VALLEY OF THE SHADOW OF DEATH: brain stem

23. DISORDERS OF ALCOHOL
Alcohol intoxication
• Alcohol intoxication occurs after the recent ingestion of alcohol and is
evidenced by behavioral changes such as impaired social or
occupational functioning, fighting, or impaired judgment.
• The client may exhibit mood changes, increased verbalization, impaired
attention span, or irritability.
• Symptoms of alcohol intoxication include slurred speech, lack of
coordination, unsteady gait, nystagmus, impaired memory, and stupor
or coma.

24. Alcohol withdrawal
• Clients generally experience clinical symptoms of alcohol withdrawal
within several hours to a few days after the cessation or reduction of
heavy and prolonged alcohol consumption.
• Autonomic hyperactivity; increased hand tremor; sleep disturbances,
insomnia, or nightmares; nausea or vomiting; transient visual, tactile, or
auditory hallucinations or illusions; psychomotor agitation; anxiety; and
grand mal seizures.

25. Severity of alcohol withdrawal.
1. Mild alcohol withdrawal: (uncomplicated)
• Occurs less than 24 hours after stopping or decreasing alcohol intake.
• It may include tremulousness, anxiety, nausea, vomiting, sweating, hyper-
reflexia and minor autonomic hyperactivity.
2. Moderate alcohol withdrawal (complicated)
• An intermediate position along the continuum with the hallmark of hallucinosis but
an otherwise clear sensorium.
3. Severe Alcohol Withdrawal
• Occurs more than 24 hours and up to 5 days after stopping or decreasing alcohol
intake.
• It is characterized by disorientation, agitation, hallucinations and severe autonomic
derangement. Withdrawal seizure: rum fits

26. WITHDRAWAL DELIRIUM: Also referred to as delirium tremens.
• Occur from 24 to 72 hours after the client's last drink.
• Elevation of vital signs accompanies restlessness, tremulousness,
agitation, and hyper-alertness.
• Any noises or quick movements are perceived as greatly exaggerated,
shadows are misinterpreted, and illusions and hallucinations frequently
occur.
• The client's speech is incoherent.

27. Alcohol dependence and alcohol abuse
• Characterized by tolerance to alcohol or by the development of withdrawal
phenomena upon cessation of or reduction in intake (Edgerton &
Campbell, 1994).
– Subtypes of dependence
• Subtype 1: young adult type
• Subtype 2: functional subtype
• Subtype 3: intermediate familial type
• Subtype 4: young antisocial type
• Subtype 5: chronic severe subtype
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2094392/)

28. EFFECTS OF BRAIN
• BIOCHEMISTRY
–No single molecular target mediator for effect of alcohol.
Theory is alcohol affects membranes of neurons. Hypothesis
is alcohol inserts into the layers of membranes and increase
fluidity of membranes, so membranes become rigid or stiff.

29. • BEHAVOIRAL
–At 0.05% blood alcohol – judgment, thought and restraint
are loosened and disrupted
–At 0.1% blood alcohol – voluntary motor action become
clumpsy
–At 0.2% blood alcohol – entire motor function is depressed,
parts that control emotions become affected.
–At 0.3% blood alcohol – confused or stuporous

30. • SLEEP
–Although evening alcohol consumption eases falling asleep,
alcohol has adverse effects on sleep architecture. Alcohol is
associated with decrease in REM and deep sleep with sleep
fragmentation and longer episodes of awakening. Thus idea
alcohol makes person sleep is myth.

31. • OTHER
– Alcohol can induce a general, nonselective, reversible depression of
the CNS.
– 80% of alcohol in one drink is processed slowly through upper GIT
into blood stream.
– Low dose alcohol can produce loss of inhibition, lack of
concentration, drowsiness, slurred speech.
– Chronic use can result in multisystem physiological impairments.

32. EFFECTS OF BODY
• PERIPHERAL NEUROPATHY:
– Results in pain, burning, tingling or pricking sensation of extremities.
– Research say it is the direct effect of Vit B deficiency, particularly
Thiamine.
– Nutritional deficiency are common due to insufficient intake of
nutrients and toxic effect of alcohol (malabsorption of nutrients).
– The process is reversible with abstinence and nutritional deficiency
restoration.
– Other wise permanent muscle wasting and paralysis can occur.

33. • ALCOHOLIC MYOPATHY:
– Can occur as acute or chronic.
– Acute – muscle pain, swelling, and weakness; rhabdomyolysis seen in
urine, rise in muscle enzyme in blood.
– Lab – elevation in CPK, LDH, ALT, AST
– Chronic – gradual wasting and weakness in skeletal muscle.
– Said as Vit B deficiency->Alc. Myopathy->peripheral neuropathy.
– Improvement seen with abstinence and nutritious diet.

34. • WERNICKE’S ENCEPHALOPATHY:
– Most serious form of thiamine deficiency.
– Symptoms are ocular muscle paralysis, diplopia, ataxia, somnolence and
stupor.
– If thiamine replacement is not done death can occur
• KORSAKOFF’S PSYCHOSIS:
– A syndrome of confusion, loss of recent memory, confabulation.
– Seen in patients recovering from Wernicke’s encephalopathy.
– In US these 2 are called together as WERNICKE’S – KORSAKOFF SYNDROME.

35. • ALCOHOLIC CARDIOMYOPATHY:
– Effect of alcohol –accumulation of lipids in myocardial cells
– Clinical findings relate to CHF or arrhythmia.
– Symptoms include decreased exercise tolerance, tachycardia, dyspnea, edema,
palpitations and non-productive cough
– Lab – elevation of CPK, AST, ALT, LDH.
– Changes of ECG seen, CHF evident on CXR
– Treatment is permanent abstinence, treatment of CHF (rest, O2, Na restriction,
diuretics).
– Prognosis is good if treated early.
– Advanced symptoms –death.

36. • ESOPHAGITIS
– it is inflammation and pain in the esophagus, because of the toxic effects
of alcohol. It also occurs because of frequent vomiting associated with
alcohol abuse.
• GASTRITIS
– Inflammation of stomach lining characterized by epigastric distress,
nausea, vomiting and distention. Alcohol breaks mucosal barrier of
stomach, allowing HCl to erode stomach wall.

37. • PANCREATITIS
– Characterized as acute or chronic. Acute pancreatitis occurs 1 or 2
days after binge consumption. Symptoms include constant, severe
epigastric pain, nausea and vomiting, and abdominal distention.
– Chronic condition leads to pancreatic insufficiency resulting in
steatorrhea, malnutrition, weight loss, and DM

38. • ALCOHOLIC HEPATITIS
– Caused by long-term heavy alcohol use.
– Manifestations are enlarged and tender liver, nausea and vomiting,
lethargy, anorexia, elevated WBC count, fever, and jaundice.
– Ascites and weight loss may be evident in severe case.
– Treatment includes strict abstinence from alcohol, proper
malnutrition and rest- the individual can experience complete
recovery.
– Severe cases can lead to cirrhosis or hepatic encephalopathy.

39. • CIRRHOSIS OF LIVER (end stage of alcoholic liver damage disease)
May be caused by anything that results in chronic injury to the liver. Results
from long term chronic alcohol abuse.
There is widespread destruction of liver cells replaced by fibrous (scar) tissue.
Manifestations include nausea, vomiting, anorexia, weight loss, abdominal
pain, jaundice, edema, anemia, blood coagulation abnormalities.
Treatment includes abstention from alcohol, correction of malnutrition, and
supportive care to prevent complications.

40. Complications are
– PORTAL HYPERTENSION
Elevation of BP through the portal circulation results from defective blood flow through the
cirrhotic liver.
– ASCITES
Ascites is in which an excessive amount of serous fluid accumulates in the abdominal
cavity, occurs in response to portal HTN. The increased pressure results in the seepage of
fluid from the surface of the liver into the abdominal cavity.
– ESOPHAGEAL VARICES
These are veins in esophagus that become distended because of excessive pressure from
defective blood flow through the cirrhotic liver. As this pressure increases, these
varicosities can rupture, resulting in hemorrhage and sometimes death.

41. – HEPATIC ENCEPHALOPATHY
This serious complication occurs as response to the inability of the
diseased liver to convert ammonia to urea for excretion.
The continued rise in serum ammonia results in progressively impaired
mental functioning, apathy, euphoria or depression, sleep disturbances,
increasing confusion, and progression to coma and eventual death.
• LEUKOPENIA
The production, function, and movement of the WBC are impaired in
chronic alcoholics.
This condition, places the individual at high risk for contracting
infections diseases as well as for complicated recovery.

42. • THROMBOCYTOPENIA
Platelet production and survival is impaired as a result of toxic
effects of alcohol. This places alcoholics at risk for hemorrhage.
Abstinence from alcohol rapidly reverses this deficiency.
• SEXUAL DYSFUNCTION
Alcohol interferes with normal production and maintaince of female
and male hormones.
For women, changes in menstrual cycles and a decreased or loss of
ability to become pregnant.
For men, the decreased sexual performance, and impaired fertility.

43. DURING PREGNANCY:-
• FETAL ALCOHOL SYNDROME: Prenatal exposure (at any stage; who are
pregnant; who could become pregnant) to alcohol can result in a broad
spectrum range of disorders to fetus, known as fetal alcohol spectrum
disorders (FASDs), the most common of which is fetal alcohol syndrome.
• FAS can cause physical, mental, behavioral, and/or learning disabilities
with lifelong implications.
• There may be problems with learning, memory, attention span,
communication, vision, hearing or a combination of these.

44. COMORBIDITY
• The psychiatric diagnoses most commonly associated but somewhat
controversial, suggest that persons with alcohol related disorder have
markedly higher suicide rate than general population.
• ANTISOCIAL PERSONALITY DISORDER:
Relation between ASPD and AUD have frequently been reported. Some
studies suggest that ASPD is common in men and precede
development of AUD. Yet some studies contra verse these studies.

45. • MOOD DISORDER:
About 30-40% persons with AUD meet diagnostic criteria for major
depressive disorder sometimes during their lifetime.
Depression is more common in women with AUD than men.
It is also suggested that daily alcohol consumption and family history of
alcohol abuse, and depression are likely to correlate.

46. • ANXIETY DISORDER:
Many use alcohol for its efficacy in alleviating anxiety. 25-50% person
with AUD have anxiety disorder. Phobia and panic disorder are most
common.
• SUICIDE:
10-50% of AUD persons are prevalent to commit suicide. Factors that
influence are presence of major depressive episodes, weak
psychological support system, a serious co-existing medical condition,
unemployment and living alone.

47. TREATMENT MODALITIES
• ALCOHOLICS ANONYMOUS:-
AA is a major self-help group for the treatment of alcoholism.
Found in 1935 (alcoholics- stockbroker, Bill Wilson; physician, Dr. Bob
Smith)
They found that they could remain sober with mutual support.
The movement grew like snowball.
Patients who have been treated unsuccessfully maintained sobriety
through AA.

48. AA are based on concept of peer support, acceptance and
understanding from others who have experienced the same
problems in their lives.
Requirement is desire to stop alcohol
Sole purpose is to help members stay sober, when sobriety is
achieved, they are expected to help others
AA has been model for various other self-help group associated with
addiction problems.
Nurses need to fully and accurately informed about these self-help
group.

49. 12 steps and traditions/principle of
Alcohol AnonymousHand out

50. • PHARMOCOTHERAPY:-
– Disulfiram (deterrant)
– Naltrexone
– Acomprosate
• COUNSELING:-
– One to one basis
– Goal directed and length varies
– Phases : assessment phase and working phase
– Referrals to AA

51. • GROUP THERAPY:-
– Powerful agent of change
– Able to share experiences
– Some are task oriented, some are educational groups
– Some teaching groups are psychotherapy groups
– Therapy groups and self groups are complementary to each other.

52. PROGNOSIS
• Between 10-40% of alcoholic persons enter some kind of formal treatment program
during the course of their alcohol problems. A number of prognostic signs are
favorable, they are
1. Absence of pre-existing ASPD
2. Evidence of general life stability with a job, continuing close family contacts, and
absence of several legal problems also bodes well for the patient.
3. Patient stays for the full course of the initial rehabilitation (perhaps 2 to 4 wks), the
chances of maintaining abstinence are good.

53. The combination of these attributes predicts atleast 60% chance for 1 or
more years of abstinence.
Researchers agree that 1 year of abstinence over an extended period.
Accurately predicting achieving or maintaining abstinence is impossible.

54. APPLICATION OF NURSING PROCESS
• Assessment : done in pre introductory phase. Use unconditional positive
regard
• Assessment tools: Includes drug history & biopsychosocial assessment
• MAST and CAGE questionnaire are developed by APA to screen
individuals for problems with substance.
• Dual diagnosis: also called as co-existing or co-occurring disorders.
– Supportive and less confrontational approach
– Peer groups are important part.
– Cognitive and behavioral therapies are helpful.

55. • Nursing care: through nursing process
1. Risk for injury related to internal and eternal environmental conditions interacting
with individuals adaptive and defensive resource.
2. Ineffective denial related to weak, underdeveloped ego
3. Ineffective coping related to previous ineffective coping skills with substitution of
drug
4. Imbalanced nutrition: less than body’s requirement related to poor intake of food,
decreased appetite
5. Risk for violence related to CNS depression
6. Impaired family coping related to situational crisis
7. Knowledge deficit regarding illness and prognosis related to ignorance, lack of
knowledge